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21,411 | <p><strong>[Moderator Edit: I'm reopening this question by request from third parties because medical staff around the world are being forced to use masks such as these.]</strong></p>
<p>How does a sanding mask compare with a disposable medical mask? I have some on hand. Would that be a reasonable thing to wear to protect myself and family members (corona virus)? Or would it give even less protection than a bandanna or a disposable medical mask?</p>
<p><a href="https://i.stack.imgur.com/qG9Tt.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/qG9Tt.jpg" alt="enter image description here"></a></p>
<p>Update: I'm asking about the range of particle and droplet size that the two types of mask keep in/out (according to specs, and disregarding particles that can enter around the edges).</p>
<p>I am not asking whether you think someone should or should not wear a mask.</p>
| [
{
"answer_id": 21550,
"author": "Graham Chiu",
"author_id": 3414,
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"text": "<h2>Particle Size-Selective Assessment of Protection of European Standard FFP Respirators and Surgical Masks against Particles-Tested with Human Subjects</h2>\n\n<blockquote>\n <p>The tested FFP respirators and SMs in this study were observed to have the worst protection against particles between 0.263 and 0.384 μm. The protection factors of FFP respirators against particles in the size range of 0.093–1.61 μm were not size dependent. The size ranges of viral and bacterial particles fall into this size range, and they are expected to have similar PFs. The FFP respirators provided about 11.5 to 15.9 times better protection than the SMs, suggesting that SMs are not a good substitute for FFP respirators when concerns exist about airborne transmission of bacterial and viral pathogens.</p>\n</blockquote>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058571/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058571/</a></p>\n\n<p>That's a FFP2 in your image and they are saying it's 12-16x better PF (Protection Factor) than a surgical mask (SM)</p>\n"
},
{
"answer_id": 24754,
"author": "Michael Altfield",
"author_id": 19986,
"author_profile": "https://health.stackexchange.com/users/19986",
"pm_score": 0,
"selected": false,
"text": "<p>For protecting against saw dust (sanding), they work great!</p>\n<p>For protecting from biological risks in a medial setting, they're up to half as effective.</p>\n<p>Assuming we're discussing the respirator in the photo you uploaded with your question, note that it has a plastic valve in its center. This is an exhilaration valve. The exhilaration valve is a one-way valve that permits air to pass unobstructed out of the respirator. This is great when doing construction work; it makes breathing (out) easier.</p>\n<p>However, respirators with exhalation valves necessarily do not filter your exhalation, so they are not very effective at preventing the spread of biological infectious agents, such as the coronavirus. In fact, the CDC recommends that if you only have an N95 mask with an exhalation valve, then you should wear it <em>along with</em> a surgical mask on the outside <sup><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/respirator-use-faq.html\" rel=\"nofollow noreferrer\">1</a></sup>.</p>\n<p>One of the biggest issues with the spread of COVID-19 is that many people who contract the virus (and can spread it to others) never experience symptoms (asymptomatic) or they can spread the virus for up to 14-days before they experience symptoms (pre-symptomatic) <sup>[<a href=\"https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200402-sitrep-73-covid-19.pdf?sfvrsn=5ae25bc7_2\" rel=\"nofollow noreferrer\">2</a>]</sup>. Therefore, it's very important that you use a respirator that filters both your inhalations and your exhalations.</p>\n<p>That said, any filter is better than no filter.</p>\n"
}
] | 2020/03/15 | [
"https://health.stackexchange.com/questions/21411",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/402/"
] |
21,442 | <p>Could one be injected with an infinitesimal amount of Covid-19 viral particles, in a way that it would trigger an immune response long enough before the virus overran the body? Could it be injected into tissue that was far enough away from the lungs, so that some immunity could build up before the virus reached the lungs?</p>
<p>I am talking about something similar to variolation, which was a method used to control the spread of smallpox. Material from smallpox sores (pustules) was given to people who had never had smallpox. This was done either by scratching the material into the arm or inhaling it through the nose.</p>
<p>People usually went on to develop the symptoms associated with smallpox. However, fewer people died than if they had acquired smallpox naturally.</p>
| [
{
"answer_id": 21450,
"author": "Mark",
"author_id": 333,
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"selected": true,
"text": "<p>What you're describing is a <a href=\"https://en.wikipedia.org/wiki/Vaccine\" rel=\"noreferrer\">live-virus vaccine</a>. The only live-virus vaccines ever used were the <a href=\"https://en.wikipedia.org/wiki/Variolation\" rel=\"noreferrer\">early smallpox vaccines</a>, which carried a significant risk of causing the disease rather than building immunity. Even attenuated vaccines (using a live but weakened form of the virus) can cause disease; most cases of polio these days are caused by the <a href=\"https://en.wikipedia.org/wiki/Polio_vaccine\" rel=\"noreferrer\">oral polio vaccine</a>. Vaccines using inactivated viruses or virus fragments are strongly preferred.</p>\n"
},
{
"answer_id": 23254,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>This isn't really an answer since you have one already accepted but it postulates one possibility, noting that we are really in an evidence free zone. If the mods think it's unacceptable they can delete it.</p>\n\n<p>The historical case fatality rate from variolation was 5%. The case fatality rate from smallpox was on average 30%. So, let's say approximately 15% of people using variolation got smallpox of whom 30% died to give us the case fatality rate of 5% from variolation.</p>\n\n<p>Now variolation was pretty crude. Now the experts think that the inoculum needed to cause COVID-19 is about a few hundred - few 1000s of virions. So applying the dose is going to be hit and miss. Given that the skin isn't thought to be a major portal of infection, and the virus attacks monocytes and probably very little else in the skin, it may not be effective at all.</p>\n\n<p>But let's say it's effective as smallpox, and we then get 15% of people who go on to develop clinical COVID-19. So, that's 15% of the population of the USA 328M which is 49M who get COVID-19 from your \"vaccine\" Assuming a case fatality rate of 1%, that's 492,000 deaths. But these people are going to infect other people as well so you're still going to end up with 49M infected people which is more than you have now in the USA.</p>\n\n<p><a href=\"https://www.fda.gov/vaccines-blood-biologics/vaccines/smallpox\" rel=\"nofollow noreferrer\">https://www.fda.gov/vaccines-blood-biologics/vaccines/smallpox</a></p>\n\n<p><a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">https://www.worldometers.info/coronavirus/</a></p>\n"
}
] | 2020/03/17 | [
"https://health.stackexchange.com/questions/21442",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17866/"
] |
21,445 | <p>Since the demand for imaging is increasing regarding COVID-19 and the number of papers describing COVID-19 patterns in computed tomography (CT) is increasing, I searched medical imaging recommendations/guidelines for the clinical routine.</p>
<p><strong>What I found</strong>:</p>
<p>Besides the American College of Radiology (ACR) <a href="https://www.acr.org/Advocacy-and-Economics/ACR-Position-Statements/Recommendations-for-Chest-Radiography-and-CT-for-Suspected-COVID19-Infection" rel="nofollow noreferrer">recommendation regarding COVID-19 and imaging</a>, I found similar recommendations (mostly from European Radiological societies), e.g.:</p>
<ul>
<li><a href="https://thoracicrad.org/wp-content/uploads/2020/03/STR-ASER-Position-Statement-1.pdf" rel="nofollow noreferrer">STR</a></li>
<li><a href="https://www.rcr.ac.uk/college/coronavirus-covid-19-what-rcr-doing/rcr-position-role-ct-patients-suspected-covid-19" rel="nofollow noreferrer">RCR</a></li>
<li><a href="https://www.bsti.org.uk/media/resources/files/COVID11.3.20_2.pdf" rel="nofollow noreferrer">BSTI</a></li>
<li><a href="https://www.ranzcr.com/our-work/coronavirus" rel="nofollow noreferrer">RANZCR</a></li>
</ul>
<p>I assume that especially countries in Asia might have a lot of experience. However, I could not find any source.</p>
<p><strong>What I am looking for</strong>:</p>
<p>Is there any medical imaging recommendation/guideline regarding COVID-19 from an Asian Radiological Society?</p>
| [
{
"answer_id": 21473,
"author": "anongoodnurse",
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"text": "<p>I don't know about official Chinese recommendations, but this might help.</p>\n\n<p>China had experience with SARS, and this new infection was looking a lot like SARS. They did not have a surfeit of testing kits for a new virus, but they knew what SARS looked like on CT scans. Therefore, symptomatic patients received CT scans of the chest <em>before being tested for coronavirus</em>. If it was positive for the new pattern of atypical pneumonia, they were <em>then</em> tested and triaged. </p>\n\n<p>Since then, we have developed other screening tests that do not involve CT scans.</p>\n\n<p>See <a href=\"https://www.bioworld.com/articles/433530-china-uses-ai-in-medical-imaging-to-speed-up-covid-19-diagnosis\" rel=\"nofollow noreferrer\">here</a> and <a href=\"https://www.contagionlive.com/news/ct-scans-provide-covid19-insight\" rel=\"nofollow noreferrer\">here</a> for more information.</p>\n"
},
{
"answer_id": 21657,
"author": "captcoma",
"author_id": 17867,
"author_profile": "https://health.stackexchange.com/users/17867",
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"text": "<p>I found a good overview of medical imaging recommendations for COVID-19 from many radiological societies. </p>\n\n<p><a href=\"https://www.myesr.org/covid-19-resources\" rel=\"nofollow noreferrer\">https://www.myesr.org/covid-19-resources</a> > Guidance for radiologists in dealing with COVID-19 patients > By country.</p>\n\n<p>Unfortunately, I could still find no recommendations from Asian radiological societies. </p>\n"
}
] | 2020/03/17 | [
"https://health.stackexchange.com/questions/21445",
"https://health.stackexchange.com",
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] |
21,453 | <p>I have ethanol , Reagent Grade 99.8% v/v</p>
<p>can i use this to make hand sanitizer ? is it safe for hand skin ?</p>
<p>I will be <a href="https://www.ncbi.nlm.nih.gov/books/NBK144054/" rel="nofollow noreferrer">following this guideline from WHO for making the sanitizer</a> << have a look at that link.</p>
<p>I am planning to dilute the Ethanol with water to get a 65% concentration .</p>
<p>Can i proceed with making the sanitizer ?
Look at the Ethanol specs on the picture below</p>
<p><a href="https://i.stack.imgur.com/IZwxD.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/IZwxD.jpg" alt="enter image description here"></a></p>
<p><a href="https://i.stack.imgur.com/MXA0C.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/MXA0C.jpg" alt="enter image description here"></a></p>
| [
{
"answer_id": 21454,
"author": "Graham Chiu",
"author_id": 3414,
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"pm_score": 4,
"selected": true,
"text": "<p>All the alcohol based sanitizers are using ethanol as the main alcohol often with isopropylalcohol. The latter is more effective against bacteria and ethanol is better against virus </p>\n\n<blockquote>\n <p>The effectiveness of alcohol as an anti-bacterial or anti-fungal disinfectant increase as the molecular weight increases. Therefore, Isopropyl alcohols, such as IPA, are more effective than ethanol alcohols, such as DE.</p>\n \n <p>Denatured Ethanol is considered more effective as a virucidal disinfectant, as isopropanol is not effective against non-enveloped viruses.</p>\n \n <p>Examples of non-enveloped viruses:\n Hepatitis A\n Rotavirus\n Adenovirus\n Examples of enveloped viruses:\n Influenza\n Ebola\n HIV\n Hepatitis B\n Rabies\n SAR virus</p>\n \n <p>Non-enveloped viruses utilize capsid proteins to mediate binding to host cells, while enveloped viruses use viral proteins for this function. Enveloped viruses are surrounded by an outer lipid membrane, while non-enveloped viruses lack this membrane.</p>\n</blockquote>\n\n<p>You should add glycerine as an emollient as alcohol and water alone are too harsh on the skin, again as per the WHO recipe you referenced.</p>\n\n<p>Summary: </p>\n\n<ul>\n<li><p>70% - 95% ethanol/propylalcohol to clean surfaces (diluted with water )</p></li>\n<li><p>60% - 95% ethanol/propylalcohol to clean hands ( diluted with glycerine, or aloe vera )</p></li>\n</ul>\n\n<p><a href=\"https://cleanroomsuppliesltd.com/ipa-de-alcohol-disinfection-guide.asp\" rel=\"nofollow noreferrer\">https://cleanroomsuppliesltd.com/ipa-de-alcohol-disinfection-guide.asp</a></p>\n"
},
{
"answer_id": 21482,
"author": "iep",
"author_id": 17861,
"author_profile": "https://health.stackexchange.com/users/17861",
"pm_score": 2,
"selected": false,
"text": "<p>Yes you can. You are safe if you use 65% ethanol mixed with 35% water or glycerine. That is what is known/sold as disinfectant hand sanitizer for viruses.</p>\n"
}
] | 2020/03/17 | [
"https://health.stackexchange.com/questions/21453",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17869/"
] |
21,457 | <blockquote>
<p>Out of nearly 45,000 confirmed cases in China through February 11, there was only one death in someone younger than 20, according to the Chinese Center for Disease Control and Prevention, and no deaths among children younger than 10.</p>
<p>Out of 731 confirmed and 1412 suspected cases of Covid-19 in children in China, one child, a 14-year-old boy, died and nearly 6% of cases were severe, compared with 18.5% of adults experiencing severe symptoms, according to a new study that will be published in the journal Pediatrics in June. Also, only 6% of cases were severe, compared with 18.5% of adult cases.</p>
</blockquote>
<p>So children are still catching the disease but just simply not being affected as much as older adults.</p>
<p>What are the dominant theories to explain this response which differs drastically from influenza?</p>
<p><a href="https://edition.cnn.com/2020/03/11/health/coronavirus-children-sick/index.html" rel="nofollow noreferrer">https://edition.cnn.com/2020/03/11/health/coronavirus-children-sick/index.html</a></p>
| [
{
"answer_id": 21454,
"author": "Graham Chiu",
"author_id": 3414,
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"pm_score": 4,
"selected": true,
"text": "<p>All the alcohol based sanitizers are using ethanol as the main alcohol often with isopropylalcohol. The latter is more effective against bacteria and ethanol is better against virus </p>\n\n<blockquote>\n <p>The effectiveness of alcohol as an anti-bacterial or anti-fungal disinfectant increase as the molecular weight increases. Therefore, Isopropyl alcohols, such as IPA, are more effective than ethanol alcohols, such as DE.</p>\n \n <p>Denatured Ethanol is considered more effective as a virucidal disinfectant, as isopropanol is not effective against non-enveloped viruses.</p>\n \n <p>Examples of non-enveloped viruses:\n Hepatitis A\n Rotavirus\n Adenovirus\n Examples of enveloped viruses:\n Influenza\n Ebola\n HIV\n Hepatitis B\n Rabies\n SAR virus</p>\n \n <p>Non-enveloped viruses utilize capsid proteins to mediate binding to host cells, while enveloped viruses use viral proteins for this function. Enveloped viruses are surrounded by an outer lipid membrane, while non-enveloped viruses lack this membrane.</p>\n</blockquote>\n\n<p>You should add glycerine as an emollient as alcohol and water alone are too harsh on the skin, again as per the WHO recipe you referenced.</p>\n\n<p>Summary: </p>\n\n<ul>\n<li><p>70% - 95% ethanol/propylalcohol to clean surfaces (diluted with water )</p></li>\n<li><p>60% - 95% ethanol/propylalcohol to clean hands ( diluted with glycerine, or aloe vera )</p></li>\n</ul>\n\n<p><a href=\"https://cleanroomsuppliesltd.com/ipa-de-alcohol-disinfection-guide.asp\" rel=\"nofollow noreferrer\">https://cleanroomsuppliesltd.com/ipa-de-alcohol-disinfection-guide.asp</a></p>\n"
},
{
"answer_id": 21482,
"author": "iep",
"author_id": 17861,
"author_profile": "https://health.stackexchange.com/users/17861",
"pm_score": 2,
"selected": false,
"text": "<p>Yes you can. You are safe if you use 65% ethanol mixed with 35% water or glycerine. That is what is known/sold as disinfectant hand sanitizer for viruses.</p>\n"
}
] | 2020/03/17 | [
"https://health.stackexchange.com/questions/21457",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/3414/"
] |
21,475 | <p>Can the US increase its capacity for COVID-19 testing fast enough to accomplish simultaneously:</p>
<p>1) slowing the spread of disease to allow hospitals to provide care for the infected, and</p>
<p>2) minimizing the impact on the economy by allowing social distancing measures to be relaxed (e.g. reopening schools and restaurants)?</p>
<p>Is there a testing strategy that can accomplish this and what kind of resources would it require?</p>
<p>See a related question <a href="https://politics.stackexchange.com/questions/50897/has-there-been-a-random-survey-of-a-population-for-covid-19">here</a>.</p>
<p>EDIT: The ACLA expects US labs to be able to do 280,000 tests per week by April 1st (<a href="https://www.acla.com/commercial-labs-step-up-capacity-collaborate-with-public-health-partners-to-respond-to-national-emergency/" rel="nofollow noreferrer">acla.com</a>). What if the full weight of the federal government was behind this ramp-up in capability?</p>
<p>EDIT2: Tom Frieden recently wrote (<a href="https://www.vox.com/2020/3/16/21181025/coronavirus-covid-19-us-testing-pandemic" rel="nofollow noreferrer">vox.com</a>) that "testing is not a panacea," but he goes on to say that</p>
<blockquote>
<p>"testing is absolutely, crucially important ...in areas with few or no cases, to inform containment and isolation strategies and facilitate contact tracing. Seattle would likely have had a much smaller outbreak if testing there had been widely available sooner."</p>
</blockquote>
<p>The containment strategy right now seems to be evolving toward one in which the entire country is on lockdown. Could we do more targeted (but equally effective) containment if we had a clearer picture of where the virus was? Note: Conversely, Frieden warns against widespread testing in areas of confirmed community transmission.</p>
| [
{
"answer_id": 21529,
"author": "Mark",
"author_id": 333,
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"text": "<p>This is basically what South Korea is doing to limit the spread of the disease, and <a href=\"https://www.worldometers.info/coronavirus/country/south-korea/\" rel=\"nofollow noreferrer\">as the graph of the new-infection rate shows</a>, it's working.</p>\n\n<p>The problem is that it requires far more testing capability than the United States currently has; by April 1, it's likely the disease will be widespread enough that a quarter-million tests a week will be insufficient for trace-and-test containment (each potentially-infected person requires multiple tests over an extended period). Instead, the US is going for Chinese-style lockdown, but doing so far less effectively.</p>\n"
},
{
"answer_id": 21543,
"author": "cbeleites unhappy with SX",
"author_id": 11479,
"author_profile": "https://health.stackexchange.com/users/11479",
"pm_score": 3,
"selected": true,
"text": "<p>Well, I'm no epidemiologist and have neither the required data nor their simulation tools at hand. However:</p>\n\n<p>While testing is of course needed, I doubt that more testing can compensate for lack of distancing now. </p>\n\n<p>Also, there is Japan with social distancing but low numbers of tests with slow curve, and South Korea does not only test but also practice social distancing.\nThere are also countries with lots of tests / inhabitant and heavy increases, Italy for example.</p>\n\n<hr>\n\n<h2>How are screening tests different from what is done now.</h2>\n\n<p>(Slight disclaimer: I'm in Germany, so I know most details about the strategy here. AFAIK, it isn't that different in the US, though. At least, also here people are complaining that they get tests refused and people are talking that test capacities are not unlimited - but it's not clear to me whether people are sent home who should be tested according to a doctor ordering that test or only those who go/drive to the test centers because <em>they</em> think they should be tested.)</p>\n\n<p>What is done right now in most countries (including Italy, Germany, South Korea) is testing populations that are at a non-negligible risk of having contracted the virus. Looking at the current (Mar 19) numbers of <a href=\"https://en.wikipedia.org/wiki/COVID-19_testing\" rel=\"nofollow noreferrer\">positive tests among all tests</a> (<a href=\"https://www.stern.de/gesundheit/covid-19--so-oft-wird-wirklich-auf-das-coronavirus-getestet-9189186.html\" rel=\"nofollow noreferrer\">Germany</a>) and using LR+ of better than 20 (below in parentheses)and expected 61 and LR- of better than 1/20 (below in parentheses), expected 1/61 (see <a href=\"https://medicalsciences.stackexchange.com/questions/21337/how-accurate-are-coronavirus-tests/21379#21379\">long explanation here</a>)</p>\n\n<pre><code> | pos tests/tests | PPV | 1-NPV\n------------+-----------------+-------------+------------------\nUSA | 11 % | 88 % (72 %) | 0.2 % (0.6 %) \nGermany | 3.9 % |\nSouth Korea | 2.8 % | 64 % (36 %) | 0.05 % (0.01 %) \n</code></pre>\n\n<p>PPV = probability of having SARS-CoV-2 after the test was positive<br>\n1-NPV = probability of having SARS-CoV-2 after the test was negative </p>\n\n<p>(There's the implicit assumption that everyone is tested with that same test - which is not true, the South Koreans by now may have better validation data, but I don't know this)</p>\n\n<p><em>Screening</em> means testing the normal population, which (still) has much lower prevalence of SARS-CoV-2. Assuming the dark number is 99 x the known case count (i.e. we have 100x as many infected as positive test results),</p>\n\n<pre><code> | 100*cases/inhabitants | PPV | 1-NPV\n------------+-----------------------+----------------+------------------\nlow risk | 1 in 10000 = 0.01 % | 0.6 % ( 0.2 %) | <0.01 %\nUSA | 0.36 % | 18 % ( 6.7 %) | 0.2 % (0.6 %) \nSouth Korea | 1.6 % | 50 % (25 %) | 0.05 % (0.01 %) \nGermany | 2.0 % | 54 (28 %) | 0.03 % (0.1 %)\nGermany* | 0.4 % | 20 % ( 7.4 %) | <0.01 % (0.02 %) \n</code></pre>\n\n<p>With that assumed large dark numbers, Germany and South Korea would both have prevalences by now where using the existing test on the general population would start to make sense, as that would mean only 1 false positive case per true positive case. On the other hand, with prevalence in the single digit percent we'd be in the region where Frieden argues that testing of the general population doesn't make sense because it makes more sense to tell people to stay at home and away from contacts (which is the case for Germany - and since the numbers aren't growing as fast in South Korea, their dark number is probably much lower). </p>\n\n<p>In the low risk population (where Frieden says testing would make sense), we'd have only correct 1 out of about 200 positive cases. The PPV is for many practical considerations too low: screening needs very good tests, with very high sensitivity and specificity. Sensitivity, because it is crucial here not to overlook truly positive cases, and specificity because the true positives are otherwise hidden in army of false positives. </p>\n\n<p>To some extent, it is often possible to trade in some sensitivity for speificity and vice versa, e.g. with HIV test for blood donors, we do exactly this: we choose a very high sensitivity (so we can be sure not to infect anyone), and accept low specificity. So low, that a blood donor with positive HIV test isn't even <em>told</em> that they were tested positive. Instead, another test is applied (preferably by another manufacturer, because that adds more information than duplicate testing with the same kit), and if that is still positive, yet another one (a more elaborate one). After that IIRC it is still more probable that the blood donor does <em>not</em> have HIV, but they's be looking into it and taking anothe blood sample. \n(And the decision for the donated blood is anyways to throw it away just to be on the safe side). </p>\n\n<p>In principle we could do the same for SARS-CoV-2. Chaining lab tests would mean an enormous burden to the health system of dealing with false positives (and possibly re-testing people) at a time where we don't have unlimited health resources and where the probability that the false positive anyways catches the virus next day or so is non-negligible. This makes this strategy that starts from testing low risk population a complete waste of ressources (even if we had unlimited capacity for testing). This may change in the future when we have tests where proper full validation has shown that they have very good specificity and a useful sensitivity.</p>\n\n<p>What we do currently, isn't very different though in principle:\nWe do currently chain two independent tests, just that the lab test comes 2nd: first a doctor comes and tests whether you are high risk group because you had contact with confirmed cases (maybe even 2nd order contacts) or you show symptoms. <em>Then</em> comes the lab test. </p>\n\n<p>Now the Germany* line in the table above is an interesting additional point. The prevalence there is from the influenza sentinel data from week 11 (last week). These are samples collected from people who were <em>not</em> sent to SARS-CoV-2 tests, but who went to a doctor with flu-like symptoms. 1 out of 251 was SARS-CoV-2 positive (and also influenza positive). The practically important point is: what did we miss because that SARS-CoV-2 case was overlooked (or would have been, had they not been in the sentinel sampling)? Actually, nothing: someone with the flu is told to stay at home and not infect anyone else pretty much like someone with SARS-CoV-2 (particularly now since it would also relieve the health system if the seasonal influenza would be overcome a bit faster). </p>\n\n<h3>Testing in areas with few infections</h3>\n\n<p>Frieden does not propose screening, though: he proposes testing people who have been in contact with infected ones. Which apparently did not work out in Seattle, from what I read due to a lack of tests - but it did work out in Germany where it allowed to completely stop the first (small) outbreak in January.</p>\n\n<p>Here, the \"had (2nd order) contact to infected person\" is the first test in the chain. This is a containment strategy, not a delay strategy. </p>\n\n<p>In order for this to work, we need a two \"ingredients\": we must be able to trace the contacts (and better also 2nd order contacts), and people sent to quarantine must obey this quarantine. </p>\n\n<h3>Comparison Germany - South Korea (mainly)</h3>\n\n<p>... the US is left as excercise to the informed reader</p>\n\n<ul>\n<li><p>South Korea apparently makes extensive use of autamated tracing of people in a fashion that would be completely unconstitutional in Germany. </p></li>\n<li><p>South Korea does use social distancing: according to <a href=\"https://en.wikipedia.org/wiki/2020_coronavirus_pandemic_in_South_Korea\" rel=\"nofollow noreferrer\">Wikipedia</a> they also shut down kindergardens, schools, and universities postponed their semester start. It did not have quite the same impact on overall economy that we see in Germany now. Their shutdown apparently was not all over the country, but earlier: they did that when they had 1000 cases. </p></li>\n<li><p>Apparently the population did a whole lot of that volountarily: the wiki page says the streets of Daegu were empty on Feb 20 (when they had a total of 100 cases).<br>\nIn contrast, Germany now has 15 k cases, and pretty much an official shutdown since the weekend in terms of kindergardens/schools/universities, pubs/clubs/... and apparently there is a sizeable sub-population that gives in to the urgent need of having their own big (!) parties since pubs are closed.<br>\n(I can only speak from what I read in the news, I live in rural Germany where my sports clubs canceled everything - but the neighbors had a 4 generation party (not that many people, but...) for their new house yesterday. (OTOH, we have 8.5 confirmed cases per 100k inhabitants here, so even with that factor 100 for dark number, we're still below 1 % prevalence <em>now</em>) </p></li>\n<li><p>What seems to be similar: in South Korea young adults are the ones who spread the virus. Similar in Germany (more middle-aged initially [those who can afford to make skiing holidays in the Alps], now the Corona-Parties are a young adult thing)</p></li>\n<li><p>I believe East Asia is in general more on the alert than we were. MERS and SARS are cited as reasons, but of course overall high population density also means a permanently increased risk of infectious disesases.</p></li>\n<li><p>The <a href=\"https://en.wikipedia.org/wiki/2020_coronavirus_pandemic_in_South_Korea\" rel=\"nofollow noreferrer\">Wiki page about COVID-19 in South Korea</a> indicates similar testing capacity for South Korea (10k tests/day; 51 mio inhabitants) and Germany (16k tests/day; 80 mio inhabitants)</p></li>\n</ul>\n\n<p>Some countries with more or less flat curves and more or less testing (per mio inhabitants):</p>\n\n<ul>\n<li>South Korea so far done about 6000 tests / mio inhabitants</li>\n<li>Italy 7300 / mio (maybe a bit late, but the main thing that was late in Italy is that for a while they didn't realize they had SARS-CoV-2)</li>\n<li>Japan only 117/mio - but they have a very slow growth, still less than 1000 cases and their curve is decidedly flattening. Japan distances socially since Feb 25th (incl. e.g. to stay at home and not go to a doctor with only mild cold-like symptoms) at 167 cases in the whole country.</li>\n<li><a href=\"https://en.wikipedia.org/wiki/2020_coronavirus_pandemic_in_Singapore\" rel=\"nofollow noreferrer\">Singapore</a> practices certain measures of social distancing since late <em>January</em> when they had < 10 cases. (Didn't find testing numbers, though)</li>\n<li><p>Norway has 6440 tests/mio inhabitants. Hopeful look at curve suggests that a slight flattening may take place. They started their lockdown at ≈700 cases, a bit more than a week ago.</p></li>\n<li><p>Germany has <a href=\"https://www.stern.de/gesundheit/covid-19--so-oft-wird-wirklich-auf-das-coronavirus-getestet-9189186.html\" rel=\"nofollow noreferrer\">≈2100 tests/mio.</a> 100 k tests were done in week 11, current capacity is about 30 k tests/day (is currently ramping up).<br>\n(substantial flattening at the earliest expected in about 2 weeks)</p></li>\n<li><p>USA: according to Wikipedia 300 / mio inhabitants, but the German newspaper cites 3.5x as many tests, that would be 1100 / mio inhabitants.<br>\n(The difference may be whether private lab tests are counted or not?)</p></li>\n</ul>\n\n<h3>The Dutch test</h3>\n\n<p>... is about antibodies whereas the other tests look for virus RNA. These tests again good for different things:</p>\n\n<ul>\n<li>The Dutch test tells whether there has been sufficient exposure to the virus (and sufficient time thereafter) to build antibodies. (Once we know more about this, it may also tell whether one is immune against SARS-CoV-2)<br>\nAs they say, this is also important for getting an idea about the dark numbers of people who have been infected, but had so mild symptoms they didn't realize it.</li>\n<li>The other tests tell whether you currently have the virus (and are contagious). \nScreening for active cases needs this test - the more so as the antibody test may become positive only a while after one is already contagious. </li>\n</ul>\n\n<h3>Simulitis</h3>\n\n<p>The Washington Post has <a href=\"https://www.washingtonpost.com/graphics/2020/world/corona-simulator/\" rel=\"nofollow noreferrer\">simulations</a> of the spread of a (easier, more basic) disease called simulitis with 4 scenarios, ranging from no measures at all over a not quite perfect quarantine to moderate and extensive social distancing (25 % and 10 % of the population run around as always, rest stays where they are). I highly recommend reading, but here are some runs I just did:</p>\n\n<p><a href=\"https://i.stack.imgur.com/TxDyR.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TxDyR.png\" alt=\"simulitis\"></a></p>\n\n<p>Brown are active cases, violet cured/immune and blue susceptible persons.</p>\n\n<p>Important findig for this question: in the first part of the quarantine simulation, the quarantine worked an noone got out (1st hump). Note that this hump has roughly the same height as the moderate social distancing hump, and leaky quarantine is worse (though the simulation doesn't get any newly infected into a new quarantine - I'd say the quarantine situation may be less like real quarantine and more like totally closed borders vs. not-quite-free movement between two countries). </p>\n"
}
] | 2020/03/18 | [
"https://health.stackexchange.com/questions/21475",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17883/"
] |
21,481 | <p><a href="https://www.sciencedaily.com/releases/2020/02/200206110703.htm" rel="noreferrer">This Science Daily article</a> states that steroids could do more harm than good in treating coronavirus (COVID-19), referring to <a href="https://doi.org/10.1016/S0140-6736(20)30317-2" rel="noreferrer">this The Lancet article</a>. </p>
<blockquote>
<p>Understanding the evidence for harm or benefit from corticosteroids in
2019-nCoV is of immediate clinical importance.</p>
</blockquote>
<p>It's unclear to me how exactly the use of corticosteroids (which is a common treatments for Asthma patients) can do harm other than the vague explanation of "steroids also impair the immune system's ability to fight viruses". </p>
<p>How exactly does the use of steroids harm the body in case of fighting a virus such as SARS-CoV-2 (2019-nCoV) that causes COVID-19?</p>
| [
{
"answer_id": 21484,
"author": "Bryan Krause",
"author_id": 8728,
"author_profile": "https://health.stackexchange.com/users/8728",
"pm_score": 5,
"selected": true,
"text": "<p>One of the primary purposes of corticosteroids is to suppress immune activity and inflammation: that's exactly why they are used in asthma.</p>\n\n<p>Of course the immune system has an actual job besides causing nuisance inflammation: fighting infection.</p>\n\n<p>For some infections, the harm to the infected person caused by the immune reaction itself is worse than that of the pathogen itself, so steroids can help prevent damage or ease symptoms while the immune system continues to mount a response, without being <em>hyper</em>active.</p>\n\n<p>For others, immune suppression may be detrimental. </p>\n\n<p>Corticosteroids mediate the immune response by suppressing a variety of cytokines and increasing others, which influences activity circulating numbers of different immune cell populations. Cortisol binds the <a href=\"https://en.wikipedia.org/wiki/Glucocorticoid_receptor\" rel=\"noreferrer\">glucocorticoid receptor</a>, causing numerous changes in gene expression, many of which are associated with the immune system. From <a href=\"https://en.wikipedia.org/wiki/Cortisol#Immune_response\" rel=\"noreferrer\">Wikipedia</a>:</p>\n\n<blockquote>\n <p>(cortisol) inhibits production of interleukin (IL)-12, interferon (IFN)-gamma, IFN-alpha, and tumor-necrosis-factor (TNF)-alpha by antigen-presenting cells (APCs) and T helper (Th)1 cells, but upregulates IL-4, IL-10, and IL-13 by Th2 cells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system (and resulting increase in cortisol and Th2 shift) seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response.</p>\n</blockquote>\n\n<p>In other words, corticosteroids work by by suppressing the generalized killing/cleanup part of the immune system mediated by <a href=\"https://en.wikipedia.org/wiki/Macrophage\" rel=\"noreferrer\">macrophages</a> and <a href=\"https://en.wikipedia.org/wiki/Cytotoxic_T_cell\" rel=\"noreferrer\">CD8+ cells</a>, while preserving the <a href=\"https://en.wikipedia.org/wiki/B_cell\" rel=\"noreferrer\">B-cell</a> part of the immune system that produces specific antibodies and the <a href=\"https://en.wikipedia.org/wiki/Neutrophil\" rel=\"noreferrer\">neutrophils</a> that phagocytose antibody- and complement-bound pathogens.</p>\n\n<p>Immune reactions are incredibly complex, so some of these basics may be violated in certain circumstances (including prolonged rather than acute dosing), and I've left out a lot of the other related immune cells. See references below (and the Wikipedia pages linked above) for more:</p>\n\n<hr>\n\n<p>Cupps, T. R., & Fauci, A. S. (1982). Corticosteroid‐mediated immunoregulation in man. Immunological reviews, 65(1), 133-155.</p>\n\n<p>McGee, S., & Hirschmann, J. (2008). Use of corticosteroids in treating infectious diseases. Archives of internal medicine, 168(10), 1034-1046.</p>\n"
},
{
"answer_id": 21579,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>The Lancet article you referenced in your question answered the questions you asked. In the trials of high dose corticosteroids used to treat SARS patients</p>\n\n<p>Corticosteroids use was: </p>\n\n<ul>\n<li>not associated with a difference in 90-day mortality (adjusted odds ratio 0·8, 95% CI 0·5–1·1; p=0·12)</li>\n<li>associated with delayed clearance of viral RNA from respiratory tract secretions (adjusted hazard ratio 0·4, 95% CI 0·2–0·7; p=0·0005).</li>\n<li>more likely to require mechanical ventilation, vasopressors, and renal replacement therapy</li>\n</ul>\n"
}
] | 2020/03/18 | [
"https://health.stackexchange.com/questions/21481",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/16786/"
] |
21,502 | <p><a href="https://cleaning.lovetoknow.com/how-kill-household-germs/do-microwaves-kill-germs-like-viruses-bacteria" rel="nofollow noreferrer">This article</a> suggests temperatures over 150 degrees Fahrenheit kill viruses. So, forgive my ignorance on the subject, but does this mean that if I microwave a potentially infected (i.e. with viruses on it) piece of, let's say, cloth, for a minute or two, it would become disinfected? </p>
<p>Thanks.</p>
| [
{
"answer_id": 21507,
"author": "Philipp Leitl",
"author_id": 17885,
"author_profile": "https://health.stackexchange.com/users/17885",
"pm_score": 4,
"selected": true,
"text": "<p>You should read the whole article: </p>\n\n<p><strong>Things You Should Never Microwave</strong><br>\n...<br>\n - Clothing and other large fabric items </p>\n\n<p>The problem with microwaves is that they are not heating any item put inside them homogeneously but create \"hot spots\" instead. The image shows a simulation of the electric field inside a microwave oven (taken from <a href=\"https://en.wikipedia.org/wiki/Microwave_oven\" rel=\"nofollow noreferrer\">wikipedia</a>).\nTherefore, microwave oven have a turning table and still it is advisable to stir your food in between of the heating process. \nA paper or cloth, however, could catch fire!</p>\n\n<p><a href=\"https://i.stack.imgur.com/4ntVd.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/4ntVd.png\" alt=\"Simulation of the electric field inside a microwave oven\"></a></p>\n\n<p>The better idea to clean cloth is obviously a washing machine. Those usually have also a program to wash at 60°C / 140°Fahrenheit, which should be sufficient, or even higher. This will not only kill most germs (denaturation of many proteins or nucleic acids starts already below 50°C) but also wash away contamination.</p>\n\n<p><strong>UPDATE</strong><br>\nDue to the current situation and the ongoing shortage of respirators the possibilities for decontamination are discussed broadly.\nThe best study on this topic seems to be from 2010:\n<a href=\"https://journals.sagepub.com/doi/abs/10.1177/155892501000500405\" rel=\"nofollow noreferrer\">Evaluation of Multiple (3-Cycle) Decontamination Processing for Filtering Facepiece Respirators</a><br>\nThey tried eight different methods including <strong>microwave-oven-generated steam</strong>.<br>\nSo it turns out, <strong>yes, it is possible</strong> to decontaminate respirators in a microwave. Two minutes with max power seem to be sufficient. But you should add a <strong>bowl with some water</strong> below the respirator. The generated steam ensures a more homogeneous temperature profile and prevents local hot spots.<br>\nBut be aware that some respirators have <strong>metal brackets</strong> at the nose part. Those can not be put in a microwave.<br>\nAnyhow, it is always stated that decontamination is not ideal and should only be an emergency solution.</p>\n"
},
{
"answer_id": 21608,
"author": "therobyouknow",
"author_id": 14092,
"author_profile": "https://health.stackexchange.com/users/14092",
"pm_score": 2,
"selected": false,
"text": "<p>To add to Philipp Leitl's good and cautionary answer:</p>\n\n<p>Microwave ovens work by causing polar molecules in the food being cooked, e.g. water and fats, to rotate, according to: </p>\n\n<p><a href=\"https://chemistry.stackexchange.com/a/21780/65464\">Why does microwave heat up things so much more quickly than visible light?</a></p>\n\n<p>This rotational movement provides the heating effect. </p>\n\n<p>I would not be sure that the chemical make-up of clothing has equivalent properties such that it can be heated in the same way as food. Indeed as Philipp Leitl points out there is danger in this approach.</p>\n\n<p>However staying on the subject of photons/electromagentic radiation, what can kill pathogens, such as the coronavirus, is Ultra-Violet light, particular, UV-C: <a href=\"https://www.bbc.com/news/business-51914722\" rel=\"nofollow noreferrer\">Coronavirus: Robots use light beams to zap hospital viruses</a></p>\n\n<p>The UV radiation must be able to get to the target, so an obstructed or dirty surface will inhibit effectiveness.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21502",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17890/"
] |
21,505 | <p>I'm wondering if cheaper alternatives are as effective in daily cleanliness of surfaces. </p>
| [
{
"answer_id": 21515,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<blockquote>\n <p>Diluted household bleach solutions can be used if appropriate for the surface. Follow manufacturer’s instructions for application and proper ventilation. Check to ensure the product is not past its expiration date. Never mix household bleach with ammonia or any other cleanser. Unexpired household bleach will be effective against coronaviruses when properly diluted.</p>\n</blockquote>\n\n<p>Prepare a bleach solution by mixing:</p>\n\n<p>5 tablespoons (1/3rd cup) bleach per gallon of water or</p>\n\n<p>4 teaspoons bleach per quart of water</p>\n\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/prepare/cleaning-disinfection.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/prepare/cleaning-disinfection.html</a></p>\n"
},
{
"answer_id": 21531,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 1,
"selected": false,
"text": "<p>There's no evidence that ozonated water is of any use for killing COVID-19 or any other disease organism. <a href=\"https://en.wikipedia.org/wiki/Ozone#Applications_2\" rel=\"nofollow noreferrer\">Gaseous ozone is effective as a disinfectant</a>, but it requires concentrations far higher than can be dissolved in water (or can be tolerated by humans -- if you were to step into a room being treated with ozone, you'd die of lung damage in short order).</p>\n\n<p><a href=\"https://www.epa.gov/pesticide-registration/list-n-disinfectants-use-against-sars-cov-2\" rel=\"nofollow noreferrer\">The EPA has a list of cleaners known to be able to kill COVID-19</a>. Common household cleaning agents on that list include concentrated ethanol (70% or higher concentration -- vodka won't cut it), hydrogen peroxide, isopropyl alcohol (listed as \"isopropanol\"), and chlorine bleach (listed as \"sodium hypochlorite\"). Note that a quick wipe won't do the job: you need to keep the surface wetted for between ten seconds and ten minutes, depending on what you're using.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21505",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/14443/"
] |
21,508 | <p>From different sources we hear that a coronavirus vaccine might be ready in weeks / April / 3 months, but that they would require testing and mass production and it won't be ready to use until 12/18 months. For example, this website states,</p>
<p><a href="https://www.cnbc.com/2020/03/12/human-trials-testing-coronavirus-vaccine-could-begin-within-a-few-weeks.html" rel="nofollow noreferrer">Human trials for a coronavirus vaccine could begin ‘within a few weeks</a></p>
<blockquote>
<p>Human trials testing a potential vaccine to prevent COVID-19 could
begin “within a few weeks” with a vaccine ready for public use within
the next 12 to 18 months, a top U.S. health official said.</p>
</blockquote>
<p>But according to,</p>
<p><a href="https://en.wikipedia.org/wiki/2009_flu_pandemic_vaccine" rel="nofollow noreferrer">2009 flu pandemic vaccine</a></p>
<blockquote>
<p>After a meeting with the WHO on 14 May 2009, pharmaceutical companies
said they were ready to begin making a swine flu vaccine</p>
</blockquote>
<p>and </p>
<blockquote>
<p>As of September 2009 a vaccine for H1N1/09 was expected to be
available starting in November 2009, with production of three billion
doses per year.</p>
<p>As of 19 November 2009, the World Health Organization (WHO) said that
65 million doses of vaccine had been administered and that it had a
similar safety profile to the seasonal flu vaccine, with no
significant differences in the adverse events produced by the
different types of vaccine</p>
</blockquote>
<p>Why it's said a coronavirus vaccine wont be ready for using in 12-18 months when for the H1N1 2009 outbreak there were vaccines available in 6 months?</p>
| [
{
"answer_id": 21515,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<blockquote>\n <p>Diluted household bleach solutions can be used if appropriate for the surface. Follow manufacturer’s instructions for application and proper ventilation. Check to ensure the product is not past its expiration date. Never mix household bleach with ammonia or any other cleanser. Unexpired household bleach will be effective against coronaviruses when properly diluted.</p>\n</blockquote>\n\n<p>Prepare a bleach solution by mixing:</p>\n\n<p>5 tablespoons (1/3rd cup) bleach per gallon of water or</p>\n\n<p>4 teaspoons bleach per quart of water</p>\n\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/prepare/cleaning-disinfection.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/prepare/cleaning-disinfection.html</a></p>\n"
},
{
"answer_id": 21531,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 1,
"selected": false,
"text": "<p>There's no evidence that ozonated water is of any use for killing COVID-19 or any other disease organism. <a href=\"https://en.wikipedia.org/wiki/Ozone#Applications_2\" rel=\"nofollow noreferrer\">Gaseous ozone is effective as a disinfectant</a>, but it requires concentrations far higher than can be dissolved in water (or can be tolerated by humans -- if you were to step into a room being treated with ozone, you'd die of lung damage in short order).</p>\n\n<p><a href=\"https://www.epa.gov/pesticide-registration/list-n-disinfectants-use-against-sars-cov-2\" rel=\"nofollow noreferrer\">The EPA has a list of cleaners known to be able to kill COVID-19</a>. Common household cleaning agents on that list include concentrated ethanol (70% or higher concentration -- vodka won't cut it), hydrogen peroxide, isopropyl alcohol (listed as \"isopropanol\"), and chlorine bleach (listed as \"sodium hypochlorite\"). Note that a quick wipe won't do the job: you need to keep the surface wetted for between ten seconds and ten minutes, depending on what you're using.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21508",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7049/"
] |
21,510 | <p>There have been a number of do-it-yourself (DIY) mask designs released and tested by both universities and other institutions on account of world wide Personal Protection Equipment (PPE) shortages. Some were designed at the time of the SARS epidemic, and use double-folded kitchen paper towels with tissue.</p>
<p>Even though double tea towel masks are more effective in reducing viral exposure, it's difficult to breathe with it on.</p>
<p>What design has been tested to provide relatively good protection while being comfortable to wear and breathe while wearing them? And it needs to use readily available materials throughout the world.</p>
| [
{
"answer_id": 21566,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<h1>DIY Designs - most do not carry efficacy data claims</h1>\n\n<p>Note that many of these are only respiratory protection designs. You also need to protect your eyes in a high risk situation eg. looking after an infected relative. Get protective goggles or your own glasses and attach a plastic shield eg. plastic pamphlet holder to the glasses for a full face shield.</p>\n\n<h2>Combined mask with face shield</h2>\n\n<h3>University of Hong Kong-Shenzen Paper Towel Mask</h3>\n\n<ul>\n<li>Claims 90% filter protection of a surgical mask</li>\n</ul>\n\n<p><a href=\"https://www.youtube.com/watch?v=aNjpH5lBZ8w\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=aNjpH5lBZ8w</a></p>\n\n<h2>Masks only</h2>\n\n<h3>Freesewing sew your own mask from cotton T-shirt etc</h3>\n\n<p><a href=\"https://freesewing.org/fu-facemask-freesewing.org.a4.pdf\" rel=\"nofollow noreferrer\">A4 PDF Pattern</a></p>\n\n<h3>CDC letter - simple mask (uses heavyweight T shirt material)</h3>\n\n<p><a href=\"https://wwwnc.cdc.gov/eid/article/12/6/05-1468_article\" rel=\"nofollow noreferrer\">CDC</a></p>\n\n<h3>Instructables Cloth Masks patterns</h3>\n\n<ul>\n<li>as with all cloth based, wash in hot water to pre-shrink</li>\n</ul>\n\n<p><a href=\"https://www.instructables.com/id/DIY-Cloth-Face-Mask/\" rel=\"nofollow noreferrer\">Instructables</a></p>\n\n<h3>Copper 3D design using PLA 3-D printer</h3>\n\n<ul>\n<li>seems to need their special filter but perhaps use HEPA material?</li>\n</ul>\n\n<p><a href=\"https://www.infoq.com/news/2020/03/3d-n95-masks/\" rel=\"nofollow noreferrer\">3d printed masks unsafe</a> poor fit or build up of CO2</p>\n\n<p><a href=\"https://copper3d.com/hackthepandemic/\" rel=\"nofollow noreferrer\">Instructions</a></p>\n\n<h2>Face shield only</h2>\n\n<ul>\n<li><p><a href=\"https://www.prusaprinters.org/prints/25857-prusa-protective-face-shield-rc2\" rel=\"nofollow noreferrer\">Prusa Printers RC2</a></p></li>\n<li><p><a href=\"https://budmen.com/?elqTrackId=946352961b79457dbc8531c8fd75da1a&elqaid=4271&elqat=2\" rel=\"nofollow noreferrer\">Budmen 3D Printed Face Sheild V2</a></p></li>\n<li><p><a href=\"http://www.amlab.co.nz/shield.html\" rel=\"nofollow noreferrer\">Laser Cut Shield - University of Auckland</a></p></li>\n</ul>\n\n<h2>Field Respirators</h2>\n\n<p><a href=\"https://enable.hp.com/us-en-3dprint-COVID-19-containment-applications\" rel=\"nofollow noreferrer\">First industrialized field 3D printed emergency respiration device to support hospitals and ICUs. </a></p>\n\n<h2>Door Handle Opener</h2>\n\n<ul>\n<li>Hands free <a href=\"https://www.materialise.com/en/hands-free-door-opener?elqTrackId=20b7e0f7116d499a97ad8f3b66dabb8b&elqaid=4271&elqat=2\" rel=\"nofollow noreferrer\">Materialise Door handle Opener</a></li>\n</ul>\n\n<h3>More Reading</h3>\n\n<p><a href=\"https://smartairfilters.com/en/blog/best-materials-make-diy-face-mask-virus/\" rel=\"nofollow noreferrer\">https://smartairfilters.com/en/blog/best-materials-make-diy-face-mask-virus/</a></p>\n"
},
{
"answer_id": 21669,
"author": "Chris",
"author_id": 17994,
"author_profile": "https://health.stackexchange.com/users/17994",
"pm_score": 2,
"selected": false,
"text": "<p>Here is a relevant link on the best materials to use in creating a handmade face mask:</p>\n\n<p><a href=\"https://www.cambridge.org/core/journals/disaster-medicine-and-public-health-preparedness/article/testing-the-efficacy-of-homemade-masks-would-they-protect-in-an-influenza-pandemic/0921A05A69A9419C862FA2F35F819D55\" rel=\"nofollow noreferrer\">https://www.cambridge.org/core/journals/disaster-medicine-and-public-health-preparedness/article/testing-the-efficacy-of-homemade-masks-would-they-protect-in-an-influenza-pandemic/0921A05A69A9419C862FA2F35F819D55</a></p>\n\n<p>Also, here is relevant study on the effectiveness of a saline solution applied to a face mask that can kill flu-like viruses (through the osmotic effect) even within five minutes:</p>\n\n<p><a href=\"https://www.thestar.com/news/canada/2020/02/11/salt-is-the-secret-ingredient-in-these-face-masks-that-could-prevent-spread-of-next-coronavirus.html\" rel=\"nofollow noreferrer\">https://www.thestar.com/news/canada/2020/02/11/salt-is-the-secret-ingredient-in-these-face-masks-that-could-prevent-spread-of-next-coronavirus.html</a></p>\n\n<p><a href=\"https://www.nature.com/articles/srep39956\" rel=\"nofollow noreferrer\">https://www.nature.com/articles/srep39956</a></p>\n"
},
{
"answer_id": 21671,
"author": "gatorback",
"author_id": 7446,
"author_profile": "https://health.stackexchange.com/users/7446",
"pm_score": 1,
"selected": false,
"text": "<p>In a scenario of being forced to choose from DIY designs (yikes!): Perhaps understanding: How are masks tested for efficacy? would provide insight into comparing DIY mask designs. </p>\n\n<p>Efficacy Test example: <a href=\"https://www.astm.org/Standards/F2101.htm\" rel=\"nofollow noreferrer\">https://www.astm.org/Standards/F2101.htm</a></p>\n\n<p>Possible Mask features that drive efficacy:</p>\n\n<ul>\n<li>physical design: does the design effectively position the filter?</li>\n<li>filter material & design: Which materials will work better than others?</li>\n<li>comfort: Will users be able to wear these for extended periods without discomfort?</li>\n</ul>\n"
},
{
"answer_id": 21754,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>From {1}:</p>\n\n<p><a href=\"https://i.stack.imgur.com/rnHgo.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/rnHgo.png\" alt=\"enter image description here\"></a></p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 23818,
"author": "RudyB",
"author_id": 12770,
"author_profile": "https://health.stackexchange.com/users/12770",
"pm_score": 2,
"selected": false,
"text": "<p>There is literature to support that wearing a mask decreases transmission of infection ([Leung, N.H.L., Chu, D.K.W., Shiu, E.Y.C. et al. Respiratory virus shedding in exhaled breath and efficacy of face masks. Nat Med 26, 676–680 (2020).<a href=\"https://doi.org/10.1038/s41591-020-0843-2\" rel=\"nofollow noreferrer\">1</a>), however, there is exceedingly limited evidence that wearing an improvised mask is anywhere near as effective as standard protective equipment (N95 respirator or better).</p>\n\n<p>However, with that said, although I wear a powered air purifying respirator at work (and my company owns the equipment specifically for my personal use, so I could in theory use it elsewhere), I use a homemade cotton mask when outside of home for routine tasks (shopping, getting the vehicle fixed, etc.).</p>\n\n<p>As others have said, wearing a mask is for protection of others from droplets that you might generate, and as such these masks function similar to how the surgical mask was designed (to protect the patient from the surgeon, not vice versa). If everyone was to wear a mask, this could be compared to the concept of \"herd immunity\" where people are protecting each other. It is a bigger concept than purely personal protection, which an improvised mask fails at any way you wish to look at it.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21510",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/3414/"
] |
21,519 | <p><a href="https://en.wikipedia.org/wiki/Oseltamivir" rel="nofollow noreferrer">Oseltamivir</a> (Tamiflu) is an antiviral medication used to treat and prevent influenza A and influenza B (flu). It is said to reduce symptom duration even when initiated more than 2 days after symptom onset. <a href="https://en.wikipedia.org/wiki/Oseltamivir" rel="nofollow noreferrer">Oseltamivir</a> does inhibit influenza virus replication and transmission following ocular-only aerosol inoculation of ferrets.</p>
<p>Can the replication and transmission of the SARS-CoV-2 (2019-nCoV) virus in humans be inhibited in a similar way by the use of <a href="https://en.wikipedia.org/wiki/Oseltamivir" rel="nofollow noreferrer">oseltamivir</a>?</p>
<hr />
<ul>
<li><p>Richard Broadhurst, Anne Mounsey, <a href="https://www.ncbi.nlm.nih.gov/pubmed/27660842" rel="nofollow noreferrer">Does oseltamivir shorten flu symptom duration?</a> [PMID: 27660842], J. Fam. Pract., August 2016.</p>
</li>
<li><p>Jessica A. Belser, Taronna R. Maines, Hannah M. Creager, Jacqueline M. Katz, Terrence M. Tumpeya, <a href="https://dx.doi.org/10.1016%2Fj.virol.2015.06.020" rel="nofollow noreferrer">Oseltamivir inhibits influenza virus replication and transmission following ocular-only aerosol inoculation of ferrets</a> [PMID: 26142497], Virology, October 2015.</p>
</li>
</ul>
| [
{
"answer_id": 21566,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<h1>DIY Designs - most do not carry efficacy data claims</h1>\n\n<p>Note that many of these are only respiratory protection designs. You also need to protect your eyes in a high risk situation eg. looking after an infected relative. Get protective goggles or your own glasses and attach a plastic shield eg. plastic pamphlet holder to the glasses for a full face shield.</p>\n\n<h2>Combined mask with face shield</h2>\n\n<h3>University of Hong Kong-Shenzen Paper Towel Mask</h3>\n\n<ul>\n<li>Claims 90% filter protection of a surgical mask</li>\n</ul>\n\n<p><a href=\"https://www.youtube.com/watch?v=aNjpH5lBZ8w\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=aNjpH5lBZ8w</a></p>\n\n<h2>Masks only</h2>\n\n<h3>Freesewing sew your own mask from cotton T-shirt etc</h3>\n\n<p><a href=\"https://freesewing.org/fu-facemask-freesewing.org.a4.pdf\" rel=\"nofollow noreferrer\">A4 PDF Pattern</a></p>\n\n<h3>CDC letter - simple mask (uses heavyweight T shirt material)</h3>\n\n<p><a href=\"https://wwwnc.cdc.gov/eid/article/12/6/05-1468_article\" rel=\"nofollow noreferrer\">CDC</a></p>\n\n<h3>Instructables Cloth Masks patterns</h3>\n\n<ul>\n<li>as with all cloth based, wash in hot water to pre-shrink</li>\n</ul>\n\n<p><a href=\"https://www.instructables.com/id/DIY-Cloth-Face-Mask/\" rel=\"nofollow noreferrer\">Instructables</a></p>\n\n<h3>Copper 3D design using PLA 3-D printer</h3>\n\n<ul>\n<li>seems to need their special filter but perhaps use HEPA material?</li>\n</ul>\n\n<p><a href=\"https://www.infoq.com/news/2020/03/3d-n95-masks/\" rel=\"nofollow noreferrer\">3d printed masks unsafe</a> poor fit or build up of CO2</p>\n\n<p><a href=\"https://copper3d.com/hackthepandemic/\" rel=\"nofollow noreferrer\">Instructions</a></p>\n\n<h2>Face shield only</h2>\n\n<ul>\n<li><p><a href=\"https://www.prusaprinters.org/prints/25857-prusa-protective-face-shield-rc2\" rel=\"nofollow noreferrer\">Prusa Printers RC2</a></p></li>\n<li><p><a href=\"https://budmen.com/?elqTrackId=946352961b79457dbc8531c8fd75da1a&elqaid=4271&elqat=2\" rel=\"nofollow noreferrer\">Budmen 3D Printed Face Sheild V2</a></p></li>\n<li><p><a href=\"http://www.amlab.co.nz/shield.html\" rel=\"nofollow noreferrer\">Laser Cut Shield - University of Auckland</a></p></li>\n</ul>\n\n<h2>Field Respirators</h2>\n\n<p><a href=\"https://enable.hp.com/us-en-3dprint-COVID-19-containment-applications\" rel=\"nofollow noreferrer\">First industrialized field 3D printed emergency respiration device to support hospitals and ICUs. </a></p>\n\n<h2>Door Handle Opener</h2>\n\n<ul>\n<li>Hands free <a href=\"https://www.materialise.com/en/hands-free-door-opener?elqTrackId=20b7e0f7116d499a97ad8f3b66dabb8b&elqaid=4271&elqat=2\" rel=\"nofollow noreferrer\">Materialise Door handle Opener</a></li>\n</ul>\n\n<h3>More Reading</h3>\n\n<p><a href=\"https://smartairfilters.com/en/blog/best-materials-make-diy-face-mask-virus/\" rel=\"nofollow noreferrer\">https://smartairfilters.com/en/blog/best-materials-make-diy-face-mask-virus/</a></p>\n"
},
{
"answer_id": 21669,
"author": "Chris",
"author_id": 17994,
"author_profile": "https://health.stackexchange.com/users/17994",
"pm_score": 2,
"selected": false,
"text": "<p>Here is a relevant link on the best materials to use in creating a handmade face mask:</p>\n\n<p><a href=\"https://www.cambridge.org/core/journals/disaster-medicine-and-public-health-preparedness/article/testing-the-efficacy-of-homemade-masks-would-they-protect-in-an-influenza-pandemic/0921A05A69A9419C862FA2F35F819D55\" rel=\"nofollow noreferrer\">https://www.cambridge.org/core/journals/disaster-medicine-and-public-health-preparedness/article/testing-the-efficacy-of-homemade-masks-would-they-protect-in-an-influenza-pandemic/0921A05A69A9419C862FA2F35F819D55</a></p>\n\n<p>Also, here is relevant study on the effectiveness of a saline solution applied to a face mask that can kill flu-like viruses (through the osmotic effect) even within five minutes:</p>\n\n<p><a href=\"https://www.thestar.com/news/canada/2020/02/11/salt-is-the-secret-ingredient-in-these-face-masks-that-could-prevent-spread-of-next-coronavirus.html\" rel=\"nofollow noreferrer\">https://www.thestar.com/news/canada/2020/02/11/salt-is-the-secret-ingredient-in-these-face-masks-that-could-prevent-spread-of-next-coronavirus.html</a></p>\n\n<p><a href=\"https://www.nature.com/articles/srep39956\" rel=\"nofollow noreferrer\">https://www.nature.com/articles/srep39956</a></p>\n"
},
{
"answer_id": 21671,
"author": "gatorback",
"author_id": 7446,
"author_profile": "https://health.stackexchange.com/users/7446",
"pm_score": 1,
"selected": false,
"text": "<p>In a scenario of being forced to choose from DIY designs (yikes!): Perhaps understanding: How are masks tested for efficacy? would provide insight into comparing DIY mask designs. </p>\n\n<p>Efficacy Test example: <a href=\"https://www.astm.org/Standards/F2101.htm\" rel=\"nofollow noreferrer\">https://www.astm.org/Standards/F2101.htm</a></p>\n\n<p>Possible Mask features that drive efficacy:</p>\n\n<ul>\n<li>physical design: does the design effectively position the filter?</li>\n<li>filter material & design: Which materials will work better than others?</li>\n<li>comfort: Will users be able to wear these for extended periods without discomfort?</li>\n</ul>\n"
},
{
"answer_id": 21754,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>From {1}:</p>\n\n<p><a href=\"https://i.stack.imgur.com/rnHgo.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/rnHgo.png\" alt=\"enter image description here\"></a></p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 23818,
"author": "RudyB",
"author_id": 12770,
"author_profile": "https://health.stackexchange.com/users/12770",
"pm_score": 2,
"selected": false,
"text": "<p>There is literature to support that wearing a mask decreases transmission of infection ([Leung, N.H.L., Chu, D.K.W., Shiu, E.Y.C. et al. Respiratory virus shedding in exhaled breath and efficacy of face masks. Nat Med 26, 676–680 (2020).<a href=\"https://doi.org/10.1038/s41591-020-0843-2\" rel=\"nofollow noreferrer\">1</a>), however, there is exceedingly limited evidence that wearing an improvised mask is anywhere near as effective as standard protective equipment (N95 respirator or better).</p>\n\n<p>However, with that said, although I wear a powered air purifying respirator at work (and my company owns the equipment specifically for my personal use, so I could in theory use it elsewhere), I use a homemade cotton mask when outside of home for routine tasks (shopping, getting the vehicle fixed, etc.).</p>\n\n<p>As others have said, wearing a mask is for protection of others from droplets that you might generate, and as such these masks function similar to how the surgical mask was designed (to protect the patient from the surgeon, not vice versa). If everyone was to wear a mask, this could be compared to the concept of \"herd immunity\" where people are protecting each other. It is a bigger concept than purely personal protection, which an improvised mask fails at any way you wish to look at it.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21519",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/16786/"
] |
21,520 | <p>There have been "suggestions" (facebook, media etc) that the novel coronavirus is heat sensitive. Specifically that the virus is "killed" or impotent when subjected to temperature of 77F. </p>
<p>Are there any peer-reviewed studies that would support such a contention?</p>
<p>More broadly, are there any peer-reviewed studies on the viability of the virus in other naturally occurring circumstances?</p>
<p>(As I am not a medical professional or researcher, I'm a bit lost on how to do my own research to find appropriate and reliable information on this - I'm not even sure that I'm using the appropriate terminology. This is why I've come to this site: for guidance on how to get the information )</p>
| [
{
"answer_id": 21578,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 2,
"selected": false,
"text": "<p><strong>Casanova LM et al. 2010, \"Effects of air temperature and relative humidity on coronavirus survival on surfaces.\"</strong>\n This study on other similar viruses -- transmissible gastroenteritis virus and mouse hepatitis virus -- showed that those viruses persisted for as long as 28 days at 4 degrees C, and stayed activated at low humidity (20% RH). But inactivation was more rapid at warmer temperature, 20 deg C. At 40 degrees, both viurses were inactivated more rapidly. Humidity was different, as there was greater survival at high (80%).\n The Abstract: Assessment of the risks posed by severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) on surfaces requires data on survival of this virus on environmental surfaces and on how survival is affected by environmental variables, such as air temperature (AT) and relative humidity (RH). The use of surrogate viruses has the potential to overcome the challenges of working with SARS-CoV and to increase the available data on coronavirus survival on surfaces. Two potential surrogates were evaluated in this study; transmissible gastroenteritis virus (TGEV) and mouse hepatitis virus (MHV) were used to determine effects of AT and RH on the survival of coronaviruses on stainless steel. At 4 degrees C, infectious virus persisted for as long as 28 days, and the lowest level of inactivation occurred at 20% RH. Inactivation was more rapid at 20 degrees C than at 4 degrees C at all humidity levels; the viruses persisted for 5 to 28 days, and the slowest inactivation occurred at low RH. Both viruses were inactivated more rapidly at 40 degrees C than at 20 degrees C. The relationship between inactivation and RH was not monotonic, and there was greater survival or a greater protective effect at low RH (20%) and high RH (80%) than at moderate RH (50%). There was also evidence of an interaction between AT and RH. The results show that when high numbers of viruses are deposited, TGEV and MHV may survive for days on surfaces at ATs and RHs typical of indoor environments. TGEV and MHV could serve as conservative surrogates for modeling exposure, the risk of transmission, and control measures for pathogenic enveloped viruses, such as SARS-CoV and influenza virus, on health care surfaces.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/20228108\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/20228108</a></p>\n"
},
{
"answer_id": 21580,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Here are studies on viability at different temperature for similar viruses</p>\n\n<p><a href=\"https://i.stack.imgur.com/lMNSL.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/lMNSL.png\" alt=\"enter image description here\"></a></p>\n\n<p><a href=\"https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext\" rel=\"nofollow noreferrer\">https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext</a></p>\n"
},
{
"answer_id": 21583,
"author": "BobE",
"author_id": 11421,
"author_profile": "https://health.stackexchange.com/users/11421",
"pm_score": 2,
"selected": false,
"text": "<p>For the sake of completeness:\n<strong>Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1</strong> (dated March 17 2020) from \n<a href=\"https://www.nejm.org/doi/full/10.1056/NEJMc2004973\" rel=\"nofollow noreferrer\">New England Journal of Medicine</a></p>\n\n<p>Begins: </p>\n\n<blockquote>\n <p>A novel human coronavirus that is now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (formerly called HCoV-19) emerged in Wuhan, China, in late 2019 and is now causing a pandemic.1 We analyzed the aerosol and surface stability of SARS-CoV-2 and compared it with SARS-CoV-1, the most closely related human coronavirus.2</p>\n \n <p>We evaluated the stability of SARS-CoV-2 and SARS-CoV-1 in aerosols and on various surfaces</p>\n</blockquote>\n"
},
{
"answer_id": 23078,
"author": "BobE",
"author_id": 11421,
"author_profile": "https://health.stackexchange.com/users/11421",
"pm_score": 3,
"selected": true,
"text": "<p>UPDATE:\nAccording to:<a href=\"https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30003-3/fulltext\" rel=\"nofollow noreferrer\">Lancet April 2 2020</a></p>\n\n<p>The concentration of SARS-COV-2 decayed thusly:<a href=\"https://i.stack.imgur.com/mqeK0.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/mqeK0.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>To my non-professional eye it appears that at 72F the concentration of SARS-COV-2 decayed by (approximately) 50% after 72 hours.</p>\n\n<p>When the same experiment was carried at at 99F the concentration decayed by 50% in 24 hours.</p>\n\n<p>The same experiment when carried out at 133 F, the concentration decayed by 50% in 10 minutes.</p>\n\n<p>The layperson's conclusion: Extraordinary heating conditions (greater than 100 F) will be required to decay the virus in a reasonable time period (less than 24 hours). </p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21520",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/11421/"
] |
21,526 | <p>The genome of Covid-19 <a href="https://www.nature.com/articles/s41586-020-2008-3" rel="nofollow noreferrer">was mapped</a> in early Feb. The gene for a protein spike was used to produce these spike proteins. 3-D microscopy of this synthesized spike has <a href="https://science.sciencemag.org/content/367/6483/1260/tab-pdf" rel="nofollow noreferrer">been produced</a>. Quoting McLellan from <a href="https://www.livescience.com/coronavirus-spike-protein-structure.html" rel="nofollow noreferrer">this article</a>:</p>
<blockquote>
<p>"the molecule looks really good; it's really well behaved; the
structure kind of demonstrates that the molecule is stable in the
correct confirmation that we were hoping for," McLellan said. "So now
we and others will use the molecule that we created as a basis for
vaccine antigen."</p>
</blockquote>
<p>Also saying:</p>
<blockquote>
<p>In theory, the spike protein itself "could be either the vaccine or
variants of a vaccine," McLellan said. When you inject this
spike-protein-based vaccine, "humans would make antibodies against the
spike, and then if they were ever exposed to the live virus,"</p>
</blockquote>
<p>The article goes on to say:</p>
<blockquote>
<p>Their colleagues at the NIH will now inject these spike proteins into
animals to see how well the proteins trigger antibody production.
Still, McLellan thinks a vaccine is likely about 18 to 24 months away.
That's "still quite fast compared to normal vaccine development, which
might take like 10 years," he said.</p>
</blockquote>
<p>My question is: Why not inject, or drink, these spike proteins for immunity to Covid-19? Why expect an 18-24 month wait? The anti-body production response should occur(and be detectable) in days?</p>
| [
{
"answer_id": 21532,
"author": "Charles",
"author_id": 12684,
"author_profile": "https://health.stackexchange.com/users/12684",
"pm_score": 3,
"selected": false,
"text": "<p>Vaccines need extensive testing before they can be used. There's essentially no medical intervention which requires more testing than vaccines, which are used in extremely large numbers of healthy patients.</p>\n\n<p>Generally this involves basic research, animal testing, Phase I testing (\"Is it safe in humans? At what dose?\"), Phase II testing (\"Is it effective? At what dose? Are there side effects?\"), and Phase III testing (\"Is it safe and effective across all different subpopulations?\").</p>\n\n<p>As just one example of what could potentially go wrong: many/most COVID-19 deaths involve <a href=\"https://en.wikipedia.org/wiki/Cytokine_release_syndrome\" rel=\"noreferrer\">cytokine storms</a> which are, roughly, damaging inflammatory immune overreactions. Priming the immune system could potentially worsen them and increase deaths by strengthening the immune response. (It doesn't seem likely, but this is why we test.)</p>\n"
},
{
"answer_id": 21570,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>We don't know if the spike proteins are an immune epitope that can be recognized by the human immune system.</p>\n\n<blockquote>\n <p>a team of researchers at La Jolla Institute for Immunology, in collaboration with researchers at the J. Craig Venter Institute, provides the first analysis of potential targets for effective immune responses against the novel coronavirus. The researchers used existing data from known coronaviruses to predict which parts of SARS-CoV-2 are capable of activating the human immune system.\n ..</p>\n \n <p>When the immune system encounters a bacterium or a virus, it zeroes in on tiny molecular features, so called epitopes, which allow cells of the immune system to distinguish between closely related foreign invaders and focus their attack. Having a complete map of viral epitopes and their immunogenicity is critical to researchers attempting to design new or improved vaccines to protect against COVID-19, the disease caused by SARS-CoV-2.</p>\n \n <p>\"Right now, we have limited information about which pieces of the virus elicit a solid human response,\" says the study's lead author Alessandro Sette, Dr. Biol.Sci, a professor in the Center for Infectious Disease and Vaccine Research at LJI. \"Knowing the immunogenicity of certain viral regions, or in other words, which parts of the virus the immune system reacts to and how strongly, is of immediate relevance for the design of promising vaccine candidates and their evaluation.\"</p>\n \n <p>While scientists currently know very little about how the human immune system responds to SARS-CoV-2, the immune response to other coronaviruses has been studied and a significant amount of epitope data is available.</p>\n</blockquote>\n\n<p><a href=\"https://marlin-prod.literatumonline.com/pb-assets/journals/research/cell-host-microbe/PDFs/CHOM_2264_S50.pdf\" rel=\"nofollow noreferrer\">https://marlin-prod.literatumonline.com/pb-assets/journals/research/cell-host-microbe/PDFs/CHOM_2264_S50.pdf</a></p>\n\n<p>There's also experimental data to suggest that strong binding of the spike proteins to the ACE2 receptor, that could cause ARDS as it blocks inhibition of AT1-R.</p>\n"
},
{
"answer_id": 22988,
"author": "Don Slowik",
"author_id": 17886,
"author_profile": "https://health.stackexchange.com/users/17886",
"pm_score": -1,
"selected": false,
"text": "<p>From <a href=\"https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30118-3/fulltext\" rel=\"nofollow noreferrer\">this paper</a> it appears that theses spikes might be used in this way.</p>\n<blockquote>\n<p>MNA delivery of either rSARS-CoV-2-S1 or rSARS-CoV-2-S1fRS09 induced\nsubstantial and statistically significant increases in\nantigen-specific antibodies responses as soon as week 2 compared to\npre-immunization and week 1 responses.</p>\n<p>The significant antibody titers we observed at the early time points\nbefore boosting strongly supports the feasibility of our\nMNA-SARS-CoV-2 vaccines,</p>\n<p>Neutralization assays are important to ensure antibody function;\nhowever, at this early timepoint, we do not have access to validated\nassays for neutralizing antibodies against SARS-CoV-2.</p>\n<p>Taken together, our studies demonstrate the speed at which vaccines\nagainst emerging infections can be designed and produced using the\nrecent advances in recombinant DNA technology. Combining emerging\nbiotechnology methods with bioengineering advances in vaccine delivery\nstrategies, it may now be possible to rapidly produce\nclinically-translatable vaccines against novel pathogens for human\ntesting and subsequent global distribution in time to significantly\nimpact the spread of disease.</p>\n</blockquote>\n<p>They discuss the benefits of using microneedle arrays(MNAs) to deliver a potential vaccine through the skin. A production strategy and timeline to create a vaccine is included.</p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21526",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17886/"
] |
21,536 | <p>There are several aggregate central trackers for the spread of COVID-19. <a href="https://www.worldometers.info/coronavirus/" rel="noreferrer">Like this one, for example.</a></p>
<p>Is there anything similar for trials? Or trials in the pipeline? Either vaccines or treatments?</p>
| [
{
"answer_id": 21553,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": true,
"text": "<p>I think you're asking about trials</p>\n\n<p>See the <a href=\"https://clinicaltrials.gov/ct2/results?cond=covid-19&term=&cntry=&state=&city=&dist=\" rel=\"nofollow noreferrer\">clinical trials database</a></p>\n"
},
{
"answer_id": 23028,
"author": "JonathanReez",
"author_id": 7314,
"author_profile": "https://health.stackexchange.com/users/7314",
"pm_score": 2,
"selected": false,
"text": "<p>Such a tracker is available on the <a href=\"https://milkeninstitute.org/covid-19-tracker\" rel=\"nofollow noreferrer\">Milken Institute website</a>. It currently lists 52 vaccine candidates and 79 treatment candidates.</p>\n<p>Update: one month later (May 4th) it lists 123 vaccine candidates and 199 potential treatments. Incredible!</p>\n<p>Update #2: there are now 202 vaccine candidates and 316 potential treatments, as of August 8th</p>\n"
},
{
"answer_id": 24385,
"author": "Adhish",
"author_id": 20184,
"author_profile": "https://health.stackexchange.com/users/20184",
"pm_score": 2,
"selected": false,
"text": "<p>As far as treatments are concerned, there is <a href=\"https://www.covid-trials.org/\" rel=\"nofollow noreferrer\">https://www.covid-trials.org/</a>. It allows you to filter results by trial status (completed, recruiting, etc.), treatment and location. It also has links to trial results (where available) and registry information.</p>\n<p>It does not have information on vaccine candidates, though.</p>\n<p><strong>Reference:</strong></p>\n<p>Thorlund A, Dron L, Park J, et al. A real-time dashboard of clinical trials for COVID-19. The Lancet Digital Health [Internet]. 2020 Apr 24 [cited 2020 Aug 9];2(6):E286–E287. Available from: <a href=\"https://www.thelancet.com/journals/landig/article/PIIS2589-7500(20)30086-8/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/landig/article/PIIS2589-7500(20)30086-8/fulltext</a></p>\n"
},
{
"answer_id": 25924,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>One more tracker for COVID-19 trials: <a href=\"https://covid19.trackvaccines.org/trials-vaccines-by-country/\" rel=\"nofollow noreferrer\">https://covid19.trackvaccines.org/trials-vaccines-by-country/</a> (<a href=\"https://web.archive.org/web/20210226194811/https://covid19.trackvaccines.org/trials-vaccines-by-country/\" rel=\"nofollow noreferrer\">mirror</a>).</p>\n<p><a href=\"https://i.stack.imgur.com/5Jg5r.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/5Jg5r.png\" alt=\"enter image description here\" /></a></p>\n"
}
] | 2020/03/19 | [
"https://health.stackexchange.com/questions/21536",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/2994/"
] |
21,544 | <p>Many countries have instructed their elderly population to stay at home because of COVID-19. Young people like myself are starting to volunteer to help deliver food and other supplies.</p>
<p>But given asymptomatic transmission and virus spread from contact with contaminated surfaces, how I can make sure I don't accidentally do more harm than good?</p>
<p>Is it enough to use hand sanitizer before I go to the store, then again use hand sanitizer when I unload the grocery bags from my car, and make sure I keep several meters of space between me and the person I deliver to? Should I wear a mask? Gloves?</p>
<p>I'm guessing most older people will want to pay in cash. Is it possible to decontaminate change (coins, bills), or is it safer to only accept exact payment?</p>
| [
{
"answer_id": 21549,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": true,
"text": "<p>The official position of the WHO is that main mechanism of disease transmission is by droplet infection onto mucosal surfaces, or, transfer of those droplets by hand to those surfaces. There is also data to suggest aerosols are generated in close proximity to infected people by coughing or mechanical means such as toilet flushing but we do not know how viable the virus is when spread in that way.</p>\n\n<p>Hand sanitizer and washing is primarily before eating to stop that virus transfer.</p>\n\n<p>If you're visiting someone whom you don't know, then you need some PPE as a mask and goggles in case they cough directly in close proximity to you. If you can't buy this, then there are DIY recipes to make masks and plastic shields.</p>\n\n<p>You can spray the outside packaging with a bleach solution to sterilize it if there's a possibility that it was contaminated at source, or the recipient can do that.</p>\n\n<p>I'd suggest you use a non-contact form of payment, such as WeChat, or whatever else is available. Avoid handling of cash/coins.</p>\n"
},
{
"answer_id": 21564,
"author": "Andreas Jansson",
"author_id": 17921,
"author_profile": "https://health.stackexchange.com/users/17921",
"pm_score": 0,
"selected": false,
"text": "<p>If any stumbles across this question, I found this great resource: <a href=\"https://wiki.queercare.network/index.php?title=Delivering_items_to_someone_in_self_isolation_protocol\" rel=\"nofollow noreferrer\">https://wiki.queercare.network/index.php?title=Delivering_items_to_someone_in_self_isolation_protocol</a></p>\n"
}
] | 2020/03/20 | [
"https://health.stackexchange.com/questions/21544",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17921/"
] |
21,558 | <p>If I understand it right, the following steps are to be taken into account:</p>
<ol>
<li><p>Taking the sample: for the proposed method more samples would have to be taken.</p>
</li>
<li><p>Transporting the sample: more samples would have to be transported.</p>
</li>
<li><p>Testing: more material, would have to be tested, but less individual tests would have to be made.</p>
</li>
</ol>
<p>Hence, it seems that 4 sub-questions can to be considered to help one answer:</p>
<ol>
<li><p>What is the bottle neck in the testing process?</p>
</li>
<li><p>Does the amount of material needed to test for COVID-19 scale rather with the number of performed tests, or with the amount of tested material?</p>
</li>
<li><p>Does the amount of time needed to test for COVID-19 scale rather with the number of performed tests, or with the amount of tested material?</p>
</li>
<li><p>Is the the <a href="https://en.wikipedia.org/wiki/Nucleic_acid_test" rel="nofollow noreferrer">nucleic acid amplification test</a> (NAAT) still reliable enough, if the virus RNA to be detected is diluted among multiple samples?</p>
</li>
</ol>
<p>So far I have read a rather general account on how the tests are conducted and I think I have a somewhat crude understanding of how NAAT works.</p>
<ul>
<li><a href="https://www.auckland.ac.nz/en/news/2020/03/18/how-testing-for-covid-19-works.html" rel="nofollow noreferrer">How testing for COVID-19 works</a>, University of Auckland, 18 March 2020.</li>
</ul>
| [
{
"answer_id": 21562,
"author": "cbeleites unhappy with SX",
"author_id": 11479,
"author_profile": "https://health.stackexchange.com/users/11479",
"pm_score": 4,
"selected": true,
"text": "<p><strong>Update Apr 2</strong>: Pooled tests are under development now (<a href=\"https://www.faz.net/aktuell/rhein-main/frankfurter-forscher-entwickeln-schnelleren-corona-test-16704912.html\" rel=\"nofollow noreferrer\">newspaper in German</a>), the plan is to pool 5 samples and to use the usual amount of each sample (and presumably dilute less) so that sensitivity is not an issue. </p>\n\n<p><strong>Update Apr 9</strong> <a href=\"https://www.nytimes.com/2020/04/04/world/europe/germany-coronavirus-death-rate.html\" rel=\"nofollow noreferrer\">NYT article</a> mentioning a pooled procedure for routine tests for health care workers (pooling 10 samples) in Germany.</p>\n\n<hr>\n\n<p>In general, pooled tests help in screening situations, that is, when very few samples are positive, so that 10+ samples can be pooled and still only a small fraction of pooled samples is positive. They require good sensitivity. </p>\n\n<p>We're <em>not</em> in a screening situation with the current SARS-CoV-2 testing, and pooling wouldn't help much right now - it would probably not be worth while the effort to develop and implment pooled tests. </p>\n\n<hr>\n\n<p>Long version:</p>\n\n<p>(update: deleted newspaper hints that logistics may be the bottleneck:)</p>\n\n<blockquote>\n <p>What is the bottle neck in the testign process?</p>\n</blockquote>\n\n<p>According to <a href=\"https://www.mdr.de/nachrichten/podcast/kekule-corona/mundschutz-besser-als-zu-hause-bleiben100.html\" rel=\"nofollow noreferrer\">Kekulé (10 min or so into the interview)</a> the \"lab machinery\" in Germany has a capacity of several 100k tests per day, but right now there are shortages in reagents but also e.g. in the swabs for taking samples (so, comparably low tech parts of the test). Pooled tests of course need just as many swabs (if not more: false negatives due to the sampling not picking up virus material is a concern, and the usual remedy is to take more swabs.)</p>\n\n<hr>\n\n<p>Anything that comes now are my guesses as a professional from a neighbouring field: analytical chemistry). I don't have any first hand experience with PCR. </p>\n\n<blockquote>\n <p>Does the amount of material needed to test for COVID-19 scale rather with the number of performed tests, or with the amount of tested material?</p>\n</blockquote>\n\n<p>I expect the reagent needs to scale (mostly) with the number of performed tests. I also expect the amount of tested material to be the same (prescribed by the method/protocol) for each run. <strike>That is, when you pool n samples, you'd take only 1/n of material from each (In practice it may be better to pool and then take out 1/n of the pooled sample). </strike> Update: The test described in the newspaper goes the opposite direction: they take n times the sample material in order to avoid trouble with low sensitivity. In consequence, this cannot be considered a \"derived\" \"variety\" of the 1-sample tests, it must be newly developed almost from scratch.</p>\n\n<blockquote>\n <p>Does the amount of time needed to test for COVID-19 scale rather with the number of performed tests, or with the amount of tested material?</p>\n</blockquote>\n\n<p>Again: the tests, mor precisely the number of batches of tests since multiple tests can be processed in parallel. </p>\n\n<blockquote>\n <p>Is the the nucleic acid amplification test still reliable enough, if the Virus RNA to be detected is dilluded among multiple samples?</p>\n</blockquote>\n\n<p>(From here on, we're back inside my professional experience)</p>\n\n<p>This I cannot answer since I don't know the typical concentration range of virus RNA in the samples of positive cases. </p>\n\n<p>The lowest concentration of virus RNA that can reliably be detected is called the limit of detection (LoD). In this context, reliably is 19 out of 20 validation samples at that concentration according to the emergency/\"shortcut\" validation procedure of the FDA (I expect other parts of the world to have similar validation procedures right now). The rFDA has a page with tests that have this emergency approval](<a href=\"https://www.fda.gov/medical-devices/emergency-situations-medical-devices/emergency-use-authorizations#covid19ivd\" rel=\"nofollow noreferrer\">https://www.fda.gov/medical-devices/emergency-situations-medical-devices/emergency-use-authorizations#covid19ivd</a>), and the Manufacturer information lists the LoD. </p>\n\n<p>One would relate the lower end of the typical concentration range to the LoD to calculate how many samples could be pooled without the test becoming unreliable. \n<strike>The linked news article hints that this may actually be a limiting factor.</strike> The test under development avoids this problem by using more sample material.</p>\n\n<hr>\n\n<p>There's another limitation to how many samples one can sensibly pool. The aim of the procedure is to save tests. Thus, we need to set up the pooling so that only a small proportion of pooled tests is positive and a large fraction of cases can be \"closed\" as negative. </p>\n\n<p>Here's the fraction of pooled samples that is positive depending on the prevalence = fraction of positive samples and the number of samples that are pooled n:</p>\n\n<p><a href=\"https://i.stack.imgur.com/gjB0v.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gjB0v.png\" alt=\"proportion of positive pooled cases\"></a> </p>\n\n<p>Contours are every 10 %points. Dashed and dotted lines are the current fractions of positive samples for Germany and Italy.</p>\n\n<p>From that, we can calculate how many samples we need to run (for every positive pooled sample, additional n tests) and from that the fraction of tests we save compared to testing each sample separately:</p>\n\n<p><a href=\"https://i.stack.imgur.com/qE797.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/qE797.png\" alt=\"fraction of samples saved by pooling\"></a></p>\n\n<p>Contours here are right to left: 0, 25 %, 50 % and 75 % \"savings\".</p>\n\n<p>So, at the current testing situation in Germany, pooling 4 samples would allow to save almost 60 % of tests. In Italy, pooling 3 samples would save less than 15 % of tests.</p>\n\n<p>A pooled test would need its own validation and one would also do some additional development to get the required sensitivity (LoD) for the desired number of pooled samples, meaning more delay until pooled tests would be available. </p>\n\n<p>In addition, pooled tests alongside the single tests that are anyways needed would mean additional logistic burden in the labs. </p>\n\n<p>I don't think developing a pooled test would be worth while right now, the more so, as other measures would give similar or better relief:</p>\n\n<p>Doing only 1 test per household would save about 50 % since the <a href=\"https://de.statista.com/statistik/daten/studie/200374/umfrage/anzahl-der-haushalte-in-deutschland-im-jahr-2010-nach-bundeslaendern/\" rel=\"nofollow noreferrer\">average size of a household in Germany is 2</a> without the need of any new test development.</p>\n\n<p>The same is true for further concentrating the tests on the vulnerable/high risk population. </p>\n\n<p>Thus, pooled tests may help in the containment phase when they'd allow to test a larger number of possible contacts. </p>\n\n<p><strong>Update:</strong> Getting back into containment phase is the aim of the current lockdown. </p>\n\n<p>We'd still have high requirements for sensitivity and specificity. This means, pooled tests would have helped most right at the beginning of the epidemic - but they always mean additional R&D and also additional validation needs to be done (and part of the validation work btw. must be done in every single lab that wants to use the test) since they need to be implemented in addition to the single sample method. This means, they'll always be available only after the single sample method is established.</p>\n"
},
{
"answer_id": 23164,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>Israel now have the capacity to pool 64 tests in one</p>\n\n<blockquote>\n <p>“According to the new pooling approach that we have currently tested, molecular testing can be performed on a “combined sample,” taken from 32 or 64 patients. This way we can significantly accelerate the testing rate. Only in those rare cases, where the joint sample is found to be positive, will we conduct an individual test for each of the specific samples,” said Dr. Yuval Gefen, director of the Rambam Clinical Microbiology Laboratory.</p>\n</blockquote>\n\n<p><a href=\"https://www.hospimedica.com/coronavirus/articles/294781273/israeli-researchers-introduce-pooling-method-for-covid-19-testing-of-over-60-patients-simultaneously.html\" rel=\"nofollow noreferrer\">https://www.hospimedica.com/coronavirus/articles/294781273/israeli-researchers-introduce-pooling-method-for-covid-19-testing-of-over-60-patients-simultaneously.html</a></p>\n\n<p>which might be useful if there is a person who contacted many hundreds of people. Eg. We have a supermarket worker who tested positive and they were working during their infectious period.</p>\n"
}
] | 2020/03/20 | [
"https://health.stackexchange.com/questions/21558",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17929/"
] |
21,568 | <p>I want to inquire if CPAP devices can act as low performance ventilators, if they are connected to an oxygen source as well.</p>
<p>I am asking this question in regards to the covid-19 pandemic. There are only two websites which cover this in the entire web. One of them only suggests that CPAP devices <a href="https://aasm.org/coronavirus-covid-19-faqs-cpap-sleep-apnea-patients/" rel="noreferrer">may increase the risk of spreading</a>. <a href="https://www.coronavirustoday.com/cpap-machines-treat-sleep-apnea" rel="noreferrer">The other one</a> notes similarities between these devices. Due to the lack of discussion reachable via google, even if the answer is "no", it might help many people.</p>
<p>I am looking for</p>
<ol>
<li>Scientific publications</li>
<li>Conventions used in field hospitals/healthcare</li>
<li>Your professional educated guess</li>
</ol>
<p>in this order. Please include which category your answer falls into.</p>
| [
{
"answer_id": 21569,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>The essence of protection is a physical barrier against air borne virus droplets splashing against your mucus membranes (eyes, nose, mouth), and against virus from being breathed in. A CPAP machine offers none of these. Even if connected to an oxygen supply some CPAP machines are just nasal and don't stop the person using their mouths. The oxygen supply needs to be mixed with air, and that air needs to be filtered for any kind of protection.</p>\n\n<p>That is my educated guess.</p>\n"
},
{
"answer_id": 21573,
"author": "user17940",
"author_id": 17940,
"author_profile": "https://health.stackexchange.com/users/17940",
"pm_score": 2,
"selected": false,
"text": "<p>The software is very different. And the capabilities of the machine. The monitoring parameters within Ventilators are much more sensitive to pressure and volume than CPAP or BIPAP machines. Below are two pages from the manufacturer with setting capabilities for a BIPAP and a ventilator.</p>\n\n<p><a href=\"https://www.usa.philips.com/c-p/HH1460_00/dreamstation-cpap-with-humidifier\" rel=\"nofollow noreferrer\">https://www.usa.philips.com/c-p/HH1460_00/dreamstation-cpap-with-humidifier</a></p>\n\n<p><a href=\"https://www.usa.philips.com/healthcare/product/HCNOCTN96/respironics-v60-non-invasive-ventilator/specifications\" rel=\"nofollow noreferrer\">https://www.usa.philips.com/healthcare/product/HCNOCTN96/respironics-v60-non-invasive-ventilator/specifications</a></p>\n"
},
{
"answer_id": 21582,
"author": "Chris Rogers",
"author_id": 7951,
"author_profile": "https://health.stackexchange.com/users/7951",
"pm_score": 2,
"selected": false,
"text": "<p>The American Academy of Sleep Medicine (AASM) is correct in what they are saying when <a href=\"https://aasm.org/coronavirus-covid-19-faqs-cpap-sleep-apnea-patients/\" rel=\"nofollow noreferrer\">they said that</a></p>\n<blockquote>\n<p>It is possible that using CPAP could increase the risk of spreading the virus to others around you.</p>\n</blockquote>\n<p>If you are suffering from COVID-19 and use a CPAP machine, the air around you is sucked into the machine and blown out of the mask. Excess air pressure is blown out of outlet holes in the elbow joint between the tubing and mask. This can carry the COVID-19 pathogen out with it at force, spreading it further around the room.</p>\n<p>Take <a href=\"https://shop.resmed.com/medias/sys_master/images/images/hfa/hef/8835700817950/p-EU-63494-ResMed-QuietAir-Quiet-CPAP-Mask-Elbow-01-Medium.jpg\" rel=\"nofollow noreferrer\">this elbow joint as example</a>, used on my CPAP mask.\n<a href=\"https://i.stack.imgur.com/X5lyC.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/X5lyC.jpg\" alt=\"CPAP mask elbow joint\" /></a></p>\n<p>When you take where the idea of using oxygen and air supplies comes from</p>\n<blockquote>\n<p>... if demand continues to grow, hospitals could use sleep apnea machines, <strong>suggests George Washington University Law professor John Banzhaf</strong></p>\n</blockquote>\n<p>This quote from the 2nd website (<a href=\"https://www.coronavirustoday.com/cpap-machines-treat-sleep-apnea\" rel=\"nofollow noreferrer\">an article supposedly checked by an MD</a> in Coronavirus Today) highlights that this is a hypothesis from a non medical professor. He may have experience working within the field of medicine but he is a medical negligence lawyer, not a medical practitioner, as highlighted by <a href=\"https://www.law.gwu.edu/john-f-banzhaf-iii\" rel=\"nofollow noreferrer\">his George Washington University Law page</a></p>\n<p>The idea of using an oxygen and air supply is "thinking outside the box" but not viable from my knowledge of CPAP/APAP machines. CPAP and APAP machines take air from the surrounding air through a filter on the side of the machine.</p>\n<p>Take for example, my CPAP machine air intake photographed in this image</p>\n<p><a href=\"https://i.stack.imgur.com/ub2Ku.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/ub2Ku.jpg\" alt=\"CPAP air intake\" /></a></p>\n<p>There is no way of connecting a bottled oxygen and air supply to this air inlet.</p>\n<h2>Using oxygen and air supply between the machine and mask</h2>\n<p>You said in the comments:</p>\n<blockquote>\n<p>I checked that as well and there is an easy way to connect oxygen. If the CPAP is not oxygen compatible, you can add an oxygen bleed adaptor between the machine tubing and the mask tubing.</p>\n</blockquote>\n<p>If you are looking to add oxygen within the air supplied to the patient, you are correct that <a href=\"https://www.cpap.com/blog/complete-guide-using-cpap-oxygen/\" rel=\"nofollow noreferrer\">you can connect an adaptor</a> between the machine and the tubing to the mask.</p>\n<p>If you are wanting to maintain a specific oxygen concentration, the way CPAP/APAP machines work is different to hospital ICU (Intensive Care Unit) ventilators.</p>\n<blockquote>\n<p>Ventilators employed in NIV [Non-Invasive Ventilation] range from ICU ventilators with full monitoring and alarm systems normally employed in the intubated patient, to light weight, free standing devices with limited alarm systems specifically designed for non-invasive respiratory support. Life support ICU ventilators separate the inspiratory and expiratory gas mixtures. This prevents rebreathing and allows monitoring of inspiratory pressure and exhaled minute ventilation on which monitoring and alarm limits are based (British Thoracic Society Standards of Care Committee, 2002).</p>\n</blockquote>\n<h2>References</h2>\n<p>British Thoracic Society Standards of Care Committee. (2002). Non-invasive ventilation in acute respiratory failure. <em>Thorax, 57</em>(3), 192. DOI: <a href=\"https://doi.org/10.1136/thorax.57.3.192\" rel=\"nofollow noreferrer\">10.1136/thorax.57.3.192</a> PMCID: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746282/\" rel=\"nofollow noreferrer\">PMC1746282</a></p>\n"
}
] | 2020/03/20 | [
"https://health.stackexchange.com/questions/21568",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17936/"
] |
21,593 | <p>Please forgive the obvious question. </p>
<p>H2O2 vapor sterilization is deadly for the layperson but should be workable for hospitals. I can't find the small Chinese study I read the other day about it. Here are two more quickly googled sources.</p>
<ol>
<li><a href="https://www.fda.gov/emergency-preparedness-and-response/mcm-regulatory-science/investigating-decontamination-and-reuse-respirators-public-health-emergencies" rel="nofollow noreferrer">https://www.fda.gov/emergency-preparedness-and-response/mcm-regulatory-science/investigating-decontamination-and-reuse-respirators-public-health-emergencies</a></li>
</ol>
<p><a href="http://wayback.archive-it.org/7993/20170113034232/http://www.fda.gov/downloads/EmergencyPreparedness/Counterterrorism/MedicalCountermeasures/MCMRegulatoryScience/UCM516998.pdf" rel="nofollow noreferrer">http://wayback.archive-it.org/7993/20170113034232/http://www.fda.gov/downloads/EmergencyPreparedness/Counterterrorism/MedicalCountermeasures/MCMRegulatoryScience/UCM516998.pdf</a></p>
<p>2.
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781738/" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781738/</a></p>
| [
{
"answer_id": 21595,
"author": "Matt Giambusso",
"author_id": 17883,
"author_profile": "https://health.stackexchange.com/users/17883",
"pm_score": 1,
"selected": false,
"text": "<p>Some hospitals are experimenting with using UV light to decontaminate respirator masks that are to be reused:</p>\n\n<p><a href=\"https://www.nytimes.com/2020/03/20/health/coronavirus-masks-reuse.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2020/03/20/health/coronavirus-masks-reuse.html</a></p>\n\n<p>EDIT\n<a href=\"https://i.stack.imgur.com/H7pRW.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/H7pRW.jpg\" alt=\"enter image description here\"></a>\nTo follow up on RudyB's answer, Battelle has been awarded a contract to use H2O2 vapor (sources: <a href=\"https://www.nytimes.com/2020/04/11/business/coronavirus-n95-mask-decontaminating-reuse.html?searchResultPosition=2\" rel=\"nofollow noreferrer\">NYtimes</a>, <a href=\"https://www.reuters.com/article/us-health-coronavirus-respirator-idUSKCN21V1WS\" rel=\"nofollow noreferrer\">Reuters</a>)</p>\n"
},
{
"answer_id": 21617,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 0,
"selected": false,
"text": "<p>The main reason is that we don't know how.</p>\n\n<p>For something like an N95 mask, a sterilization process needs to be designed so that it (a) kills any contaminating microbes, and (b) doesn't compromise the effectiveness of the mask.</p>\n\n<p>UV sterilization may not be able to light up every contaminated surface of the mask, or it might damage the filter material or the straps that hold the mask in place.</p>\n\n<p>Hydrogen peroxide vapor might not penetrate the filter material sufficiently, or residual hydrogen peroxide might remain in the filter to harm the user.</p>\n\n<p>Heat-based sterilization could warp the edges of the mask or the outflow valve so they no longer provide a tight seal, and superheated steam might also collapse the filter material into an air-tight barrier -- or expand it into a fluff that viruses have no trouble passing through.</p>\n\n<p>Any sterilization method needs to be tested for safety and effectiveness, and historically, it's been faster and cheaper to simply discard a contaminated mask and use a new one.</p>\n"
},
{
"answer_id": 21755,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>From {1}:</p>\n\n<blockquote>\n <ul>\n <li>It is unknown how wearing the same mask multiple times effects the fit of N95 masks [NIOSH]</li>\n <li>NIOSH states “there is no way of determining the maximum possible number of safe reuses for an\n N95 respirator as a generic number to be applied in all cases” and advise to “discard N95\n respirators following use during aerosol generating procedures.”</li>\n <li>Some methods of N95 mask disinfection can maintain filtration efficiency. Their effect on mask fit\n is unknown, and these methods are not approved by NIOSH.</li>\n </ul>\n</blockquote>\n\n<p>Their summary on sanitizing methods:</p>\n\n<blockquote>\n <p>In summary bleach and microwaves were failures at point of care because the bleach\n gases (skin and respiratory irritants) remained after multiple strategies were used to\n remove them, the microwave melted the masks and soaking them first led to reduced\n filtration. EtO, UVGI, and hydrogen peroxide decontamination were safe and effective in\n the models tested but it is not known if they would retain filtration, material strength,\n and airflow integrity with repeated use. EtO, UVGI, and hydrogen peroxide limitations\n include time from decontamination to reuse and available space and materials to\n decontaminate in an OR setting. 70C /158F heating in an oven (not your home oven) for\n 30min, or hot water vapor from boiling water for 10 min, are additional effective\n decontamination methods.</p>\n</blockquote>\n\n<p>Also, from <a href=\"https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/\" rel=\"nofollow noreferrer\">https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/</a> (<a href=\"https://web.archive.org/web/20200331090651/https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/\" rel=\"nofollow noreferrer\">mirror</a>):</p>\n\n<blockquote>\n <p>Duke University thinks it has found a solution using vaporized hydrogen peroxide to decontaminate the masks.</p>\n \n <p>The process uses specialized equipment to vaporize hydrogen peroxide, which can then infuse all the layers of the mask to kill germs (including viruses) without degrading mask material.</p>\n</blockquote>\n\n<p>This Google Document goes over several papers on mask disinfection: <a href=\"https://docs.google.com/document/d/1YJ2MXeMSSIpm8Wxk8vN7zQ5SQJK9ukOh3wa-UhCJ6ZU/edit\" rel=\"nofollow noreferrer\">https://docs.google.com/document/d/1YJ2MXeMSSIpm8Wxk8vN7zQ5SQJK9ukOh3wa-UhCJ6ZU/edit</a> </p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 22805,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p><a href=\"https://web.archive.org/web/20210506231433/https://cnet4.cbsistatic.com/img/97VLceTKgeLDbT5OmoUnRk2rNew=/2020/04/07/3ec6ead4-acd0-4fcc-9660-f7c33defd992/vlcsnap-2020-04-07-13h39m12s930.png\" rel=\"nofollow noreferrer\"><img src=\"https://web.archive.org/web/20210506231433/https://cnet4.cbsistatic.com/img/97VLceTKgeLDbT5OmoUnRk2rNew=/2020/04/07/3ec6ead4-acd0-4fcc-9660-f7c33defd992/vlcsnap-2020-04-07-13h39m12s930.png\" alt=\"\" /></a></p>\n<blockquote>\n<p>Dr. Peter Tsai, the INVENTOR of the filtration fabric in the N95 mask. N95 masks are made of polypropylene material and are designed to tightly fit over your face with little leakage around the edge of the mask.</p>\n</blockquote>\n<h1>method 1</h1>\n<blockquote>\n<p>When reusing N95 masks, leave a used respirator in dry, atmosphere air for 3-4 days to dry it out. Polypropylene in N95 masks is hydrophobic and contains zero moisture. COVID-19 needs a host to survive–it can survive on a metal surface for up to 48 hours, on plastic for 72 hours, and on cardboard for 24 hours. When the respirator is dry in 3-4 days, the virus will not have survived.</p>\n</blockquote>\n<p>Take four N95 masks, and number them (#1-4).</p>\n<p>On day 1, use mask #1, then let it dry it out for 3-4 days.</p>\n<p>On day 2, use mask #2, then let it dry out for 3-4 days.</p>\n<p>Same for day 3, and day 4…</p>\n<h1>method 2</h1>\n<blockquote>\n<p>You can also sterilize the N95 mask by hanging it in the oven (without contacting metal) at 70C (158F) for 30 minutes-it is reported that COVID-19 cannot survive at 65C (149F) for 30 minutes.</p>\n<p>Use a wood clip to hang the respirator in the kitchen oven to do the sterilization.</p>\n</blockquote>\n<p>Experimentally though this time is much less when incubating virus in transport media</p>\n<blockquote>\n<p>With the incubation temperature increased to 70°C, the time for virus inactivation was reduced to 5 mins.</p>\n</blockquote>\n<h1>UV light</h1>\n<blockquote>\n<p>When sterilizing N95 masks, be wary of using UV light–keep N95 masks away from UV light / sunlight. N95 masks are degraded by UV light because it damages the electrostatic charges in the polypropylene material. It is unclear how long the masks can be exposed to UV light before they are ineffective.</p>\n</blockquote>\n<p>Read more details at the link</p>\n<p><a href=\"https://www.sages.org/n-95-re-use-instructions/\" rel=\"nofollow noreferrer\">https://www.sages.org/n-95-re-use-instructions/</a></p>\n<p>We do have more data now on UV and what levels are safe to use</p>\n<h2>Ultraviolet germicidal irradiation </h2>\n<blockquote>\n<p>UVGI disinfection involves placing respirators in direct line with UV-C lamps. Any exposed surface of the mask will be disinfected. This process generally requires the masks to be flipped after some period to ensure both sides of a mask are disinfected or requires a setup involving two UV-C lamps on either side of the respirator.</p>\n<p>For samples of FFR filters treated with SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome) viruses, no viable virus was found following a dose of 1 joule per square centimeter (J/cm2) of short wavelength (254 nanometers) UV-C light, even in the presence of artificial skin oil and saliva.11 Researchers found no impact of doses ranging from 3 to 20 J/cm2 on filter performance.9-12</p>\n<p>A similar dose range did not compromise fit on three N95 FFRs worn by 10 volunteers.12 Doses ranging from 3 to 6.5 J/cm2 did not alter fit performance on human subjects; doses up to 20 J/cm2 did not significantly change fit performance on respirators mounted on a static head form connected to a breathing machine.11</p>\n<p>Lindsley et al13 tested the impact of much higher doses, ranging from 120 to 950 J/cm2, on respirator filter samples and 590 to 2,360 J/cm2 on respirator straps. For most samples, filter efficiency decreased after UVGI treatment but remained above 95% at all dose levels for the four tested respirator models. Strength of the different layers decreased at all doses, with more layers showing decreased strength with increasing dose. The breaking strength of straps also decreased at all doses, ranging from a loss of 10% to 21% at the lowest dose of 590 J/cm2 and 20% to 51% at the highest dose of 2,360 J/cm2. Respirators treated with a single decontamination of UVGI showed no significant difference from untreated respirators in odor, donning ease, comfort, and respirator fit.9</p>\n<p>Altogether, these data suggest that respirators could be decontaminated by UVGI for up to 20 cycles at a dose of 1 J/cm2 per cycle, if the fit performance data from Heimbuch and Harnish11 using a static head form are representative of fit on humans. Limited human data on a small number of N95 FFR models suggest that 3 cycles at this dose will not degrade fit.</p>\n<p>While respirator filter performance (and perhaps fit) were not adversely affected at the higher doses studied by Lindsley et al,13 because the lowest dose level of 120 J/cm2 caused a loss of strength of at least one filter layer, extending UVGI treatment beyond 20 cycles does not seem appropriate at this time.</p>\n</blockquote>\n<p><a href=\"https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-respirators-can-be-reused-decontamination-not-well-studied\" rel=\"nofollow noreferrer\">https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-respirators-can-be-reused-decontamination-not-well-studied</a></p>\n<p><a href=\"https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30003-3/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30003-3/fulltext</a></p>\n<p><a href=\"https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-face-mask-materials/\" rel=\"nofollow noreferrer\">https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-face-mask-materials/</a></p>\n"
},
{
"answer_id": 23124,
"author": "RudyB",
"author_id": 12770,
"author_profile": "https://health.stackexchange.com/users/12770",
"pm_score": 1,
"selected": false,
"text": "<p>Some hospitals are sanitizing (not sterilizing) their N95 respirators (not masks) already.</p>\n\n<p><a href=\"https://newyork.cbslocal.com/2020/04/03/coronavirus-sterilizing-n95-masks-long-island-nyc/\" rel=\"nofollow noreferrer\">Coronavirus Update: Massive N95 Mask Sterilizing Machines Now Running on Long Island</a></p>\n\n<p><a href=\"https://whyy.org/articles/doylestown-hospital-has-a-sterile-solution-to-the-n95-mask-shortage/\" rel=\"nofollow noreferrer\">Doylestown Hospital has solution to coronavirus mask shortage - WHYY</a></p>\n\n<p>As others have pointed out, for an item that is usually $2-3 at most, the time and effort involved had not previously been worth even investigating sanitization and re-use until now. Quite literally, in some areas even up to last month people used to use one of these respirators for 3 minutes and throw it out.</p>\n"
}
] | 2020/03/22 | [
"https://health.stackexchange.com/questions/21593",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17956/"
] |
21,607 | <p>I'm trying to wrap my head around some of the information I'm reading about how to fight Covid-19 and conflicting opinions about how much "social distancing" is required to avert a disaster, or whether social distancing works at all. (my training is in IT and Mathematics, not biology or medicine) </p>
<ul>
<li><p>Can social distancing (without hard quarantines, tracking as many cases as possible, and instantly isolating any new cases discovered, etc...) actually lead to 0 < 1 and therefore reduce the number of infections as opposed to just spreading them out to a manageable rate? </p></li>
<li><p>I think the answer is "No", because of small world network theory: The majority of people respect prefect social distancing, i.e. they maintain zero social contact with anybody outside of their immediate family and the the people they interact with for procuring life essentials. Because the number of people who cannot practice social distancing due to their essential role in society (grocery and pharmacy employees, health care professionals, law enforcement, etc...) will still experience very high transmission rates, a small world phenomenon occurs, where the average chain of transmission is still very short between any two individuals in an impacted area. What is wrong with this line of reasoning? </p></li>
<li>In general, is 0 < 1 achievable without a cure, a vaccine, herd immunity, or the ability to track infections with very high accuracy and isolating them instantly? </li>
</ul>
| [
{
"answer_id": 21595,
"author": "Matt Giambusso",
"author_id": 17883,
"author_profile": "https://health.stackexchange.com/users/17883",
"pm_score": 1,
"selected": false,
"text": "<p>Some hospitals are experimenting with using UV light to decontaminate respirator masks that are to be reused:</p>\n\n<p><a href=\"https://www.nytimes.com/2020/03/20/health/coronavirus-masks-reuse.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2020/03/20/health/coronavirus-masks-reuse.html</a></p>\n\n<p>EDIT\n<a href=\"https://i.stack.imgur.com/H7pRW.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/H7pRW.jpg\" alt=\"enter image description here\"></a>\nTo follow up on RudyB's answer, Battelle has been awarded a contract to use H2O2 vapor (sources: <a href=\"https://www.nytimes.com/2020/04/11/business/coronavirus-n95-mask-decontaminating-reuse.html?searchResultPosition=2\" rel=\"nofollow noreferrer\">NYtimes</a>, <a href=\"https://www.reuters.com/article/us-health-coronavirus-respirator-idUSKCN21V1WS\" rel=\"nofollow noreferrer\">Reuters</a>)</p>\n"
},
{
"answer_id": 21617,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 0,
"selected": false,
"text": "<p>The main reason is that we don't know how.</p>\n\n<p>For something like an N95 mask, a sterilization process needs to be designed so that it (a) kills any contaminating microbes, and (b) doesn't compromise the effectiveness of the mask.</p>\n\n<p>UV sterilization may not be able to light up every contaminated surface of the mask, or it might damage the filter material or the straps that hold the mask in place.</p>\n\n<p>Hydrogen peroxide vapor might not penetrate the filter material sufficiently, or residual hydrogen peroxide might remain in the filter to harm the user.</p>\n\n<p>Heat-based sterilization could warp the edges of the mask or the outflow valve so they no longer provide a tight seal, and superheated steam might also collapse the filter material into an air-tight barrier -- or expand it into a fluff that viruses have no trouble passing through.</p>\n\n<p>Any sterilization method needs to be tested for safety and effectiveness, and historically, it's been faster and cheaper to simply discard a contaminated mask and use a new one.</p>\n"
},
{
"answer_id": 21755,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>From {1}:</p>\n\n<blockquote>\n <ul>\n <li>It is unknown how wearing the same mask multiple times effects the fit of N95 masks [NIOSH]</li>\n <li>NIOSH states “there is no way of determining the maximum possible number of safe reuses for an\n N95 respirator as a generic number to be applied in all cases” and advise to “discard N95\n respirators following use during aerosol generating procedures.”</li>\n <li>Some methods of N95 mask disinfection can maintain filtration efficiency. Their effect on mask fit\n is unknown, and these methods are not approved by NIOSH.</li>\n </ul>\n</blockquote>\n\n<p>Their summary on sanitizing methods:</p>\n\n<blockquote>\n <p>In summary bleach and microwaves were failures at point of care because the bleach\n gases (skin and respiratory irritants) remained after multiple strategies were used to\n remove them, the microwave melted the masks and soaking them first led to reduced\n filtration. EtO, UVGI, and hydrogen peroxide decontamination were safe and effective in\n the models tested but it is not known if they would retain filtration, material strength,\n and airflow integrity with repeated use. EtO, UVGI, and hydrogen peroxide limitations\n include time from decontamination to reuse and available space and materials to\n decontaminate in an OR setting. 70C /158F heating in an oven (not your home oven) for\n 30min, or hot water vapor from boiling water for 10 min, are additional effective\n decontamination methods.</p>\n</blockquote>\n\n<p>Also, from <a href=\"https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/\" rel=\"nofollow noreferrer\">https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/</a> (<a href=\"https://web.archive.org/web/20200331090651/https://techcrunch.com/2020/03/27/duke-university-uses-vaporized-hydrogen-peroxide-to-clean-n95-face-masks-for-reuse/\" rel=\"nofollow noreferrer\">mirror</a>):</p>\n\n<blockquote>\n <p>Duke University thinks it has found a solution using vaporized hydrogen peroxide to decontaminate the masks.</p>\n \n <p>The process uses specialized equipment to vaporize hydrogen peroxide, which can then infuse all the layers of the mask to kill germs (including viruses) without degrading mask material.</p>\n</blockquote>\n\n<p>This Google Document goes over several papers on mask disinfection: <a href=\"https://docs.google.com/document/d/1YJ2MXeMSSIpm8Wxk8vN7zQ5SQJK9ukOh3wa-UhCJ6ZU/edit\" rel=\"nofollow noreferrer\">https://docs.google.com/document/d/1YJ2MXeMSSIpm8Wxk8vN7zQ5SQJK9ukOh3wa-UhCJ6ZU/edit</a> </p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 22805,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p><a href=\"https://web.archive.org/web/20210506231433/https://cnet4.cbsistatic.com/img/97VLceTKgeLDbT5OmoUnRk2rNew=/2020/04/07/3ec6ead4-acd0-4fcc-9660-f7c33defd992/vlcsnap-2020-04-07-13h39m12s930.png\" rel=\"nofollow noreferrer\"><img src=\"https://web.archive.org/web/20210506231433/https://cnet4.cbsistatic.com/img/97VLceTKgeLDbT5OmoUnRk2rNew=/2020/04/07/3ec6ead4-acd0-4fcc-9660-f7c33defd992/vlcsnap-2020-04-07-13h39m12s930.png\" alt=\"\" /></a></p>\n<blockquote>\n<p>Dr. Peter Tsai, the INVENTOR of the filtration fabric in the N95 mask. N95 masks are made of polypropylene material and are designed to tightly fit over your face with little leakage around the edge of the mask.</p>\n</blockquote>\n<h1>method 1</h1>\n<blockquote>\n<p>When reusing N95 masks, leave a used respirator in dry, atmosphere air for 3-4 days to dry it out. Polypropylene in N95 masks is hydrophobic and contains zero moisture. COVID-19 needs a host to survive–it can survive on a metal surface for up to 48 hours, on plastic for 72 hours, and on cardboard for 24 hours. When the respirator is dry in 3-4 days, the virus will not have survived.</p>\n</blockquote>\n<p>Take four N95 masks, and number them (#1-4).</p>\n<p>On day 1, use mask #1, then let it dry it out for 3-4 days.</p>\n<p>On day 2, use mask #2, then let it dry out for 3-4 days.</p>\n<p>Same for day 3, and day 4…</p>\n<h1>method 2</h1>\n<blockquote>\n<p>You can also sterilize the N95 mask by hanging it in the oven (without contacting metal) at 70C (158F) for 30 minutes-it is reported that COVID-19 cannot survive at 65C (149F) for 30 minutes.</p>\n<p>Use a wood clip to hang the respirator in the kitchen oven to do the sterilization.</p>\n</blockquote>\n<p>Experimentally though this time is much less when incubating virus in transport media</p>\n<blockquote>\n<p>With the incubation temperature increased to 70°C, the time for virus inactivation was reduced to 5 mins.</p>\n</blockquote>\n<h1>UV light</h1>\n<blockquote>\n<p>When sterilizing N95 masks, be wary of using UV light–keep N95 masks away from UV light / sunlight. N95 masks are degraded by UV light because it damages the electrostatic charges in the polypropylene material. It is unclear how long the masks can be exposed to UV light before they are ineffective.</p>\n</blockquote>\n<p>Read more details at the link</p>\n<p><a href=\"https://www.sages.org/n-95-re-use-instructions/\" rel=\"nofollow noreferrer\">https://www.sages.org/n-95-re-use-instructions/</a></p>\n<p>We do have more data now on UV and what levels are safe to use</p>\n<h2>Ultraviolet germicidal irradiation </h2>\n<blockquote>\n<p>UVGI disinfection involves placing respirators in direct line with UV-C lamps. Any exposed surface of the mask will be disinfected. This process generally requires the masks to be flipped after some period to ensure both sides of a mask are disinfected or requires a setup involving two UV-C lamps on either side of the respirator.</p>\n<p>For samples of FFR filters treated with SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome) viruses, no viable virus was found following a dose of 1 joule per square centimeter (J/cm2) of short wavelength (254 nanometers) UV-C light, even in the presence of artificial skin oil and saliva.11 Researchers found no impact of doses ranging from 3 to 20 J/cm2 on filter performance.9-12</p>\n<p>A similar dose range did not compromise fit on three N95 FFRs worn by 10 volunteers.12 Doses ranging from 3 to 6.5 J/cm2 did not alter fit performance on human subjects; doses up to 20 J/cm2 did not significantly change fit performance on respirators mounted on a static head form connected to a breathing machine.11</p>\n<p>Lindsley et al13 tested the impact of much higher doses, ranging from 120 to 950 J/cm2, on respirator filter samples and 590 to 2,360 J/cm2 on respirator straps. For most samples, filter efficiency decreased after UVGI treatment but remained above 95% at all dose levels for the four tested respirator models. Strength of the different layers decreased at all doses, with more layers showing decreased strength with increasing dose. The breaking strength of straps also decreased at all doses, ranging from a loss of 10% to 21% at the lowest dose of 590 J/cm2 and 20% to 51% at the highest dose of 2,360 J/cm2. Respirators treated with a single decontamination of UVGI showed no significant difference from untreated respirators in odor, donning ease, comfort, and respirator fit.9</p>\n<p>Altogether, these data suggest that respirators could be decontaminated by UVGI for up to 20 cycles at a dose of 1 J/cm2 per cycle, if the fit performance data from Heimbuch and Harnish11 using a static head form are representative of fit on humans. Limited human data on a small number of N95 FFR models suggest that 3 cycles at this dose will not degrade fit.</p>\n<p>While respirator filter performance (and perhaps fit) were not adversely affected at the higher doses studied by Lindsley et al,13 because the lowest dose level of 120 J/cm2 caused a loss of strength of at least one filter layer, extending UVGI treatment beyond 20 cycles does not seem appropriate at this time.</p>\n</blockquote>\n<p><a href=\"https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-respirators-can-be-reused-decontamination-not-well-studied\" rel=\"nofollow noreferrer\">https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-respirators-can-be-reused-decontamination-not-well-studied</a></p>\n<p><a href=\"https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30003-3/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30003-3/fulltext</a></p>\n<p><a href=\"https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-face-mask-materials/\" rel=\"nofollow noreferrer\">https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-face-mask-materials/</a></p>\n"
},
{
"answer_id": 23124,
"author": "RudyB",
"author_id": 12770,
"author_profile": "https://health.stackexchange.com/users/12770",
"pm_score": 1,
"selected": false,
"text": "<p>Some hospitals are sanitizing (not sterilizing) their N95 respirators (not masks) already.</p>\n\n<p><a href=\"https://newyork.cbslocal.com/2020/04/03/coronavirus-sterilizing-n95-masks-long-island-nyc/\" rel=\"nofollow noreferrer\">Coronavirus Update: Massive N95 Mask Sterilizing Machines Now Running on Long Island</a></p>\n\n<p><a href=\"https://whyy.org/articles/doylestown-hospital-has-a-sterile-solution-to-the-n95-mask-shortage/\" rel=\"nofollow noreferrer\">Doylestown Hospital has solution to coronavirus mask shortage - WHYY</a></p>\n\n<p>As others have pointed out, for an item that is usually $2-3 at most, the time and effort involved had not previously been worth even investigating sanitization and re-use until now. Quite literally, in some areas even up to last month people used to use one of these respirators for 3 minutes and throw it out.</p>\n"
}
] | 2020/03/22 | [
"https://health.stackexchange.com/questions/21607",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17968/"
] |
21,620 | <p>During the COVID-19 pandemic, ventilators are in short supply. As an engineer, I am interested in learning the risks/challenges of designing an OpenSource ventilator. And how it could be tested for proper functionality.</p>
<p>Medical equipment has to rise to the highest standards, especially when it is required to work flawlessly in an emergency situation.</p>
<p>Are there existing OpenSource ventilators projects? What requirements would a OpenSource ventilator have to fullfil?</p>
| [
{
"answer_id": 21630,
"author": "gatorback",
"author_id": 7446,
"author_profile": "https://health.stackexchange.com/users/7446",
"pm_score": 4,
"selected": true,
"text": "<p>In the <strong>United States</strong>, any ventilator must fulfill:</p>\n\n<ol>\n<li>Safety and </li>\n<li>Efficacy </li>\n</ol>\n\n<p>requirements as set forth in <a href=\"https://www.meddeviceonline.com/doc/an-introduction-to-international-medical-device-standards-0001\" rel=\"nofollow noreferrer\">Medical Device Standards</a>. </p>\n\n<p>Sales of medical devices are regulated by the FDA: a lengthy (data intensive) and paperwork intensive process. FDA <a href=\"https://www.fda.gov/medical-devices/letters-health-care-providers/ventilator-supply-mitigation-strategies-letter-health-care-providers\" rel=\"nofollow noreferrer\">ventilator specific guidance</a> within the context of COVID respirator demand </p>\n\n<p>I would suggest that you identify testable system requirements. The quickest way to learn is to operate an existing device: if you have access to a healthcare professional (Anesthesiologist or Respiratory Therapist), he / she would be the best functional resource. A good starting point (do your homework before talking to anyone) is this <a href=\"https://www.youtube.com/watch?v=gk_Qf-JAL84\" rel=\"nofollow noreferrer\">functional explanation on youTube</a>. </p>\n\n<p>Challenges for hacking a ventilator for the COVID crisis comprises:</p>\n\n<ol>\n<li>A design where parts (Bill of Materials) are readily available (100K to 1M devices needed)</li>\n<li>A testbed to demonstrate Safety and Efficacy testing + any required regulatory approval</li>\n<li>Skilled labor to manufacture assemble and test </li>\n</ol>\n\n<h1>UPDATE</h1>\n\n<p>April 8 2020: <a href=\"https://techcrunch.com/2020/03/30/medtronic-is-sharing-its-portable-ventilator-design-specifications-and-code-for-free-to-all/\" rel=\"nofollow noreferrer\">Medtronic is sharing its portable ventilator design specifications and code for free to all</a> That being said, a 510K and all the document would be required by the FDA ensure requirements discussed above are met.</p>\n"
},
{
"answer_id": 23109,
"author": "Dale Mahalko",
"author_id": 7949,
"author_profile": "https://health.stackexchange.com/users/7949",
"pm_score": 0,
"selected": false,
"text": "<p>This is not my work, but there is now a Youtube video that goes into the complex details of actual medical ventilators, and what needs to be done for a DIY device to do it safely.</p>\n\n<p><strong>A Guide To Designing Low-Cost Ventilators for COVID-19</strong></p>\n\n<p>By Real Engineering, published April 4, 2020</p>\n\n<p><a href=\"https://www.youtube.com/watch?v=7vLPefHYWpY\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=7vLPefHYWpY</a></p>\n"
}
] | 2020/03/22 | [
"https://health.stackexchange.com/questions/21620",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17972/"
] |
21,625 | <p>One of the most commonly used masks/recommended to protect against COVID-19 is N95.</p>
<p><strong>Is there any upside of using N95 masks instead of N99 or N100 to protect against COVID-19?</strong></p>
<p>N95 which filter 95% of particulates, while N99 or N100 filter 99% and 99.97%, respectively.</p>
<p>For <a href="https://www.cnbc.com/2020/03/16/who-considers-airborne-precautions-for-medical-staff-after-study-shows-coronavirus-can-survive-in-air.html" rel="nofollow noreferrer">example</a>:</p>
<blockquote>
<p>Health officials recommend medical staff wear so-called N95 masks because they filter out about 95% of all liquid or airborne particles.</p>
</blockquote>
<p>The N95 equivalent in Europe is FFP2, the N99/100 equivalent in Europe is FFP3, and the N95 equivalent in South Korea is KF94.</p>
<hr />
<p><strong>Prior research:</strong></p>
<p><a href="https://www.health.com/condition/infectious-diseases/n95-respirator-mask-coronavirus" rel="nofollow noreferrer">https://www.health.com/condition/infectious-diseases/n95-respirator-mask-coronavirus</a></p>
<blockquote>
<p>Infectious disease expert Amesh A. Adalja, MD, senior scholar at the Johns Hopkins Center for Health Security, tells Health that the N95 is still the recommended face mask for health professionals, because it has the capacity to filter out very small particles that could possibly contain the virus. “This is different than a surgical mask, which can only stop larger droplets,” says Dr. Adalja.</p>
</blockquote>
<p><a href="http://emag.medicalexpo.com/which-masks-actually-protect-against-coronavirus/" rel="nofollow noreferrer">http://emag.medicalexpo.com/which-masks-actually-protect-against-coronavirus/</a></p>
<blockquote>
<p>In the United States, respirators must meet NIOSH (National Institute for Occupational Safety and Health) standards. Within this standard, there are several classes of respirators depending on the degree of oil resistance:</p>
<p>Class N: no oil resistance. A distinction is made between N95, N99 and N100. The number after the letter indicates the percentage of filtration of suspended particles</p>
</blockquote>
<p><a href="https://www.businessinsider.com/wuhan-coronavirus-face-masks-not-entirely-effective-2020-1" rel="nofollow noreferrer">https://www.businessinsider.com/wuhan-coronavirus-face-masks-not-entirely-effective-2020-1</a></p>
<blockquote>
<p>When worn correctly, N95 respirators block out at least 95% of small airborne particles. So the respirators can filter out some droplets carrying coronavirus. The coronavirus itself measures between .05 and 0.2 microns in diameter, according to a recent article in The Lancet.</p>
</blockquote>
<hr />
<p>I have cross-posted the question at:</p>
<ul>
<li><a href="https://qr.ae/pNvXM4" rel="nofollow noreferrer">Quora</a></li>
<li><a href="https://redd.it/fng99n" rel="nofollow noreferrer">Reddit</a></li>
</ul>
| [
{
"answer_id": 21630,
"author": "gatorback",
"author_id": 7446,
"author_profile": "https://health.stackexchange.com/users/7446",
"pm_score": 4,
"selected": true,
"text": "<p>In the <strong>United States</strong>, any ventilator must fulfill:</p>\n\n<ol>\n<li>Safety and </li>\n<li>Efficacy </li>\n</ol>\n\n<p>requirements as set forth in <a href=\"https://www.meddeviceonline.com/doc/an-introduction-to-international-medical-device-standards-0001\" rel=\"nofollow noreferrer\">Medical Device Standards</a>. </p>\n\n<p>Sales of medical devices are regulated by the FDA: a lengthy (data intensive) and paperwork intensive process. FDA <a href=\"https://www.fda.gov/medical-devices/letters-health-care-providers/ventilator-supply-mitigation-strategies-letter-health-care-providers\" rel=\"nofollow noreferrer\">ventilator specific guidance</a> within the context of COVID respirator demand </p>\n\n<p>I would suggest that you identify testable system requirements. The quickest way to learn is to operate an existing device: if you have access to a healthcare professional (Anesthesiologist or Respiratory Therapist), he / she would be the best functional resource. A good starting point (do your homework before talking to anyone) is this <a href=\"https://www.youtube.com/watch?v=gk_Qf-JAL84\" rel=\"nofollow noreferrer\">functional explanation on youTube</a>. </p>\n\n<p>Challenges for hacking a ventilator for the COVID crisis comprises:</p>\n\n<ol>\n<li>A design where parts (Bill of Materials) are readily available (100K to 1M devices needed)</li>\n<li>A testbed to demonstrate Safety and Efficacy testing + any required regulatory approval</li>\n<li>Skilled labor to manufacture assemble and test </li>\n</ol>\n\n<h1>UPDATE</h1>\n\n<p>April 8 2020: <a href=\"https://techcrunch.com/2020/03/30/medtronic-is-sharing-its-portable-ventilator-design-specifications-and-code-for-free-to-all/\" rel=\"nofollow noreferrer\">Medtronic is sharing its portable ventilator design specifications and code for free to all</a> That being said, a 510K and all the document would be required by the FDA ensure requirements discussed above are met.</p>\n"
},
{
"answer_id": 23109,
"author": "Dale Mahalko",
"author_id": 7949,
"author_profile": "https://health.stackexchange.com/users/7949",
"pm_score": 0,
"selected": false,
"text": "<p>This is not my work, but there is now a Youtube video that goes into the complex details of actual medical ventilators, and what needs to be done for a DIY device to do it safely.</p>\n\n<p><strong>A Guide To Designing Low-Cost Ventilators for COVID-19</strong></p>\n\n<p>By Real Engineering, published April 4, 2020</p>\n\n<p><a href=\"https://www.youtube.com/watch?v=7vLPefHYWpY\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=7vLPefHYWpY</a></p>\n"
}
] | 2020/03/22 | [
"https://health.stackexchange.com/questions/21625",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/43/"
] |
21,647 | <p>If I read Figure 2 of <a href="https://www.ijidonline.com/article/S1201-9712(19)30328-5/fulltext" rel="nofollow noreferrer">… the impact of influenza on excess mortality …</a> correctly, the excess mortality due to flu
in Italy during the peak weeks of the flu epidemic of 2016–2017 was about 800 deaths/day. This is way more than what is happening
with Covid-19 now. How come the health system is so stressed now?</p>
<p>Is it due to geographical distribution (Lombardy!) which Italy could not compensate by moving resources? Or is it a different
distribution of deaths vs. being in intensive care? Or what?</p>
| [
{
"answer_id": 21652,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 1,
"selected": false,
"text": "<p>You're misreading the study. It's not measuring the number of deaths due to influenza, it's measuring the excess mortality rate during the flu season. This covers not just direct deaths from infection, but secondary deaths such as someone getting the flu, recovering, and then dying from a heart attack caused by the stress of being sick. It can even include highly indirect deaths, such as someone isolating themselves to avoid infection, and dying because they fell down, broke their leg, and couldn't contact anyone for help.</p>\n\n<p>Excess mortality rate is calculated by estimating how many deaths there would have been in the absence of a given cause (eg. a flu season) and then comparing that to the actual number of deaths.</p>\n"
},
{
"answer_id": 21654,
"author": "Bryan Krause",
"author_id": 8728,
"author_profile": "https://health.stackexchange.com/users/8728",
"pm_score": 3,
"selected": true,
"text": "<p>The big difference in Italy today is that <em>many younger, otherwise healthier patients need critical care</em> and more generally that <em>patients need critical care for a long time</em>. These patients are not necessarily dying after they get care, but the extent to which the surviving patients require ventilators and supplemental oxygen is nothing like a seasonal flu and is likely inflating the death rate substantially among those who could otherwise be treated.</p>\n\n<p>From NEJM: <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMp2005492\" rel=\"nofollow noreferrer\">https://www.nejm.org/doi/full/10.1056/NEJMp2005492</a></p>\n\n<blockquote>\n <p>Contributing to the resource scarcity is the prolonged intubation many of these patients require as they recover from pneumonia — often 15 to 20 days of mechanical ventilation, with several hours spent in the prone position and then, typically, a very slow weaning. In the midst of the outbreak’s peak in northern Italy, as physicians struggled to wean patients off ventilators while others developed severe respiratory decompensation, hospitals had to lower the age cutoff — from 80 to 75 at one hospital, for instance.</p>\n</blockquote>\n"
},
{
"answer_id": 23030,
"author": "Ilya Zakharevich",
"author_id": 17982,
"author_profile": "https://health.stackexchange.com/users/17982",
"pm_score": 0,
"selected": false,
"text": "<p>Adding another possible explanation (supporting what Mark said): according to an article in <a href=\"https://www.ecodibergamo.it/stories/bergamo-citta/coronavirus-the-real-death-tool-4500-victims-in-one-month-in-the-province-of_1347414_11/\" rel=\"nofollow noreferrer\">L’Eco di Bergamo</a>, the excess mortality from Covid-19 seems to be about 2.2 times more than the official mortality numbers. (Mostly due to the shortage of testing and the rules for ascribing reasons for death. The data is restricted to the most affected region only.)</p>\n"
}
] | 2020/03/23 | [
"https://health.stackexchange.com/questions/21647",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17982/"
] |
21,681 | <p>In this link</p>
<p><a href="https://www.dw.com/en/covid-19-recovered-patients-have-partially-reduced-lung-function/a-52859671" rel="nofollow noreferrer">https://www.dw.com/en/covid-19-recovered-patients-have-partially-reduced-lung-function/a-52859671</a></p>
<p>we can see</p>
<blockquote>
<p>Now researchers in Hong Kong have said that recovered coronavirus patients can be left with damaged lungs.</p>
<p>A small study of 12 patients discharged from hospital showed that two or three had reduced lung function. However, it is too early to confirm any long-term effects.</p>
<p>"In some patients, lung function could decline by about 20 to 30% after recovery," says Dr. Owen Tsang Tak-yin, medical director of the Infectious Diseases Centre at Princess Margaret Hospital in Hong Kong.</p>
<p>Computer tomography have shown fluid- or debris-filled sacs in the lungs, which may get progressively worse as the illness develops.</p>
</blockquote>
<p>What can determine the <em>long term effects</em>?</p>
<p>Why can this:</p>
<p>"In some patients, lung function could decline by about 20 to 30% after recovery," happen?</p>
<p>Are elderly more likely to this? or it could happen to anyone?</p>
<p>Does this only happen if you had severe symptoms?</p>
| [
{
"answer_id": 21682,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>The best theoretical model we have is that the SARS and SARS-CoV-2 viruses knock out the ACE2 receptor found on numerous tissues including alveolar cells, and myocytes, and intestinal luminal cells.</p>\n\n<p>If those cells have died then they need to be replaced, and if and until when that happens there will be reduced organ function.</p>\n\n<p>CT scans of recovered patients show some have ground glass changes pointing to extensive damage and scarring which may be irreversible.</p>\n\n<p><a href=\"https://www.businessinsider.com.au/coronavirus-recovery-damage-lung-function-gasping-air-hong-kong-doctors-2020-3?r=US&IR=T\" rel=\"nofollow noreferrer\">https://www.businessinsider.com.au/coronavirus-recovery-damage-lung-function-gasping-air-hong-kong-doctors-2020-3?r=US&IR=T</a></p>\n\n<p><a href=\"https://www.theatlantic.com/science/archive/2020/03/biography-new-coronavirus/608338/\" rel=\"nofollow noreferrer\">https://www.theatlantic.com/science/archive/2020/03/biography-new-coronavirus/608338/</a></p>\n"
},
{
"answer_id": 21750,
"author": "nick012000",
"author_id": 17893,
"author_profile": "https://health.stackexchange.com/users/17893",
"pm_score": 1,
"selected": false,
"text": "<p><a href=\"https://www.youtube.com/watch?v=BtN-goy9VOY\" rel=\"nofollow noreferrer\">This video</a> by Kurzgesagt gives a good overview of how the COVID-19 infection process works. The damage it causes to the lungs seems to the result of it damaging the cells that create a protective lining of your lungs; this happens both directly as a result of their infections of these cells, as well as by causing the immune system to attack healthy cells. By killing large numbers of these cells, bacteria that this lining would normally protect from are now able to invade the lungs and cause issues like pneumonia. Additionally, the damage that is done during the initial phase can cause significant amounts of scarring within the lungs as the body tries to recover from the damage.</p>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21681",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
21,684 | <p>I'm searching for data sets about Covid-19 patients, where the column "age" occurs for each patient. All the sets I find are summarized, like the one from the <a href="https://github.com/CSSEGISandData/COVID-19" rel="nofollow noreferrer">John Hopkins University</a>.</p>
| [
{
"answer_id": 23549,
"author": "ukemi",
"author_id": 19586,
"author_profile": "https://health.stackexchange.com/users/19586",
"pm_score": 2,
"selected": false,
"text": "<p>The <a href=\"https://news.bugbank.uk/2020/04/interpreting-uk-biobank-covid-19-test.html\" rel=\"nofollow noreferrer\">UK Biobank</a> (cohort study of 500,000 participants) incorporates SARS-CoV-2 test result data. It contains age, as well as entire medical history information for each participant.</p>\n\n<p><strong>Ref:</strong> <a href=\"https://doi.org/10.6084/m9.figshare.12091455\" rel=\"nofollow noreferrer\">Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank</a> (2020) *</p>\n\n<hr>\n\n<p><sup>* Disclaimer: I have worked on this project.</sup></p>\n"
},
{
"answer_id": 23627,
"author": "Marcus D",
"author_id": 19626,
"author_profile": "https://health.stackexchange.com/users/19626",
"pm_score": 1,
"selected": false,
"text": "<p><a href=\"https://opendata.stackexchange.com/questions/16251/covid-19-clinical-data-or-statistics\">This question</a> in opendata.SE has answers that might help. </p>\n\n<p>There are three answers at the time of writing</p>\n\n<ul>\n<li><a href=\"https://opendata.stackexchange.com/a/17298/10235\">Anthem XPRIZE</a></li>\n<li><a href=\"https://opendata.stackexchange.com/a/17321/10235\">Github large dataset</a></li>\n<li><a href=\"https://opendata.stackexchange.com/a/17366/10235\">South Korean data</a></li>\n</ul>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21684",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18002/"
] |
21,689 | <p>In WHO official website "<a href="https://www.who.int/news-room/q-a-detail/q-a-coronaviruses" rel="nofollow noreferrer">What can I do to protect myself and prevent the spread of disease?"</a>, it doesn't mention that wearing mask an effective measure to protect people. </p>
<p>I don't understand why wearing mask is not good way to prevent infection of COVID-19.
Is it just because masks are out of stock?</p>
| [
{
"answer_id": 21697,
"author": "paulj",
"author_id": 16600,
"author_profile": "https://health.stackexchange.com/users/16600",
"pm_score": 2,
"selected": false,
"text": "<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/infection-control/control-recommendations.html\" rel=\"nofollow noreferrer\">CDC website</a>:\nBlanks labels</p>\n<blockquote>\n<p>PPE is the least effective control because it involves a high level\nof worker involvement and is highly dependent on proper fit and\ncorrect, consistent use.</p>\n</blockquote>\n<p>e.g. The likelihood for untrained personalto properly use PPE is not realistic, so it would be negligent of the WHOto suggest this to the public for this use.?</p>\n<p>This does not address reducing transmission. Though, masks, used by those untrained, are not realistic in <strong>halting</strong> the spread. One method that has proven to halt the spread is self-quarantine (both healthy and non-healthy) and social distancing and the other recommendations listed in the link provided.</p>\n"
},
{
"answer_id": 21698,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
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"text": "<p>Update: April 2 <a href=\"https://www.bbc.com/news/science-environment-52126735\" rel=\"nofollow noreferrer\">news</a> is that the WHO has now commissioned a panel to study the problem further:</p>\n<blockquote>\n<p>Should more of us wear face masks to help slow the spread of coronavirus?</p>\n<p>This question is to be assessed by a panel of advisers to the World Health Organization (WHO).</p>\n<p>The group will weigh up research on whether the virus can be projected further than previously thought; <a href=\"https://doi.org/10.1001/jama.2020.4756\" rel=\"nofollow noreferrer\">a study</a> in the US suggests coughs can reach 6m and sneezes up to 8m.</p>\n<p>The panel's chair, Prof David Heymann, told BBC News that the new research may lead to a shift in advice about masks.</p>\n<p>The former director at the WHO explained: "The WHO is opening up its discussion again looking at the new evidence to see whether or not there should be a change in the way it's recommending masks should be used."</p>\n</blockquote>\n<p>Original answer below:</p>\n<hr />\n<p>The effectiveness of masks in the general population, as opposed to use by HCW (health-case workers) has not been studied a lot. Some such studies involved "home use" which may or may not be equivalent to "going shopping" use, so we don't have a lot of clear data on how people might be using masks in the present pandemic.</p>\n<p>But some facts that <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4868614/\" rel=\"nofollow noreferrer\">were reported</a>...</p>\n<blockquote>\n<p>In the 1919 influenza pandemic, masks were available and were dispensed to populations, but they had no impact on the epidemic curve.</p>\n</blockquote>\n<p>There was no clear idea how to design masks at that point, a "germ-proof" surgical mask was only <a href=\"https://doi.org/10.1086/647501\" rel=\"nofollow noreferrer\">available</a> from the 1930s onward.</p>\n<p>And some "home use" RCTs; <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2662657/\" rel=\"nofollow noreferrer\">MacIntyre et al. (2009)</a></p>\n<blockquote>\n<p>We conducted a prospective cluster-randomized trial comparing surgical masks, non–fit-tested P2 masks, and no masks in prevention of influenza-like illness (ILI) in households. [...] Adherence to mask use was associated with a significantly reduced risk of ILI-associated infection. We concluded that <strong>household use of masks is associated with low adherence and is ineffective in controlling seasonal ILI. If adherence were greater, mask use might reduce transmission during a severe influenza pandemic.</strong></p>\n</blockquote>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/19652172/\" rel=\"nofollow noreferrer\">Cowling et al. (2009)</a></p>\n<blockquote>\n<p>INTERVENTION: Lifestyle education (control) (134 households), hand hygiene (136 households), or surgical facemasks plus hand hygiene (137 households) for all household members.</p>\n<p>RESULTS: Sixty (8%) contacts in the 259 households had RT-PCR-confirmed influenza virus infection in the 7 days after intervention. <strong>Hand hygiene with or without facemasks seemed to reduce influenza transmission</strong>, but the differences compared with the control group were not significant. In 154 households in which interventions were implemented within 36 hours of symptom onset in the index patient, <strong>transmission of</strong> RT-PCR-<strong>confirmed infection seemed reduced, an effect attributable to fewer infections among participants using facemasks plus hand hygiene</strong> [...]. Adherence to interventions varied.</p>\n</blockquote>\n<p>Basically, masks can work for the "average Joe" but note that some effect of hand hygiene was observed even without masks, but not vice-versa.</p>\n<p>Here's the full summary table from the review of <a href=\"https://www.bmj.com/content/350/bmj.h694\" rel=\"nofollow noreferrer\">MacIntyre and Chughtai (2015)</a> on household/community settings studies. (Paper found by Vladimir F.)</p>\n<p><a href=\"https://i.stack.imgur.com/x7xvx.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/x7xvx.png\" alt=\"enter image description here\" /></a></p>\n<p>As you can see, most report no significant differences for masks alone. The review says that a meta-analysis is not possible due to varying study design(s). It also says the studies may have been underpowered. They discuss the studies in a bit more detail (including the two I've already mentioned above). Since the ones inside a household are pretty similar to each other, let me quote just what they say on two studies on a slightly different setting:</p>\n<blockquote>\n<p>Two RCTs in university residence halls in the United\nStates over two influenza seasons randomised well students\ninto medical masks plus hand hygiene, medical\nmasks alone, or control. <strong>Influenza-like illness and\nlaboratory confirmed influenza were not significantly\nreduced after either intervention, although during the first\nfour to six weeks, influenza-like illness was significantly\nlower in the medical masks plus hand hygiene arm in\nboth trials (P<0.05). This suggests that hand hygiene\nmight have been the major contributor to protection.</strong></p>\n</blockquote>\n<p>(Those are the two studies by Aiello et al. [2010, 2012] in that big table.)</p>\n<p>The review also says:</p>\n<blockquote>\n<p>The routine use of facemasks is not recommended by WHO,\nthe CDC, or the ECDC in the community setting. However,\n[citing the same guidelines] the use of facemasks is recommended in crowded settings\n(such as public transport) and for those at high risk\n(older people, pregnant women, and those with a medical\ncondition) during an outbreak or pandemic.</p>\n</blockquote>\n<p>However... looking at the actual sources cited <a href=\"https://www.cdc.gov/h1n1flu/masks.htm\" rel=\"nofollow noreferrer\">2009 CDC page</a> and <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291414/\" rel=\"nofollow noreferrer\">2006 WHO paper</a>... what they actually say (the CDC in particular) is that <em>both</em> criteria (crowded setting and vulnerable person) have to be met simultaneously for the mask to be recommended.</p>\n<p><a href=\"https://i.stack.imgur.com/UxGl4.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/UxGl4.png\" alt=\"enter image description here\" /></a></p>\n"
},
{
"answer_id": 21699,
"author": "Vladimir F Героям слава",
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"text": "<p>The prevalent claim is that these masks do not really protect (as opposed to a respirator) the individual wearing it and should be only be worn by sick people and by medical personel. The wearer must be trained and there is a shortage of proffesional made masks and community usage might increase the shortage.</p>\n\n<p>However, there are also studies that offer a view differing from those referenced by @Fizz. For example: </p>\n\n<p><a href=\"https://fas.org/rlg/060306-facemasks.pdf\" rel=\"nofollow noreferrer\">https://fas.org/rlg/060306-facemasks.pdf</a> </p>\n\n<blockquote>\n <p>Improvised masks or reuse of disposable masks when in contact with\n other people might well be sufficient to quench a flu pandemic, when\n combined with hand sanitation.</p>\n</blockquote>\n\n<p><a href=\"https://www.bmj.com/content/350/bmj.h694.full\" rel=\"nofollow noreferrer\">https://www.bmj.com/content/350/bmj.h694.full</a> </p>\n\n<blockquote>\n <p>Of the nine trials of facemasks identified in community settings, in\n all but one, facemasks were used for respiratory protection of well\n people. They found that facemasks and facemasks plus hand hygiene may\n prevent infection in community settings, subject to early use and\n compliance.</p>\n</blockquote>\n\n<p><a href=\"https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1539-6924.2010.01428.x\" rel=\"nofollow noreferrer\">https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1539-6924.2010.01428.x</a></p>\n\n<p>This study was based on modelling: </p>\n\n<blockquote>\n <p>We conclude that population-wide use of face masks could make\n animportant contribution in delaying an influenza pandemic. Mask use\n also reduces the repro-duction number, possibly even to levels\n sufficient for containing an influenza outbreak.</p>\n</blockquote>\n\n<p>Several countries, such as the Czech Republic and Slovakia are now using face masks for general public in an effort to lower the reproduction number and thus slow the epidemics. One peculiar aspect of COVID-19 is spreading by people who do not know they are sick so the suggestion for the masks to be worn only by sick people is problematic even if we assume zero protection for the wearer. Certain training in proper usage of these masks can and is being done by media and in social media.</p>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21689",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18003/"
] |
21,691 | <p>A few weeks ago the UK has been debating about <em>herd immunity</em>. </p>
<p>I understand that when most people are immune to a disease, then the disease is harder to spread. However, how are they going to implement that? Protecting the majority with the minority (old people, people with bad immune systems, etc) doesn't seem to be an ethical thing to do. (Think of this case. It's kind of like putting the pain of everybody onto a single innocent person. )</p>
<p>Without a vaccine, most people will be infected in herd immunity (if I am wrong, please consider answering how a community can get herd immunity otherwise). That means that there will be more people who are infected, so there will be more deaths. </p>
<p>Maybe do they mean to attempt to social-distance vulnerable people like old people but let other healthy people get an infection? Wouldn't that <em>also</em> overflow the hospital?</p>
| [
{
"answer_id": 21692,
"author": "motosubatsu",
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"selected": true,
"text": "<blockquote>\n <p>Protecting the majority with the minority (old people, people with bad immune systems, etc) doesn't seem to be an ethical thing to do. (Think of this case. It's kind of like putting the pain of everybody onto a single innocent person. )</p>\n</blockquote>\n\n<p>Essentially the idea was to do the <em>reverse</em> i.e. if the majority get infected -> gain immunity then if you can keep the (vulnerable) minority from being exposed while the infection->immunity process happens they won't <em>need</em> to get immunity because they will then be protected by the immunity of the majority (i.e. the herd).</p>\n\n<p>In the same way that there are always going to be people who can't be vaccinated for a disease like measles (immunocompromised, too young, etc) but if a sufficient majority are vaccinated that prevents the disease ever getting an opportunity to get to them in the first place.</p>\n\n<blockquote>\n <p>That means that there will be more people who are infected, so there will be more deaths.</p>\n</blockquote>\n\n<p>If more people <em>total</em> get infected but less <em>vulnerable</em> people then you can still see less overall deaths.</p>\n\n<blockquote>\n <p>Maybe do they mean to attempt to social-distance vulnerable people like old people but let other healthy people get an infection? Wouldn't that also overflow the hospital?</p>\n</blockquote>\n\n<p>That was basically the initial UK plan - the idea being that if you could keep the spread amongst \"healthy\" people slow enough you'd \"flatten the peak\" and while the same eventual number would get the virus less would have it any one time, therefore (hopefully) avoiding an overload on the health infrastructure. This has sort of (although not entirely) gone out of the window now as it wasn't slow enough - and too many vulnerable people were getting infected.</p>\n\n<p>The difference between this so-called \"mitigation\" approach and the China-style \"suppression\" approach is that in a suppression you're aiming to reduce the number of people that each infected person can subsequently infect to less than 1.</p>\n\n<p>The change in tack to more intensive measures was driven mainly by modelling done by a team at <a href=\"https://www.imperial.ac.uk/media/imperial-college/medicine/sph/ide/gida-fellowships/Imperial-College-COVID19-NPI-modelling-16-03-2020.pdf\" rel=\"nofollow noreferrer\">Imperial College London</a>, where they predicted that at the rate the virus was spreading the NHS would be overwhelmed and concluded:</p>\n\n<blockquote>\n <p>We therefore conclude that epidemic suppression is the only viable strategy at the current time.</p>\n</blockquote>\n\n<p>Hence why more drastic lockdown measures are now being implemented. Suppression brings its own challenges - namely that if it is successful the population at large remains non-immune and when you ease the suppression measures off too soon and you get any new cases introduced into the population it can spread very quickly again and you're back where you started.</p>\n"
},
{
"answer_id": 21743,
"author": "not2qubit",
"author_id": 17628,
"author_profile": "https://health.stackexchange.com/users/17628",
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"text": "<p>Unfortunately the ideas about herd-immunity have become a populist term to down-play serious diseases, by many people who do not understand the conditions where this can be applied. Just straight off, it can only <em>work</em> within western ethical standards when:</p>\n\n<ol>\n<li>The disease doesn't kill a large percentage of the infected.</li>\n<li>The infected are not infectious for a long time.</li>\n<li>The incubation time is very short.</li>\n<li>The virus causing the disease does not mutate fast.</li>\n</ol>\n\n<p>Unfortunately <strong>none</strong> of the above are true for COVID-19. Which make the arguments for applying <em>herd-immunity</em>, in that case, macabre.</p>\n\n<hr>\n\n<p>PS. For those who will immediately scream for references, please google and search here or in the <a href=\"https://biology.stackexchange.com/\">biology SE</a>, where you will find hundreds of answers to the above statements. </p>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21691",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18004/"
] |
21,700 | <p>Current statistics on number of cases will always be a few days behind reality due to the time between infection and going to get tested, asymptomatic people, etc. But why not take a random sample of a few thousand people people, and test all of them to see how many of them have the virus? Would that not give us a picture of the proportion of people who have the virus?</p>
| [
{
"answer_id": 21701,
"author": "Fizz",
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"text": "<p>Italy has 60 million people and around 70 thousand (known) cases. That's barely more than 1 in 1000 <a href=\"https://en.wikipedia.org/wiki/Prevalence\" rel=\"noreferrer\">prevalence</a>. For most countries it's less than this. So, you'd need a huge sample for a good estimate. And those tests/resources are better deployed where suspected cases are, for the time being.</p>\n<p>And sensible or not, I've heard this from a colleague, and it's <a href=\"https://www.nineoclock.ro/2020/03/26/pilot-project-for-testing-10500-people-in-bucharest-for-the-novel-coronavirus/\" rel=\"noreferrer\">confirmed</a> by the news that Romania's capital Bucharest plans to randomly test a sample of 10,500 people to determine the extent of the virus spread over there.</p>\n<blockquote>\n<p>Manager of the “Matei Bals” Infectious Diseases Institute Adrian Streinu-Cercel has announced that a pilot project for testing 10,500 persons for the novel coronavirus will start in Bucharest within a scientific study to detect those infected with SARS CoV-2 virus, from the desire to thus prevent the severe forms of illness.</p>\n<p>Streinu-Cercel mentioned that, for a population of approximately 2 million inhabitants, the testing of 9,558 persons is necessary, with a correction of 10% being applied to this number. He also stated that the sample can be resized along the way. In this regard, Streinu-Cercel referred to the recommendations of the World Health Organization, which asked that testing be conducted to detect COVID 19. The manager of the “Matei Bals” Institute showed that it is necessary to test the medical staff and patients, but also the population, in order to know if “it’s healthy, if it is currently infected or went through the infection” with this virus, these three pieces of information completely changing how this pandemic is approached in the near future. [...]</p>\n<p>Streinu-Cercel underscored that, in lack of screening, the mild forms can go undetected, generating subsequent forms of severe infections. He also mentioned that the Minister of Health approved this project and stressed that this is a study with “scientific value,” not a simple testing. At the same time, he mentioned that in Bucharest there are 188 people diagnosed positively.</p>\n</blockquote>\n<p>Note that ~200 cases in 2M is 1:10,000.</p>\n<p>Ha, ha, the more amusing part is that this <a href=\"https://www.romaniajournal.ro/society-people/pm-about-testing-10000-in-bucharest-for-covid-19-just-stories-testing-algorithm-updated-what-categories-take-priority/\" rel=\"noreferrer\">turned out</a> to be "fake news!" But it's actually informative to read the "retraction/information" as to why they are not actually doing such a study [obviously: insufficient testing capacity for the proposed sample.]</p>\n<blockquote>\n<p>After the manager of the “Matei Bals” Institute for Infectious Diseases, Adrian Streinu-Cercel and Bucharest mayor Gabriela Firea had announced on Thursday that 10,514 people from 5 different age groups in Bucharest will be tested for the novel Coronavirus, PM Ludovic Orban reacted and said this is not possible.</p>\n<p>“We cannot establish the people to be tested randomly. Selecting 10,000 are just stories, there is a priority list for testing, it depends on how the situation and the testing capacity are developing,” the PM told a conference at the Health Ministry’s HQs.</p>\n<p>Orban said that the medical staff and those targeted by the epidemiological inquiries are qualifying for testing first, adding that “Romania has not been ready and the testing capacity has been limited”.</p>\n<p>The premier said that “the testing capacity in Romania will increase up to 2,000 next week” and will gradually rise, but to select 10,000 people “are just stories”, the more the death toll has been low in Romania.</p>\n</blockquote>\n<p>In <a href=\"https://www.thehindubusinessline.com/news/icmr-500-random-tests-for-covid-19-come-up-negative/article31092901.ece\" rel=\"noreferrer\">older news</a> I see that India conducted a random test on 500 of their citizens. Rather predictably, they all came out negative.</p>\n<p>And for some more official objections of the same kind <a href=\"https://www.dw.com/en/germanys-coronavirus-response-separating-fact-from-fiction/a-53053822\" rel=\"noreferrer\">DW reported on Apr 7</a>...</p>\n<blockquote>\n<p>Germany's center for disease control, the Robert Koch Institute, has criticized Germany's methods of testing, complaining for example that too many asymptomatic individuals were being tested. The RKI called for an end to this practice on the grounds that <strong>Germany could risk running out of tests</strong>. Therefore, asymptomatic people are currently not being recommended for testing.</p>\n</blockquote>\n<p>By the way, if what you want to find out are the proportion of asymptomatic cases, there are some studies (albeit on fairly contained populations) that may have an answer to that, <a href=\"https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.10.2000180\" rel=\"noreferrer\">e.g. one</a> on the Diamond Princess (the cruise ship quarantined off Japan):</p>\n<blockquote>\n<p>[Overall:] Our estimated asymptomatic proportion is at 17.9% (95%CrI: 15.5–20.2%), which overlaps with a recently derived estimate of 33.3% (95% confidence interval: 8.3–58.3%) from data of Japanese citizens evacuated from Wuhan.</p>\n<p>[Caveat:] Considering that most of the passengers were 60 years and older, the nature of the age distribution may lead to underestimation if older individuals tend to experience more symptoms.</p>\n</blockquote>\n<p>From a <a href=\"https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.12.2000256\" rel=\"noreferrer\">2nd study</a> on the Diamond Princess, it's informative to read the testing strategy/order:</p>\n<blockquote>\n<p>Overall 3,063 PCR tests were performed among [the 3,711] passengers and crew members. Testing started among the elderly passengers, descending by age.</p>\n</blockquote>\n<p>An interesting counterpoint to the healthcare providers' perspective is that economists seem to <a href=\"http://www.igmchicago.org/surveys/testing-for-coronavirus-infections-and-antibodies/\" rel=\"noreferrer\">strongly agree</a> on the need for random testing (or better said, per some comments which corrected the question, population-representative testing) in order to calibrate the length of the lockdown from their perspective, of limiting "economic damage" caused by the lockdowns themselves.</p>\n"
},
{
"answer_id": 21714,
"author": "cbeleites unhappy with SX",
"author_id": 11479,
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"text": "<blockquote>\n <p>Would that not give us a picture of the proportion of people who have the virus?</p>\n</blockquote>\n\n<p>Yes, but: at the moment, this is probably not worth while in most countries. </p>\n\n<ul>\n<li>As Fizz explained, tests are scarce, so we need to use them where the outcome of the test does make a difference in treatment and/or for containing the disease/slowing down the spread.</li>\n<li>Right now, the development of Covid-19 case numbers is quite dynamic in many countries. The percentage we find by testing today will be outdated if not tomorrow then by the end of the week. </li>\n<li><p>In order to get good estimates of a <em>low</em> prevalence, we need to test large numbers of people and we need tests that have both high sensitivity and specificity. Right now, the tests that are used have not undergone a full validation procedure (in order to have them available asap). </p>\n\n<p>One consequence of that is that while we can know that they work sufficiently well to be useful for testing high risk patients, e.g. for some test we may know that sensitivity is better than 94% and specificity is better than 97%. If we test a general population with a prevalence of 1 in 1000 using a test with 97% specificity, we'll get around 30 false positives and 1 true positive (with 94% sensitivity). In other words, rather than measuring the prevalence of SARS-CoV-2 infections in the general population, we measured 1 - specificity of the test. Unfortunately, we wouldn't know this. </p></li>\n</ul>\n\n<p>As a rule of thumb, we can measure prevalences that are >> 1 - specificity of the test. So if we expect a prevalence of 1 : 1000, we'd ask for a test that has specificity at least 99.95 % (with that, we'd observe 1.5 positive in 1000). In order to know that a test has a specificity > 99.95 %, we'd need to validate it with at least 10000 truly negative patients all of which would need to be recognized correctly. Right now, the test may have been validated with 100 negative samples. If you want to read more background about this, I have long answers to <a href=\"https://medicalsciences.stackexchange.com/q/21337/11479\">How accurate are coronavirus tests?</a> and <a href=\"https://medicalsciences.stackexchange.com/q/21318/11479\">Why are people with COVID-19 symptoms being denied tests in the US?</a></p>\n\n<hr>\n\n<p><strong>Sentinel Samples</strong></p>\n\n<p>While we do not have such a random sampling scheme from the population right now, we have something that goes into this direction here in Germany: samples from so-called sentinel practices. Sentinel practices are medical practices throughout the country that send patient samples to a central lab where they are analyzed for a number of viruses as part of influenza surveillance. The tested viruses now include also SARS-CoV-2. </p>\n\n<p>These samples are not a random sample of the population you ask for: </p>\n\n<ul>\n<li>they are taken of patients that show up at the doctor's with acute respiratory disease, </li>\n<li>and right now with the further systematic restriction that these are patients that were not thought to be at a particularly high risk of having Covid-19 (those are sent to the SARS-CoV-2 testing).</li>\n</ul>\n\n<p>In week 12 (Mar 16 - 22), 3 of the 193 sentinel samples that were tested for SARS-CoV-2 were positive. That's a prevalence of 1,6 %, 95 % confidence interval roughly being 0.4 - 4 % (in other words, we have an order of magnitude). </p>\n\n<p>I don't have information on the specificity of the SARS-CoV-2 test used for the sentinel samples, but the published data reports two weeks with 0 positive among 191 + 229 = 420 samples, and if we take those as true negatives, specificity would be better than 99 %.</p>\n\n<hr>\n\n<p>I expect that studies will be done once the first wave of Covid-19 is over and once properly validated antibody tests are available. In contrast to the RNA tests now (which test an active infection), antibody tests can say whether someone had such an infection recently (possibly as recent as right now) or a while ago. </p>\n\n<p>The specificity requirements are the same regardless of whether RNA or antibodies are tested.</p>\n"
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"answer_id": 21729,
"author": "Franck Dernoncourt",
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"pm_score": 2,
"selected": false,
"text": "<blockquote>\n<p>why not take a random sample of a few thousand people people, and test all of them to see how many of them have the virus?</p>\n</blockquote>\n<p>Iceland did it, see <a href=\"https://english.alarabiya.net/en/features/2020/03/25/Coronavirus-Iceland-s-mass-testing-finds-half-of-carriers-show-no-symptoms\" rel=\"nofollow noreferrer\">https://english.alarabiya.net/en/features/2020/03/25/Coronavirus-Iceland-s-mass-testing-finds-half-of-carriers-show-no-symptoms</a>:</p>\n<blockquote>\n<p>As of Sunday night, the country’s health authorities and the biotechnology firm deCode Genetics have tested more than 10,300 people. That might not sound like a large number, compared to the around 350,000 Americans who have been tested for coronavirus according to the COVID Tracking Project, but it is a far higher percentage of tests per capita - a ratio Icelandic authorities have claimed is the highest in the world.</p>\n<p>But it is not just the numbers of people being tested that is unusual about Iceland’s approach.</p>\n<p>Unlike other countries, where people are only tested if they exhibit symptons of coronavirus or have come into contact with known spreaders, the country is testing thousands of people from the general population who don’t exhibit any symptoms of the virus whatsoever – helping to reveal information about the nature of the pathogen and its symptoms.</p>\n</blockquote>\n<p>This was also done in a city in Italy:</p>\n<blockquote>\n<p>In COVID-19, The University of Padua, Veneto Region and the Red Cross tested the populationof Vò, Italy, 3300 people, to establish the natural history of the virus, the transmission dynamicsand categories of risk. " they found >50 of those who tested positive to be asymptomatic” according to Professor Sergio Romagnani.</p>\n</blockquote>\n<p>The same question was asked on politics.SE:\n<a href=\"https://politics.stackexchange.com/q/50897/2231\">Has there been a random survey of a population for COVID-19?</a></p>\n<p>Update (2020-11-01): <a href=\"https://www.theguardian.com/world/2020/nov/01/half-slovakia-population-covid-tested-covid-one-day\" rel=\"nofollow noreferrer\">More than 2.5 million Slovaks took swab tests on Saturday, with 25,850 testing positive</a></p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 23065,
"author": "JonathanReez",
"author_id": 7314,
"author_profile": "https://health.stackexchange.com/users/7314",
"pm_score": 1,
"selected": false,
"text": "<p>Denmark did this recently and found that <a href=\"https://www.dr.dk/nyheder/indland/blodbanker-tester-om-donorer-har-haft-coronavirus\" rel=\"nofollow noreferrer\">2.7% of Danes living in the Capital region already have antibodies for the disease</a>. This isn't randomized per se as these samples are from people donating blood, but so far it's as good as it gets.</p>\n"
},
{
"answer_id": 23237,
"author": "Vladimir F Героям слава",
"author_id": 17979,
"author_profile": "https://health.stackexchange.com/users/17979",
"pm_score": 0,
"selected": false,
"text": "<p>It is being done. The Czech Republic is currently preparing such a study }to begin on the 20th April) to find out the number of asymptomatic patients to better predict the future evolution of the number of infected people. A bit older source in English <a href=\"https://news.expats.cz/coronavirus-in-the-czech-republic/czech-covid-19-central-control-team-plans-blanket-testing-in-sample-of-prague-population/\" rel=\"nofollow noreferrer\">https://news.expats.cz/coronavirus-in-the-czech-republic/czech-covid-19-central-control-team-plans-blanket-testing-in-sample-of-prague-population/</a> Much more updated information exists in Czech <a href=\"https://www.seznamzpravy.cz/clanek/prazdniny-podle-prymuly-v-ceskem-hotelu-s-vylety-po-hradech-a-bez-festivalu-99893\" rel=\"nofollow noreferrer\">https://www.seznamzpravy.cz/clanek/prazdniny-podle-prymuly-v-ceskem-hotelu-s-vylety-po-hradech-a-bez-festivalu-99893</a></p>\n\n<p>\"Testování vzorku 17 tisíc lidí v České republice na protilátky proti koronaviru začne v pondělí 20. dubna, do dalšího pondělí budeme znát výsledky.\" \"Testing of the sample of 17 thousand people in the Czech Republic for antigens against coronavirus will begin on Monday 20th April. By the next Monday we will know the results.\"</p>\n"
},
{
"answer_id": 24375,
"author": "curiousdannii",
"author_id": 11080,
"author_profile": "https://health.stackexchange.com/users/11080",
"pm_score": 1,
"selected": false,
"text": "<p>One technique that is also being trialled is <a href=\"https://www.csiro.au/en/News/News-releases/2020/Australian-researchers-trace-sewage-for-early-warning-COVID-19-spread\" rel=\"nofollow noreferrer\">testing wastewater/sewerage</a> for RNA from the SARS-CoV2 virus. This won't help you identify who has the virus, but it could inform a city that had previously eliminated the virus that someone has brought the virus back again.</p>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21700",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18008/"
] |
21,716 | <p>I don't own a working bike, but I do have a bike-sharing system membership. My city's bike-sharing system has many stations. I can borrow a bike and ride it to any other station.</p>
<p>There's currently a worldwide pandemic caused by the SARS-CoV-2 novel coronavirus. So far, only 27 people in my country have died from confirmed COVID-19 cases. <a href="https://www.canada.ca/en/public-health/services/diseases/2019-novel-coronavirus-infection.html" rel="nofollow noreferrer">(Source.)</a> Unfortunately, infectious diseases tend to spread exponentially, at least at first. <a href="https://www.wired.com/story/the-promising-math-behind-flattening-the-curve/" rel="nofollow noreferrer">(Source.)</a></p>
<p>During the COVID-19 pandemic, is it safe for me to use bike-sharing or bike-rental services? If so, must I follow any special safety precautions?</p>
| [
{
"answer_id": 21717,
"author": "unforgettableidSupportsMonica",
"author_id": 575,
"author_profile": "https://health.stackexchange.com/users/575",
"pm_score": 2,
"selected": false,
"text": "<p>This answer was written on Mar. 25; things can change quickly. By the time you read this answer, it may or may not still be correct.</p>\n\n<h1>Summary</h1>\n\n<ul>\n<li>Bike sharing is probably <strong>safe and healthy</strong>, as long as you take certain <strong>hygiene</strong> and <strong>disinfection</strong> precautions, as explained in later sections.</li>\n<li><strong>Don't ride when sick.</strong></li>\n<li>Exercise, in moderation, may <strong>strengthen the immune system</strong>.</li>\n<li>Sun exposure may help you synthesize <strong>vitamin D</strong>. It's possible that this vitamin somewhat <strong>helps protect against COVID-19</strong>.</li>\n</ul>\n\n<h1>Introduction</h1>\n\n<p>It's probably safe and healthy to use bike-sharing during the COVID-19 pandemic — as long as you take some simple precautions.</p>\n\n<p>If you take these precautions, bike-sharing is probably safer than public transit during the pandemic. <a href=\"https://www.consumerreports.org/electric-scooters/avoid-coronavirus-when-riding-a-rented-electric-scooter/\" rel=\"nofollow noreferrer\">(Source.)</a></p>\n\n<p>Please note: If you're sick, please don't use bike sharing. Please use your own car or bike. Or, better yet, please stay home. <a href=\"https://www.mobibikes.ca/en/news/covid-19-updates\" rel=\"nofollow noreferrer\">(Source.)</a></p>\n\n<h1>Hygiene</h1>\n\n<ul>\n<li>After riding, wash your hands for 20 seconds with soap and water. <a href=\"https://www.bicycling.com/news/a31469228/cycling-during-coronavirus/\" rel=\"nofollow noreferrer\">(Source.)</a></li>\n<li>If you can't access soap or water, carry and use hand sanitizer instead.</li>\n</ul>\n\n<h1>Disinfecting handlebars</h1>\n\n<p>You might have thought it unnecessary to disinfect handlebars, for three reasons.</p>\n\n<ul>\n<li>The CDC <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/prepare/transmission.html\" rel=\"nofollow noreferrer\">writes</a>: \"It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes. But this is not thought to be the main way the virus spreads.\"</li>\n<li>On stainless steel, coronavirus particles can survive for two days, but virus titers start to plummet after just four hours. <a href=\"https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/\" rel=\"nofollow noreferrer\">(Source.)</a></li>\n<li>Ultraviolet (UV) light from the sun seems to destroy coronaviruses. <a href=\"https://www.sciencemag.org/news/2020/03/does-disinfecting-surfaces-really-prevent-spread-coronavirus\" rel=\"nofollow noreferrer\">(Source.)</a></li>\n</ul>\n\n<p>However, during the pandemic, <a href=\"https://www.consumerreports.org/electric-scooters/avoid-coronavirus-when-riding-a-rented-electric-scooter/\" rel=\"nofollow noreferrer\">various</a> <a href=\"https://www.bicycling.com/news/a31469228/cycling-during-coronavirus/\" rel=\"nofollow noreferrer\">experts</a> do recommend that you disinfect bike-share bike handlebars and brake levers. If a sick person used a bike right before you, they might have left their germs on the handlebars; disinfection can kill these germs. <a href=\"https://www.bicycling.com/news/a31469228/cycling-during-coronavirus/\" rel=\"nofollow noreferrer\">(Source.)</a></p>\n\n<p>70% rubbing alcohol solution is probably a good disinfectant to use here.</p>\n\n<ul>\n<li>At home:\n\n<ul>\n<li>Dampen a clean rag, or some paper towels, with 70% rubbing alcohol solution.</li>\n<li>Store the result an air-tight bag, so that the alcohol doesn't evaporate.</li>\n</ul></li>\n<li>Later, at the bike-share station:\n\n<ul>\n<li>Dampen the handlebars and brake levers with the solution. Let them stay damp for at least 30 seconds.</li>\n</ul></li>\n</ul>\n\n<p>In theory, alcohol probably shouldn't damage most rubber items. <a href=\"https://chemistry.stackexchange.com/questions/1092/will-alcohol-or-soap-damage-plastic-or-rubber#1095\">(Source.)</a> But please see the comments on this post.</p>\n\n<p>Disinfecting wipes containing benzalkonium chloride (e.g. Lysol wipes) are another option. Benzalkonium chloride <a href=\"https://aem.asm.org/content/84/17/e01201-18\" rel=\"nofollow noreferrer\">may promote antibiotic resistance</a> and <a href=\"https://aem.asm.org/content/85/13/e00377-19\" rel=\"nofollow noreferrer\">is toxic to fish</a>. If you do use Lysol wipes, wash your hands after use and before eating.</p>\n\n<p>If there are shortages of disinfecting wipes or rubbing alcohol in your city: Please consider leaving these items for sick people who truly need them. Instead, please avoid touching your face, and wash your hands after riding.</p>\n\n<h1>Exercise may strengthen the immune system</h1>\n\n<p>The research literature suggests that exercise, if done in moderation, probably strengthens the immune system. <a href=\"https://doi.org/10.1371/journal.pone.0002108\" rel=\"nofollow noreferrer\">(Source.)</a> During a pandemic, experts recommend against exercising in crowded spaces, or beyond the point of exhaustion, or when feeling flu-like symptoms. <a href=\"https://www.marketwatch.com/story/how-much-exercise-is-ok-during-the-coronavirus-pandemic-whats-too-risky-2020-03-23\" rel=\"nofollow noreferrer\">(Source.)</a></p>\n\n<h1>Sun exposure may protect against COVID-19</h1>\n\n<p>When your skin is exposed to moderate amounts of sunlight, it may synthesize vitamin D. (Don't get sunburned; this <a href=\"https://www.healthline.com/health-news/heres-how-much-damage-a-really-bad-sunburn-can-do\" rel=\"nofollow noreferrer\">increases</a> your risk of skin cancer.) Getting enough vitamin D may reduce, but not eliminate, your risk of catching COVID-19. (Source: <a href=\"https://www.youtube.com/watch?v=gmqgGwT6bw0\" rel=\"nofollow noreferrer\">a MedCram video</a> citing <a href=\"https://doi.org/10.1136/bmj.i6583\" rel=\"nofollow noreferrer\">a BMJ meta-analysis</a>. Please see also <a href=\"https://www.bmj.com/company/newsroom/vitamin-d-supplements-acute-respiratory-infections/\" rel=\"nofollow noreferrer\">this BMJ press release</a> and <a href=\"https://www.bmj.com/content/368/bmj.m810/rr-9\" rel=\"nofollow noreferrer\">this post</a>.) Regular outdoor exercise may help you to get more sun and to synthesize more vitamin D.</p>\n\n<p>There are other ways to get vitamin D, such as from daily pills; but the details are beyond the scope of this post.</p>\n\n<h1>Notes</h1>\n\n<p>I'm not a doctor. This thread is for educational purposes only; it is not intended as a substitute for personalized advice from a doctor.</p>\n"
},
{
"answer_id": 21718,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>The latest data suggests virus can be recovered from surfaces at <a href=\"https://medicalsciences.stackexchange.com/questions/21655/how-long-can-sars-cov-2-persist-on-surfaces/21656#21656\">17 days</a></p>\n\n<p>I suggest spraying everything with a <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/prepare/cleaning-disinfection.html\" rel=\"nofollow noreferrer\">bleach</a> solution which has also been recommended by the CDC. That should disable the virus.</p>\n"
}
] | 2020/03/25 | [
"https://health.stackexchange.com/questions/21716",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/575/"
] |
21,721 | <p>I know that there's no immune response/adaptation of some (relatively) new viruses like HIV for which it's <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253032/" rel="nofollow noreferrer">estimated</a> that it would take at least 32,000 years for humans to develop a non-pathogenic response similar to that that some monkeys have to SIV. </p>
<p>But for more "run of the mill" viruses like new strains of influenza etc., do doses below the <a href="https://link.springer.com/article/10.1007/s12560-011-9056-7" rel="nofollow noreferrer">minimum infective dose</a> (MID) sometimes act like a vaccine, i.e triggering immune system adaptation that later helps preventing a pathogenic response to a higher dose (above MID)?</p>
| [
{
"answer_id": 21738,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>There are clearly people who have antibodies to viruses such as SARS-CoV-2 who have no history of clinical symptoms. Presumably, they have been exposed to a low viral load which has been sufficient to trigger an immune response without the virus infecting sufficient cells to cause symptoms.</p>\n<p>That is why they are saying that you don't need testing if you have been closer than 2 m to an infected person but have stayed there less than 10-15 minutes ( depending on the hospital issuing that information ).</p>\n<blockquote>\n<p>Close contact can occur while caring for a patient, including:</p>\n<p>being within approximately 6 feet (2 meters) of a patient with COVID-19 for a prolonged period of time.</p>\n<p>having direct contact with infectious secretions from a patient with COVID-19. Infectious secretions may include sputum, serum, blood, and respiratory droplets.\nIf close contact occurs while not wearing all recommended PPE, healthcare personnel may be at risk of infection.</p>\n</blockquote>\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/caring-for-patients.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/hcp/caring-for-patients.html</a></p>\n"
},
{
"answer_id": 21740,
"author": "not2qubit",
"author_id": 17628,
"author_profile": "https://health.stackexchange.com/users/17628",
"pm_score": -1,
"selected": false,
"text": "<p>The answer is <strong>NO</strong>. It only take one successful viroid particle to start an infection. Then you can always argue about how many particles you need to breath in, in order to ensure (<em>statistically</em>) that one sticks to your cellular lining and membrane to actually start the infection process. That's a different question.</p>\n"
}
] | 2020/03/26 | [
"https://health.stackexchange.com/questions/21721",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/10980/"
] |
21,744 | <p>This page <a href="https://www.scripps.edu/newsandviews/e_20060213/bleach.html" rel="noreferrer">Bleach</a> claims </p>
<blockquote>
<p>Bleach is more effective at killing germs when diluted than when used
straight out of the bottle.</p>
</blockquote>
<p>this other page (Spanish) <a href="http://www.prensa.mendoza.gov.ar/coronavirus-alcohol-y-lavandina-son-mas-efectivos-si-se-diluyen-en-agua/" rel="noreferrer">Alcohol and Bleach are more effective against Coronavirus diluted</a> claims the same</p>
<blockquote>
<p>Disinfectants like bleach and alcohol alter the virus structure and
prevent it from infecting us. Their effects will depend in the right
concentration</p>
</blockquote>
<p>But this other page, <a href="http://madsci.org/posts/archives/2013-01/1359009191.Cb.r.html" rel="noreferrer">Does liquid bleach has to be diluted to be effective as a virus killer?</a></p>
<p>claims </p>
<blockquote>
<p>So, all things being equal, undiluted bleach is more effective at
killing stubborn bacteria.</p>
</blockquote>
<p>I know, he says bacteria and not virus but, </p>
<blockquote>
<p>The data of viruses is a little more straight forward � viruses are
simply not cut out to defend against the bleach onslaught! A group of
scientists in New York studied the effects of very dilute
concentrations of bleach on the respiratory syncytial virus (RSV). A
tenfold dilution of bleach, which subsequently mixed with an equal
volume of RSV-containing medium (so in fact a twentyfold dilution)
eradicated all of the virus. A 100-fold dilution of bleach killed 100%
of the virus half of the time, and decreased the number of live viral
particles by greater than three logs in the other half of the tests.
This was all after five minutes of treatment.</p>
<p>So at least for viruses, you can probably dilute the bleach tenfold
without worrying too much about decreased antimicrobial activity.</p>
</blockquote>
<p>Personally, I don't find any logic why bleach would be more effective diluted, the opposite makes more sense to me. Is there any explanation for this to be so? Or it's just a wrong idea?</p>
| [
{
"answer_id": 21746,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Household bleach is usually at 5% concentration of sodium hypochlorite. Data from disinfection of other coronaviruses indicates that dilutions of 1:100 are still effective. Higher concentrations of bleach are difficult to manage as they release chlorine gas and are irritant to the mucous membranes, lungs and eyes.</p>\n\n<p>The bleach works as a potent oxidizer of the viral capsule and its contents. <strong>The oxidation relies on the amount of free chlorine molecules available</strong> which is why bleach solutions need to be made up and used in 24 hours as potency drops with time. Normal contact time is 30 seconds to 10 minutes for most microorganisms.</p>\n\n<p>So, this clearly means the higher the concentration the greater the efficacy, but also the greater the risk to the user on account of off gassing of chlorine gas.</p>\n\n<p>Alcohol is different. It requires water to enter the virus so that is why more than 95% concentrations are not recommended. But chlorine just needs to oxidize the outside of the virus to disrupt the viral capsule, and then that opens up the virus RNA which can then be oxidized.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK214356/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/books/NBK214356/</a></p>\n\n<p><a href=\"https://ehs.unc.edu/files/2015/09/coronavirus.pdf\" rel=\"nofollow noreferrer\">Use of 10% Ultra Chlorox regular bleach mixed with liquids containing virus to give 5% final concentration</a> to treat coronavirus waste.</p>\n\n<p><a href=\"https://cen.acs.org/biological-chemistry/infectious-disease/How-we-know-disinfectants-should-kill-the-COVID-19-coronavirus/98/web/2020/03\" rel=\"nofollow noreferrer\">https://cen.acs.org/biological-chemistry/infectious-disease/How-we-know-disinfectants-should-kill-the-COVID-19-coronavirus/98/web/2020/03</a></p>\n"
},
{
"answer_id": 21756,
"author": "PejoPhylo",
"author_id": 18031,
"author_profile": "https://health.stackexchange.com/users/18031",
"pm_score": 2,
"selected": false,
"text": "<p>The text does <strong>not</strong> say that <strong>more diluted</strong> bleach is <strong>more effective</strong> at killing viruses (or bacteria, or yeast, for that matter). </p>\n\n<p>I'm quoting:</p>\n\n<p>...A tenfold dilution of bleach, which subsequently mixed with an equal volume of RSV-containing medium (so in fact a <strong>twentyfold dilution</strong>) <strong>eradicated all of the virus</strong>. A <strong>100-fold dilution</strong> of bleach <strong>killed 100% of the virus half of the time</strong>, and <strong>decreased the number of live viral particles by greater than three logs in the other half of the tests</strong>. This was all after five minutes of treatment...</p>\n\n<p>So a 20-fold dilution kills all virus always; a 100-fold dilution kills 100% of the virus 50% of the time and kills most of them in the other cases. </p>\n\n<p>I think form this we can conclude that more highly concentrated bleach is more deadly to viruses than more diluted bleach. </p>\n"
}
] | 2020/03/26 | [
"https://health.stackexchange.com/questions/21744",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7049/"
] |
21,762 | <p>Even CDC site does not seem to mention uv as a method of sterilization.</p>
<ol>
<li><p>The only authoritative source of uv disinfection of COVID type virus I found was in '<a href="https://www.ncbi.nlm.nih.gov/pubmed/14631830" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/14631830</a>'. But it does not mention the most effective wavelength or a duration. Can somebody point me in the right direction?</p></li>
<li><p>If 1 hour of appropriate UV exposure is sufficient to eradicate it, can head safety shields be reused after that period of time of exposure? I understand there might be limited # of cycles that polycarbonate shields can be reused, since the plastic will loose some transparency after repeated exposure.</p></li>
<li><p>Can UV exposure be used for face respiration soft masks (N95 or plain) for disinfection?</p></li>
</ol>
<p>If this has been covered here already - I'll remove.</p>
<p>EDIT1: Actually Franck's reference to <a href="https://medicalsciences.stackexchange.com/questions/21593/why-arent-we-sterilizing-n95-masks?noredirect=1&lq=1">Why aren't we sterilizing n95 masks?</a>
is relevant. Mark's answer does mention UV sterilization, but does not provide authoritative link/ref.</p>
<p>So, the other question of UV use for covid-19 sterilization of face shield is still open.</p>
| [
{
"answer_id": 21765,
"author": "user431378",
"author_id": 18042,
"author_profile": "https://health.stackexchange.com/users/18042",
"pm_score": 0,
"selected": false,
"text": "<p>There are <a href=\"https://www.crr.columbia.edu/research/using-power-light-preventing-airborne-spread-coronavirus-and-influenza-virus\" rel=\"nofollow noreferrer\">some reports</a> suggesting that UVC light IS effective</p>\n"
},
{
"answer_id": 21768,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 2,
"selected": true,
"text": "<p>From {1}:</p>\n<blockquote>\n<p>[The <a href=\"https://en.wikipedia.org/wiki/Coronavirus_disease_2019\" rel=\"nofollow noreferrer\">SARS-CoV-2 virus</a> virus] will be killed by UV, estimated survival in direct sunlight is 10% after 2–3h exposure</p>\n<ul>\n<li>90% of flu virus dies after 6h sunlight at spring equinox (3/21) at Bay Area latitude (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/17880524\" rel=\"nofollow noreferrer\">Pubmed 17880524</a>).</li>\n<li>Coronaviruses are 2–3x more sensitive to UV than flu virus (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16254359\" rel=\"nofollow noreferrer\">Pubmed 16254359</a>)</li>\n</ul>\n</blockquote>\n<p>Regarding:</p>\n<blockquote>\n<p>Can UV exposure be used for face respiration soft masks (N95 or plain) for disinfection?</p>\n</blockquote>\n<p>See <a href=\"https://medicalsciences.stackexchange.com/q/21593/43\">Why aren't we sterilizing n95 masks?</a></p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
},
{
"answer_id": 22871,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 0,
"selected": false,
"text": "<p>The inventor of the N95 filter material, Dr Peter Tsai, has said UV irradiation of the mask will destroy the electrostatic charge in the material rendering it much less effective. But then in this later interview he is less sure and says it needs to be tested as to whether the charge is affected.</p>\n\n<p><a href=\"https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-masks-against-covid-19/\" rel=\"nofollow noreferrer\">https://utrf.tennessee.edu/information-faqs-performance-protection-sterilization-of-masks-against-covid-19/</a></p>\n"
}
] | 2020/03/27 | [
"https://health.stackexchange.com/questions/21762",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18035/"
] |
21,767 | <p>It's been mentioned in <a href="https://medicalsciences.stackexchange.com/a/21729/43">another answer</a> that</p>
<blockquote>
<p>In COVID-19, The University of Padua, Veneto Region and the Red Cross tested the population of Vò, Italy, 3300 people, to establish the natural history of the virus, the transmission dynamics and categories of risk. " they found >50 of those who tested positive to be asymptomatic” according to Professor Sergio Romagnani.</p>
</blockquote>
<p>I'm aware that a Covid-19 prevalence study on the [entire population of the] Diamond Princess ship (3,711 passengers and crew) <a href="https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.10.2000180" rel="nofollow noreferrer">has been published</a> in <em>Eurosurveillance</em>. Has this comparable (in size) study on an entire Italian town been published somewhere?</p>
<p>(I see a later issue of <em>Eurosurveillance</em> has a <a href="https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.12.2000293" rel="nofollow noreferrer">larger study on Lombardy</a>, but it doesn't mention Vò specifically. Also, this latter issue has a <a href="https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.12.2000256" rel="nofollow noreferrer">2nd study</a> on the Diamond Princess.)</p>
| [
{
"answer_id": 21769,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 2,
"selected": false,
"text": "<p>As far I know, no. Only an open letter has been published so far:</p>\n\n<p><a href=\"https://corrierefiorentino.corriere.it/firenze/notizie/cronaca/20_marzo_15/dobbiamo-cambiare-rotta-ef23a500-669a-11ea-a40a-86d505f82a96.shtml\" rel=\"nofollow noreferrer\">https://corrierefiorentino.corriere.it/firenze/notizie/cronaca/20_marzo_15/dobbiamo-cambiare-rotta-ef23a500-669a-11ea-a40a-86d505f82a96.shtml</a></p>\n"
},
{
"answer_id": 21780,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>The data has also been discussed in this report</p>\n\n<blockquote>\n <p>Sergio Romagnani, a professor of clinical immunology at the University of Florence, has reported how blanket testing in a completely isolated village of roughly 3000 people in northern Italy saw the number of people with covid-19 symptoms fall by over 90% within 10 days.</p>\n</blockquote>\n\n<p>So by isolating those that were asymptomatic and testing positive to the virus, they dropped the symptomatic infection rate by 90%.</p>\n\n<p><a href=\"https://www.bmj.com/content/368/bmj.m1165\" rel=\"nofollow noreferrer\">https://www.bmj.com/content/368/bmj.m1165</a></p>\n"
},
{
"answer_id": 21781,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 0,
"selected": false,
"text": "<p>In a <em>Nature</em> roundup, the following (mid April) draft paper has been highlighted as the main scientific publication on that town/survey:</p>\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.04.17.20053157v1\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.17.20053157v1</a></p>\n<blockquote>\n<p>On the 21st of February 2020 a resident of the municipality of Vo, a small town near Padua, died of pneumonia due to SARS-CoV-2 infection. This was the first COVID-19 death detected in Italy since the emergence of SARS-CoV-2 in the Chinese city of Wuhan, Hubei province. In response, the regional authorities imposed the lockdown of the whole municipality for 14 days. <strong>We collected information on the demography, clinical presentation, hospitalization, contact network and presence of SARS-CoV-2 infection in nasopharyngeal swabs for 85.9% and 71.5% of the population of Vo at two consecutive time points. On the first survey, which was conducted around the time the town lockdown started, we found a prevalence of infection of 2.6% (95% confidence interval (CI) 2.1-3.3%). On the second survey, which was conducted at the end of the lockdown, we found a prevalence of 1.2% (95% CI 0.8-1.8%). <em>Notably, 43.2% (95% CI 32.2-54.7%) of the confirmed SARS-CoV-2 infections detected across the two surveys were asymptomatic.</em></strong> The mean serial interval was 6.9 days (95% CI 2.6-13.4). We found no statistically significant difference in the viral load (as measured by genome equivalents inferred from cycle threshold data) of symptomatic versus asymptomatic infections (p-values 0.6 and 0.2 for E and RdRp genes, respectively, Exact Wilcoxon-Mann-Whitney test). Contact tracing of the newly infected cases and transmission chain reconstruction revealed that most new infections in the second survey were infected in the community before the lockdown or from asymptomatic infections living in the same household. This study sheds new light on the frequency of asymptomatic SARS-CoV-2 infection and their infectivity (as measured by the viral load) and provides new insights into its transmission dynamics, the duration of viral load detectability and the efficacy of the implemented control measures.</p>\n</blockquote>\n<p>The 43% asymptomatic is a bit less than what was reported from the Princess, but it overlaps it in the 95% CI 32.2-54.7%.</p>\n<hr />\n<p>End or March answer, largely obsolete now, but leaving it for some press coverage:</p>\n<p>Also March 20 coverage <a href=\"https://www.theguardian.com/commentisfree/2020/mar/20/eradicated-coronavirus-mass-testing-covid-19-italy-vo\" rel=\"nofollow noreferrer\">in the Guardian</a>, which is of course not a science venue, but had even more details than even the BMJ coverage; the "opinion piece" in the Guardian was apparently written by the researchers/epidemiologists involved:</p>\n<blockquote>\n<p>in the last two weeks, a promising pilot study here has produced results that may be instructive for other countries trying to control coronavirus. Beginning on 6 March , along with researchers at the University of Padua and the Red Cross, we tested all residents of Vò, a town of 3,000 inhabitants near Venice – including those who did not have symptoms. This allowed us to quarantine people before they showed signs of infection and stop the further spread of coronavirus. In this way, we eradicated coronavirus in under 14 days. [...]</p>\n<p>Our experiment came to be by chance. The Italian authorities had a strong emotional reaction to news of the country’s first death – which was in Vò. The whole town was put into quarantine and every inhabitant was tested. The tests were processed by us at the University of Padua. [...]</p>\n<p>In the first round of testing, 89 people tested positive. In the second round, the number had dropped to six, who remained in isolation. In this way, we managed to eradicate coronavirus from Vò, achieving a 100% recovery rate for those previously infected while recording no further cases of transmission.</p>\n</blockquote>\n<p>Strong claims here. They also say/claim that</p>\n<blockquote>\n<p>asymptomatic or quasi-symptomatic subjects represent a good 70% of all virus-infected people</p>\n</blockquote>\n<p>referring to COVID-19.</p>\n<p>About the authors, the Guardian notes:</p>\n<blockquote>\n<p>Andrea Crisanti is professor of microbiology at the University of Padua; Antonio Cassone is a former director of the department of infectious diseases at the Italian institute of health.</p>\n</blockquote>\n<p>I guess I now know whose publications to look at (in the future).</p>\n<p>There's a longer interview with Crisanti <a href=\"https://www.cbc.ca/radio/asithappens/as-it-happens-tuesday-edition-1.5508052/how-one-italian-town-managed-to-stop-the-coronavirus-in-its-tracks-1.5508059\" rel=\"nofollow noreferrer\">on CBC.ca</a>. An intersting bit:</p>\n<blockquote>\n<p>I want to draw a comparison. If you remember the Diamond Princess. They started with few cases. They did the tests only to those [who] were symptomatic. So you develop a symptom, you test positive, you were taken out of the ship.</p>\n<p>But day by day, cases, if you remember, they increased up to more than 700. So in this way, they couldn't stop the disease. That couldn't stop the disease in spite of the fact that they were isolated, they were kind of quarantined. And the reason why they couldn't stop it is because the ship was full of asymptomatic people that [were] spreading the virus.</p>\n<p>Q: [When you started this in February], the protocol was that you tested people only if they … were returning from a foreign place, or from China, or if they had symptoms. ... You ignored that and went to everybody.</p>\n<p>Yeah, we ignored that because we weren't convinced that the disease was transmitted only by symptomatic individuals. We found this quite implausible. And so this is the reason why we tested everybody.</p>\n</blockquote>\n"
},
{
"answer_id": 24417,
"author": "Jonas Heidelberg",
"author_id": 19739,
"author_profile": "https://health.stackexchange.com/users/19739",
"pm_score": 2,
"selected": true,
"text": "<p>It took a while, but it has now been published in <strong>Nature</strong>:</p>\n<p><a href=\"https://www.nature.com/articles/s41586-020-2488-1\" rel=\"nofollow noreferrer\">"Suppression of a SARS-CoV-2 outbreak in the Italian municipality of Vo’"</a></p>\n<p>by Enrico Lavezzo, Elisa Franchin, […]Andrea Crisanti, Nature (2020). Published: 30 June 2020</p>\n<p>This seems to be the same content as the preprint linked and discussed by @Fizz in <a href=\"https://medicalsciences.stackexchange.com/a/21781/19739\">their answer</a>.</p>\n<p>Abstract</p>\n<blockquote>\n<p>On 21 February 2020, a resident of the municipality of Vo’, a small\ntown near Padua (Italy), died of pneumonia due to severe acute\nrespiratory syndrome coronavirus 2 (SARS-CoV-2) infection1. This was\nthe first coronavirus disease 19 (COVID-19)-related death detected in\nItaly since the detection of SARS-CoV-2 in the Chinese city of Wuhan,\nHubei province2. In response, the regional authorities imposed the\nlockdown of the whole municipality for 14 days3. Here we collected\ninformation on the demography, clinical presentation, hospitalization,\ncontact network and the presence of SARS-CoV-2 infection in\nnasopharyngeal swabs for 85.9% and 71.5% of the population of Vo’ at\ntwo consecutive time points. From the first survey, which was\nconducted around the time the town lockdown started, we found a\nprevalence of infection of 2.6% (95% confidence interval (CI):\n2.1–3.3%). From the second survey, which was conducted at the end of the lockdown, we found a prevalence of 1.2% (95% CI: 0.8–1.8%).\nNotably, 42.5% (95% CI: 31.5–54.6%) of the confirmed SARS-CoV-2\ninfections detected across the two surveys were asymptomatic (that is,\ndid not have symptoms at the time of swab testing and did not develop\nsymptoms afterwards). The mean serial interval was 7.2 days (95% CI:\n5.9–9.6). We found no statistically significant difference in the viral load of symptomatic versus asymptomatic infections (P = 0.62 and\n0.74 for E and RdRp genes, respectively, exact Wilcoxon–Mann–Whitney test). This study sheds light on the frequency of asymptomatic\nSARS-CoV-2 infection, their infectivity (as measured by the viral\nload) and provides insights into its transmission dynamics and the\nefficacy of the implemented control measures.</p>\n</blockquote>\n"
}
] | 2020/03/27 | [
"https://health.stackexchange.com/questions/21767",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/10980/"
] |
21,794 | <p>I have been preparing bleach disinfectant lately in a spray bottle and have been spraying on my couch, door mat, door knots, etc...
I don't rinse it... So I assume there is bleach residue left after evaporation. Is it safe to leave the residue?</p>
<p>I felt some very mild burn like feeling on my arms when putting my arms on my couch lately; I don't know if this is some kind of placebo effect or if it is real.</p>
| [
{
"answer_id": 22791,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<blockquote>\n <p> In its manufacturing process, hypochlorite bleach begins as salt and water. After use, the compound breaks down mainly into salt and water during or quickly after use.</p>\n</blockquote>\n\n<p>So it's table salt left behind, NaCl, as well as the similar NaClO3 and NaOCl.</p>\n\n<p><a href=\"https://www.infectioncontroltoday.com/environmental-hygiene/dispelling-myths-about-bleach-odors\" rel=\"nofollow noreferrer\">https://www.infectioncontroltoday.com/environmental-hygiene/dispelling-myths-about-bleach-odors</a></p>\n"
},
{
"answer_id": 22800,
"author": "timpin",
"author_id": 19056,
"author_profile": "https://health.stackexchange.com/users/19056",
"pm_score": 2,
"selected": false,
"text": "<p>In the UK most bleach contains NaOH and NaClO. The hypochlorite (which is the bit that does the bleaching) breaks down to common salt and free oxygen. The hydroxide doesn't. So it's possible you are experiencing some kind of chemical burn.</p>\n"
}
] | 2020/03/28 | [
"https://health.stackexchange.com/questions/21794",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/18052/"
] |
22,793 | <p>In this <a href="https://www.youtube.com/watch?v=8q6nM1bT9o0" rel="nofollow noreferrer">YouTube video</a> min 0:32, Dr. Samir Gupta, says </p>
<blockquote>
<p>It typically would last for 12 to 18 months</p>
</blockquote>
<p>In <em><a href="https://www.theatlantic.com/health/archive/2020/03/how-will-coronavirus-end/608719/" rel="nofollow noreferrer">How the Pandemic Will End</a></em> in the <strong>ll. The Endgame</strong> section:</p>
<blockquote>
<p>No matter which strategy is faster, Berkley and others estimate that it will take 12 to 18 months to develop a proven vaccine, and then longer still to make it, ship it, and inject it into people’s arms.</p>
</blockquote>
<p>Why?</p>
| [
{
"answer_id": 22898,
"author": "WinEunuuchs2Unix",
"author_id": 17751,
"author_profile": "https://health.stackexchange.com/users/17751",
"pm_score": 1,
"selected": false,
"text": "<p>The last flu pandemic (<a href=\"https://en.wikipedia.org/wiki/Spanish_flu\" rel=\"nofollow noreferrer\">Spanish Flu</a>), lasted from January 1918 until December 1920. If my human calculator is correct that is three years. So 1 to 1.5 years seems almost optimistic. </p>\n\n<p><a href=\"https://www.cnbc.com/2020/03/11/top-federal-health-official-says-coronavirus-outbreak-is-going-to-get-worse-in-the-us.html\" rel=\"nofollow noreferrer\">Top US health official says the coronavirus is 10 times ‘more lethal’ than the seasonal flu</a> would be 500 million assuming Spanish Flu was 50 million and Novel Coronavirus is 10 times worse. On the other hand maybe the Spanish Flu was just like the Coronavirus, we simply do not know. That said the experts \"guesstimate\" of 12 to 18 months might be too pessimistic like you hope or too optimistic compared to the Spanish Flu.</p>\n\n<p>The good news is if every nation could be like China and attempt to catch every single case the virus will end. </p>\n\n<p>The bad news is <a href=\"https://globalnews.ca/news/6756926/coronavirus-77-alberta-health-care-workers-infected-with-new-coronavirus/\" rel=\"nofollow noreferrer\">more than 10% of infections</a> in Alberta (where I live) are healthcare workers who spread it at home and when they go shopping. In the old days they lived in <a href=\"https://www.cbc.ca/news/canada/edmonton/health-region-renovates-residences-to-attract-nurses-1.690579\" rel=\"nofollow noreferrer\">hospital residence</a>. In efforts to make things better we are unwittingly making them worse.</p>\n\n<p>China on the other hand took <a href=\"https://www.cnbc.com/2020/02/22/coronavirus-latest-updates-china-covid-19.html\" rel=\"nofollow noreferrer\">seven idled cruise ships</a> and moored them for healthcare workers to live in comfort. It's not just Alberta that has healthcare transmission, <a href=\"https://abcnews.go.com/Health/wireStory/collapsing-virus-pummels-medics-spain-italy-69789413\" rel=\"nofollow noreferrer\">13.6% of Spain's infected</a> are healthcare professionals and <a href=\"https://www.newsweek.com/more-50-doctors-italy-have-now-died-coronavirus-1494781\" rel=\"nofollow noreferrer\">51 doctors have died in Italy</a>.</p>\n\n<p>The moral of the story is if you stop the spread you stop the virus. If you don't stop the spread you accelerate the virus.</p>\n\n<p>Finally consider the current strategy is to slow the spread, not to test for the spread. (I can provide sources if desired). This means it could lengthen the disease duration until herd immunity, unless a miracle wipes it out.</p>\n\n<hr>\n\n<p>April 3, 2020 Update</p>\n\n<p>Today Ontario said the <a href=\"https://globalnews.ca/news/6773486/ontario-coronavirus-covid19-number-modelling/\" rel=\"nofollow noreferrer\">Pandemic would last 2 years</a> but praised themselves for reducing 5,000 deaths to 1,600 deaths for the month of April.. But of course it was all fiction because it was based on \"what ifs\".</p>\n\n<p>Personally I hope we can wrap things up with an action plan in 30 days but barring no plan I suspect 3 years and not 2 years like Ontario forecasts or 1 to 1.5 years like OP forecasts.</p>\n\n<p>Sadly it appears no one is in charge.</p>\n"
},
{
"answer_id": 23506,
"author": "Peter",
"author_id": 19523,
"author_profile": "https://health.stackexchange.com/users/19523",
"pm_score": 2,
"selected": false,
"text": "<p>Under the assumption that infected people become permanently immune and stop transmitting the disease, the virus will eventually just run out of people to infect. Currently the <a href=\"https://www.telegraph.co.uk/global-health/science-and-disease/what-r-value-means-help-lift-coronavirus-lockdown-uk/\" rel=\"nofollow noreferrer\">\"R\" value</a>, which measures the average number of people that an infected person contaminates, is somewhere around 2.5 if people behave normally. R below 1 means there will be less and less infections until there are no more infected.</p>\n\n<p>In this graph of the spread in Germany from February to early May (<a href=\"https://www.worldometers.info/coronavirus/country/germany/\" rel=\"nofollow noreferrer\">source</a>) you can observe R > 1 in the left half and R < 1 in the right half:</p>\n\n<p><a href=\"https://i.stack.imgur.com/Bg3Mul.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Bg3Mul.png\" alt=\"source: https://www.worldometers.info/coronavirus/#countries\"></a></p>\n\n<p>There are 3 ways this can happen:</p>\n\n<ul>\n<li><p>A: If a significant percentage of the population catches the disease and becomes immune, the R factor will drop (if you are infected and half the people you would have infected are immune, you will infect half as many people as you otherwise would have infected, thus R is now cut in half). In some countries <a href=\"https://www.theguardian.com/science/occams-corner/2014/may/15/real-reason-british-public-chickenpox-vaccine-shingles\" rel=\"nofollow noreferrer\">this approach is practiced against chickenpox</a>.</p></li>\n<li><p>B: <a href=\"https://www.historyofvaccines.org/content/herd-immunity-0\" rel=\"nofollow noreferrer\">Vaccination</a> can provide herd immunity just like A, but requires a safe vaccine without side effects, that must be manufactured in massive quantities. It's <a href=\"https://www.bbc.com/news/health-51665497\" rel=\"nofollow noreferrer\">estimated that the development of such a vaccine will take 12-18 months</a>, but this time frame isn't guaranteed.</p></li>\n<li><p>C: Temporary changes to society (contact tracing, quarantines, social distancing, masks), or the environment (heat, humidity) can significantly modify the R factor. If the changes push the R factor below 1 and are sustained until the virus is gone, this will end the pandemic. <a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30129-8/fulltext\" rel=\"nofollow noreferrer\">This is what stopped SARS</a>.</p></li>\n</ul>\n\n<p>In countries that practice C to some extent, A is not going to happen this year. Because there is no consensus among countries to eradicate the virus by means of C, C isn't going to happen in the foreseeable future. Which leaves B as the most probable outcome at this time. And B is widely reported in the news media to be ready in 12-18 months time.</p>\n\n<p>Things will change when there are significant changes to the projected timeline for B.</p>\n"
}
] | 2020/03/28 | [
"https://health.stackexchange.com/questions/22793",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
22,796 | <p>Reading numerous news articles about COVID-19, I got confused as to what is its main transmission route. In particular, I am confused as to whether it is</p>
<ul>
<li>direct landing of respiratory droplets in mouths and noses,</li>
<li>contaminated surfaces,</li>
<li>aerosols (i.e., suspensions of the virus in the air rather than respiratory droplets quickly landing in mouths or noses or on surfaces), or</li>
<li>something else.</li>
</ul>
<p>On the one hand, the website of the Centers for Disease Control and Prevention (CDC) says that contaminated surfaces are not thought to be the main transmission route:</p>
<blockquote>
<p>It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes, but this is not thought to be the main way the virus spreads. (<a href="https://www.cdc.gov/coronavirus/2019-ncov/prepare/transmission.html" rel="noreferrer">Link</a>)</p>
</blockquote>
<p>The same website appears to suggest that the main transmission route is direct landing of respiratory droplets in mouths and noses:</p>
<blockquote>
<p>The virus is thought to spread mainly from person-to-person.</p>
<ul>
<li><p>Between people who are in close contact with one another (within about 6 feet).</p>
</li>
<li><p>Through respiratory droplets produced when an infected person coughs or sneezes.</p>
</li>
</ul>
<p>These droplets can land in the mouths or noses of people who are nearby or possibly be inhaled into the lungs.</p>
</blockquote>
<p>On the other hand, the World Health Organization (WHO), like many other agencies, puts the main emphasis on washing hands. Here is the WHO's first and foremost piece of advice on how to prevent getting infected with the virus:</p>
<blockquote>
<p>Regularly and thoroughly clean your hands with an alcohol-based hand rub or wash them with soap and water. Why? Washing your hands with soap and water or using alcohol-based hand rub kills viruses that may be on your hands. (<a href="https://www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public" rel="noreferrer">Link</a>)</p>
</blockquote>
<p>Social distancing is mentioned on that webpage only as a second piece of advice, and, furthermore, the webpage implies that it is safe to approach coughing people as close as 1 meter away:</p>
<blockquote>
<p>Maintain at least 1 metre (3 feet) distance between yourself and anyone who is coughing or sneezing.</p>
</blockquote>
<p>Furthermore, I found an article saying that the virus wasn't detected in the air of hospital rooms with COVID-19 patients, but was detected on surfaces:</p>
<blockquote>
<p>When researchers in Singapore tested the air in the rooms of three Covid-19 patients, they found no virus particles on cleaned surfaces or in the air even when they took samples on days the patients were symptomatic and presumably shedding virus into the air, they reported this month in the Journal of the American Medical Association. In the room of the third patient, who shed more virus, virus particles were present on ventilation fans and numerous surfaces — but all air samples were negative. (<a href="https://www.statnews.com/2020/03/16/coronavirus-can-become-aerosol-doesnt-mean-doomed" rel="noreferrer">Link</a>)</p>
</blockquote>
<p>But the same article also says that Chinese researchers found COVID-19 aerosols near patients' toilets.</p>
<p>My question: Actually what is the main way COVID-19 spreads?</p>
| [
{
"answer_id": 22799,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 5,
"selected": true,
"text": "<p>The confusion exists because there are conflicting pronouncements from various authoritative sources but also conflicting pronouncements from the same authority.</p>\n\n<p>Covid-19 is a respiratory infection spread by droplets that can be aerosolized (nuclear droplets) in certain situations such as by flushing toilets or in certain medical procedures such as intubation. However, it reaches the air it contaminates surfaces and this allows for the infection to be caught through the eyes nose and mouth with the virus being transferred from the hand.</p>\n\n<p>The data from Singapore and Taiwan show that handwashing and social distancing are successful in preventing disease transmission. However, if social distancing is not rigorously enforced then you will need to wear a mask. The head of the Chinese CDC, Dr George Gao, has recommended that everyone wear a mask which is advice that contradicts most countries health ministries. This is so that the infected are not shedding as many viral particles into the environment. His advice is based on the fact that there is a high degree of asymptomatic infection in the community and these people are spreading the virus by droplets just by talking and exhaling. The contrary advice is because they feel users are wearing masks to protect themselves, and, in the absence of training, they are almost certainly less effective at providing protection. But trained users have a similar degree of protection with both surgical masks and N95 masks.</p>\n\n<p>So the main way of disease transmission is by respiratory droplet. But the fact that health workers, NYPD officers (currently over 500) and others are getting infected wearing masks points to surface contamination as the second main mode of infection, or, possibly lack of training in wearing the masks and/or poor hand washing, or, that aerosol transmission is indeed important.</p>\n\n<p><a href=\"https://www.sciencemag.org/news/2020/03/not-wearing-masks-protect-against-coronavirus-big-mistake-top-chinese-scientist-says#\" rel=\"nofollow noreferrer\">https://www.sciencemag.org/news/2020/03/not-wearing-masks-protect-against-coronavirus-big-mistake-top-chinese-scientist-says#</a></p>\n\n<p><a href=\"https://www.bostonglobe.com/2020/03/19/opinion/guidance-against-wearing-masks-coronavirus-is-wrong-you-should-cover-your-face/\" rel=\"nofollow noreferrer\">https://www.bostonglobe.com/2020/03/19/opinion/guidance-against-wearing-masks-coronavirus-is-wrong-you-should-cover-your-face/</a></p>\n"
},
{
"answer_id": 24307,
"author": "chongman",
"author_id": 19917,
"author_profile": "https://health.stackexchange.com/users/19917",
"pm_score": 2,
"selected": false,
"text": "<p>The main way COVID19 spreads (according to experts) is either <strong>droplets</strong> (short distance, <6ft. short duration, <5 seconds from emission) OR <strong>aerosols</strong> (long distance, 20ft+, whole room. long duration, >60minutes)</p>\n<p>Unfortunately, as of July 2020, we still don't know.</p>\n<p>WHO has updated their modes of transmission: <a href=\"https://www.who.int/news-room/commentaries/detail/transmission-of-sars-cov-2-implications-for-infection-prevention-precautions\" rel=\"nofollow noreferrer\">https://www.who.int/news-room/commentaries/detail/transmission-of-sars-cov-2-implications-for-infection-prevention-precautions</a></p>\n<p>July 9.</p>\n<p>They say there isn't hard evidence of for <code>H1: aerosol>droplet</code>, so they are sticking to their null hypothesis <code>H0: droplet > aerosol</code>. However, the detractors say there isn't hard evidence for <code>H0</code> either.</p>\n<p>After talking to several doctors and chemists and reading about 5-10 articles, my conclusion (i.e. educated guess) is that it's about a tie between droplets and aerosols.</p>\n<p>The key details can be found in the OPTIONAL section of this 10 minute science communication piece (<a href=\"http://tinyurl.com/covid3particles\" rel=\"nofollow noreferrer\">http://tinyurl.com/covid3particles</a>).</p>\n<h3>It's endogenous -- the main mode of transmission depends on what protective practices are in place.</h3>\n<ul>\n<li>If you 100% protect against droplets, then aerosols will probably be the main mode.</li>\n<li>If you use no protection, then droplets are probably the main mode.</li>\n<li>If you are never in someone else's room (except after airing it out), then fomites (surfaces) might be the main route. But only because you eliminated everything else.</li>\n</ul>\n<p>You can also look at the CHAIN model. (tinyurl.com/CHAINmodel) especially the end of the article.</p>\n<h3>Surfaces and soap are, unfortunately, not foolproof/complete protection.</h3>\n<p>There are many people who wash their hand religiously. They still can get sick. So, we know that perfect hand washing won't stop it.</p>\n<p>PS: Agree with @Graham's answer</p>\n"
}
] | 2020/03/28 | [
"https://health.stackexchange.com/questions/22796",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19055/"
] |
22,813 | <p>In this <a href="https://www.health.harvard.edu/diseases-and-conditions/covid-19-basics" rel="nofollow noreferrer">link</a>, in the section <em>How long is it between when a person is exposed to the virus and when they start showing symptoms?</em> mentions</p>
<blockquote>
<p>Recently published research found that on average, the time from exposure to symptom onset (known as the incubation period) is about five to six days. However, studies have shown that symptoms could appear as soon as three days after exposure to as long as 13 days later. </p>
</blockquote>
<p>I have seen this other <a href="https://www.worldometers.info/coronavirus/coronavirus-incubation-period/" rel="nofollow noreferrer">link</a> where we can see that the incubation could vary from 0 to 27 days.</p>
<p>Now <a href="https://www.thesun.co.uk/news/11193056/how-to-treat-coronavirus/" rel="nofollow noreferrer">here</a> mentions how long it last if you have got it, which says its 22 days.</p>
<p><a href="https://i.stack.imgur.com/DtsNk.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/DtsNk.jpg" alt="enter image description here"></a></p>
<p>If the Covid-19 goes after 22 days, then could be possible that one gets it and showing no symptoms at all, not even feeling bad at all, the whole time on the Covid-19 process? </p>
<p>If yes, is there a way to know that you already had it?</p>
<p>Thanks in advance. </p>
| [
{
"answer_id": 22815,
"author": "Thomas",
"author_id": 19070,
"author_profile": "https://health.stackexchange.com/users/19070",
"pm_score": 2,
"selected": false,
"text": "<p>Yes, it is possible to have no symptoms and be infected, various sources, e. g. <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/32179137\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/32179137</a>.</p>\n\n<p>As for testing after 'clearing the infection', this would be what a serological scarring test would look for, e. g.: </p>\n\n<ul>\n<li><a href=\"https://www.statnews.com/2020/03/27/serological-tests-reveal-immune-coronavirus/\" rel=\"nofollow noreferrer\">https://www.statnews.com/2020/03/27/serological-tests-reveal-immune-coronavirus/</a></li>\n<li><a href=\"https://www.contagionlive.com/news/florian-krammer-phd-discusses-new-coronavirus-serological-assay\" rel=\"nofollow noreferrer\">https://www.contagionlive.com/news/florian-krammer-phd-discusses-new-coronavirus-serological-assay</a>.</li>\n</ul>\n"
},
{
"answer_id": 22817,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 1,
"selected": false,
"text": "<p>From {1}:</p>\n\n<blockquote>\n <p>In COVID-19, The University of Padua, Veneto Region and the Red Cross tested the populationof Vò, Italy, 3300 people, to establish the natural history of the virus, the transmission dynamicsand categories of risk. \"<strong>they found >50 of those who tested positive to be asymptomatic</strong>” according to Professor Sergio Romagnani. </p>\n</blockquote>\n\n<p>FYI: <a href=\"https://medicalsciences.stackexchange.com/q/21723/43\">How can one predict whether an individual infected with the SARS-CoV-2 virus will be asymptomatic?</a></p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n"
}
] | 2020/03/29 | [
"https://health.stackexchange.com/questions/22813",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
22,823 | <p>A model from the University of Washington predicts that new COVID-19 cases and deaths will drop to zero shortly after July 1:
<a href="https://covid19.healthdata.org/projections" rel="nofollow noreferrer">https://covid19.healthdata.org/projections</a></p>
<p>I assume that's because the virus runs out of new people to infect, if people who have had it before can't get it again, and if we assume it doesn't mutate.</p>
<p>But then I don't understand what is the point of developing a vaccine that won't be ready for 12-18 months anyway. What does it achieve, if all of the deaths from COVID-19 will have already occurred by this July? And if the reason the deaths level off in July is because so many people have the antibodies by then that we have herd immunity, then who is the vaccine for?</p>
<p>I understand the virus could mutate so that people who have antibodies from the current version will not be immune. But if the eventual vaccine is going to be based on the current version, doesn't that mean that if it mutates, people who get the vaccine won't be immune either?</p>
<p>I can think of some possible answers that would make sense (by which I only mean they would make logical sense as an answer; I don't mean that they make scientific sense):</p>
<p>1) The UW model represents a rogue view and people are working on the vaccine because they don't think it's correct.</p>
<p>2) Even if we achieve herd immunity at 75%, the vaccine is to protect the remaining 25%. (I would call this a special case of #1, contradicting the UW model, because it seems to assume there is a significant number of preventable deaths lying to the right of July 2020.)</p>
<p>3) People who get the SARS-CoV-2 virus will only be immune to the current version, but the vaccine can be developed in a way that it might also provide immunity against other mutated versions.</p>
<p>4) The vaccine is not going to be ready in time to make a difference against the current SARS-CoV-2, but we're working on a general strategy for identifying any mutated strains that might appear next year, so that we can respond quickly with a vaccine, similar to what we do with the flu.</p>
<p>5) Even though we think our bodies will retain the antibodies from SARS-CoV-2 indefinitely, there's a chance that they might not (similar to norovirus), so the vaccine is to cover that possibility.</p>
<p>Or something else?</p>
| [
{
"answer_id": 22825,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>You've misinterpreted the modelling you refer to above. The modelling is based on the premise that the USA population adopts <strong>assuming full social distancing through May 2020</strong>. This means that the majority of the USA population will remain susceptible to infection because the social distancing has kept them away from the virus.</p>\n\n<p>Furthermore, there are millions of people in other countries that will need vaccination. Take for instance China where the majority of the population remains immune naive because they have shut down the pandemic inside China.</p>\n\n<p>Furthermore, the risks of future coronavirus pandemics remains high. The main reason the SARS vaccine was not developed was because they ran out of people to test the vaccine on. With a SARS-Cov-2 vaccine that will help the development of new vaccines. The influenza vaccine is able to be developed yearly because the expertise is there, but we lack that expertise at present with the novel coronaviruses.</p>\n"
},
{
"answer_id": 25405,
"author": "Acccumulation",
"author_id": 12695,
"author_profile": "https://health.stackexchange.com/users/12695",
"pm_score": 1,
"selected": false,
"text": "<p>If by the model being "correct", you mean that the model will correctly predict what happens, then my understanding is it's mostly your first point. But if you consider a model correctly predicting what <em>would</em> happen if its assumptions turn out to be accurate, but those assumptions turn out to be false, then that's a separate points. Other points:</p>\n<p>It's downright foolish to not work on all possible responses simply because you think they won't be needed. Even if people thought that there was, say, a 60% chance of cases going to zero by July, it would be silly to say "Well, there's only a 40% chance we'll need this vaccine, so no point working on it." When you're facing the possibility of millions of deaths, the probability of that doesn't need to be very high for it to warrant working to address.</p>\n<p>It doesn't take 18 months to develop a vaccine. It took a few weeks to create a vaccine, and then several more months to test it, and it will take several months after that to deploy it.</p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22823",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19075/"
] |
22,837 | <p>As specified in <a href="https://www.theguardian.com/world/2020/mar/19/coronavirus-testing-explained-how-does-it-work-and-how-quickly-can-you-get-a-response-in-australia" rel="nofollow noreferrer">this link</a>, COVID-19 tests start with taking samples from the nose or back or throat of people.</p>
<p>Based on growth rate of this disease, I thought what if those samples are not positive (showing infection with COVID-19), but that person has that virus in other parts of his body, because he's in the early stages of the infection.</p>
<p>So is it possible to be infected with COVID-19 and have no virus in nose and throat, and if it's possible, how long would it take to be certain that a sample shows the reality and a negative answer can be trusted?</p>
| [
{
"answer_id": 22838,
"author": "Bob Ortiz",
"author_id": 16786,
"author_profile": "https://health.stackexchange.com/users/16786",
"pm_score": 2,
"selected": false,
"text": "<p>You are searching for the false-negative rate of these tests. <em>A test resulting in a negative outcome while it should have been a positive outcome.</em> </p>\n\n<p>A recent article stated that most of the false-negatives of COVID-19 tests are actually caused by not properly taking the samples from nose and throat. While I cannot find the original article I've got this information from, I've added two other relevant quotes. So yes false-negatives are possible but are likely caused by samples that are not properly collected.</p>\n\n<blockquote>\n <p>The rollout of COVID-19 testing is accelerating as more kits become available. However, a leading pathologist who was director of virology at Stanford, points out that the results are not 100% accurate. \"It's not that these tests can't detect virus,\" said Dr. Bruce Patterson. \"My concern is that the sampling involved in detecting the virus can lead to clinical false negatives.\" - <a href=\"https://abc7news.com/6053940/\" rel=\"nofollow noreferrer\">https://abc7news.com/6053940/</a></p>\n</blockquote>\n\n<p>Also, the false-negative rate can vary based on the test method used and its quality and accuracy.</p>\n\n<blockquote>\n <p>COVID-19 tests are new, and assessing their accuracy is challenging. PCR tests may produce false negatives, failing to identify evidence of SARS-CoV-2. Sometimes false negatives result from human error or problems with the procedure. Giving the test too early or late, for example, can lead to a false negative. - <a href=\"https://www.medicalnewstoday.com/articles/coronavirus-testing#accuracy\" rel=\"nofollow noreferrer\">https://www.medicalnewstoday.com/articles/coronavirus-testing#accuracy</a></p>\n</blockquote>\n"
},
{
"answer_id": 22840,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>The SARS-CoV-2 virus infects cells that possess the ACE2 receptor but this is described as being present mainly in pneumocytes lining the alveoli, vascular endothelium, cardiac tissue, and small bowel luminal cells. The virus appears to preferentially attack well differentiated cells. There are also some ACE2 containing cells in the respiratory epithelium. Nevertheless virus can be detected from nasal and oropharyngeal swabs indicating infection there. The tests themselves are only about 75% sensitive which suggests there is not a high concentration of virus in the upper respiratory tract,though it may also relate to the time the swab is taken as greatest viral shedding in the upper airways occurs in the pre-symptomatic phase.</p>\n\n<p>So a positive test may relate to when it was taken, and test sensitivity.</p>\n\n<p>A deep sputum test is best but dangerous to obtain as large amounts of virus are exhaled or coughed into the environment endangering medical staff.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/</a></p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22837",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19079/"
] |
22,846 | <p>As I understand, Aortic stenosis restricts the blood flow from the left ventricle to the aorta, this restriction should cause a disruption in the pumping of blood. That would cause the heart to beat at a faster rate. If this happens over a long period of time, can it lead to cardiac arrhythmia?</p>
| [
{
"answer_id": 23031,
"author": "Sudhanshu Sharma",
"author_id": 19201,
"author_profile": "https://health.stackexchange.com/users/19201",
"pm_score": 0,
"selected": false,
"text": "<p>Yes , I feel so . As AS will cause pressure overLoad in LV which will further cause increase pressure for pumping the blood, so chronically which leads to arrhythmic activity </p>\n"
},
{
"answer_id": 23040,
"author": "Brian",
"author_id": 19203,
"author_profile": "https://health.stackexchange.com/users/19203",
"pm_score": 1,
"selected": false,
"text": "<p>In the long term, aortic stenosis (AS), especially when untreated, can cause structural changes to the heart that can contribute to arrhythmia. </p>\n\n<p>More specifically, left ventricular (LV) outflow obstruction caused by AS can cause pressure buildup in the LV, which over time can cause LV concentric hypertrophy (I.e., the heart muscle thickens uniformly). Such thickening of the heart can lead to a disruption of normal cardiac electrical activity and can lead to ventricular arrhythmias. An example of a study supporting this in a clinical population is Wolfe et al. 1993 in <em>Circulation</em> (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8425327\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/8425327</a>).</p>\n\n<p>In a genetic condition somewhat similar to aortic stenosis, hypertrophic cardiomyopathy, individuals are predisposed to ventricular arrhythmias in a similar fashion, which is a leading cause of sudden cardiac death in these individuals (<a href=\"https://europepmc.org/article/med/1728506\" rel=\"nofollow noreferrer\">https://europepmc.org/article/med/1728506</a>).</p>\n\n<p>It is also possible that long-term untreated AS can lead to a backup of pressure into the left atrium, leading to left atrial enlargement, which can cause atrial fibrillation (<a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0002914915018457\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/abs/pii/S0002914915018457</a>).</p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22846",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19268/"
] |
22,850 | <p>How can a competition among computer programmers be helpful to find a vaccine against corona?</p>
<p>HackZurich, under the patronage of the Federal Department of Home Affairs (FDHA), aims to use the collective intelligence of researchers, experts, technology specialists and fellow citizens to develop fresh ideas and solutions for dealing with and combating the Coronavirus.</p>
<p><a href="https://inf.ethz.ch/news-and-events/spotlights/2020/03/codevscovid19.html" rel="nofollow noreferrer">https://inf.ethz.ch/news-and-events/spotlights/2020/03/codevscovid19.html</a></p>
<p>My idea is: is a virtual virus similar with a real virus that an antivirus to covid-19 can be developed analogous to the construction of a virtual virus?</p>
<p>Is this a kind of bionics?</p>
<p><a href="https://en.wikipedia.org/wiki/Bionics" rel="nofollow noreferrer">https://en.wikipedia.org/wiki/Bionics</a></p>
<p>Edit: this question has been closed as opinion based.</p>
<p>But this answer by Thomas is the proof that there is evidence and scientific research:</p>
<p>Yes, they can, see e. g. <a href="https://www.ncbi.nlm.nih.gov/pubmed/30905159" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/30905159</a> (field of cheminformatics) re the possiblity of drug discovery in general via machine learning</p>
| [
{
"answer_id": 23031,
"author": "Sudhanshu Sharma",
"author_id": 19201,
"author_profile": "https://health.stackexchange.com/users/19201",
"pm_score": 0,
"selected": false,
"text": "<p>Yes , I feel so . As AS will cause pressure overLoad in LV which will further cause increase pressure for pumping the blood, so chronically which leads to arrhythmic activity </p>\n"
},
{
"answer_id": 23040,
"author": "Brian",
"author_id": 19203,
"author_profile": "https://health.stackexchange.com/users/19203",
"pm_score": 1,
"selected": false,
"text": "<p>In the long term, aortic stenosis (AS), especially when untreated, can cause structural changes to the heart that can contribute to arrhythmia. </p>\n\n<p>More specifically, left ventricular (LV) outflow obstruction caused by AS can cause pressure buildup in the LV, which over time can cause LV concentric hypertrophy (I.e., the heart muscle thickens uniformly). Such thickening of the heart can lead to a disruption of normal cardiac electrical activity and can lead to ventricular arrhythmias. An example of a study supporting this in a clinical population is Wolfe et al. 1993 in <em>Circulation</em> (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8425327\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/8425327</a>).</p>\n\n<p>In a genetic condition somewhat similar to aortic stenosis, hypertrophic cardiomyopathy, individuals are predisposed to ventricular arrhythmias in a similar fashion, which is a leading cause of sudden cardiac death in these individuals (<a href=\"https://europepmc.org/article/med/1728506\" rel=\"nofollow noreferrer\">https://europepmc.org/article/med/1728506</a>).</p>\n\n<p>It is also possible that long-term untreated AS can lead to a backup of pressure into the left atrium, leading to left atrial enlargement, which can cause atrial fibrillation (<a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0002914915018457\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/abs/pii/S0002914915018457</a>).</p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22850",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17790/"
] |
22,857 | <p>I've been trying to think of the simplest, pre-existing item that could be used as a ventilator to support coronavirus patients that require it. I have come across this useful specification regarding what ventilators should ideally comply to: <a href="https://www.gov.uk/government/publications/specification-for-rapidly-manufactured-cpap-system-to-be-used-during-the-coronavirus-covid-19-outbreak" rel="nofollow noreferrer">https://www.gov.uk/government/publications/specification-for-rapidly-manufactured-cpap-system-to-be-used-during-the-coronavirus-covid-19-outbreak</a></p>
<p>Unfortunately I do not have the equipment to measure the effectiveness of using a bike pump with respect to this specification.</p>
<p><strong>Could a bike pump be used (are you in a position to test one against the above spec)? Otherwise, is there another common/household product that could be a successful substitute?</strong></p>
| [
{
"answer_id": 22858,
"author": "Thomas",
"author_id": 19070,
"author_profile": "https://health.stackexchange.com/users/19070",
"pm_score": 1,
"selected": false,
"text": "<ul>\n<li>Airway pressure is a lot less than what a bike pump produces during a single pump action (in the usual setting of how its used).</li>\n<li>Even though ventilators work in a similar way (cf. <a href=\"https://i.stack.imgur.com/PgmEZ.png\" rel=\"nofollow noreferrer\">https://i.stack.imgur.com/PgmEZ.png</a>), CPAP by definition needs to maintain a continuous airway pressure (CPAP = continuous positive airway pressure). The pressure to be held should be between around 3 mbar up to around 20-25 mbar. These are, again, exceedingly small pressures and need to be adjustable very explicitly.</li>\n</ul>\n\n<p>One simple way of generating the kind of pressure in the airway one would want is trying to exhale against lips firmly pressed against each other; this produces around 20-40 mbar (depending on where you read about it).</p>\n\n<p>Generally respiratory physiology is not a trivial subject, unfortunately. If you are interested, there are West's lectures, which are very accessible and free of charge: <a href=\"https://meded.ucsd.edu/ifp/jwest/resp_phys/\" rel=\"nofollow noreferrer\">https://meded.ucsd.edu/ifp/jwest/resp_phys/</a></p>\n"
},
{
"answer_id": 22859,
"author": "Eike Pierstorff",
"author_id": 19089,
"author_profile": "https://health.stackexchange.com/users/19089",
"pm_score": 2,
"selected": false,
"text": "<p>Even a cursory reading of the spec indicates that this will not work.</p>\n\n<blockquote>\n <p>Specification</p>\n \n <p><strong>Must: Defines the minimum viable product clinically acceptable by clinicians [...]</strong></p>\n \n <ul>\n <li>RMCPAP must deliver inspired oxygen concentration in the range 35 – 80% to the patient, selectable by the user. [...]</li>\n <li>All gas connectors and hoses must comply with BS EN ISO 5359:2014+A1:2017, ISO 5359:2014/AMD 1:2017 and BS 2050: 1978\n Electrical Conductivity [...]</li>\n <li>Must connect to wall pipeline oxygen supply via BS 5682:2015 compatible probes [...]</li>\n <li>Must maintain a nearly constant airway pressure of between 5–15 cmH2O, with the ability to adjust the pressure [...]</li>\n <li>Must either alarm or be provided with a suitable air entrainment system if the fresh gas supply fails [...]</li>\n <li>Must have as low a resistance to expiration as possible [...]</li>\n <li>Expiratory gas must be able to pass through an appropriate filter [...]</li>\n <li>Must have a pressure safety release valve to protect the patient from high pressures, having a release pressure of no greater than 25\n cmH2O. [...]</li>\n <li>Must be securely attached to the gas outlet</li>\n </ul>\n</blockquote>\n\n<p>A bike pump does not meet any of those criteria, this isn't even the complete list of \"musts\", and failing on a single criteria would already mean that the pump is not suitable. Adding enough peripherals to meet even some of the criteria would in all likelihood impossible, and if possible the resulting device would no longer resemble a bike pump. </p>\n\n<p>You could probably use a bike pump to pump air into a lung, but given that a bike pump is designed to deliver up to 160 psi (\"<a href=\"https://www.ems.com/f/ea-how-to-choose-a-bike-pump.html\" rel=\"nofollow noreferrer\">Portable pump psi ratings can vary. Some offer 90 psi, others up to 160 psi</a>\"), that's just an interesting way to kill a person, which is not usually what ventilators are for. </p>\n\n<p>The closest to this plan I could find was a plan to <a href=\"https://scitechdaily.com/mit-posts-free-plans-online-for-an-emergency-ventilator-that-can-be-built-for-100/\" rel=\"nofollow noreferrer\">convert an ambu bag into a ventilator</a>. My experience with ventilators is rather more practical than theoretical, and given what fickle machines even state of the art ventilators are, I would probably choose death over that sort of improvised machine.</p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22857",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19088/"
] |
22,860 | <p>We know there is no cure for Covid-19 (currently) and the
treatment focuses on managing symptoms as the virus runs its course.</p>
<p>The main <a href="https://www.cdc.gov/coronavirus/2019-ncov/symptoms-testing/symptoms.html" rel="nofollow noreferrer">symptoms of Covid-19</a> are</p>
<p>-Fever</p>
<p>-Cough</p>
<p>-Shortness of breath</p>
<p>There's no need to seek medical attention unless</p>
<p>-Trouble breathing</p>
<p>-Persistent pain or pressure in the chest</p>
<p>-New confusion or inability to arouse</p>
<p>-Bluish lips or face</p>
<hr>
<p>From <a href="https://www.healthline.com/health/coronavirus-covid-19#treatment" rel="nofollow noreferrer">healthline</a> the examples of therapies used for these illnesses include:</p>
<ul>
<li>antiviral or retroviral medications</li>
<li>breathing support, such as mechanical ventilation</li>
<li>steroids to reduce lung swelling</li>
<li>blood plasma transfusions</li>
</ul>
<p>But there's no mention of specific medications.</p>
<p>I have checked other pages and again, no specific medications.</p>
<p>I know there is a lot of medication of antivirals, to treat cough, fever, etc. </p>
<p>But is a special medication to treat these symptoms that came particularly from Covid-19 infection?</p>
<p>Or it doesn't matter that the symptoms came from Covid-19? they could be treated as a common cough or common fever, etc.?</p>
| [
{
"answer_id": 22861,
"author": "Graham Chiu",
"author_id": 3414,
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"text": "<p>There are no specific proven drug treatments for Covid-19 disease but quite a few claims based on very limited experience which is why the WHO is arranging a mega trial called SOLIDARITY to test 4 protocols. </p>\n\n<ul>\n<li><p>Remdesivir, an anti-Ebola drug, a RNA polymerase inhibitor</p></li>\n<li><p>Hydroxychloroquine - a drug used in SLE/Rheumatoid arthritis that may have some ACE2 blocking ability by glycosylating the spike protein and the ACE2 receptor</p></li>\n<li><p>Ritonavir and lopinavir, a combination of common anti-AIDS drugs </p></li>\n<li><p>Interferon beta + ritonavir and lopinavir- interferons are released by cells to fight viruses</p></li>\n</ul>\n\n<p><a href=\"https://www.medicalnewstoday.com/articles/who-launch-trial-testing-4-potential-covid-19-treatments\" rel=\"nofollow noreferrer\">https://www.medicalnewstoday.com/articles/who-launch-trial-testing-4-potential-covid-19-treatments</a></p>\n\n<p><a href=\"https://www.nature.com/articles/s41421-020-0156-0\" rel=\"nofollow noreferrer\">https://www.nature.com/articles/s41421-020-0156-0</a></p>\n"
},
{
"answer_id": 22899,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 1,
"selected": false,
"text": "<p><a href=\"https://www.genengnews.com/a-lists/how-to-conquer-coronavirus-top-35-treatments-in-development/\" rel=\"nofollow noreferrer\">https://www.genengnews.com/a-lists/how-to-conquer-coronavirus-top-35-treatments-in-development/</a> has a list of 35 treatments being considered / in development.</p>\n\n<blockquote>\n <p>A new survey by Genetic Engineering & Biotechnology News (GEN) reveals 35 active drug development programs in North America, Europe, and China. Those 35 include treatments that have received the greatest public attention in recent days, being developed by companies that range from pharma giants like GlaxoSmithKline and Sanofi, to small and large biotechs such as Moderna and Gilead Sciences. Gilead has begun clinical trials in China after peer-reviewed journals showed its antiviral candidate, remdesivir, having positive results in a case involving an American patient and Chinese in vitro tests.</p>\n</blockquote>\n\n<p>Also, interesting summary of what supplements David Sinclair takes to reduce COVID-19 risk: <a href=\"https://podcastnotes.org/bulletproof-radio/david-sinclair-covid-19-supplements-immune-system/\" rel=\"nofollow noreferrer\">https://podcastnotes.org/bulletproof-radio/david-sinclair-covid-19-supplements-immune-system/</a> </p>\n"
}
] | 2020/03/30 | [
"https://health.stackexchange.com/questions/22860",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
22,869 | <p>An article from 2008: <a href="https://www.livescience.com/7472-kill-viruses-shake-death.html" rel="nofollow noreferrer">New way to kill virus: Shake them to death</a>.
Can ultrasound have the potential to treat COVID-19 infected humans at large-scale (because it does not require anesthesia)?</p>
<p>I went through an answer on <a href="https://www.quora.com/Are-ultrasonic-waves-harmful-to-the-human-body" rel="nofollow noreferrer">Quora</a>. Is it a good idea to make a cavity with ultrasound for humans, specifically targeting the respiratory organs?</p>
<p>My apologies if this seems dope, I myself am an engineer, but this COVID-19 seems to affect the future generations as well so I thought of asking here. Please validate it.</p>
<p>References:
<a href="https://books.google.co.in/books?id=AXArBgAAQBAJ&pg=PA229&lpg=PA229&dq=whitewater%20electronics%20ultrasound&source=bl&ots=b5ehLFwUBM&sig=ACfU3U2EiR92YBGO77GV4mcU11_6hIEVwg&hl=en&sa=X&ved=2ahUKEwierYfI0rnoAhXvxzgGHa2NCywQ6AEwAHoECAoQAQ#v=onepage&q=whitewater%20electronics%20ultrasound&f=false" rel="nofollow noreferrer">Effects of ultrasound on living organisms</a></p>
| [
{
"answer_id": 22870,
"author": "Graham Chiu",
"author_id": 3414,
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"text": "<p>Sounds like science fiction and not much use for treating patients. They talk about shining laser light on the virus to induce the resonant frequency to shatter the virus.</p>\n\n<p>But, Covid-19 is a deep tissue infection, and I can't imagine how lasers could possibly get inside the lung, heart and other tissues affected by this virus.</p>\n"
},
{
"answer_id": 23037,
"author": "Melissa Y",
"author_id": 19202,
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"text": "<p>[High intensity focused ultrasound][1] can be quite targeted and get into deep parts of the body, including into the brain. But while it would likely kill the virus, I don't think it's very realistic to be sonicating everywhere the virus might be, because it isn't very localized. You can't use FUS on the entire lung, as that would cause far too much damage if you were to have any impact on reducing viral load. This is just my opinion, but I do think that a good antiviral treatment for SARS COV 2 will need systemic effects, not localized.</p>\n"
}
] | 2020/03/31 | [
"https://health.stackexchange.com/questions/22869",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19091/"
] |
22,901 | <p>Prior to the SARS-CoV-2 epidemic I was under the impression that viruses fall into two categories:</p>
<ol>
<li><p>Diseases from which you recover and afterwards become fully immune. When reinfected with a mutated version of the virus, you do get sick again, but it's a milder form. (common cold, influenza)</p></li>
<li><p>Diseases which are impossible to recover from (HIV, HPV), so you don't really gain immunity</p></li>
</ol>
<p>Are there diseases which fall into a third bucket: you do recover, but can be reinfected immediately with the same strain? Note that I'm not asking about whether or not this is possible with COVID-19 - this question is purely about other diseases that we know of.</p>
| [
{
"answer_id": 22902,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
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"selected": false,
"text": "<p>Seasonal coronaviruses come back year after year and we continue to suffer with them</p>\n<blockquote>\n<p>Researchers do know that reinfection is an issue with the four seasonal coronaviruses that cause about 10 to 30% of common colds. These coronaviruses seem to be able to sicken people again and again, even though people have been exposed to them since childhood.</p>\n<p>"Almost everybody walking around, if you were to test their blood right now, they would have some levels of antibody to the four different coronaviruses that are known," says Ann Falsey of the University of Rochester Medical Center.</p>\n<p>After infection with one of these viruses, she says, antibodies are produced but then the levels slowly decline and people become susceptible again.</p>\n</blockquote>\n<p>Similarly, the Herpes Zoster or chicken pox virus you recover from but when your antibody levels drop, it can reappear as shingles.</p>\n<p><a href=\"https://www.npr.org/sections/goatsandsoda/2020/03/20/819038431/do-you-get-immunity-after-recovering-from-a-case-of-coronavirus\" rel=\"nofollow noreferrer\">https://www.npr.org/sections/goatsandsoda/2020/03/20/819038431/do-you-get-immunity-after-recovering-from-a-case-of-coronavirus</a></p>\n<p><a href=\"https://www.cdc.gov/shingles/about/transmission.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/shingles/about/transmission.html</a></p>\n"
},
{
"answer_id": 22909,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
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"text": "<p>Short answer seems to be that there is such a category and it includes most respiratory viruses, <a href=\"https://jvi.asm.org/content/89/6/2995\" rel=\"nofollow noreferrer\">including</a> coronaviruses:</p>\n<blockquote>\n<p>Although the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) epidemic was controlled by nonvaccine measures, coronaviruses remain a major threat to human health. The design of optimal coronavirus vaccines therefore remains a priority. Such vaccines present major challenges: <strong>coronavirus immunity often wanes rapidly,</strong> individuals needing to be protected include the elderly, and vaccines may exacerbate rather than prevent coronavirus lung immunopathology.</p>\n</blockquote>\n<p>Alas this paper considers it such a well-known fact that they don't actually bother to cite any studies in support of that particular claim. (So, if you want to further challenge this, Skeptics SE awaits you...)</p>\n<p>And regarding the closest know relatives of SARS-CoV-2, that is SARS (and MERS) the data on long-term immunity is not very encouraging either, as a March 18, <em>Nature</em> editorial <a href=\"https://www.nature.com/articles/d41586-020-00798-8\" rel=\"nofollow noreferrer\">relates</a>:</p>\n<blockquote>\n<p><strong>Immunity is short-lived for the coronaviruses that cause common colds</strong>; even people who have high levels of antibodies against these viruses can still become infected, says Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City.</p>\n<p><strong>The evidence is more equivocal for the two other coronaviruses that have triggered epidemics: those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).</strong> Perlman says his team has found that after people recover from MERS, their antibodies against the virus drop precipitously. He also says that his team has gathered data — not yet published — showing that SARS antibodies are still present in the body 15 years after infection. <strong>But it’s not clear whether this immune response is enough to prevent reinfection.</strong> “We don’t have good evidence of long-lasting immunity, but we also don’t have really good data from both SARS and MERS,” Perlman adds.</p>\n</blockquote>\n<hr />\n<p>More tangential info below:</p>\n<p>The immune system can be damaged by some pathogens making them vulnerable to others, even if you had prior exposure to those. Besides the well-known HIV which causes general immunodeficiency, measles can do this to some extent as well, and you do get cured from measles proper. This from a <a href=\"https://www.nytimes.com/2019/10/31/health/measles-vaccine-immune-system.html\" rel=\"nofollow noreferrer\">NYT article</a>, I haven't checked the actual science publications:</p>\n<blockquote>\n<p>Measles is far more dangerous than most people realize, new research shows.</p>\n<p>The disease itself can cause a severe and sometimes deadly illness, but two new studies published on Thursday found that even when patients recover, the virus can inflict lasting harm on their immune systems.</p>\n<p>The weakened immunity leaves a child vulnerable for several years to other dangerous infections like flu and pneumonia. The damage occurs because the virus kills cells that make antibodies, which are crucial to fighting off infections.</p>\n<p>Scientists call the effect “immune amnesia.” During childhood, as colds, flu, stomach bugs and other illnesses come and go, the immune system forms something akin to a memory that it uses to attack those germs if they try to invade again. The measles virus erases that memory, leaving the patient prone to catching the diseases all over again.</p>\n</blockquote>\n<p>Technically this a bit besides what you're asking about. The technical term is "immunomodulation".</p>\n<p>Also, the adaptive response <a href=\"https://www.virology.ws/2009/12/28/reinfection-with-2009-influenza-h1n1/\" rel=\"nofollow noreferrer\">takes</a> a bit longer than people might suspect:</p>\n<blockquote>\n<p>These individuals were likely resusceptible to reinfection with the same strain of influenza virus due to a confluence of unusual events. First, all three were reinfected within three weeks, before their primary adaptive response had sufficiently matured. Another contributing factor was the high level of circulation of the pandemic strain. [...]</p>\n<p>Could reinfection also occur after immunization with influenza vaccine? Yes, if the immunized individual encounters the virus before the primary antibody response matures, which occurs in 3-4 weeks. This is more likely to occur during pandemic influenza when circulation of the virus is more extensive than in non-pandemic years.</p>\n<p>[Citing:]</p>\n<ul>\n<li>Perez CM, Ferres M, & Labarca JA (2010). Pandemic (H1N1) 2009 Reinfection, Chile. Emerging infectious diseases, 16 (1), 156-7 PMID: 20031070</li>\n</ul>\n</blockquote>\n<p>And it's suspected that it's not actually true (as claimed in the question) that prior exposure to a family of viruses, e.g. influenza, always makes subsequent infections with different influenza strains milder. In fact, there's <a href=\"https://academic.oup.com/emph/article/2019/1/18/5298310\" rel=\"nofollow noreferrer\">some evidence</a> that the W shaped mortality curve (by age) for the 1918 influenza was due to the exposure in infancy of some age groups (but not others) to a somewhat similar viruses that primed a overreaction of the immune response, which was often responsible for the rapid swelling of the lungs:</p>\n<blockquote>\n<p>The 1918 pandemic was caused by an H1N1 virus (with a Group 1 HA). Those whose first exposure had been to a putative H3N8 (Group 2) virus that emerged in 1889 were at high risk of death [20]. Crucially, because children born several years prior to a newly emerged IAV strain can experience that virus as their first (or among their first) IAV infections, one should not expect a clean demarcation of increased risk to coincide with the year of emergence of that H3N8 strain. Although the young-adult mortality rate from the 1918 virus has a sharp peak in those born very near 1889, it stretches back to include those born up to a decade or so prior to 1889 (Fig. 3b). Interestingly, it also stretches forward only a decade or so, possibly because a new H1 virus emerged in the early years of the 20th century, displacing the 1889 H3 virus [20, 24]. This idea is supported by the lack of evidence of anti-H3 antibodies in those born after the turn of the century—despite clear evidence of N8 reactivities until shortly before 1918—as well as by the low mortality during the 1968 H3N2 pandemic in those born before, but not after, about 1900 [20].</p>\n<p>[...] Nevertheless, results indicating that the 1918 virus is unusually lethal in mice [27], along with the fact that introduction of all new internal proteins in the 1918 virus could have played some role in its unusual virulence (due, e.g., to absent cellular immunity to new T cell epitopes) [20], suggest that the overall virulence of the 1918 virus may have been affected by factors other than antigenic imprinting in childhood. These uncertainties make the recovery of archival viral strains from prior to 1918 particularly attractive: exposing experimental animals such as ferrets, pigs or mice to reconstructed versions of putative H3N8 and H1N8 viruses that may have provided distinct imprinting of different cohorts in 1918 [20] may be the only way to resolve these questions and answer, finally, why this pandemic was so catastrophic.</p>\n</blockquote>\n<p>Unfortunately no genomes of pre-1918 influenzas have been reconstructed insofar, so it's presently impossible to experimentally verify this kind of "kindling" hypothesis, at least for 1918 pandemic.</p>\n<p>And more generally, <a href=\"https://www.statnews.com/2020/02/04/two-scenarios-if-new-coronavirus-isnt-contained/\" rel=\"nofollow noreferrer\">it's suspected</a> that nobody becomes "fully immune" to coronaviruses and some other respiratory viruses like the RSV:</p>\n<blockquote>\n<p>The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, [Richard] Webby, an influenza expert at St. Jude Children’s Research Hospital] said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.</p>\n<p>“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.</p>\n<p>“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.</p>\n</blockquote>\n<p>I'll try to find some actual studies on this as it's the most central issue relating to the question. There are lot of papers in pubmed about <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/?term=waning+immunity\" rel=\"nofollow noreferrer\">"waning immunity"</a> but most are about vaccines, so that may or may not fully answer your question. But to <a href=\"https://academic.oup.com/jid/article/217/6/851/4833004\" rel=\"nofollow noreferrer\">pick an example</a> (of such a paper on vaccines waning):</p>\n<blockquote>\n<p>For mumps, protection appears to wane over decades, prompting the use of additional doses of vaccine for outbreak control [18]. Transmission models have been used to study long-term age-specific time trends of pertussis and mumps. The best-fitting models require waning immunity, leading to the inference that vaccine protection does indeed wane, as well as providing an estimate of the rate of waning [19, 20].</p>\n</blockquote>\n<p>I think I found some <a href=\"https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2006601\" rel=\"nofollow noreferrer\">research</a> that might satisfy you a bit more, but it's alas not about influenzas etc.:</p>\n<blockquote>\n<p>Determining the duration of protective immunity requires quantifying the magnitude and rate of loss of antibodies to different virus and vaccine antigens. A key complication is heterogeneity in both the magnitude and decay rate of responses of different individuals to a given vaccine, as well as of a given individual to different vaccines. We analyzed longitudinal data on antibody titers in 45 individuals to characterize the extent of this heterogeneity and used models to determine how it affected the longevity of protective immunity to measles, rubella, vaccinia, tetanus, and diphtheria. Our analysis showed that the magnitude of responses in different individuals varied between 12- and 200-fold (95% coverage) depending on the antigen. Heterogeneity in the magnitude and decay rate contribute comparably to variation in the longevity of protective immunity between different individuals. We found that some individuals have, on average, slightly longer-lasting memory than others—on average, they have higher antibody levels with slower decay rates. We identified different patterns for the loss of protective levels of antibodies to different vaccine and virus antigens. Specifically, we found that for the first 25 to 50 years, virtually all individuals have protective antibody titers against diphtheria and tetanus, respectively, but about 10% of the population subsequently lose protective immunity per decade. In contrast, at the outset, not all individuals had protective titers against measles, rubella, and vaccinia. However, these antibody titers wane much more slowly, with a loss of protective immunity in only 1% to 3% of the population per decade. Our results highlight the importance of long-term longitudinal studies for estimating the duration of protective immunity and suggest both how vaccines might be improved and how boosting schedules might be reevaluated.</p>\n</blockquote>\n"
}
] | 2020/04/01 | [
"https://health.stackexchange.com/questions/22901",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
22,920 | <p><strong>Sensitivity and specificity</strong>.
These are the links I used to know about these two terms:</p>
<p><a href="https://en.wikipedia.org/wiki/Sensitivity_and_specificity" rel="nofollow noreferrer">https://en.wikipedia.org/wiki/Sensitivity_and_specificity</a></p>
<p><a href="https://m.youtube.com/watch?v=FnJ3L-63Cf8" rel="nofollow noreferrer">https://m.youtube.com/watch?v=FnJ3L-63Cf8</a></p>
<p><a href="https://m.youtube.com/watch?v=Z5TtopYX1Gc" rel="nofollow noreferrer">https://m.youtube.com/watch?v=Z5TtopYX1Gc</a></p>
<p>What I understand is that we want to know:</p>
<blockquote>
<p>how many members of a collection can be detected by a detector</p>
</blockquote>
<p>In other words: </p>
<pre><code>detector's detection rate = detected members / all members which are the same
</code></pre>
<p>Now, how comes that they are named differently? I fail to see their distinction. In other words both can be called <em>sensitivity</em> or <em>specificity</em> or <em>detection rate</em>. And of course when we have detection rate, non-detection rate becomes 1 minus the detection rate. Still it's not a distinguishing factor.</p>
| [
{
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"text": "<p>I would say the best distinction for me is that of <strong>what you detect</strong>, versus <strong>how good you are at detecting</strong> it.</p>\n"
},
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"answer_id": 22970,
"author": "cbeleites unhappy with SX",
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"text": "<p>In your terminology, they are detection rates for *different types of <code>all members which are the same</code>.</p>\n\n<p>You may say, they both* answer questions of the type \"What fraction of cases do we correctly recognize?\". But the difference is in the denominator of the fraction (the population this figure of merit refers to):</p>\n\n<ul>\n<li><strong>Sensitivity</strong> answers the question: Of all patients that truly have the disease, what fraction do we correctly recognize as diseased.<br>\nYou may say, sensitivity is the detection rate of diseased patients.</li>\n<li><strong>Specificitiy</strong> answers the question: Of all patients that truly do <strong>not</strong> have the disease, what fraction do we correctly recognize as <strong>not</strong> diseased.<br>\nYou may say, specificity is the detection rate of healthy people.</li>\n</ul>\n\n<p>So they look at disjunct (sub)populations, and their denominators do have <em>nothing</em> in common. This makes them in first approximation independent of each other:</p>\n\n<ul>\n<li>A good test has <em>both</em> high sensitivity and high specificity (A in the diagram below), and</li>\n<li><p>a test that has <em>both</em> low sensitivity and low specificity is a bad test (C).</p></li>\n<li><p>It is often possible to some extent to trade-off some sensitivity for increased specificity and vice versa (this is what the 2nd video is about). For test B, this trade-off is along the dotted line. The dotted line will always go from high specificity and low sensitivity to high sensitivity and low specificity, never from \"bad\" to \"very good\".<br>\nIt is still important as in some situations sensitivity is more important and in others specificity is more important (sometimes false negatives are worse than false positives, sometimes it is the other way round)-</p></li>\n</ul>\n\n<pre><code>^ sensitivity\n| . . . * very good test A\n| . . . \n| * test B\n| . \n| . \n| .\n| * bad test C .\n+------------------> specificity\n\n\n</code></pre>\n\n<hr>\n\n<p>* there are more such \"What fraction do we get correct?\"-type figures of merit that use yet different denominators, e.g. the predictive values in the 1st video.</p>\n"
}
] | 2020/04/01 | [
"https://health.stackexchange.com/questions/22920",
"https://health.stackexchange.com",
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22,924 | <p>Would I change sodalime after each patient or are the filters enough?</p>
| [
{
"answer_id": 22926,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>This advice is about cleaning of anaesthetic equipment after a Covid-19 patient</p>\n<blockquote>\n<p>Short Answer: Cleaning procedures are the same for all patients if high quality viral filters are used to protect the machine. Discard disposable items – breathing circuit, reservoir bag, patient mask, gas sampling tubing, filters placed at the airway and elsewhere if supply is sufficient. Wipe all exposed surfaces. Manufacturers’ cleaning recommendations are useful for individual devices.</p>\n<p>As noted previously, a high quality viral filter will protect the internal components of the anesthesia machine from contamination. Single use items must be discarded and not used between patients. Practices of using an HMEF and reusing the breathing circuit between patients are not desirable in part because it is virtually impossible to decontaminate the external surfaces of the circuit. Some practices in Europe are reusing circuits by just changing the airway filter after use with patients at low risk for COVID 19 infection. Manufacturers typically have recommendations for cleaning solutions that are safe and effective for cleaning between patients. Usual practices for surface cleaning are acceptable.</p>\n</blockquote>\n<p><a href=\"https://www.apsf.org/faq-on-anesthesia-machine-use-protection-and-decontamination-during-the-covid-19-pandemic/#cleaning\" rel=\"noreferrer\">https://www.apsf.org/faq-on-anesthesia-machine-use-protection-and-decontamination-during-the-covid-19-pandemic/#cleaning</a></p>\n"
},
{
"answer_id": 22927,
"author": "Community",
"author_id": -1,
"author_profile": "https://health.stackexchange.com/users/-1",
"pm_score": 4,
"selected": false,
"text": "<p>I refer to the American Society of Anesthesiologists </p>\n\n<blockquote>\n <ol>\n <li>Does the anesthesia machine need to be decontaminated after use on a COVID-19 patient? We have HEPA filters in the circuit and the gas sampling line.</li>\n </ol>\n \n <p>Please refer to ASA Guidance that states, “After the case, clean and disinfect high-touch surfaces on the anesthesia machine and anesthesia work area with an EPA-approved hospital disinfectant.” The internal components of the anesthesia machine and breathing system do not need “terminal cleaning” if breathing circuit filters have been used as directed. Please also see guidance from the APSF on decontaminiation. </p>\n</blockquote>\n\n<p>For further information see the American Society of Anesthesiologists <a href=\"https://www.asahq.org/about-asa/governance-and-committees/asa-committees/committee-on-occupational-health/coronavirus/clinical-faqs\" rel=\"noreferrer\">COVID-19 FAQs</a></p>\n"
}
] | 2020/04/01 | [
"https://health.stackexchange.com/questions/22924",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19117/"
] |
22,936 | <p>In the highly cited <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291398/" rel="nofollow noreferrer">2006 review</a> of <a href="https://en.wikipedia.org/wiki/Jeffery_Taubenberger" rel="nofollow noreferrer">Taubenberger</a> and Morens it is mentioned that:</p>
<blockquote>
<p>The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics. [Until Covid-19]</p>
<p>With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. <strong>But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer</strong> (9). They continue to circulate endemically and epidemically.</p>
</blockquote>
<p>It citest a <a href="https://www.ncbi.nlm.nih.gov/pubmed/82293/" rel="nofollow noreferrer">somewhat obscure paper</a> for that 1977 event. I've actually read the 1978 paper (now) but it leaves me somewhat more confused. It says this about the putative origins of the re-emergence:</p>
<blockquote>
<p>The close similarity in both the HA and
NA of A/USSR/77-like strains with a 1950
reference virus raises many questions as to
the origin of the current H1N1 genes. Because
antigenic drift has been observed in
animal influenza viruses of several subgroups
that have been isolated over a period
of years ((16) and R. G. Webster, personal
communication), it has been considered
unlikely that the H1N1 virus could
have been maintained in an animal reservoir
for a quarter century without undergoing
detectable mutation. Therefore, some
have speculated that the epidemic may
have resulted from a man-made event.
However, it must be noted that the Hav1
antigen of fowl plague virus and the Heq1
antigen of equine influenza virus, which
appear to be distantly related (17), have
been stable for many years in viruses isolated from birds and horses, respectively
((18) and unpublished results). Chemical
studies of all genes in the A/USSR/77-like
isolates are, therefore, being done to further
examine the question of the origin of this
virus (personal communication from Drs.
W. Bean, P. Palese, and C. Scholtissek).</p>
<p>The contrast between the homogeneity
of antigenic specificity of the HA in
1977-1978 isolates of H1N1 influenza and
the antigenic heterogeneity of the HA in
viruses in the 1950-1951 epidemics does
suggest, however, that current H1N1 viruses
arose from a single source. This is
also supported by the observed uniformity
of avidity of the HAS in 1977-1978 isolates,
since avidity also is believed to be a genetic
characteristic of influenza viruses (7). Variant
viruses that co-circulated in 1950-1951
presumably arose by mutation and evolution
from strains widely seeded in the human
population during the preceding years,
as has also been observed more recently for
H3N2 influenza A strains (19).</p>
<p>Note added in proof: Preliminary results
of analysis of about 500 H1N1 strains of
influenza A virus isolated from about February
to May 1978 suggest that approximately
5% of the viruses exhibit minor antigenic
drift away from the A/USSR/77
reference strain, and that several distinguishable
groups of such variants may be
detected. None of the variants, however,
appear to resemble A/England/1/51 or
other H1N1 strains isolated in the period of
former prevalence of such viruses. Presumably,
therefore, the newer variants represent
examples of mutants of the A/USSR/77-like virus which have appeared following its spread through large segments
of the human population.</p>
</blockquote>
<p>While this paper entertains the idea of a laboratory release, it doesn't quite seem to fully back it up. So, has any additional research been done since then on the matter, that can (better) explain what Taubenberger and Morens [seem to] claim about the 1977 event?</p>
| [
{
"answer_id": 23265,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 1,
"selected": false,
"text": "<p>According to a <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC372859/\" rel=\"nofollow noreferrer\">1992 review</a> the conclusion of release from a freezer is one obtained by elimination of alternatives:</p>\n\n<blockquote>\n <p>Where was this virus for 27 years? The\n possible explanations include preservation in a frozen state,\n preservation in an animal reservoir, or retention in an\n integrated, as yet undetected form in the genetic material of\n a human or lower animal. The animal reservoir option is\n unlikely, for the accumulation of mutations would have\n continued. There is no evidence for integration of influenza\n genetic material into the host genome, leaving the most\n likely explanation that in 1977 the H1N1 virus was reintroduced\n to humans from a frozen source.</p>\n</blockquote>\n\n<p>According to a <a href=\"https://www.virology.ws/2009/03/02/origin-of-current-influenza-h1n1-virus/\" rel=\"nofollow noreferrer\">2009 (academic) blog</a> the actual lab/source of the release was never found and the Chinese and Russians/Soviets strongly denied it came from one of their labs:</p>\n\n<blockquote>\n <p>This possibility has been denied by Chinese and Russian scientists, but remains to this day the only scientifically plausible explanation.</p>\n</blockquote>\n"
},
{
"answer_id": 23271,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": true,
"text": "<p>We have a more plausible reason for the reappearance in 1977 of H1N1. The thesis is that a live attenuated version of H1N1 (LAIV) was used by Chinese scientists who innoculated several 1000s military recruits. It likely was not attenuated correctly and reverted to a more virulent form in-vivo leading to the epidemic.</p>\n\n<blockquote>\n <p>Between 1962 and 1973, almost 40,000 children participated in eight LAIV trials in the USSR (13). Scientists at the Peking Vaccine and Serum Institute in China also carried out clinical trials using live vaccines during the same time period (1). Additionally, there are records of the mass production of a live H1N1 vaccine in Odessa, USSR, in 1977 (14, 15). In the early days of research in the 1940s, LAIVs were often able to regain virulence upon administration to humans and cause disease (16). In addition, many strains isolated from the 1977 outbreak (for example, the A/Tientsin/78/77 isolate) were temperature sensitive (ts), meaning that the virus could not replicate at higher temperatures. Temperature sensitivity generally occurs only after a series of laboratory manipulations, typical in generation of LAIVs, and is used as a biological marker of attenuation. While not all of the 1977-1978 strains were temperature sensitive, a comparison of all 1977 strains shows a higher prevalence of the ts phenotype than in 1950 strains, supporting the claim that the outbreak may have resulted from attempts at attenuation for vaccine purposes (1, 17). The possibility that the 1977-1978 strain could have resulted from a LAIV trial was also mentioned in a personal communication from C. M. Chu, renowned virologist and the former director of the Chinese Academy of Medical Sciences to Peter Palese, who described “the introduction of this 1977 virus [as] the result of vaccine trials in the Far East involving the challenge of several thousand military recruits with live H1N1 virus” (18). Whether this involved an ineffectively attenuated vaccine or a laboratory-cultivated challenge strain, the deliberate infection of several thousand people with H1N1 would be a plausible spark for the outbreak.</p>\n</blockquote>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4542197/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4542197/</a></p>\n"
},
{
"answer_id": 23280,
"author": "helpmeplease",
"author_id": 19247,
"author_profile": "https://health.stackexchange.com/users/19247",
"pm_score": 0,
"selected": false,
"text": "<p>Found this in Wikipedia long ago although might not be what you're looking for.</p>\n\n<p><em>The 1977–1978 Russian flu epidemic was caused by strain Influenza A/USSR/90/77 (H1N1). It infected mostly children and young adults under 23; because a similar strain was prevalent in 1947–57, most adults had substantial immunity. Because of a striking similarity in the viral RNA of both strains – one which is unlikely to appear in nature due to antigenic drift – it was speculated that the later outbreak was due to a laboratory incident in Russia or Northern China, though this was denied by scientists in those countries. The virus was included in the 1978–79 influenza vaccine.</em></p>\n\n<p><a href=\"http://www.epi.hss.state.ak.us/bulletins/docs/b1978_09.pdf\" rel=\"nofollow noreferrer\">http://www.epi.hss.state.ak.us/bulletins/docs/b1978_09.pdf</a></p>\n"
}
] | 2020/04/02 | [
"https://health.stackexchange.com/questions/22936",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/10980/"
] |
22,937 | <p>Presuming that we were able to find a person who was never exposed to any of the human seasonal coronaviruses (part of the viruses that cause the common cold), would the virus be just as deadly for that person as the SARS-CoV-2 currently circulating around the world? Or is SARS-CoV-2 uniquely dangerous?</p>
| [
{
"answer_id": 22938,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 6,
"selected": true,
"text": "<p>The seasonal coronaviruses attach exclusively to cells with a ciliated epithelium.</p>\n<blockquote>\n<p>Coronaviruses invade the respiratory tract via the nose. After an incubation period of about 3 days, they cause the symptoms of a common cold, including nasal obstruction, sneezing, runny nose, and occasionally cough (Figs. 60-1 and 60-2). The disease resolves in a few days, during which virus is shed in nasal secretions. There is some evidence that the respiratory coronaviruses can cause disease of the lower airways but it is unlikely that this is due to direct invasion. Other manifestations of disease such as multiple sclerosis have been attributed to these viruses but the evidence is not clear-cut.</p>\n<p>Studies in both organ cultures and human volunteers show that <strong>coronaviruses are extremely fastidious and grow only in differentiated respiratory epithelial cells</strong>. Infected cells become vacuolated, show damaged cilia, and may form syncytia. Cell damage triggers the production of inflammatory mediators, which increase nasal secretion and cause local inflammation and swelling. These responses in turn stimulate sneezing, obstruct the airway, and raise the temperature of the mucosa.</p>\n</blockquote>\n<p>So, the mechanism of infection is such that they only attack the upper airways.</p>\n<p>The SARS-CoV-2 is totally different. It attaches to the ACE2 surface receptor which is found deep in alveolar pneumocytes. Their damage causes loss of surfactant in the alveoli, the collapse of these air cells that perform oxygen exchange and subsequently ARDS.</p>\n<p>So, seasonal coronaviruses give you a runny nose but don't kill. SARS-CoV-2 collapses the air sacs that allow oxygenation to occur.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK7782/\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/books/NBK7782/</a></p>\n"
},
{
"answer_id": 22964,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>I should add here that there <a href=\"https://www.hindawi.com/journals/criid/2018/6796839/\" rel=\"nofollow noreferrer\">has been</a> a case of ARDS reported for the alphacoronavirus 229E (i.e. a \"common cold\" coronavirus) in 2018. But ARDS occurrences are of course, much less common in these \"common colds\" than in Covid-19 infections. The case report for 229E discusses the few other such occurrences:</p>\n\n<blockquote>\n <p>HCoV-229E has been associated with bronchitis, acute exacerbations of COPD, and pneumonia in infants, children, and elderly persons with underlying illnesses [11–13]. Life-threatening infections have only been described in immunocompromised patients [7, 8], but the correlation of HCoV-229E with LRTI in healthy adult individuals is uncertain [9]. An adult patient with pneumonia tested positive for HCoV-229E has been described in a study conducted in rural Thailand, but it is not made clear if other comorbidities were present [14]. Nine Italian patients hospitalized with LRTI have also been tested positive for HCoV-229E; however, their age is not specified [15]. Αlthough numerous studies have tentatively linked 229E infections to severe respiratory tract illness over many years, no study controlling for age and underlying illness has demonstrated an epidemiologic association between infection with HcoV-229E in healthy adults and any illness other than the common cold. Furthermore, <strong>no case of HCoV-229E-associated ARDS has been reported in immunocompetent adults.</strong> Only a few cases of pulmonary infection and ARDS have been described in a 76-year-old woman infected with the closely related alpha coronavirus HCoV-NL63 [16] and in a 39-year-old woman with poorly controlled DM and infected with the beta coronavirus HCoV-OC43.</p>\n</blockquote>\n\n<p>For severely immunocompromised patients however, there have been cases of 229E infection, triggering pneumonia e.g. as reported in (the papers referenced from the prviousone):</p>\n\n<ul>\n<li><a href=\"https://academic.oup.com/cid/article/37/7/929/422314\" rel=\"nofollow noreferrer\">\"Coronavirus 229E-Related Pneumonia in Immunocompromised Patients\"</a>\n\n<blockquote>\n <p>Here we report 2 well-documented cases of pneumonia related to coronavirus 229E, each with a different clinical presentation.</p>\n</blockquote></li>\n<li>or <a href=\"https://journal.chestnet.org/article/S0012-3692(16)35674-4/fulltext\" rel=\"nofollow noreferrer\">\"Coronavirus Pneumonia Following Autologous Bone Marrow Transplantation for Breast Cancer\"</a>\n\n<blockquote>\n <p>Rarely has coronavirus been linked, either by serology or nasal wash, to pneumonia. We report a case of a young woman who, following treatment for stage IIIA breast cancer using a high-dose chemotherapy regimen followed by autologous bone marrow and stem cell transplantation, developed respiratory failure and was found to have coronavirus pneumonia as diagnosed by electron microscopy from BAL fluid. </p>\n</blockquote></li>\n</ul>\n\n<p>But this is like a handful of cases in toto (for 229E).</p>\n\n<p>The ARDS case cited/mentioned in that (first) paper for NL63 was <a href=\"https://www.atsjournals.org/doi/full/10.1164/rccm.201506-1239LE\" rel=\"nofollow noreferrer\">reported in 2016</a>. This was also diagnosed by <a href=\"https://en.wikipedia.org/wiki/Bronchoalveolar_lavage\" rel=\"nofollow noreferrer\">BAL</a> + electron microscopy. This latter paper also suggests that in immunocompromised patients NL63 may be a bit more problematic (than 229E):</p>\n\n<blockquote>\n <p>In 2010, a case of fatal HCoV-NL63 pulmonary infection during the late-engraftment phase was reported (6). An Australian study reported that 2% of patients presenting to the hospital because of respiratory symptoms tested positive for HCoV-NL63, and 81% of these patients were diagnosed with lower respiratory tract disease; all of them required admission to the hospital, 56% had an abnormal chest xray, and one immunocompromised patient died, yet none of these patients had ARDS (7).</p>\n</blockquote>\n"
}
] | 2020/04/02 | [
"https://health.stackexchange.com/questions/22937",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
22,950 | <p>In this <a href="http://www.vdh.virginia.gov/coronavirus/coronavirus/what-to-do-if-you-have-confirmed-or-suspected-coronavirus-disease-covid-19/" rel="nofollow noreferrer">link</a></p>
<p>Mentions</p>
<blockquote>
<h1>Take these steps to monitor your health while you stay home and practice social distancing:</h1>
<p><strong>Stay home, except to get medical care. Get rest and drink plenty of fluids.</strong></p>
</blockquote>
<p>...</p>
<blockquote>
<ul>
<li>Get rest and drink plenty of water or clear liquids. Avoid alcohol or drinks with caffeine, such as sodas, tea, and coffee.</li>
</ul>
</blockquote>
<p>...</p>
<p>Why?</p>
<p>Why to avoid coffee?</p>
<p>And what would happen if I drink coffee?</p>
<p>What's the worst thing that could happen?</p>
| [
{
"answer_id": 22938,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 6,
"selected": true,
"text": "<p>The seasonal coronaviruses attach exclusively to cells with a ciliated epithelium.</p>\n<blockquote>\n<p>Coronaviruses invade the respiratory tract via the nose. After an incubation period of about 3 days, they cause the symptoms of a common cold, including nasal obstruction, sneezing, runny nose, and occasionally cough (Figs. 60-1 and 60-2). The disease resolves in a few days, during which virus is shed in nasal secretions. There is some evidence that the respiratory coronaviruses can cause disease of the lower airways but it is unlikely that this is due to direct invasion. Other manifestations of disease such as multiple sclerosis have been attributed to these viruses but the evidence is not clear-cut.</p>\n<p>Studies in both organ cultures and human volunteers show that <strong>coronaviruses are extremely fastidious and grow only in differentiated respiratory epithelial cells</strong>. Infected cells become vacuolated, show damaged cilia, and may form syncytia. Cell damage triggers the production of inflammatory mediators, which increase nasal secretion and cause local inflammation and swelling. These responses in turn stimulate sneezing, obstruct the airway, and raise the temperature of the mucosa.</p>\n</blockquote>\n<p>So, the mechanism of infection is such that they only attack the upper airways.</p>\n<p>The SARS-CoV-2 is totally different. It attaches to the ACE2 surface receptor which is found deep in alveolar pneumocytes. Their damage causes loss of surfactant in the alveoli, the collapse of these air cells that perform oxygen exchange and subsequently ARDS.</p>\n<p>So, seasonal coronaviruses give you a runny nose but don't kill. SARS-CoV-2 collapses the air sacs that allow oxygenation to occur.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK7782/\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/books/NBK7782/</a></p>\n"
},
{
"answer_id": 22964,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>I should add here that there <a href=\"https://www.hindawi.com/journals/criid/2018/6796839/\" rel=\"nofollow noreferrer\">has been</a> a case of ARDS reported for the alphacoronavirus 229E (i.e. a \"common cold\" coronavirus) in 2018. But ARDS occurrences are of course, much less common in these \"common colds\" than in Covid-19 infections. The case report for 229E discusses the few other such occurrences:</p>\n\n<blockquote>\n <p>HCoV-229E has been associated with bronchitis, acute exacerbations of COPD, and pneumonia in infants, children, and elderly persons with underlying illnesses [11–13]. Life-threatening infections have only been described in immunocompromised patients [7, 8], but the correlation of HCoV-229E with LRTI in healthy adult individuals is uncertain [9]. An adult patient with pneumonia tested positive for HCoV-229E has been described in a study conducted in rural Thailand, but it is not made clear if other comorbidities were present [14]. Nine Italian patients hospitalized with LRTI have also been tested positive for HCoV-229E; however, their age is not specified [15]. Αlthough numerous studies have tentatively linked 229E infections to severe respiratory tract illness over many years, no study controlling for age and underlying illness has demonstrated an epidemiologic association between infection with HcoV-229E in healthy adults and any illness other than the common cold. Furthermore, <strong>no case of HCoV-229E-associated ARDS has been reported in immunocompetent adults.</strong> Only a few cases of pulmonary infection and ARDS have been described in a 76-year-old woman infected with the closely related alpha coronavirus HCoV-NL63 [16] and in a 39-year-old woman with poorly controlled DM and infected with the beta coronavirus HCoV-OC43.</p>\n</blockquote>\n\n<p>For severely immunocompromised patients however, there have been cases of 229E infection, triggering pneumonia e.g. as reported in (the papers referenced from the prviousone):</p>\n\n<ul>\n<li><a href=\"https://academic.oup.com/cid/article/37/7/929/422314\" rel=\"nofollow noreferrer\">\"Coronavirus 229E-Related Pneumonia in Immunocompromised Patients\"</a>\n\n<blockquote>\n <p>Here we report 2 well-documented cases of pneumonia related to coronavirus 229E, each with a different clinical presentation.</p>\n</blockquote></li>\n<li>or <a href=\"https://journal.chestnet.org/article/S0012-3692(16)35674-4/fulltext\" rel=\"nofollow noreferrer\">\"Coronavirus Pneumonia Following Autologous Bone Marrow Transplantation for Breast Cancer\"</a>\n\n<blockquote>\n <p>Rarely has coronavirus been linked, either by serology or nasal wash, to pneumonia. We report a case of a young woman who, following treatment for stage IIIA breast cancer using a high-dose chemotherapy regimen followed by autologous bone marrow and stem cell transplantation, developed respiratory failure and was found to have coronavirus pneumonia as diagnosed by electron microscopy from BAL fluid. </p>\n</blockquote></li>\n</ul>\n\n<p>But this is like a handful of cases in toto (for 229E).</p>\n\n<p>The ARDS case cited/mentioned in that (first) paper for NL63 was <a href=\"https://www.atsjournals.org/doi/full/10.1164/rccm.201506-1239LE\" rel=\"nofollow noreferrer\">reported in 2016</a>. This was also diagnosed by <a href=\"https://en.wikipedia.org/wiki/Bronchoalveolar_lavage\" rel=\"nofollow noreferrer\">BAL</a> + electron microscopy. This latter paper also suggests that in immunocompromised patients NL63 may be a bit more problematic (than 229E):</p>\n\n<blockquote>\n <p>In 2010, a case of fatal HCoV-NL63 pulmonary infection during the late-engraftment phase was reported (6). An Australian study reported that 2% of patients presenting to the hospital because of respiratory symptoms tested positive for HCoV-NL63, and 81% of these patients were diagnosed with lower respiratory tract disease; all of them required admission to the hospital, 56% had an abnormal chest xray, and one immunocompromised patient died, yet none of these patients had ARDS (7).</p>\n</blockquote>\n"
}
] | 2020/04/02 | [
"https://health.stackexchange.com/questions/22950",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
22,974 | <p>Would it make sense from the public safety point of view to allow the persons already having the antibodies to move more freely than the persons not having the antibodies? Or it is more of an ethical question than a medical one?</p>
| [
{
"answer_id": 22975,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>I would think that this is a reasonable possibility. We assume that they are largely immune but there is a possibility that this is not the case in 100% of recovered patients.</p>\n\n<blockquote>\n <p>But some Wuhan residents who had tested positive earlier and then recovered from the disease are testing positive for the virus a second time. Based on data from several quarantine facilities in the city, which house patients for further observation after their discharge from hospitals, about 5%-10% of patients pronounced \"recovered\" have tested positive again.</p>\n</blockquote>\n\n<p><a href=\"https://www.npr.org/sections/goatsandsoda/2020/03/27/822407626/mystery-in-wuhan-recovered-coronavirus-patients-test-negative-then-positive\" rel=\"nofollow noreferrer\">https://www.npr.org/sections/goatsandsoda/2020/03/27/822407626/mystery-in-wuhan-recovered-coronavirus-patients-test-negative-then-positive</a></p>\n"
},
{
"answer_id": 22977,
"author": "Albrecht Hügli",
"author_id": 17790,
"author_profile": "https://health.stackexchange.com/users/17790",
"pm_score": 1,
"selected": true,
"text": "<p>Projects for broad-based antibody blood tests are currently springing up like mushrooms.\nBut the first test series available will be needed for the staff of health care.</p>\n\n<p>of course there are other interests for antibody tests: virological, epidemiological and as your question implies economical. </p>\n\n<p><em>Antibody blood tests should provide information about the spread of the corona virus so that the measures taken by the authorities can be adapted. A nationwide initiative is now putting pressure.</em></p>\n\n<p><a href=\"https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic\" rel=\"nofollow noreferrer\">https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic</a></p>\n\n<p><em>For example, if a selected group of people were tested for Sars-CoV-2 antibodies every two weeks, the course of the epidemic would be clearly visible.</em></p>\n\n<p><em>The interest, especially in business circles, is huge. Everyone urgently wanted to know where they were in the pandemic, who was at best already immune and could therefore probably move around and work safely again.</em> </p>\n\n<p><a href=\"https://www.srf.ch/news/schweiz/coronavirus-antikoerper-tests-ein-schweizweites-projekt-wird-aufgegleist\" rel=\"nofollow noreferrer\">https://www.srf.ch/news/schweiz/coronavirus-antikoerper-tests-ein-schweizweites-projekt-wird-aufgegleist</a></p>\n\n<p><em>Such data could inform practical issues such as whether and how to reopen schools that have been closed. Relatively few cases have been diagnosed among children, but it isn’t clear whether that’s because they don’t get infected or because their infections are generally so mild that they go unnoticed. Testing children for SARS-CoV-2 antibodies should resolve that.</em></p>\n\n<p><a href=\"https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic\" rel=\"nofollow noreferrer\">https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic</a></p>\n\n<p>Authorities are still afraid of a roll back of the wave when people start moving freely again. It must have a great acceptance and also be respected by those who should still stay at home. </p>\n"
}
] | 2020/04/03 | [
"https://health.stackexchange.com/questions/22974",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19140/"
] |
22,982 | <p>Many news outlets are reporting total COVID-19 cases by country and then comparing them to other countries. For example, comparing the total cases in the <a href="https://www.bbc.com/news/world-us-canada-52056586" rel="nofollow noreferrer">United States vs the total cases in China</a>. As of April 3rd, 2020 this shows that the U.S. has more cases than China. However, there is virtually no mention of comparing <a href="https://www.statista.com/chart/21176/covid-19-infection-density-in-countries-most-total-cases/" rel="nofollow noreferrer">total cases of each country by population</a> which would put the U.S. far below the top. Is there a reason why comparing cases by population wouldn't be significant (from a medical or statistical point of view)? These statistics seem to be ignored by news outlets or are not mentioned at all. </p>
| [
{
"answer_id": 22984,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>It's the simplest measure, the absolute number of cases. The second graph you showed gives us the relative case rate based on a per million of population. Now if for instance the while population of a country succumbed to the disease, the population is now zero. So their number of cases now becomes zero because everyone is decreased. So, that's extreme but the absolute number doesn't have that fault in it.</p>\n\n<p>Most people are more interested in the acceleration curves which is simply the number of diagnosed cases over time. And that's what they show us. </p>\n\n<p>There's no perfect statistic.</p>\n"
},
{
"answer_id": 22985,
"author": "Bryan Krause",
"author_id": 8728,
"author_profile": "https://health.stackexchange.com/users/8728",
"pm_score": 2,
"selected": true,
"text": "<p>As long as the numbers are small, the per capita numbers don't really matter much. Epidemics of infectious diseases spread initially in localized populations, so imagine the case of a disease spreading mostly around a hospital, which is common early on:</p>\n\n<ul>\n<li><p>In one country, a hospital at the epicenter has 50 infected patients. That country has 5,000,000 people.</p></li>\n<li><p>In another country, a hospital at the epicenter has 50 infected patients. That country has 500,000,000 people.</p></li>\n</ul>\n\n<p>The situation is basically the same in both countries: they have a single epicenter with a bunch of patients. There are probably a similar number of unknown cases in the community. If you divided by the total population, you might think one situation is 100X worse, but it really isn't: it's one center. The vast majority of both are still unaffected, and the severity at the epicenter is exactly the same.</p>\n\n<p>Now we are at the point of extensive community spread in many places. So now per capita might start to be meaningful, but there are some remaining limitations:</p>\n\n<p><strong>Testing is not uniform</strong></p>\n\n<p>100 cases in a place with extensive testing does not mean the same as 100 cases in a place without, so case counts aren't very informative. When the numerators aren't comparable it doesn't matter so much that the denominators are different: you have to consider each number on a case-by-case basis (and the \"race\" in the media is not really that relevant).</p>\n\n<p>Some argue <a href=\"https://www.nytimes.com/interactive/2020/03/21/upshot/coronavirus-deaths-by-country.html\" rel=\"nofollow noreferrer\">deaths are a better measure</a>, and I would agree, but those are also limited by reporting differences.</p>\n\n<p><strong>Cases are not distributed randomly within borders</strong></p>\n\n<p>Taking the United States as an example, the US per capita number of cases doesn't tell the whole story, which is that certain geographic locations like New York City and New Orleans have substantially more cases per capita than the rest of the country. Same for Lombardy in Italy; Wuhan in China. Averaging those cases over the entire country doesn't do much to reflect the concentration of cases in places where the health care system is stressed to its limit.</p>\n\n<hr>\n\n<p>So what should we use instead? In many cases I would recommend looking at logarithmic scale data. These tell you what the rate of change is. Even these are not perfect, as both testing and mortality can vary over time (both because of availability of tests and triage as the situation gets more serious), and they may not be the best data for a specific purpose. What they do show is how the rate of increase differs in different countries, and how the rate of increase changes over time in a single country.</p>\n\n<p>For the US, these data: <a href=\"https://www.us-covid-tracker.com/?log=0&consistentY=1&per100k=1&field=deaths&time=1mo\" rel=\"nofollow noreferrer\">https://www.us-covid-tracker.com/?log=0&consistentY=1&per100k=1&field=deaths&time=1mo</a> might be helpful for assessing the extent to which different states have been affected (and shows why California is not making as much news despite having a lot of cases). I think this is one case where non-log-scale per-capita data are informative.</p>\n"
},
{
"answer_id": 22991,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 0,
"selected": false,
"text": "<p>Percentage and raw counts serve different purpose:</p>\n\n<ul>\n<li>Raw counts are one way to get a feeling of the impact on the population (50k deaths gives a different perspective than 0.1%, especially for people who don't know population sizes).</li>\n<li>Percentage are another way to get a feeling of the impact on the population (e.g., black plague is estimated to have wiped out up to 50% of the European population) and also allow for comparison (e.g., a random walk in Switzerland is significantly more dangerous than in China).</li>\n</ul>\n\n<p>Note that, as {1} mentions, case and death counts depend on how testing is done and on how testing is done and how to decide that a death is due to COVID-19.</p>\n\n<p>FYI, updated percentages for all countries: <a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">https://www.worldometers.info/coronavirus/</a> </p>\n\n<hr>\n\n<p>References:</p>\n\n<ul>\n<li>{1} Onder, Graziano, Giovanni Rezza, and Silvio Brusaferro. \"Case-Fatality Rate and Characteristics of Patients Dying in Relation to COVID-19 in Italy.\" JAMA (2020). <a href=\"http://jamanetwork.com/article.aspx?doi=10.1001/jama.2020.4683\" rel=\"nofollow noreferrer\">http://jamanetwork.com/article.aspx?doi=10.1001/jama.2020.4683</a></li>\n</ul>\n"
}
] | 2020/04/03 | [
"https://health.stackexchange.com/questions/22982",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/2282/"
] |
22,986 | <p>It is well-known that South-Korea has developed a powerful system of drive-through testing allowing them to test hundreds of thousands of person in the past two months. I was wondering whether the test-subjects all visit those testing stations on a voluntary basis (because they are worried about their health) or whether true random samples of the population are being tested, supposedly requiring a government order to have certain people take a test on a (semi)compulsory basis.</p>
<p>To summarize: <strong>Is SK conducting random covid-19 tests on sizeable random samples of its population? Is any other country with a major outbreak doing such a thing?</strong></p>
<p>This question arose in my mind in the light of rumours that the covid-19 epidemic would have a tendency to create a pool of infected <a href="https://www.medrxiv.org/content/10.1101/2020.03.14.20036178v1" rel="nofollow noreferrer">10 times larger</a> than reported because alledgedly the main bulk of the infected don't experience grave symptoms and do not seek out a test or diagnosis. </p>
| [
{
"answer_id": 22990,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 3,
"selected": true,
"text": "<blockquote>\n <p>Is SK conducting random covid-19 tests on sizeable random samples of its population? </p>\n</blockquote>\n\n<p>Not currently (source: South Korean friends).</p>\n\n<blockquote>\n <p>Is any other country with a major outbreak doing such a thing?</p>\n</blockquote>\n\n<p>See <a href=\"https://medicalsciences.stackexchange.com/q/21700/43\">Why don't we take a random sample of the population to estimate the amount of COVID-19 cases?</a></p>\n"
},
{
"answer_id": 22993,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>South Korea has adopted a highly technical and transparent approach to Covid-19. By sharing where infected people have been, citizens can see if they have been in contact or near contact with the infected person, and then request a test.</p>\n<blockquote>\n<p>Since the first cases were confirmed, Korean public health authorities and local governments collaborated to precisely document the movement of infected people down to the minute. Authorities sought testimony, watched closed-circuit television, investigated smartphone GPS data and more, publicizing the so-called moving histories of Covid-19 patients. All local governments share information through websites, text messages, and media. Companies have developed apps that allow users to visualize the information. Koreans can now learn where infected people went, when they were there, and how they got there. If someone learns they might have been exposed, they can quickly visit a doctor and begin self-quarantine if they have similar symptoms.</p>\n<p>On February 4, the Korea Centers for Disease Control and Prevention took advantage of the post-MERS reform and authorized an unlicensed Covid-19 test; the government went on to test an extraordinary number of people. By February 26, Korea had tested 46,127 cases, while by that point, Japan had tested just 1,846 cases and the United States only 426. Tests still remain hard to come by in the United States, despite the Trump administration’s repeated suggestions that widespread testing is imminent.</p>\n</blockquote>\n<p>There are few countries as technologically advanced as South Korea that are able to adopt this approach without a wide spread lockdown. And it helped that they allowed the use of an unapproved tests whereas in the USA the CDC blocked the use of independent tests which has lead to their current deplorable state of testing.</p>\n<blockquote>\n<p>Following the end of the MERS outbreak, South Korea enacted a new law in 2016 that allows laboratories to use unapproved in-vitro diagnostic kits in the case of a public health emergency.</p>\n</blockquote>\n<p>and</p>\n<blockquote>\n<p>“Testing is absolutely critical with a fast-travelling virus like this,” says Kang. “We have tested over 350,000 cases so far – some patients are tested many times before they are released, so we can say they are fully cured. Altogether, we’re talking about one out of 145 or one out of 150 people having been tested so far.”</p>\n</blockquote>\n<p><a href=\"https://thebulletin.org/2020/03/south-korea-learned-its-successful-covid-19-strategy-from-a-previous-coronavirus-outbreak-mers/\" rel=\"nofollow noreferrer\">https://thebulletin.org/2020/03/south-korea-learned-its-successful-covid-19-strategy-from-a-previous-coronavirus-outbreak-mers/</a></p>\n<p><a href=\"https://www.weforum.org/agenda/2020/03/south-korea-covid-19-containment-testing/\" rel=\"nofollow noreferrer\">https://www.weforum.org/agenda/2020/03/south-korea-covid-19-containment-testing/</a></p>\n"
}
] | 2020/04/03 | [
"https://health.stackexchange.com/questions/22986",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17835/"
] |
23,020 | <p>I've read the article:</p>
<p><a href="https://www.upmc.com/media/news/040220-falo-gambotto-sars-cov2-vaccine" rel="nofollow noreferrer">https://www.upmc.com/media/news/040220-falo-gambotto-sars-cov2-vaccine</a></p>
<p>regarding a prospective method of immunization against sars-cov-2 using the spike protein of the virus and micro-needle array delivery (MNA) and I've wondered if using the virus instead of the spike protein makes sense. What are the trade-offs? Is the risk of the virus spreading through the bloodstream in the body very high? Is culturing the virus or producing the spike protein more expensive? Can the sars-cov-2 virus be de-activated after being produced to make it safer?</p>
| [
{
"answer_id": 23163,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": true,
"text": "<p>Using weakened virus, or attenuated virus, is very old biotechnology to create vaccines. I doubt that there is any ethics committee that would sanction the use of live attenuated virus as a vaccine through whatever route as there is no data on safety via this route.</p>\n\n<p>Also, you would want to be able inject enough virions to induce an immune response without killing the patient.</p>\n\n<p>The latest technology is to use mRNA which would be used by the body to create the proteins seen on the virus, and the body would then create the antibodies against these proteins.</p>\n\n<blockquote>\n <p>Moderna is studying its messenger RNA (mRNA) vaccine in the US, and CanSino Biologics has begun a trial of its adenoviral vector vaccine in China.</p>\n</blockquote>\n\n<p><a href=\"https://cen.acs.org/pharmaceuticals/vaccines/coronavirus-help-mRNA-DNA-vaccines/98/i14\" rel=\"nofollow noreferrer\">https://cen.acs.org/pharmaceuticals/vaccines/coronavirus-help-mRNA-DNA-vaccines/98/i14</a> </p>\n"
},
{
"answer_id": 30627,
"author": "Gerry Creager",
"author_id": 21548,
"author_profile": "https://health.stackexchange.com/users/21548",
"pm_score": -1,
"selected": false,
"text": "<p>The Moderna and Pfizer-BioNTech mRNA vaccines, which use several protein fragments from the S1 protein and the receptor binding domain as primary antigenic targets to trigger production of antibodies. In general, whole (attenuated or killed) virus vaccines are pretty specific to that virus, and this works well for a virus that doesn't mutate or vary readily. Measles is a good example. the mRNA vaccines tend to provide more separate targets for antibody creation because they use smaller protein fragments. Thus, mutations and variants are more likely to see some positive effect from prior immunization than if a whole-virus response was created.</p>\n"
}
] | 2020/04/05 | [
"https://health.stackexchange.com/questions/23020",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19140/"
] |
23,029 | <p>Does the anti-parasitic Ivermectin work in actual human studies versus the Petri dish in vitro studies, when treating coronavirus COVID-19 infection? And if so, is it safe in humans?</p>
<p>An <a href="https://www.sciencedirect.com/science/article/pii/S0166354220302011" rel="noreferrer">in vitro study</a> was done.</p>
| [
{
"answer_id": 23042,
"author": "Brian",
"author_id": 19203,
"author_profile": "https://health.stackexchange.com/users/19203",
"pm_score": 1,
"selected": false,
"text": "<p>This in-vitro study reveals exciting data regarding Ivermectin, which is typically used for treatment of scabies. </p>\n\n<p>I was unable to find any clinical data to support use of Ivermectin for COVID-19. But this study definitely supports starting a clinical trial given the widespread availability of Ivermectin. Overall ivermectin is well-tolerated in both children and adults, with rash being one of the most common side effects. It may have fewer severe adverse effects than hydroxychloroquine, which can cause fatal arrhythmias like Torsades de Pointes(though this is more with chronic use; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16615675\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/16615675</a>). This supports ivermectin as a good candidate drug to study.</p>\n\n<p>It is important to note, however, that many drugs that have shown to be effective in-vitro will fail to produce any clinical benefit when given to animals or humans. For instance, for ebola virus, chloroquine was effective in-vitro but not in guinea pigs (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26459826\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/26459826</a>). There are many factors that could contribute to these discrepancies, including issues with bioavailability, distribution to the appropriate tissues, entrance into cells, and breakdown of the drug by cellular or viral mechanisms. </p>\n"
},
{
"answer_id": 25015,
"author": "Blue Various",
"author_id": 16820,
"author_profile": "https://health.stackexchange.com/users/16820",
"pm_score": 2,
"selected": false,
"text": "<p>There is a paper which suggest that ivermectin is unlikely to be an effective antiviral vs. SARS-CoV-2 at recommended dosing.</p>\n<blockquote>\n<p>Please find this <a href=\"https://www.medrxiv.org/content/10.1101/2020.04.21.20073262v1\" rel=\"nofollow noreferrer\">preprint</a> or this <a href=\"https://ascpt.onlinelibrary.wiley.com/doi/10.1002/cpt.1889\" rel=\"nofollow noreferrer\">paper</a>.</p>\n</blockquote>\n<p>This paper has the following description.</p>\n<blockquote>\n<p>Recently, an article by Caly et al. reported that ivermectin inhibited severe acute respiratory syndrome‐coronavirus (SARS‐CoV‐2) in vitro causing an ~ <strong>5,000‐fold reduction in viral RNA at 48 hours with ivermectin at 5 μM</strong>. The concentration resulting in <strong>50% inhibition (IC50) of 2 μM</strong> (1,750 ng/mL) is > 35× higher than the <strong>maximum plasma concentration (Cmax) of 0.05 µM</strong> (46.6 ng/mL)2 after oral administration of the approved dose (~ 200 μg/kg) and ivermectin showed little to no activity 1 μM in vitro. Because ivermectin is highly bound to serum albumin (93%), the IC50 is orders of magnitude higher than the <strong>unbound plasma Cmax after approved doses of ivermectin (0.0035 µM; 3.26 ng/mL)</strong>.</p>\n</blockquote>\n<p>Therefore, a large estimate is that the plasma concentration is 2 μM /0.0035 µM =571 times insufficient.</p>\n<p>I think the key points of above paper are as follows;</p>\n<ul>\n<li>The development of methods to realize enough concentrations of ivermectin in the lungs/plasma.</li>\n<li>Is ivermectin still safe when the enough concentration is achieved in the lungs/plasma?</li>\n</ul>\n<p>These questions follow naturally from the preprint/paper above.</p>\n<p>However, as described in the @Matthew Elvey 's answer, as of December 5, 2020, <strong>there are many clinical results which suggest that we can get enough efficiency</strong> with far less dosage than would be assumed from pharmacokinetic considerations; formulas that combine several things such as zinc and vitamins seem to be more desirable.(Added on December 5, 2020)</p>\n<p>The gap between inadequate blood levels and a strong clinical effect is one puzzle. It is an exciting scientific topic. This gap will be bridged as the mechanism of action of ivermectin is elucidated.</p>\n<p>So far, various mechanisms have been proposed, but it has not been decided which one is the mainstay. That's what Satoshi Omura said in his <a href=\"https://www.youtube.com/watch?v=aETVHbqlDbo?t=1:10:07\" rel=\"nofollow noreferrer\">open youtube lecture</a> (In Japanese, the relevant part has been headed out.) at <a href=\"https://en.wikipedia.org/wiki/Showa_Pharmaceutical_University\" rel=\"nofollow noreferrer\">Showa Pharmaceutical University</a> at the end of October, 2020.</p>\n<p>The following is a summary of the <a href=\"https://www.youtube.com/watch?v=aETVHbqlDbo?t=1:10:07\" rel=\"nofollow noreferrer\">youtube lecture</a> by Satoshi Omura.</p>\n<blockquote>\n<ul>\n<li>There are various proposed mechanisms of action by which ivermectin inhibits coronaviruses, and it is not clear which theory is definitively correct. He introduced the following two mechanisms <strong>as examples</strong>.</li>\n<li>One is that ivermectin inhibits the process by which the viral spike joins <a href=\"https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2\" rel=\"nofollow noreferrer\">ACE2</a> and enters the cell. This is an example of the idea of inhibiting viral entry. (Figure 1, left)</li>\n<li>Dr. Maruta and colleagues in Australia have proposed a different mechanism. In that theory ivermectin acts on the human body. Briefly, when the virus binds to receptors such as <a href=\"https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2\" rel=\"nofollow noreferrer\">ACE2</a>, a kinase called <a href=\"https://en.wikipedia.org/wiki/PAK1\" rel=\"nofollow noreferrer\">PAK1</a> is induced. This is a release kinase, which appears to be released when infection occurs and suppresses the immune system. Their idea seems to be that ivermectin also protects the immune system by inhibiting PAK1. (Figure 1, right)</li>\n</ul>\n</blockquote>\n<h2><a href=\"https://i.stack.imgur.com/6SknF.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/6SknF.png\" alt=\"enter image description here\" /></a><br>\n<strong>Fig.1</strong> Examples of proposed mechanisms of action. Adapted from a <a href=\"https://www.youtube.com/watch?v=aETVHbqlDbo?t=1:10:07\" rel=\"nofollow noreferrer\">lecture</a> given by Satoshi Omura at the end of October 2020, partially written in Japanese.</h2>\n<hr />\n<p>In September 2020, Japan's <a href=\"https://en.wikipedia.org/wiki/Kitasato_University\" rel=\"nofollow noreferrer\">Kitasato University</a> appears to have begun a physician-led clinical trial for COVID-19. Kitasato University is where <a href=\"https://en.wikipedia.org/wiki/Satoshi_%C5%8Cmura\" rel=\"nofollow noreferrer\">Satoshi Omura</a>, one of the discoverers of ivermectin, is affiliated.</p>\n<ul>\n<li><a href=\"https://jrct.niph.go.jp/en-latest-detail/jRCT2031200120\" rel=\"nofollow noreferrer\">jRCT2031200120</a>:A placebo-controlled, randomized, double-blind study in Covid-19\npatients with ivermectin; An investigator initiated trial</li>\n</ul>\n<p>They will administer the Ivermectin Tablets, sold under the brand name <a href=\"https://www.rad-ar.or.jp/siori/english/kekka_plain.cgi?n=40911\" rel=\"nofollow noreferrer\">STROMECTOL</a>, orally.\nAccording to a Japanese newspaper <a href=\"https://yakuyomi.jp/industry_news/20200923a/\" rel=\"nofollow noreferrer\">article</a> (written in Japanese), the trial is expected to be completed in March 2021. (Completion = LPI?)</p>\n<p>On the other hand, scandalous clinical data also exists. It seems that one data analysis company, <a href=\"https://en.wikipedia.org/wiki/Surgisphere\" rel=\"nofollow noreferrer\">Surgisphere</a> published a preprint saying that ivermectin was beneficial based on analysis of real world data, but it was later retracted. According to this <a href=\"https://www.sciencemag.org/news/2020/06/mysterious-company-s-coronavirus-papers-top-medical-journals-may-be-unraveling\" rel=\"nofollow noreferrer\">article</a>, it seems to have pointed out many unnatural aspects of the data.</p>\n<hr />\n<p>By the way, Ivermectin's 'birthplace' features hot news about Ivermectin. Note that a bit slow in terms of information; as of 5 December 2020, the introduction of the paper published on 10 November is the most recent. Even more unfortunate is that the information is in Japanese. However, it will be helpful to see the trends. For many people, though, they may need the help of machine translation.<br>\n<a href=\"https://kitasato-infection-control.info/\" rel=\"nofollow noreferrer\">https://kitasato-infection-control.info/</a>\n(Written in Japanese)</p>\n"
},
{
"answer_id": 25237,
"author": "WHO's NoToOldRx4CovidIsMurder",
"author_id": 17268,
"author_profile": "https://health.stackexchange.com/users/17268",
"pm_score": 2,
"selected": false,
"text": "<p>Yes. Prevents it too. 100% in some studies, but not others, but then, the vaccines aren't proven stop it 100%, and ivermectin's safety profile is far superior.</p>\n<p>What's established/true has changed a lot since this question was asked and initially answered.</p>\n<h2>CHEST</h2>\n<p>Does CHEST only publish results of INvalid clinical evidence? No. It's v. reputable. Yes, this retrospective study shows it works, and likely works much better than the other treatments already in use.</p>\n<p>Chest Article : <a href=\"https://journal.chestnet.org/article/S0012-3692(20)34898-4/fulltext\" rel=\"nofollow noreferrer\">Use of Ivermectin Is Associated With Lower Mortality in Hospitalized Patients With Coronavirus Disease 2019</a> (Title, Link)</p>\n<hr />\n<h2>FLCCC review</h2>\n<p>And in addition to reliable clinical evidence (which Cochrane says evidence shows is as reliable as RCT evidence) there are a great many preprint results from RCT and published results from RCT. Rather than put up a static, soon to be wrong summary, I point to this:</p>\n<p>The <strong>FLCCC</strong>'s <a href=\"https://covid19criticalcare.com/flccc-ivermectin-in-the-prophylaxis-and-treatment-of-covid-19/\" rel=\"nofollow noreferrer\"><strong>comprehensive review of the emerging evidence for Ivermectin use in our I-MASK+ protocol</strong> (PDF, continuously updated)</a> (It recently had 87 citations and resolves to <a href=\"https://covid19criticalcare.com/wp-content/uploads/2020/11/FLCCC-Ivermectin-in-the-prophylaxis-and-treatment-of-COVID-19.pdf\" rel=\"nofollow noreferrer\">this URL</a> but that has changed or is sure to change.)</p>\n<p>Also, it is more than an incredibly popular preprint that has surely saved tens of thousands of lives; it has now passed peer review for publication in <em>Frontiers in Pharmacology</em>. doi: 10.3389/fphar.2021.643369.</p>\n<p>They put it thus in their review:</p>\n<blockquote>\n<p>To our knowledge, the current review is the earliest to compile\nsufficient clinical data to demonstrate a strong signal of therapeutic\nefficacy based on numerous clinical trials in multiple disease phases,\nhowever it is limited by the fact that only a minority of studies have\nbeen published in peer-reviewed publications, with the majority of\nresults compiled from manuscripts uploaded to medicine pre-print\nservers or from registered trials that have posted preliminary results\non clinicaltrials.gov.</p>\n</blockquote>\n<p>] But "minority" != 0. Overall, the results are largely highly significant. Results from 16 clinical trials and 3 large case series are reviewed.</p>\n<p>They even mention:</p>\n<blockquote>\n<p>Two manuscripts reviewing the scientific rationale and evolving\npublished clinical evidence base in support of the MATH+ protocol\npassed peer review and have been accepted for publication in major\nmedical journals at two different time points in the pandemic (2, 3).</p>\n</blockquote>\n<h1>E-BMC for Cochrane's <strong>Tess Lawrie</strong></h1>\n<p><a href=\"https://www.e-bmc.co.uk/#comp-k86k1hw8\" rel=\"nofollow noreferrer\"> e-bmc.co.uk </a> : This organization has published a meta-analysis to the rigorous standards of the WHO by these extremely experienced and prolific Cochrane authors.</p>\n<p>Their Tess Lawrie <a href=\"https://www.youtube.com/watch?v=rHPkR6QRcCc\" rel=\"nofollow noreferrer\">discusses it here. ESSENTIAL</a>.</p>\n<h2>Ivermectin has helped Billions of patients, is helping Millions fight the pandemic.</h2>\n<p>People have already received far over three billion < sic > doses, and the record of significant adverse reports indicates is about as safe as medicine gets.</p>\n<p>Another retrospective study is based on over 1 million doses distributed in one of each of several <strong>paired Brazilian cities</strong>. Another compares <strong>regions in Paraguay</strong> that did and didn't receive ivermectin. Another compares <strong>African states</strong> where ivermectin is and isn't distributed nationwide. In each study, cases and deaths, tracked over time, diverge, strongly according to ivermectin distribution.</p>\n<p>There are now several literature reviews and meta-analyses by several groups of doctors including the from FLCCC - who are some of the most experienced in emergency medicine. These are confirmed by their clinical experience as well as large population studies and medical groups in several countries on the latest research.</p>\n<h1>100% prevention???</h1>\n<p>Yup. The 100% figure comes from <a href=\"https://doi.org/10.31546/2633-8653.1007\" rel=\"nofollow noreferrer\">Carvallo</a>. It reports:</p>\n<blockquote>\n<p>The overall infection rate in health care workers recruited for this study was 20% with 237 testing positive for CoViD 19 during the 3 month study recruitment. Of those infected, all patients were from the comparator group of using PPE alone. This represented an overall infection rate of 58.2% ( 237 of 407) in the PPE group.\n<strong>No patients of the 788 treated with [IVERMECTIN] tested positive for CoViD 19 during the study.</strong></p>\n</blockquote>\n<p>I.e. 100% did not. And this was a multi-center study in 4 major hospitals, including the pilot, with 1,424 <strong>health care workers</strong>. <strong>Of the 919 who got ivermectin, 100% remained CoViD-19-free.</strong></p>\n<h2>WHO endorsements</h2>\n<p>There are two recent WHO-originated and funded endorsements of ivermectin. First, <a href=\"https://www.who.int/news/item/17-12-2020-a-parasitic-infection-that-can-turn-fatal-with-administration-of-corticosteroids\" rel=\"nofollow noreferrer\">on the WHO website, ivermectin is recommended</a> for treatment of Covid-19 patients when they are being treated with immunosuppressants.</p>\n<p>Secondly the WHO funded an evaluation of the evidence to date and Dr Hill, the expert consultant the WHO relies on for such evaluations of evidence to be used as the basis for official WHO recommendations has spoken very encouragingly regarding the evidence from randomized controlled trials demonstrating the utility of Ivermectin in treating Covid-19 that his work so far has uncovered:</p>\n\n<p>Andrew Hill for WHO: <a href=\"https://m.youtube.com/watch?v=yOAh7GtvcOs\" rel=\"nofollow noreferrer\">https://m.youtube.com/watch?v=yOAh7GtvcOs</a> (censored)\nOriginal is at <a href=\"https://medincell.com/IvermectinWorkshop/AndrewHill.mp4\" rel=\"nofollow noreferrer\">https://medincell.com/IvermectinWorkshop/AndrewHill.mp4</a>, (works) and I have a copy as well. <a href=\"https://www.dropbox.com/s/li4i3pyl52t88dy/AndrewHill%20WebOpt%2Ch265%2C0%2C-fps%2CRF31%2C%20placebo%2C%20to1920x1k%20-36%2C106%2C-94%2C-4%2CnoALL%2CHE-AAC40kbps.m4v?dl=0\" rel=\"nofollow noreferrer\">https://www.dropbox.com/s/li4i3pyl52t88dy/AndrewHill%20WebOpt%2Ch265%2C0%2C-fps%2CRF31%2C%20placebo%2C%20to1920x1k%20-36%2C106%2C-94%2C-4%2CnoALL%2CHE-AAC40kbps.m4v?dl=0</a> (works; sign-up/login NOT needed)</p>\n<p><a href=\"https://www.who.int/news/item/17-12-2020-a-parasitic-infection-that-can-turn-fatal-with-administration-of-corticosteroids\" rel=\"nofollow noreferrer\">https://www.who.int/news/item/17-12-2020-a-parasitic-infection-that-can-turn-fatal-with-administration-of-corticosteroids</a></p>\n<p>--\n(The ~Sphere data-derived paper is obviously garbage and merits scant not attention outside the tabloids.)</p>\n<p>From Hill's presentation:\n<img src=\"https://i.stack.imgur.com/Yc722.jpg\" alt=\"Sources\" /></p>\n"
},
{
"answer_id": 25504,
"author": "WHO's NoToOldRx4CovidIsMurder",
"author_id": 17268,
"author_profile": "https://health.stackexchange.com/users/17268",
"pm_score": 0,
"selected": false,
"text": "<p>(What's true has changed even further!! A lot changed AGAIN - since this question was asked and initially answered, AND THEN since it was (last month) initially answered by me! So time for another new answer!)</p>\n<p>YES! In addition to several literature reviews by several groups of doctors including some of the most experienced in emergency medicine, and confirmed by their clinical experience as well as large population studies and medical groups in several countries on the latest research, there are two recent WHO-originated and funded endorsements of ivermectin. First, on the WHO website, ivermectin is recommended for treatment of Covid-19 patients when they are being treated with immunosuppressants. Secondly The WHO funded an evaluation of the evidence to date and the expert consultant the WHO relies on for such evaluations of evidence to be used as the basis for official WHO recommendations has spoken very encouragingly regarding the evidence from randomized controlled trials demonstrating the utility of Ivermectin in treating Covid-19 that his work so far has uncovered.</p>\n\n<p>Andrew Hill for WHO: <a href=\"https://m.youtube.com/watch?v=yOAh7GtvcOs\" rel=\"nofollow noreferrer\">https://m.youtube.com/watch?v=yOAh7GtvcOs</a> (censored)\nOriginal is at <a href=\"https://medincell.com/IvermectinWorkshop/AndrewHill.mp4\" rel=\"nofollow noreferrer\">https://medincell.com/IvermectinWorkshop/AndrewHill.mp4</a>, (works) and I have a copy as well. <a href=\"https://www.dropbox.com/s/li4i3pyl52t88dy/AndrewHill%20WebOpt%2Ch265%2C0%2C-fps%2CRF31%2C%20placebo%2C%20to1920x1k%20-36%2C106%2C-94%2C-4%2CnoALL%2CHE-AAC40kbps.m4v?dl=0\" rel=\"nofollow noreferrer\">https://www.dropbox.com/s/li4i3pyl52t88dy/AndrewHill%20WebOpt%2Ch265%2C0%2C-fps%2CRF31%2C%20placebo%2C%20to1920x1k%20-36%2C106%2C-94%2C-4%2CnoALL%2CHE-AAC40kbps.m4v?dl=0</a> (works; sign-up/login NOT needed)</p>\n<p><a href=\"https://www.who.int/news/item/17-12-2020-a-parasitic-infection-that-can-turn-fatal-with-administration-of-corticosteroids\" rel=\"nofollow noreferrer\">https://www.who.int/news/item/17-12-2020-a-parasitic-infection-that-can-turn-fatal-with-administration-of-corticosteroids</a></p>\n<p><img src=\"https://i.stack.imgur.com/Yc722.jpg\" alt=\"Sources\" /></p>\n"
},
{
"answer_id": 25754,
"author": "Narusan",
"author_id": 8212,
"author_profile": "https://health.stackexchange.com/users/8212",
"pm_score": 2,
"selected": false,
"text": "<h2>We do not know. Until there is a phase 3 clinical trial and ivermectin gets FDA approval, it is too early to draw definite conclusions.</h2>\n<p>[The NIH has selected some of the studies performed and combined them into a table][1]. <strong>At the time, all of them</strong> had one or more methodical disadvantage or limitation such as no peer review, no randomisation or a small sample size (20 patients in each arm) and were deemed insufficient to draw a conclusion.</p>\n<p>The <a href=\"https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930464-8\" rel=\"nofollow noreferrer\">most recent study published in The Lancet</a> (one of the most prestigious scientific journals) found no statistically significant difference in clinical endpoints for the usage of ivermectin, and maybe smaller viral loads but no difference in vital signs etc. This study also had a very small sample size (12 patients in each arm, all at low risk).</p>\n<p>[1]: <a href=\"https://www.covid19treatmentguidelines.nih.gov/tables/table-2c/\" rel=\"nofollow noreferrer\">Table 2c. Ivermectin: <strong>Selected</strong> Clinical Data. NIH.gov\nLast Updated: February 11, 2021</a>.</p>\n"
}
] | 2020/04/05 | [
"https://health.stackexchange.com/questions/23029",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17942/"
] |
23,035 | <p>I don't know if this is the right place to ask this question. I feel like a lot of people are asking a very similar question, and all we have are deadlines for quarantines (as of writing this question, <a href="https://www.theguardian.com/world/2020/apr/01/italy-extends-lockdown-amid-signs-coronavirus-infection-rate-is-easing" rel="nofollow noreferrer">Italy is under quarantine until 13 April</a>), rather than deadlines for the impact.</p>
<p>I want to purchase a flight to Italy while the prices are very low (as of writing this, prices are less than $700). However, I don't want to fly there during this pandemic, for obvious reasons. So what is the general forecast for COVID-19? Does such a thing exist? </p>
| [
{
"answer_id": 23041,
"author": "I likeThatMeow",
"author_id": 17725,
"author_profile": "https://health.stackexchange.com/users/17725",
"pm_score": 0,
"selected": false,
"text": "<blockquote>\n <p>So what is the general forecast for COVID-19? Does such a thing exist?</p>\n</blockquote>\n\n<p>Yes, such thing exists.</p>\n\n<p>It is predicted that COVID-19 will end within 12-18 months:</p>\n\n<blockquote>\n <blockquote>\n <p>In <em><a href=\"https://www.theatlantic.com/health/archive/2020/03/how-will-coronavirus-end/608719/\" rel=\"nofollow noreferrer\">How the Pandemic Will End</a></em> in the <strong>ll. The Endgame</strong> section:</p>\n \n <p>No matter which strategy is faster, Berkley and others estimate that it will take 12 to 18 months to develop a proven vaccine, and then longer still to make it, ship it, and inject it into people’s arms.</p>\n </blockquote>\n</blockquote>\n"
},
{
"answer_id": 23524,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 0,
"selected": false,
"text": "<p>I'm not aware of a forecast for the world as a whole, other than a vague \"12 to 18 months\". For individual countries and regions, a number of groups are making forecasts of the progression of the disease. For example, the <a href=\"http://www.healthdata.org/\" rel=\"nofollow noreferrer\">Institute for Health Metrics and Evaluation</a> at the University of Washington predicts that under current conditions, the <a href=\"https://covid19.healthdata.org/italy\" rel=\"nofollow noreferrer\">outbreak in Italy</a> will be effectively over (0 deaths per day) no later than June 7.</p>\n\n<p>Quarantine deadlines are mostly unrelated to the progress of the pandemic. For example, in the United States, it's common for the law to limit the duration of emergency orders. In New York, for example, <a href=\"https://www.nysenate.gov/legislation/laws/EXC/29-A\" rel=\"nofollow noreferrer\">emergency orders cannot last longer than 30 days, but they can be renewed at that time</a>.</p>\n"
},
{
"answer_id": 23561,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 1,
"selected": false,
"text": "<p>As of May 2020, many governmental timelines are being developed as the result of COVID-19 forecasting models from public health authorities, although others may be politically or economically influenced as well.</p>\n\n<p>While the IHME models have been featured, others including the Northeastern University models developed by Prof Alessandro Vespignani have been used to develop regional forecasts. This group has led the <a href=\"https://covid19.gleamproject.org/\" rel=\"nofollow noreferrer\">GLEAM project</a> seeking to forecast the pandemic not only based on traditional epidemiology models known as “compartment” SEIR or SIR models, but also randomized simulations.</p>\n\n<p>Many of these models are forecasting the peak death time period and capacity utilization of hospital ICUs though, rather than general risk to the public. Similarly, because other past epidemics have seen a second wave, for a variety of reasons, many models are being re-run to look for and predict any resurgence, which may also be influenced by weather factors as well as people’s behavior to move indoors to more social contact during colder months if people begin to stop social distancing measures.</p>\n"
}
] | 2020/04/05 | [
"https://health.stackexchange.com/questions/23035",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/6576/"
] |
23,048 | <p>What is the purpose of using vaccines against commonly found bacteria? Since the human immune system develops at birth and shortly thereafter (via colostrum) natural defenses against common bacteria, presumably the body already has antibodies against common bacteria. What purpose is there in "innoculating" someone against such bacteria?</p>
<p>For example, bacteria like pneumococcus endemically colonize everyone's lungs. <a href="https://rupress.org/jem/article/53/4/535/10121/THE-EPIDEMIOLOGY-OF-PNEUMOCOCCUS-INFECTION-THE" rel="nofollow noreferrer">In one study pneumococci were found in 80% of the healthy patients studied</a>. Of course, that is just the bacteria that were <em>found</em>. Undoubtedly the other 20% of the healthy patients had various colonies of pneumococcus which simply went undiscovered. So, obviously the human body is well adapted to constantly defend against pneumococcus, yet there are varieties of <a href="https://en.wikipedia.org/wiki/Pneumococcal_vaccine" rel="nofollow noreferrer">pneumococcal vaccine</a> anyway. Why would this be? To make money, or is there a proven biological action that implies a benefit? By a "biological action" I mean an explanation of the immunological mechanism by which the innoculation significantly augments pre-existing T-cell/B-cell receptors for common bacteria such as pneumococcus, and has a real benefit which is not merely reduplicative. </p>
| [
{
"answer_id": 23053,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>There are two immune responses to an infection, primary and secondary. Vaccination makes it possible for the body to immediately switch to a secondary response. So that's why young adults are vaccinated again meningococcal disease so that they don't die from meningitis while the body is still mounting its primary immune response.</p>\n<blockquote>\n<p>The secondary immune responses can usually prevent disease, because the pathogen is detected, attacked and destroyed before symptoms appear. In general, adults respond more rapidly to infection than children. They are able to prevent disease or reduce the severity of the disease by mounting a rapid and strong immune response to antigens they have previously experienced. In contrast, children have not experienced as many antigens and are more likely to get sick.</p>\n<p>Memory of the infection is reinforced and long lived antibodies remain in circulation. Some infections, such as chickenpox, induce a life-long memory of infection. Other infections, such as influenza, vary from season to season to such an extent that even an adult is unable to adapt.</p>\n</blockquote>\n<p><a href=\"https://www.immune.org.nz/immunisation/immune-system-vaccination\" rel=\"nofollow noreferrer\">https://www.immune.org.nz/immunisation/immune-system-vaccination</a></p>\n"
},
{
"answer_id": 23056,
"author": "Charles E. Grant",
"author_id": 18010,
"author_profile": "https://health.stackexchange.com/users/18010",
"pm_score": 2,
"selected": false,
"text": "<p>As @BryanKrause points out in a comment, there are many, many, <a href=\"https://en.wikipedia.org/wiki/Strain_(biology)\" rel=\"nofollow noreferrer\">strains</a> of Pneumococcus, many of which <strong>do not cause disease in otherwise healthy humans</strong>. The paper you referred to looked at 500 strains of Pneumococcus: \"They formed smooth colonies and were <strong>for the most part avirulent</strong> for mice.\" That is, most of the strains they looked were not disease causing! You may be more familiar with this phenomena with E. coli and food borne disease. All of us have guts full of E. coli which we live in a symbiotic relationship with. However, if you pick up the wrong strain from a contaminated salad bar, you can get very, very, sick. </p>\n\n<p>For bacteria, the species level is a fairly gross classification, and each strain may have subtle variations in the proteins presented at the surface of the bacterium. These surface proteins can play a key role in both the virulence of the bacteria, and our immune response to it. The <a href=\"https://www.cdc.gov/vaccines/hcp/adults/downloads/fs-pneumo-hcp.pdf\" rel=\"nofollow noreferrer\">CDC tracks 90 strains of Pneumococcus that are responsible for most serious human disease. The current pneumococcal polysaccharide vaccine is effective against 23 of those strains.</a>. Having been exposed to one of the non-disease causing strains does not necessarily confer immunity to a disease causing train. It depends on the details of the differences between the strains.</p>\n\n<p>In addition, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582124/\" rel=\"nofollow noreferrer\">our immune systems tend to fail as we get older</a>. As we age our immune systems have a lessened ability to respond to new infections, and they can even \"forget\" how to respond to pathogens that have already been seen. That's why the CDC recommends this vaccine for adults over the age of 65, and younger adults with compromised immune systems. It isn't generally offered to healthy young people.</p>\n"
}
] | 2020/04/05 | [
"https://health.stackexchange.com/questions/23048",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/5371/"
] |
23,059 | <p>I would add my own research if I could to respect site rules, but I can't. There are no studies on SARS-CoV-2, all I can find is for SARS-CoV-1 and some Chinese information based studies. </p>
<p>My government is planning to do massive testing (when tests are available) and transfer and isolate every asymptomatic person in buildings such as hotels. The right is in arms saying this is like gulags and saying now they don't want to do the test.</p>
<p>My question, I hope generically, is: if someone is infected but asymptomatic, could the exposure to a high virus load lead to COVID-19 disease? </p>
<p>Or conversely: if your immune system is already coping well with the virus, the addition of more virus load can't worsen your diagnosis.</p>
| [
{
"answer_id": 23060,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>Doing such an experiment on humans would obviously be unethical in the present circumstances. There has been <a href=\"https://www.livescience.com/monkeys-cannot-get-reinfected-with-coronavirus-study.html\" rel=\"nofollow noreferrer\">a report</a> that monkeys who recovered and were later re-infected with mega-doses of the Covid-19 virus didn't get sick again. This is not terribly conclusive, because monkeys don't get severe symptoms from SARS like we do, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC521815/\" rel=\"nofollow noreferrer\">for example</a>. (SARS is the closest relevant relative to the Covid-19 virus aka SARS-CoV-2.)</p>\n<p>Immunity to a pathogen, <a href=\"https://www.virology.ws/2009/12/28/reinfection-with-2009-influenza-h1n1/\" rel=\"nofollow noreferrer\">in general</a> takes about 3-4 weeks to develop to develop fully, so if you [get] re-infect[ed] with a larger dose within this window, even a after a vaccine, you can cause/get the disease, although it's apparently a pretty rare occurrence.</p>\n<blockquote>\n<p>These individuals were likely resusceptible to reinfection with the same strain of influenza virus due to a confluence of unusual events. First, all three were reinfected within three weeks, before their primary adaptive response had sufficiently matured. Another contributing factor was the high level of circulation of the pandemic strain. [...]</p>\n<p>Could reinfection also occur after immunization with influenza vaccine? Yes, if the immunized individual encounters the virus before the primary antibody response matures, which occurs in 3-4 weeks. This is more likely to occur during pandemic influenza when circulation of the virus is more extensive than in non-pandemic years.</p>\n<p>[Citing:]</p>\n<p>Perez CM, Ferres M, & Labarca JA (2010). Pandemic (H1N1) 2009 Reinfection, Chile. Emerging infectious diseases, 16 (1), 156-7 PMID: 20031070</p>\n</blockquote>\n<hr />\n<p>About the Fangcang-style hospitals (i.e. make-shift hospitals for those with mild or asymptomatic infections), which China <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\">says it closed</a> the last one on March 10 (after there were 13 opened in Wuhan at the peak); it <a href=\"https://politics.stackexchange.com/questions/52494/are-any-countries-besides-china-planning-to-use-fangcang-hospitals-to-relocate\">turns out</a> they used now in other countries, and they are even a <a href=\"https://www.who.int/publications-detail/home-care-for-patients-with-suspected-novel-coronavirus-(ncov)-infection-presenting-with-mild-symptoms-and-management-of-contacts\" rel=\"nofollow noreferrer\">WHO recommendation</a> of sorts (as of March 17):</p>\n<blockquote>\n<p>WHO recommends that all laboratory confirmed cases be isolated and cared for in a health care facility.</p>\n<p>[...]</p>\n<p>If all mild cases cannot be isolated in health facilities, then those with mild illness and no risk factors may need to be isolated in non-traditional facilities, such as repurposed hotels, stadiums or gymnasiums where they can remain until their symptoms resolve and laboratory tests for COVID-19 virus are negative.</p>\n</blockquote>\n<p>According to the (April 2) <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\"><em>Lancet</em> paper</a> on Fangcang hospitals, they Chinese took various precautions to prevent cross-infection with other diseases in such settings. How strictly these measures have been implemented and how well replicated in non-Chines Fangcangs elsewhere, I won't venture to comment here, but <a href=\"https://edition.cnn.com/2020/02/22/asia/china-coronavirus-roundup-intl-hnk/index.html\" rel=\"nofollow noreferrer\">CNN had</a> a somewhat disparaging article about Fangcang hospitals back in February, outlining their shortcomings. Since then, the US has been arranging similarly looking facilities <a href=\"https://www.youtube.com/watch?v=ncC6KnVzKu0\" rel=\"nofollow noreferrer\">in the NY area</a>, but I don't know how they intend to use them.</p>\n"
},
{
"answer_id": 23061,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 5,
"selected": true,
"text": "<p>What your government is proposing is a lot less than what was actually done in China. There, and perhaps that is still the case, large numbers of asymptomatic infected people were housed together in halls with only social separation between them, and masks to prevent others from infecting others.</p>\n\n<p>Your government is proposing to house the asymptomatic infected in hotels, presumably in separate rooms.</p>\n\n<p>We know that people who are infected because they have virus identified using PCR swabs of their upper airways. CT scans can show pulmonary lesions present even without cough or fever. And even speaking can aerosolize virus though you are likely most infective at about days 4-5 before your own antibody production has ramped up significantly.</p>\n\n<p>So, it's likely you are exhaling virus, and inhaling again the virus that you exhale, as well as spreading virus in your blood to other tissues. It seems less likely that you're going to inhale a viral load that already exceeds the amount of virus coating your mucus membranes and alveloli. At least you will have some antibody production after day 5 or so on average to provide some protection.</p>\n\n<p>Note also that even within family groups housed together in Guangzhou, the incidence of cross infection was only 10%.</p>\n\n<p>And there are likely to be host factors at work. We know that women and younger people have a less severe course generally. So, even with a higher viral load on re-exposure, that may not change the underlying host factors that might =give them some protection eg. higher levels of ACE2 receptors, Group O blood group etc.</p>\n\n<p><a href=\"https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf\" rel=\"noreferrer\">https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf</a></p>\n"
},
{
"answer_id": 23069,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 2,
"selected": false,
"text": "<p>You may find this article to be helpful in some way. Dr. Siddhartha Mukharjee The New Yorker April 6 2020 issue. “How does the Coronavirus Behave Inside a Patient”</p>\n\n<p>The title I think is a bit misleading. The article does not cover the whole course of the illness! I think. It is interesting <a href=\"https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient\" rel=\"nofollow noreferrer\">https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient</a></p>\n\n<p>This covers more first, early, early repeat exposures. </p>\n\n<p>The inoculum viral load and such is discussed. </p>\n\n<p>I don’t think this a perfect answer to OP’s question but it may be helpful in some way. </p>\n\n<p>Author bio: <a href=\"https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee</a></p>\n"
}
] | 2020/04/06 | [
"https://health.stackexchange.com/questions/23059",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/-1/"
] |
23,086 | <p>Assuming I've contracted COVID-19 this January and made a full recovery and the antibodies have already left my body again. Now, I come into contact with someone who is sick and I inhale some COVID-19 viruses.</p>
<p>They will multiply and spread for a little while, but my body will detect them and produce antibodies again, but very fast this time. However, there will be a time delay, and the number of viruses in my body will peak at some point. Is there a chance, that this peak is high enough to be contagious to other people?</p>
| [
{
"answer_id": 23060,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>Doing such an experiment on humans would obviously be unethical in the present circumstances. There has been <a href=\"https://www.livescience.com/monkeys-cannot-get-reinfected-with-coronavirus-study.html\" rel=\"nofollow noreferrer\">a report</a> that monkeys who recovered and were later re-infected with mega-doses of the Covid-19 virus didn't get sick again. This is not terribly conclusive, because monkeys don't get severe symptoms from SARS like we do, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC521815/\" rel=\"nofollow noreferrer\">for example</a>. (SARS is the closest relevant relative to the Covid-19 virus aka SARS-CoV-2.)</p>\n<p>Immunity to a pathogen, <a href=\"https://www.virology.ws/2009/12/28/reinfection-with-2009-influenza-h1n1/\" rel=\"nofollow noreferrer\">in general</a> takes about 3-4 weeks to develop to develop fully, so if you [get] re-infect[ed] with a larger dose within this window, even a after a vaccine, you can cause/get the disease, although it's apparently a pretty rare occurrence.</p>\n<blockquote>\n<p>These individuals were likely resusceptible to reinfection with the same strain of influenza virus due to a confluence of unusual events. First, all three were reinfected within three weeks, before their primary adaptive response had sufficiently matured. Another contributing factor was the high level of circulation of the pandemic strain. [...]</p>\n<p>Could reinfection also occur after immunization with influenza vaccine? Yes, if the immunized individual encounters the virus before the primary antibody response matures, which occurs in 3-4 weeks. This is more likely to occur during pandemic influenza when circulation of the virus is more extensive than in non-pandemic years.</p>\n<p>[Citing:]</p>\n<p>Perez CM, Ferres M, & Labarca JA (2010). Pandemic (H1N1) 2009 Reinfection, Chile. Emerging infectious diseases, 16 (1), 156-7 PMID: 20031070</p>\n</blockquote>\n<hr />\n<p>About the Fangcang-style hospitals (i.e. make-shift hospitals for those with mild or asymptomatic infections), which China <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\">says it closed</a> the last one on March 10 (after there were 13 opened in Wuhan at the peak); it <a href=\"https://politics.stackexchange.com/questions/52494/are-any-countries-besides-china-planning-to-use-fangcang-hospitals-to-relocate\">turns out</a> they used now in other countries, and they are even a <a href=\"https://www.who.int/publications-detail/home-care-for-patients-with-suspected-novel-coronavirus-(ncov)-infection-presenting-with-mild-symptoms-and-management-of-contacts\" rel=\"nofollow noreferrer\">WHO recommendation</a> of sorts (as of March 17):</p>\n<blockquote>\n<p>WHO recommends that all laboratory confirmed cases be isolated and cared for in a health care facility.</p>\n<p>[...]</p>\n<p>If all mild cases cannot be isolated in health facilities, then those with mild illness and no risk factors may need to be isolated in non-traditional facilities, such as repurposed hotels, stadiums or gymnasiums where they can remain until their symptoms resolve and laboratory tests for COVID-19 virus are negative.</p>\n</blockquote>\n<p>According to the (April 2) <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\"><em>Lancet</em> paper</a> on Fangcang hospitals, they Chinese took various precautions to prevent cross-infection with other diseases in such settings. How strictly these measures have been implemented and how well replicated in non-Chines Fangcangs elsewhere, I won't venture to comment here, but <a href=\"https://edition.cnn.com/2020/02/22/asia/china-coronavirus-roundup-intl-hnk/index.html\" rel=\"nofollow noreferrer\">CNN had</a> a somewhat disparaging article about Fangcang hospitals back in February, outlining their shortcomings. Since then, the US has been arranging similarly looking facilities <a href=\"https://www.youtube.com/watch?v=ncC6KnVzKu0\" rel=\"nofollow noreferrer\">in the NY area</a>, but I don't know how they intend to use them.</p>\n"
},
{
"answer_id": 23061,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 5,
"selected": true,
"text": "<p>What your government is proposing is a lot less than what was actually done in China. There, and perhaps that is still the case, large numbers of asymptomatic infected people were housed together in halls with only social separation between them, and masks to prevent others from infecting others.</p>\n\n<p>Your government is proposing to house the asymptomatic infected in hotels, presumably in separate rooms.</p>\n\n<p>We know that people who are infected because they have virus identified using PCR swabs of their upper airways. CT scans can show pulmonary lesions present even without cough or fever. And even speaking can aerosolize virus though you are likely most infective at about days 4-5 before your own antibody production has ramped up significantly.</p>\n\n<p>So, it's likely you are exhaling virus, and inhaling again the virus that you exhale, as well as spreading virus in your blood to other tissues. It seems less likely that you're going to inhale a viral load that already exceeds the amount of virus coating your mucus membranes and alveloli. At least you will have some antibody production after day 5 or so on average to provide some protection.</p>\n\n<p>Note also that even within family groups housed together in Guangzhou, the incidence of cross infection was only 10%.</p>\n\n<p>And there are likely to be host factors at work. We know that women and younger people have a less severe course generally. So, even with a higher viral load on re-exposure, that may not change the underlying host factors that might =give them some protection eg. higher levels of ACE2 receptors, Group O blood group etc.</p>\n\n<p><a href=\"https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf\" rel=\"noreferrer\">https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf</a></p>\n"
},
{
"answer_id": 23069,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 2,
"selected": false,
"text": "<p>You may find this article to be helpful in some way. Dr. Siddhartha Mukharjee The New Yorker April 6 2020 issue. “How does the Coronavirus Behave Inside a Patient”</p>\n\n<p>The title I think is a bit misleading. The article does not cover the whole course of the illness! I think. It is interesting <a href=\"https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient\" rel=\"nofollow noreferrer\">https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient</a></p>\n\n<p>This covers more first, early, early repeat exposures. </p>\n\n<p>The inoculum viral load and such is discussed. </p>\n\n<p>I don’t think this a perfect answer to OP’s question but it may be helpful in some way. </p>\n\n<p>Author bio: <a href=\"https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee</a></p>\n"
}
] | 2020/04/07 | [
"https://health.stackexchange.com/questions/23086",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19241/"
] |
23,089 | <p>Could you create a system that continually filters viral particles out of a patient's blood like in the following diagram?</p>
<p>Corona virus particles are 100nm to 160nm, while the smallest blood cells are 2 to 3 microns. So they could be separated by an appropriate sized filter.</p>
<p>Reasonably high doses of UVC at 250nm will deactivate viruses.</p>
<p>Alternatively, or in combination, a second filter this time 50nm could be used to remove the virus particles from the flow.</p>
<p>Then the blood cells and the sterilized portion of the flow could be recombined and put back into the patient in a continuous flow.</p>
<p>Is this system viable, and could it help treat viral diseases like COVID-19? Cheers!</p>
<pre><code>Cannula Outflow
|
0.5 micron Osmosis
| \
Blood Cells Viral Particles
| |
| UVC 250nm Irradiation
| /
Recombination of Parts
|
Cannula Inflow
</code></pre>
<p>Edit: There's a company called Aethlon Medical looking into this with their Hemopurifer device. They used a special filter in a dialysis machine to treat ebola successfully. <a href="https://www.aethlonmedical.com/the-hemopurifier/the-hemopurifier-in-infectious-disease" rel="nofollow noreferrer">Here's their statement on applying the technology to COVID-19</a>. See answers for more context.</p>
| [
{
"answer_id": 23060,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>Doing such an experiment on humans would obviously be unethical in the present circumstances. There has been <a href=\"https://www.livescience.com/monkeys-cannot-get-reinfected-with-coronavirus-study.html\" rel=\"nofollow noreferrer\">a report</a> that monkeys who recovered and were later re-infected with mega-doses of the Covid-19 virus didn't get sick again. This is not terribly conclusive, because monkeys don't get severe symptoms from SARS like we do, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC521815/\" rel=\"nofollow noreferrer\">for example</a>. (SARS is the closest relevant relative to the Covid-19 virus aka SARS-CoV-2.)</p>\n<p>Immunity to a pathogen, <a href=\"https://www.virology.ws/2009/12/28/reinfection-with-2009-influenza-h1n1/\" rel=\"nofollow noreferrer\">in general</a> takes about 3-4 weeks to develop to develop fully, so if you [get] re-infect[ed] with a larger dose within this window, even a after a vaccine, you can cause/get the disease, although it's apparently a pretty rare occurrence.</p>\n<blockquote>\n<p>These individuals were likely resusceptible to reinfection with the same strain of influenza virus due to a confluence of unusual events. First, all three were reinfected within three weeks, before their primary adaptive response had sufficiently matured. Another contributing factor was the high level of circulation of the pandemic strain. [...]</p>\n<p>Could reinfection also occur after immunization with influenza vaccine? Yes, if the immunized individual encounters the virus before the primary antibody response matures, which occurs in 3-4 weeks. This is more likely to occur during pandemic influenza when circulation of the virus is more extensive than in non-pandemic years.</p>\n<p>[Citing:]</p>\n<p>Perez CM, Ferres M, & Labarca JA (2010). Pandemic (H1N1) 2009 Reinfection, Chile. Emerging infectious diseases, 16 (1), 156-7 PMID: 20031070</p>\n</blockquote>\n<hr />\n<p>About the Fangcang-style hospitals (i.e. make-shift hospitals for those with mild or asymptomatic infections), which China <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\">says it closed</a> the last one on March 10 (after there were 13 opened in Wuhan at the peak); it <a href=\"https://politics.stackexchange.com/questions/52494/are-any-countries-besides-china-planning-to-use-fangcang-hospitals-to-relocate\">turns out</a> they used now in other countries, and they are even a <a href=\"https://www.who.int/publications-detail/home-care-for-patients-with-suspected-novel-coronavirus-(ncov)-infection-presenting-with-mild-symptoms-and-management-of-contacts\" rel=\"nofollow noreferrer\">WHO recommendation</a> of sorts (as of March 17):</p>\n<blockquote>\n<p>WHO recommends that all laboratory confirmed cases be isolated and cared for in a health care facility.</p>\n<p>[...]</p>\n<p>If all mild cases cannot be isolated in health facilities, then those with mild illness and no risk factors may need to be isolated in non-traditional facilities, such as repurposed hotels, stadiums or gymnasiums where they can remain until their symptoms resolve and laboratory tests for COVID-19 virus are negative.</p>\n</blockquote>\n<p>According to the (April 2) <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\"><em>Lancet</em> paper</a> on Fangcang hospitals, they Chinese took various precautions to prevent cross-infection with other diseases in such settings. How strictly these measures have been implemented and how well replicated in non-Chines Fangcangs elsewhere, I won't venture to comment here, but <a href=\"https://edition.cnn.com/2020/02/22/asia/china-coronavirus-roundup-intl-hnk/index.html\" rel=\"nofollow noreferrer\">CNN had</a> a somewhat disparaging article about Fangcang hospitals back in February, outlining their shortcomings. Since then, the US has been arranging similarly looking facilities <a href=\"https://www.youtube.com/watch?v=ncC6KnVzKu0\" rel=\"nofollow noreferrer\">in the NY area</a>, but I don't know how they intend to use them.</p>\n"
},
{
"answer_id": 23061,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 5,
"selected": true,
"text": "<p>What your government is proposing is a lot less than what was actually done in China. There, and perhaps that is still the case, large numbers of asymptomatic infected people were housed together in halls with only social separation between them, and masks to prevent others from infecting others.</p>\n\n<p>Your government is proposing to house the asymptomatic infected in hotels, presumably in separate rooms.</p>\n\n<p>We know that people who are infected because they have virus identified using PCR swabs of their upper airways. CT scans can show pulmonary lesions present even without cough or fever. And even speaking can aerosolize virus though you are likely most infective at about days 4-5 before your own antibody production has ramped up significantly.</p>\n\n<p>So, it's likely you are exhaling virus, and inhaling again the virus that you exhale, as well as spreading virus in your blood to other tissues. It seems less likely that you're going to inhale a viral load that already exceeds the amount of virus coating your mucus membranes and alveloli. At least you will have some antibody production after day 5 or so on average to provide some protection.</p>\n\n<p>Note also that even within family groups housed together in Guangzhou, the incidence of cross infection was only 10%.</p>\n\n<p>And there are likely to be host factors at work. We know that women and younger people have a less severe course generally. So, even with a higher viral load on re-exposure, that may not change the underlying host factors that might =give them some protection eg. higher levels of ACE2 receptors, Group O blood group etc.</p>\n\n<p><a href=\"https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf\" rel=\"noreferrer\">https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf</a></p>\n"
},
{
"answer_id": 23069,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 2,
"selected": false,
"text": "<p>You may find this article to be helpful in some way. Dr. Siddhartha Mukharjee The New Yorker April 6 2020 issue. “How does the Coronavirus Behave Inside a Patient”</p>\n\n<p>The title I think is a bit misleading. The article does not cover the whole course of the illness! I think. It is interesting <a href=\"https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient\" rel=\"nofollow noreferrer\">https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient</a></p>\n\n<p>This covers more first, early, early repeat exposures. </p>\n\n<p>The inoculum viral load and such is discussed. </p>\n\n<p>I don’t think this a perfect answer to OP’s question but it may be helpful in some way. </p>\n\n<p>Author bio: <a href=\"https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Siddhartha_Mukherjee</a></p>\n"
}
] | 2020/04/07 | [
"https://health.stackexchange.com/questions/23089",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19243/"
] |
23,094 | <p>The current prognosis for a COVID-19 vaccine to become available is "12-18 months" and a big part of the reason for such a long timeline is the fact that scientists want to ensure that the vaccine is safe enough. But did this ever happen in practice? An article on CNN mentions the <a href="https://www.cnn.com/2020/03/31/us/coronavirus-vaccine-timetable-concerns-experts-invs/index.html" rel="noreferrer">fiasco of the 1976 vaccine</a>: </p>
<blockquote>
<p>In 1976, President Gerald Ford's administration reacted at speed to a novel swine flu outbreak, ignoring the World Health Organization's words of caution and vowing to vaccinate "every man, woman and child in the United States." After 45 million people were vaccinated, the flu turned out to be mild. Worse, researchers discovered that a disproportionately high number of the vaccinated -- roughly 450 in all -- had developed Guillain-Barré syndrome, a rare disorder in which the body's immune system attacks the nerves, leading to paralysis. At least 30 people died. Upon discovery of the risk, the program was terminated in late 1976. A crush of lawsuits against the federal government followed.</p>
</blockquote>
<p>However this looks like a very rare complication, only causing problems for 1 in 100,000 patients. And even that complication could've been detected <a href="https://www.nytimes.com/2009/05/09/health/09vaccine.html" rel="noreferrer">quickly with enough volunteers</a>:</p>
<blockquote>
<p><strong>About a week</strong> after getting the swine flu shot, she recalled, “I was so weak I couldn’t push down the toaster button.” She spent a month in the hospital, paralyzed from the neck down, before gradually recovering.</p>
</blockquote>
<p>So has there ever been a vaccine trial satisfying the following conditions?</p>
<ol>
<li>Significant side effects were detected</li>
<li>Those side effects appeared in otherwise healthy candidates after more than 3 months since they were injected with the vaccine</li>
<li>These side effects were something other than birth defects (those obviously take up to 9 months to show up)</li>
</ol>
<p>If not, what causes scientists to be so cautious about testing a new vaccine quickly?</p>
| [
{
"answer_id": 23107,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>I think the unclarity in this question (and ironically that it's getting upvoted while the answers to it are getting downvoted) is that the question doesn't specify in its numbered premises that the side effect has to be <strong>commonly</strong> reported <em>but only after a long time</em>. A <em>very rare</em> side effect is statistically hard to find, so it's natural that it may take a long time to find some cases, even if it does show up fairly quickly in susceptible individual.</p>\n<p>The question then makes the following blurring/confusion: it goes from a trial in which effects were (not) found to a rollout which vastly expands the population/sample. The question is then misleadingly phrased as</p>\n<blockquote>\n<p>If not, what causes scientists to be so cautious about testing a new vaccine quickly?</p>\n</blockquote>\n<p>There's no reluctance to test a vaccine quickly enough in a small sample (e.g. phase II trials) if the vaccine "passes the smell test" in some preclinical trials etc. But e.g. phase II trials may not find all the rare side effects. The question probably wants to ask why does it take longer to get the vaccine <em>rolled out</em>, but it phrases that as "scientists to be so cautious about <strong>testing</strong>". Basically the caution is about testing (with or without scare quotes) with a large sample all of a sudden, e.g. in an extreme case roll-out after successful pre-clinical trials. Increasing the sample size (as in phase III trials) gives more power to detect rarer side effects. In a <a href=\"https://uk.gsk.com/en-gb/research/trials-in-people/clinical-trial-phases/\" rel=\"nofollow noreferrer\">nutshell</a></p>\n<blockquote>\n<p>The first time a new treatment or vaccine is tested in humans, it will usually be given to a small group of healthy volunteers. [...]</p>\n<p>The principle objectives in Phase I are to:</p>\n<ul>\n<li>make sure that the new medicine presents no <strong>major</strong> safety issues\n[...]</li>\n</ul>\n<p>If Phase I is successful, approval will be sought for a trial involving a larger group of people. Phase II trials will usually (but not always) include patients who have the condition the potential medicine is targeting, and aim to establish: [...]</p>\n<ul>\n<li>effectiveness in preventing the condition (if the volunteer does not already have it)\n[...]</li>\n</ul>\n<p>Phase III</p>\n<p>If the results from Phase II are encouraging, we will seek to start a Phase III trial. This will be a much larger trial, often involving hundreds, possibly thousands of participants coming from a range of different countries.</p>\n<p>The principle objectives in Phase III are to:</p>\n<ul>\n<li><p>demonstrate the <strong>safety and effectiveness</strong> of the new medicine or vaccine in the typical patient likely to use it</p>\n</li>\n<li><p>identify side effects or reasons why the treatment should not be given to people with the condition in question (known as <strong>‘contraindications’</strong>)</p>\n</li>\n</ul>\n</blockquote>\n<p>Emphasis mine.</p>\n<p>Obviously when you increase the sample size even further (roll out) you may even find very rare side effects that were even missed in phase III. Sometimes <a href=\"http://www.genetherapynet.com/clinical-trial-phases.html\" rel=\"nofollow noreferrer\">there are</a> so-called phase IV studies</p>\n<blockquote>\n<p>Phase IV studies may be required by regulatory authorities or may be undertaken by the sponsoring company for competitive (finding a new market for the drug) or other reasons (for example, the drug may not have been tested for interactions with other drugs, or on certain population groups such as pregnant women, who are unlikely to subject themselves to trials).</p>\n<p><strong>The safety surveillance is designed to detect any rare or long-term adverse effects over a much larger patient population and longer time period than was possible during the Phase I-III clinical trials.</strong> Harmful effects discovered by Phase IV trials may result in a drug being no longer sold, or restricted to certain uses.</p>\n</blockquote>\n<p>So the last part of the question is based on (a lot) of misphrasing and/or bad (logical) premises, lumping everything (including roll out) under the word "testing". The level of caution/reluctance is proportional with the size of the population being tested (on).</p>\n<hr />\n<p>So, how long can it take to figure it out if a vaccine gives <em>any</em> bad side effects? <a href=\"https://www.virology.ws/2015/09/10/why-do-we-still-use-sabin-poliovirus-vaccine/\" rel=\"nofollow noreferrer\">How about 20 years?</a> Because deciding if the observed side effects are caused by a vaccine or not is not actually trivial:</p>\n<blockquote>\n<p>all three of Sabin’s OPV strains were approved for use in the US, and in 1961-62 they replaced IPV for routine immunization against poliomyelitis.</p>\n<p>As soon as OPV was used in mass immunizations in the US, cases of vaccine-associated paralysis were described. Initially Sabin decried these findings, arguing that temporal association of paralysis with vaccine administration was not sufficient to implicate OPV. He suggested that the observed paralysis was caused by wild-type viruses, not his vaccine strains.</p>\n<p>A breakthrough in our understanding of vaccine-associated paralysis came in the early 1980s when the recently developed DNA sequencing methods were used to determine the nucleotide sequences of the genomes of the Sabin type 3 vaccine, the neurovirulent virus from which it was derived, and a virus isolated from a child who had developed paralysis after administration of OPV. The results enumerated for the first time the mutations that distinguish the Sabin vaccine from its neurovirulent parent. More importantly, the genome sequence of the vaccine-associated isolate proved that it was derived from the Sabin vaccine and was not a wild-type poliovirus.</p>\n<p>We now understand that every recipient of OPV excretes, within a few days, viruses that are more neurovirulent that the vaccine strains. This evolution occurs because during replication of the OPV strains in the human intestine, the viral genome undergoes mutation and recombination that eliminate the attenuating mutations that Sabin so carefully selected by passage in different hosts.</p>\n<p>From 1961 to 1989 there were an average of 9 cases (range, 1-25 cases) of vaccine-associated paralytic poliomyelitis (VAPP) in the United States, in vaccine recipients or their contacts, or 1 VAPP case per 2.9 million doses of OPV distributed (illustrated). Given this serious side effect, the use of OPV was evaluated several times by the Institute of Medicine, the Centers for Disease Control and Prevention, and the Advisory Committee on Immunization Practices. Each time it was decided that the risks associated with the use of OPV justified the cases of VAPP. It was believed that a switch to IPV would lead to outbreaks of poliomyelitis, because: OPV was better than IPV at protecting non-immunized recipients; the need to inject IPV would lead to reduced compliance; and IPV was known to induce less protective mucosal immunity than OPV.</p>\n</blockquote>\n<p>And yeah whether the benefits outweigh the risks of severe albeit seldom-encountered side effects is a balancing matter:</p>\n<blockquote>\n<p>After the WHO began its poliovirus eradication initiative in 1988, the risk of poliovirus importation into the US slowly decreased until it became very difficult to justify routine use of OPV. In 1996 the Advisory Committee on Immunization Practices decided that the US would transition to IPV and by 2000 IPV had replaced OPV for the routine prevention of poliomyelitis. As a consequence VAPP has been eliminated from the US.</p>\n</blockquote>\n<p>Yes, yes, I can see the objections already that with the current state of biology/medicine we'd figure it out faster now. YMMV, i.e. it's down to "expert opinion" whether we could completely avoid a repeat of VAPP.</p>\n"
},
{
"answer_id": 23580,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 3,
"selected": false,
"text": "<p>Historically, vaccines eg 1955 polio vaccine had side effects due to manufacturing issues allowing live virus to appear in the vaccine in the Cutter company’s vaccine. In 1976, a swine flu vaccine was shown to have a risk of 1 in 100,000 of Guillaine-Barre Syndrome, a transient but serious neuromuscular syndrome. The 1998 rotavirus vaccine was shown to prevent serious life-threatening diarrheal illness in infants, but later studies suggested a risk of a rare form of bowel obstruction called intussusception. The recommendation for RotaShield vaccine was withdrawn.</p>\n\n<p>These side effects generally appeared within weeks, months or a few years of the vaccine administrative. </p>\n\n<p>Source:\n<a href=\"https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html\" rel=\"noreferrer\">https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html</a></p>\n\n<p>Over time this led to significant increase in safety oversight including the FDA VAERS (vaccine adverse event reporting system). Many long-term vaccine safety studies and monitoring systems have been built since then.</p>\n\n<p>For example, the Kaiser vaccine study center looked at hundreds of thousands of MMRV vaccine doses, for example. They found no long term side effects, but in this case the goal was to understand side effects relative to MMR & V(aricella) vaccines given separately versus together.</p>\n\n<p>Source: \n<a href=\"https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe\" rel=\"noreferrer\">https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe</a></p>\n\n<p>Long term side effects can be a complication of any medical intervention, such as medications or devices also, as well as compared to the risk of untreated disease not prevented or not treated. As a result, scientists and clinicians weigh the risks, benefits and alternatives and ideally partner with patients, parents and caregivers in informed consent. Where information has not yet been gathered about long-term safety — or durability of the effect — large long term safety studies have generally been required, and are also possible to detect with such systems as the <a href=\"https://www.fda.gov/vaccines-blood-biologics/biologics-post-market-activities/cbers-sentinel-program\" rel=\"noreferrer\">FDA Sentinel system launched in 2008</a> and other similar safety systems available now (2020) that were not previously available. These systems permit longer range, larger population monitoring of both safety and effectiveness of vaccines and other medical treatments, and further detail by subgroups who may be at higher risk of side effects, or who may be at higher chance of benefiting from vaccines or medications.</p>\n"
},
{
"answer_id": 26372,
"author": "endolith",
"author_id": 13428,
"author_profile": "https://health.stackexchange.com/users/13428",
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"text": "<blockquote>\n<p>Live attenuated varicella vaccines do contain actual varicella zoster virus (Oka strain), which can establish infection in hosts and undergo latency like other herpesviruses including the unattenuated virus. As a result they can very rarely cause shingles or meningitis years after the receipt of the vaccine. This is a consequence of 2 things: the use of a live vaccine, and the ability of herpesviruses like varicella to undergo latency</p>\n</blockquote>\n<p><a href=\"https://edwardnirenberg.medium.com/long-term-effects-of-covid-19-vaccines-should-you-be-worried-c3c3a547b565\" rel=\"nofollow noreferrer\">Long-Term Effects of COVID-19 Vaccines: Should You Be Worried?</a></p>\n"
}
] | 2020/04/07 | [
"https://health.stackexchange.com/questions/23094",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,100 | <p>Once a virus infects a mammal, how quickly do viral particles multiply within their bodies? In other words, what is the expected doubling time of viral particles once a mammal is infected?</p>
<p>If this question is too broad, consider the influenza virus within the human body or a well studied virus within a lab animal.</p>
| [
{
"answer_id": 23107,
"author": "Fizz",
"author_id": 10980,
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"text": "<p>I think the unclarity in this question (and ironically that it's getting upvoted while the answers to it are getting downvoted) is that the question doesn't specify in its numbered premises that the side effect has to be <strong>commonly</strong> reported <em>but only after a long time</em>. A <em>very rare</em> side effect is statistically hard to find, so it's natural that it may take a long time to find some cases, even if it does show up fairly quickly in susceptible individual.</p>\n<p>The question then makes the following blurring/confusion: it goes from a trial in which effects were (not) found to a rollout which vastly expands the population/sample. The question is then misleadingly phrased as</p>\n<blockquote>\n<p>If not, what causes scientists to be so cautious about testing a new vaccine quickly?</p>\n</blockquote>\n<p>There's no reluctance to test a vaccine quickly enough in a small sample (e.g. phase II trials) if the vaccine "passes the smell test" in some preclinical trials etc. But e.g. phase II trials may not find all the rare side effects. The question probably wants to ask why does it take longer to get the vaccine <em>rolled out</em>, but it phrases that as "scientists to be so cautious about <strong>testing</strong>". Basically the caution is about testing (with or without scare quotes) with a large sample all of a sudden, e.g. in an extreme case roll-out after successful pre-clinical trials. Increasing the sample size (as in phase III trials) gives more power to detect rarer side effects. In a <a href=\"https://uk.gsk.com/en-gb/research/trials-in-people/clinical-trial-phases/\" rel=\"nofollow noreferrer\">nutshell</a></p>\n<blockquote>\n<p>The first time a new treatment or vaccine is tested in humans, it will usually be given to a small group of healthy volunteers. [...]</p>\n<p>The principle objectives in Phase I are to:</p>\n<ul>\n<li>make sure that the new medicine presents no <strong>major</strong> safety issues\n[...]</li>\n</ul>\n<p>If Phase I is successful, approval will be sought for a trial involving a larger group of people. Phase II trials will usually (but not always) include patients who have the condition the potential medicine is targeting, and aim to establish: [...]</p>\n<ul>\n<li>effectiveness in preventing the condition (if the volunteer does not already have it)\n[...]</li>\n</ul>\n<p>Phase III</p>\n<p>If the results from Phase II are encouraging, we will seek to start a Phase III trial. This will be a much larger trial, often involving hundreds, possibly thousands of participants coming from a range of different countries.</p>\n<p>The principle objectives in Phase III are to:</p>\n<ul>\n<li><p>demonstrate the <strong>safety and effectiveness</strong> of the new medicine or vaccine in the typical patient likely to use it</p>\n</li>\n<li><p>identify side effects or reasons why the treatment should not be given to people with the condition in question (known as <strong>‘contraindications’</strong>)</p>\n</li>\n</ul>\n</blockquote>\n<p>Emphasis mine.</p>\n<p>Obviously when you increase the sample size even further (roll out) you may even find very rare side effects that were even missed in phase III. Sometimes <a href=\"http://www.genetherapynet.com/clinical-trial-phases.html\" rel=\"nofollow noreferrer\">there are</a> so-called phase IV studies</p>\n<blockquote>\n<p>Phase IV studies may be required by regulatory authorities or may be undertaken by the sponsoring company for competitive (finding a new market for the drug) or other reasons (for example, the drug may not have been tested for interactions with other drugs, or on certain population groups such as pregnant women, who are unlikely to subject themselves to trials).</p>\n<p><strong>The safety surveillance is designed to detect any rare or long-term adverse effects over a much larger patient population and longer time period than was possible during the Phase I-III clinical trials.</strong> Harmful effects discovered by Phase IV trials may result in a drug being no longer sold, or restricted to certain uses.</p>\n</blockquote>\n<p>So the last part of the question is based on (a lot) of misphrasing and/or bad (logical) premises, lumping everything (including roll out) under the word "testing". The level of caution/reluctance is proportional with the size of the population being tested (on).</p>\n<hr />\n<p>So, how long can it take to figure it out if a vaccine gives <em>any</em> bad side effects? <a href=\"https://www.virology.ws/2015/09/10/why-do-we-still-use-sabin-poliovirus-vaccine/\" rel=\"nofollow noreferrer\">How about 20 years?</a> Because deciding if the observed side effects are caused by a vaccine or not is not actually trivial:</p>\n<blockquote>\n<p>all three of Sabin’s OPV strains were approved for use in the US, and in 1961-62 they replaced IPV for routine immunization against poliomyelitis.</p>\n<p>As soon as OPV was used in mass immunizations in the US, cases of vaccine-associated paralysis were described. Initially Sabin decried these findings, arguing that temporal association of paralysis with vaccine administration was not sufficient to implicate OPV. He suggested that the observed paralysis was caused by wild-type viruses, not his vaccine strains.</p>\n<p>A breakthrough in our understanding of vaccine-associated paralysis came in the early 1980s when the recently developed DNA sequencing methods were used to determine the nucleotide sequences of the genomes of the Sabin type 3 vaccine, the neurovirulent virus from which it was derived, and a virus isolated from a child who had developed paralysis after administration of OPV. The results enumerated for the first time the mutations that distinguish the Sabin vaccine from its neurovirulent parent. More importantly, the genome sequence of the vaccine-associated isolate proved that it was derived from the Sabin vaccine and was not a wild-type poliovirus.</p>\n<p>We now understand that every recipient of OPV excretes, within a few days, viruses that are more neurovirulent that the vaccine strains. This evolution occurs because during replication of the OPV strains in the human intestine, the viral genome undergoes mutation and recombination that eliminate the attenuating mutations that Sabin so carefully selected by passage in different hosts.</p>\n<p>From 1961 to 1989 there were an average of 9 cases (range, 1-25 cases) of vaccine-associated paralytic poliomyelitis (VAPP) in the United States, in vaccine recipients or their contacts, or 1 VAPP case per 2.9 million doses of OPV distributed (illustrated). Given this serious side effect, the use of OPV was evaluated several times by the Institute of Medicine, the Centers for Disease Control and Prevention, and the Advisory Committee on Immunization Practices. Each time it was decided that the risks associated with the use of OPV justified the cases of VAPP. It was believed that a switch to IPV would lead to outbreaks of poliomyelitis, because: OPV was better than IPV at protecting non-immunized recipients; the need to inject IPV would lead to reduced compliance; and IPV was known to induce less protective mucosal immunity than OPV.</p>\n</blockquote>\n<p>And yeah whether the benefits outweigh the risks of severe albeit seldom-encountered side effects is a balancing matter:</p>\n<blockquote>\n<p>After the WHO began its poliovirus eradication initiative in 1988, the risk of poliovirus importation into the US slowly decreased until it became very difficult to justify routine use of OPV. In 1996 the Advisory Committee on Immunization Practices decided that the US would transition to IPV and by 2000 IPV had replaced OPV for the routine prevention of poliomyelitis. As a consequence VAPP has been eliminated from the US.</p>\n</blockquote>\n<p>Yes, yes, I can see the objections already that with the current state of biology/medicine we'd figure it out faster now. YMMV, i.e. it's down to "expert opinion" whether we could completely avoid a repeat of VAPP.</p>\n"
},
{
"answer_id": 23580,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 3,
"selected": false,
"text": "<p>Historically, vaccines eg 1955 polio vaccine had side effects due to manufacturing issues allowing live virus to appear in the vaccine in the Cutter company’s vaccine. In 1976, a swine flu vaccine was shown to have a risk of 1 in 100,000 of Guillaine-Barre Syndrome, a transient but serious neuromuscular syndrome. The 1998 rotavirus vaccine was shown to prevent serious life-threatening diarrheal illness in infants, but later studies suggested a risk of a rare form of bowel obstruction called intussusception. The recommendation for RotaShield vaccine was withdrawn.</p>\n\n<p>These side effects generally appeared within weeks, months or a few years of the vaccine administrative. </p>\n\n<p>Source:\n<a href=\"https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html\" rel=\"noreferrer\">https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html</a></p>\n\n<p>Over time this led to significant increase in safety oversight including the FDA VAERS (vaccine adverse event reporting system). Many long-term vaccine safety studies and monitoring systems have been built since then.</p>\n\n<p>For example, the Kaiser vaccine study center looked at hundreds of thousands of MMRV vaccine doses, for example. They found no long term side effects, but in this case the goal was to understand side effects relative to MMR & V(aricella) vaccines given separately versus together.</p>\n\n<p>Source: \n<a href=\"https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe\" rel=\"noreferrer\">https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe</a></p>\n\n<p>Long term side effects can be a complication of any medical intervention, such as medications or devices also, as well as compared to the risk of untreated disease not prevented or not treated. As a result, scientists and clinicians weigh the risks, benefits and alternatives and ideally partner with patients, parents and caregivers in informed consent. Where information has not yet been gathered about long-term safety — or durability of the effect — large long term safety studies have generally been required, and are also possible to detect with such systems as the <a href=\"https://www.fda.gov/vaccines-blood-biologics/biologics-post-market-activities/cbers-sentinel-program\" rel=\"noreferrer\">FDA Sentinel system launched in 2008</a> and other similar safety systems available now (2020) that were not previously available. These systems permit longer range, larger population monitoring of both safety and effectiveness of vaccines and other medical treatments, and further detail by subgroups who may be at higher risk of side effects, or who may be at higher chance of benefiting from vaccines or medications.</p>\n"
},
{
"answer_id": 26372,
"author": "endolith",
"author_id": 13428,
"author_profile": "https://health.stackexchange.com/users/13428",
"pm_score": 3,
"selected": true,
"text": "<blockquote>\n<p>Live attenuated varicella vaccines do contain actual varicella zoster virus (Oka strain), which can establish infection in hosts and undergo latency like other herpesviruses including the unattenuated virus. As a result they can very rarely cause shingles or meningitis years after the receipt of the vaccine. This is a consequence of 2 things: the use of a live vaccine, and the ability of herpesviruses like varicella to undergo latency</p>\n</blockquote>\n<p><a href=\"https://edwardnirenberg.medium.com/long-term-effects-of-covid-19-vaccines-should-you-be-worried-c3c3a547b565\" rel=\"nofollow noreferrer\">Long-Term Effects of COVID-19 Vaccines: Should You Be Worried?</a></p>\n"
}
] | 2020/04/08 | [
"https://health.stackexchange.com/questions/23100",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,113 | <p>So according to the <a href="https://www.worldometers.info/coronavirus/" rel="nofollow noreferrer">current data</a>, around 80k people died worldwide to COVID-19. But afaik a big portion of them didn't actually die because of the virus directly, but they instead were infected with it in the past and in the fight between the immune system and the virus the immune got so weak, that other viruses could attack the body with its defences down. So the person technically died to other viruses and only indirectly to the coronavirus.</p>
<p>My question now is, how we can actually detect whether a person died to a virus because he was previously hit by COVID-19, or died to a virus (flu, etc.) without having been infected by corona in the past.</p>
<p>~Okaghana</p>
| [
{
"answer_id": 23107,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>I think the unclarity in this question (and ironically that it's getting upvoted while the answers to it are getting downvoted) is that the question doesn't specify in its numbered premises that the side effect has to be <strong>commonly</strong> reported <em>but only after a long time</em>. A <em>very rare</em> side effect is statistically hard to find, so it's natural that it may take a long time to find some cases, even if it does show up fairly quickly in susceptible individual.</p>\n<p>The question then makes the following blurring/confusion: it goes from a trial in which effects were (not) found to a rollout which vastly expands the population/sample. The question is then misleadingly phrased as</p>\n<blockquote>\n<p>If not, what causes scientists to be so cautious about testing a new vaccine quickly?</p>\n</blockquote>\n<p>There's no reluctance to test a vaccine quickly enough in a small sample (e.g. phase II trials) if the vaccine "passes the smell test" in some preclinical trials etc. But e.g. phase II trials may not find all the rare side effects. The question probably wants to ask why does it take longer to get the vaccine <em>rolled out</em>, but it phrases that as "scientists to be so cautious about <strong>testing</strong>". Basically the caution is about testing (with or without scare quotes) with a large sample all of a sudden, e.g. in an extreme case roll-out after successful pre-clinical trials. Increasing the sample size (as in phase III trials) gives more power to detect rarer side effects. In a <a href=\"https://uk.gsk.com/en-gb/research/trials-in-people/clinical-trial-phases/\" rel=\"nofollow noreferrer\">nutshell</a></p>\n<blockquote>\n<p>The first time a new treatment or vaccine is tested in humans, it will usually be given to a small group of healthy volunteers. [...]</p>\n<p>The principle objectives in Phase I are to:</p>\n<ul>\n<li>make sure that the new medicine presents no <strong>major</strong> safety issues\n[...]</li>\n</ul>\n<p>If Phase I is successful, approval will be sought for a trial involving a larger group of people. Phase II trials will usually (but not always) include patients who have the condition the potential medicine is targeting, and aim to establish: [...]</p>\n<ul>\n<li>effectiveness in preventing the condition (if the volunteer does not already have it)\n[...]</li>\n</ul>\n<p>Phase III</p>\n<p>If the results from Phase II are encouraging, we will seek to start a Phase III trial. This will be a much larger trial, often involving hundreds, possibly thousands of participants coming from a range of different countries.</p>\n<p>The principle objectives in Phase III are to:</p>\n<ul>\n<li><p>demonstrate the <strong>safety and effectiveness</strong> of the new medicine or vaccine in the typical patient likely to use it</p>\n</li>\n<li><p>identify side effects or reasons why the treatment should not be given to people with the condition in question (known as <strong>‘contraindications’</strong>)</p>\n</li>\n</ul>\n</blockquote>\n<p>Emphasis mine.</p>\n<p>Obviously when you increase the sample size even further (roll out) you may even find very rare side effects that were even missed in phase III. Sometimes <a href=\"http://www.genetherapynet.com/clinical-trial-phases.html\" rel=\"nofollow noreferrer\">there are</a> so-called phase IV studies</p>\n<blockquote>\n<p>Phase IV studies may be required by regulatory authorities or may be undertaken by the sponsoring company for competitive (finding a new market for the drug) or other reasons (for example, the drug may not have been tested for interactions with other drugs, or on certain population groups such as pregnant women, who are unlikely to subject themselves to trials).</p>\n<p><strong>The safety surveillance is designed to detect any rare or long-term adverse effects over a much larger patient population and longer time period than was possible during the Phase I-III clinical trials.</strong> Harmful effects discovered by Phase IV trials may result in a drug being no longer sold, or restricted to certain uses.</p>\n</blockquote>\n<p>So the last part of the question is based on (a lot) of misphrasing and/or bad (logical) premises, lumping everything (including roll out) under the word "testing". The level of caution/reluctance is proportional with the size of the population being tested (on).</p>\n<hr />\n<p>So, how long can it take to figure it out if a vaccine gives <em>any</em> bad side effects? <a href=\"https://www.virology.ws/2015/09/10/why-do-we-still-use-sabin-poliovirus-vaccine/\" rel=\"nofollow noreferrer\">How about 20 years?</a> Because deciding if the observed side effects are caused by a vaccine or not is not actually trivial:</p>\n<blockquote>\n<p>all three of Sabin’s OPV strains were approved for use in the US, and in 1961-62 they replaced IPV for routine immunization against poliomyelitis.</p>\n<p>As soon as OPV was used in mass immunizations in the US, cases of vaccine-associated paralysis were described. Initially Sabin decried these findings, arguing that temporal association of paralysis with vaccine administration was not sufficient to implicate OPV. He suggested that the observed paralysis was caused by wild-type viruses, not his vaccine strains.</p>\n<p>A breakthrough in our understanding of vaccine-associated paralysis came in the early 1980s when the recently developed DNA sequencing methods were used to determine the nucleotide sequences of the genomes of the Sabin type 3 vaccine, the neurovirulent virus from which it was derived, and a virus isolated from a child who had developed paralysis after administration of OPV. The results enumerated for the first time the mutations that distinguish the Sabin vaccine from its neurovirulent parent. More importantly, the genome sequence of the vaccine-associated isolate proved that it was derived from the Sabin vaccine and was not a wild-type poliovirus.</p>\n<p>We now understand that every recipient of OPV excretes, within a few days, viruses that are more neurovirulent that the vaccine strains. This evolution occurs because during replication of the OPV strains in the human intestine, the viral genome undergoes mutation and recombination that eliminate the attenuating mutations that Sabin so carefully selected by passage in different hosts.</p>\n<p>From 1961 to 1989 there were an average of 9 cases (range, 1-25 cases) of vaccine-associated paralytic poliomyelitis (VAPP) in the United States, in vaccine recipients or their contacts, or 1 VAPP case per 2.9 million doses of OPV distributed (illustrated). Given this serious side effect, the use of OPV was evaluated several times by the Institute of Medicine, the Centers for Disease Control and Prevention, and the Advisory Committee on Immunization Practices. Each time it was decided that the risks associated with the use of OPV justified the cases of VAPP. It was believed that a switch to IPV would lead to outbreaks of poliomyelitis, because: OPV was better than IPV at protecting non-immunized recipients; the need to inject IPV would lead to reduced compliance; and IPV was known to induce less protective mucosal immunity than OPV.</p>\n</blockquote>\n<p>And yeah whether the benefits outweigh the risks of severe albeit seldom-encountered side effects is a balancing matter:</p>\n<blockquote>\n<p>After the WHO began its poliovirus eradication initiative in 1988, the risk of poliovirus importation into the US slowly decreased until it became very difficult to justify routine use of OPV. In 1996 the Advisory Committee on Immunization Practices decided that the US would transition to IPV and by 2000 IPV had replaced OPV for the routine prevention of poliomyelitis. As a consequence VAPP has been eliminated from the US.</p>\n</blockquote>\n<p>Yes, yes, I can see the objections already that with the current state of biology/medicine we'd figure it out faster now. YMMV, i.e. it's down to "expert opinion" whether we could completely avoid a repeat of VAPP.</p>\n"
},
{
"answer_id": 23580,
"author": "Henry Wei",
"author_id": 17942,
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"pm_score": 3,
"selected": false,
"text": "<p>Historically, vaccines eg 1955 polio vaccine had side effects due to manufacturing issues allowing live virus to appear in the vaccine in the Cutter company’s vaccine. In 1976, a swine flu vaccine was shown to have a risk of 1 in 100,000 of Guillaine-Barre Syndrome, a transient but serious neuromuscular syndrome. The 1998 rotavirus vaccine was shown to prevent serious life-threatening diarrheal illness in infants, but later studies suggested a risk of a rare form of bowel obstruction called intussusception. The recommendation for RotaShield vaccine was withdrawn.</p>\n\n<p>These side effects generally appeared within weeks, months or a few years of the vaccine administrative. </p>\n\n<p>Source:\n<a href=\"https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html\" rel=\"noreferrer\">https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html</a></p>\n\n<p>Over time this led to significant increase in safety oversight including the FDA VAERS (vaccine adverse event reporting system). Many long-term vaccine safety studies and monitoring systems have been built since then.</p>\n\n<p>For example, the Kaiser vaccine study center looked at hundreds of thousands of MMRV vaccine doses, for example. They found no long term side effects, but in this case the goal was to understand side effects relative to MMR & V(aricella) vaccines given separately versus together.</p>\n\n<p>Source: \n<a href=\"https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe\" rel=\"noreferrer\">https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe</a></p>\n\n<p>Long term side effects can be a complication of any medical intervention, such as medications or devices also, as well as compared to the risk of untreated disease not prevented or not treated. As a result, scientists and clinicians weigh the risks, benefits and alternatives and ideally partner with patients, parents and caregivers in informed consent. Where information has not yet been gathered about long-term safety — or durability of the effect — large long term safety studies have generally been required, and are also possible to detect with such systems as the <a href=\"https://www.fda.gov/vaccines-blood-biologics/biologics-post-market-activities/cbers-sentinel-program\" rel=\"noreferrer\">FDA Sentinel system launched in 2008</a> and other similar safety systems available now (2020) that were not previously available. These systems permit longer range, larger population monitoring of both safety and effectiveness of vaccines and other medical treatments, and further detail by subgroups who may be at higher risk of side effects, or who may be at higher chance of benefiting from vaccines or medications.</p>\n"
},
{
"answer_id": 26372,
"author": "endolith",
"author_id": 13428,
"author_profile": "https://health.stackexchange.com/users/13428",
"pm_score": 3,
"selected": true,
"text": "<blockquote>\n<p>Live attenuated varicella vaccines do contain actual varicella zoster virus (Oka strain), which can establish infection in hosts and undergo latency like other herpesviruses including the unattenuated virus. As a result they can very rarely cause shingles or meningitis years after the receipt of the vaccine. This is a consequence of 2 things: the use of a live vaccine, and the ability of herpesviruses like varicella to undergo latency</p>\n</blockquote>\n<p><a href=\"https://edwardnirenberg.medium.com/long-term-effects-of-covid-19-vaccines-should-you-be-worried-c3c3a547b565\" rel=\"nofollow noreferrer\">Long-Term Effects of COVID-19 Vaccines: Should You Be Worried?</a></p>\n"
}
] | 2020/04/08 | [
"https://health.stackexchange.com/questions/23113",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19263/"
] |
23,114 | <p>The CDC has <a href="https://www.cdc.gov/nchs/nvss/vsrr/COVID19/index.htm" rel="nofollow noreferrer">a webpage</a> that lists "Table 1. Deaths involving coronavirus disease 2019 (COVID-19) and pneumonia reported to NCHS by week ending date, United States. Week ending 2/1/2020 to 4/4/2020.*" with column "All COVID-19 Deaths (U07.1)" showing 3307 deaths.</p>
<p>But on the CDC <a href="https://www.cdc.gov/coronavirus/2019-ncov/cases-updates/cases-in-us.html" rel="nofollow noreferrer">page "Cases in the US"</a>, it says the total deaths for just COVID-19 is 12,064. </p>
<p>Why does the CDC website say there are ~9,000 more deaths when not tracking pneumonia?</p>
| [
{
"answer_id": 23107,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>I think the unclarity in this question (and ironically that it's getting upvoted while the answers to it are getting downvoted) is that the question doesn't specify in its numbered premises that the side effect has to be <strong>commonly</strong> reported <em>but only after a long time</em>. A <em>very rare</em> side effect is statistically hard to find, so it's natural that it may take a long time to find some cases, even if it does show up fairly quickly in susceptible individual.</p>\n<p>The question then makes the following blurring/confusion: it goes from a trial in which effects were (not) found to a rollout which vastly expands the population/sample. The question is then misleadingly phrased as</p>\n<blockquote>\n<p>If not, what causes scientists to be so cautious about testing a new vaccine quickly?</p>\n</blockquote>\n<p>There's no reluctance to test a vaccine quickly enough in a small sample (e.g. phase II trials) if the vaccine "passes the smell test" in some preclinical trials etc. But e.g. phase II trials may not find all the rare side effects. The question probably wants to ask why does it take longer to get the vaccine <em>rolled out</em>, but it phrases that as "scientists to be so cautious about <strong>testing</strong>". Basically the caution is about testing (with or without scare quotes) with a large sample all of a sudden, e.g. in an extreme case roll-out after successful pre-clinical trials. Increasing the sample size (as in phase III trials) gives more power to detect rarer side effects. In a <a href=\"https://uk.gsk.com/en-gb/research/trials-in-people/clinical-trial-phases/\" rel=\"nofollow noreferrer\">nutshell</a></p>\n<blockquote>\n<p>The first time a new treatment or vaccine is tested in humans, it will usually be given to a small group of healthy volunteers. [...]</p>\n<p>The principle objectives in Phase I are to:</p>\n<ul>\n<li>make sure that the new medicine presents no <strong>major</strong> safety issues\n[...]</li>\n</ul>\n<p>If Phase I is successful, approval will be sought for a trial involving a larger group of people. Phase II trials will usually (but not always) include patients who have the condition the potential medicine is targeting, and aim to establish: [...]</p>\n<ul>\n<li>effectiveness in preventing the condition (if the volunteer does not already have it)\n[...]</li>\n</ul>\n<p>Phase III</p>\n<p>If the results from Phase II are encouraging, we will seek to start a Phase III trial. This will be a much larger trial, often involving hundreds, possibly thousands of participants coming from a range of different countries.</p>\n<p>The principle objectives in Phase III are to:</p>\n<ul>\n<li><p>demonstrate the <strong>safety and effectiveness</strong> of the new medicine or vaccine in the typical patient likely to use it</p>\n</li>\n<li><p>identify side effects or reasons why the treatment should not be given to people with the condition in question (known as <strong>‘contraindications’</strong>)</p>\n</li>\n</ul>\n</blockquote>\n<p>Emphasis mine.</p>\n<p>Obviously when you increase the sample size even further (roll out) you may even find very rare side effects that were even missed in phase III. Sometimes <a href=\"http://www.genetherapynet.com/clinical-trial-phases.html\" rel=\"nofollow noreferrer\">there are</a> so-called phase IV studies</p>\n<blockquote>\n<p>Phase IV studies may be required by regulatory authorities or may be undertaken by the sponsoring company for competitive (finding a new market for the drug) or other reasons (for example, the drug may not have been tested for interactions with other drugs, or on certain population groups such as pregnant women, who are unlikely to subject themselves to trials).</p>\n<p><strong>The safety surveillance is designed to detect any rare or long-term adverse effects over a much larger patient population and longer time period than was possible during the Phase I-III clinical trials.</strong> Harmful effects discovered by Phase IV trials may result in a drug being no longer sold, or restricted to certain uses.</p>\n</blockquote>\n<p>So the last part of the question is based on (a lot) of misphrasing and/or bad (logical) premises, lumping everything (including roll out) under the word "testing". The level of caution/reluctance is proportional with the size of the population being tested (on).</p>\n<hr />\n<p>So, how long can it take to figure it out if a vaccine gives <em>any</em> bad side effects? <a href=\"https://www.virology.ws/2015/09/10/why-do-we-still-use-sabin-poliovirus-vaccine/\" rel=\"nofollow noreferrer\">How about 20 years?</a> Because deciding if the observed side effects are caused by a vaccine or not is not actually trivial:</p>\n<blockquote>\n<p>all three of Sabin’s OPV strains were approved for use in the US, and in 1961-62 they replaced IPV for routine immunization against poliomyelitis.</p>\n<p>As soon as OPV was used in mass immunizations in the US, cases of vaccine-associated paralysis were described. Initially Sabin decried these findings, arguing that temporal association of paralysis with vaccine administration was not sufficient to implicate OPV. He suggested that the observed paralysis was caused by wild-type viruses, not his vaccine strains.</p>\n<p>A breakthrough in our understanding of vaccine-associated paralysis came in the early 1980s when the recently developed DNA sequencing methods were used to determine the nucleotide sequences of the genomes of the Sabin type 3 vaccine, the neurovirulent virus from which it was derived, and a virus isolated from a child who had developed paralysis after administration of OPV. The results enumerated for the first time the mutations that distinguish the Sabin vaccine from its neurovirulent parent. More importantly, the genome sequence of the vaccine-associated isolate proved that it was derived from the Sabin vaccine and was not a wild-type poliovirus.</p>\n<p>We now understand that every recipient of OPV excretes, within a few days, viruses that are more neurovirulent that the vaccine strains. This evolution occurs because during replication of the OPV strains in the human intestine, the viral genome undergoes mutation and recombination that eliminate the attenuating mutations that Sabin so carefully selected by passage in different hosts.</p>\n<p>From 1961 to 1989 there were an average of 9 cases (range, 1-25 cases) of vaccine-associated paralytic poliomyelitis (VAPP) in the United States, in vaccine recipients or their contacts, or 1 VAPP case per 2.9 million doses of OPV distributed (illustrated). Given this serious side effect, the use of OPV was evaluated several times by the Institute of Medicine, the Centers for Disease Control and Prevention, and the Advisory Committee on Immunization Practices. Each time it was decided that the risks associated with the use of OPV justified the cases of VAPP. It was believed that a switch to IPV would lead to outbreaks of poliomyelitis, because: OPV was better than IPV at protecting non-immunized recipients; the need to inject IPV would lead to reduced compliance; and IPV was known to induce less protective mucosal immunity than OPV.</p>\n</blockquote>\n<p>And yeah whether the benefits outweigh the risks of severe albeit seldom-encountered side effects is a balancing matter:</p>\n<blockquote>\n<p>After the WHO began its poliovirus eradication initiative in 1988, the risk of poliovirus importation into the US slowly decreased until it became very difficult to justify routine use of OPV. In 1996 the Advisory Committee on Immunization Practices decided that the US would transition to IPV and by 2000 IPV had replaced OPV for the routine prevention of poliomyelitis. As a consequence VAPP has been eliminated from the US.</p>\n</blockquote>\n<p>Yes, yes, I can see the objections already that with the current state of biology/medicine we'd figure it out faster now. YMMV, i.e. it's down to "expert opinion" whether we could completely avoid a repeat of VAPP.</p>\n"
},
{
"answer_id": 23580,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 3,
"selected": false,
"text": "<p>Historically, vaccines eg 1955 polio vaccine had side effects due to manufacturing issues allowing live virus to appear in the vaccine in the Cutter company’s vaccine. In 1976, a swine flu vaccine was shown to have a risk of 1 in 100,000 of Guillaine-Barre Syndrome, a transient but serious neuromuscular syndrome. The 1998 rotavirus vaccine was shown to prevent serious life-threatening diarrheal illness in infants, but later studies suggested a risk of a rare form of bowel obstruction called intussusception. The recommendation for RotaShield vaccine was withdrawn.</p>\n\n<p>These side effects generally appeared within weeks, months or a few years of the vaccine administrative. </p>\n\n<p>Source:\n<a href=\"https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html\" rel=\"noreferrer\">https://www.cdc.gov/vaccinesafety/concerns/concerns-history.html</a></p>\n\n<p>Over time this led to significant increase in safety oversight including the FDA VAERS (vaccine adverse event reporting system). Many long-term vaccine safety studies and monitoring systems have been built since then.</p>\n\n<p>For example, the Kaiser vaccine study center looked at hundreds of thousands of MMRV vaccine doses, for example. They found no long term side effects, but in this case the goal was to understand side effects relative to MMR & V(aricella) vaccines given separately versus together.</p>\n\n<p>Source: \n<a href=\"https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe\" rel=\"noreferrer\">https://www.webmd.com/children/vaccines/news/20150107/long-term-study-finds-measles-vaccines-safe</a></p>\n\n<p>Long term side effects can be a complication of any medical intervention, such as medications or devices also, as well as compared to the risk of untreated disease not prevented or not treated. As a result, scientists and clinicians weigh the risks, benefits and alternatives and ideally partner with patients, parents and caregivers in informed consent. Where information has not yet been gathered about long-term safety — or durability of the effect — large long term safety studies have generally been required, and are also possible to detect with such systems as the <a href=\"https://www.fda.gov/vaccines-blood-biologics/biologics-post-market-activities/cbers-sentinel-program\" rel=\"noreferrer\">FDA Sentinel system launched in 2008</a> and other similar safety systems available now (2020) that were not previously available. These systems permit longer range, larger population monitoring of both safety and effectiveness of vaccines and other medical treatments, and further detail by subgroups who may be at higher risk of side effects, or who may be at higher chance of benefiting from vaccines or medications.</p>\n"
},
{
"answer_id": 26372,
"author": "endolith",
"author_id": 13428,
"author_profile": "https://health.stackexchange.com/users/13428",
"pm_score": 3,
"selected": true,
"text": "<blockquote>\n<p>Live attenuated varicella vaccines do contain actual varicella zoster virus (Oka strain), which can establish infection in hosts and undergo latency like other herpesviruses including the unattenuated virus. As a result they can very rarely cause shingles or meningitis years after the receipt of the vaccine. This is a consequence of 2 things: the use of a live vaccine, and the ability of herpesviruses like varicella to undergo latency</p>\n</blockquote>\n<p><a href=\"https://edwardnirenberg.medium.com/long-term-effects-of-covid-19-vaccines-should-you-be-worried-c3c3a547b565\" rel=\"nofollow noreferrer\">Long-Term Effects of COVID-19 Vaccines: Should You Be Worried?</a></p>\n"
}
] | 2020/04/08 | [
"https://health.stackexchange.com/questions/23114",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19264/"
] |
23,148 | <p>I found this pic <a href="https://www.bild.de/news/inland/news-inland/coronavirus-news-im-ticker-drei-wichtige-rki-studien-spahn-lockerung-moeglich-69855062.bild.html" rel="nofollow noreferrer">here</a>. Aren't these Koreans overkilling by wearing half face disposable respirators, inside their 3M powered air respirators? Isn't a 3M powered air respirator enough? </p>
<p><a href="https://i.stack.imgur.com/K1AXV.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/K1AXV.jpg" alt="enter image description here"></a></p>
| [
{
"answer_id": 23150,
"author": "goodside",
"author_id": 138,
"author_profile": "https://health.stackexchange.com/users/138",
"pm_score": 3,
"selected": false,
"text": "<p>Raymond J. Roberge (2008) discusses the rationale for concurrent use of N95 FFR masks and PAPR hoods. The primary benefit is to reduce the number of particles the wearer inhales, and secondarily to provide backup protection in the event of power loss in the PAPR.</p>\n\n<p>PDF link: <a href=\"https://www.ajicjournal.org/article/S0196-6553(07)00594-9/pdf\" rel=\"noreferrer\">https://www.ajicjournal.org/article/S0196-6553(07)00594-9/pdf</a></p>\n"
},
{
"answer_id": 23156,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>It's not clear that they are actually wearing a <a href=\"https://www.3m.com/3M/en_US/company-us/all-3m-products/%7E/All-3M-Products/Safety/Worker-Health-Safety/Personal-Protective-Equipment/Powered-Supplied-Air-Respirators/?N=5002385+8709322+8711017+8711405+8720539+8720547+3291536454+3294857497&rt=r3\" rel=\"nofollow noreferrer\">3M powered air purifying respirator system</a> as those have a valve and filter at the front of the mask.</p>\n<p>Anyway, even if it is a 3M PAPR the data suggests you get a lot more protection</p>\n<blockquote>\n<p>Objective: To determine if using an N95 filtering face-piece respirator concurrently with a loose-fitting powered air-purifying respirator (PAPR) offers additional protection to the wearer.</p>\n<p>Methods: We used a breathing mannequin programmed to deliver minute volumes of 25 L/min and 40 L/min. We measured the baseline protection factor of the PAPR with its motor operational and then deactivated (to simulate mechanical or battery failure). We tested 3 replicates of 3 different N95 models. We glued each N95 to the breathing mannequin and obtained a minimum protection factor of 100 at 25 L/min. We then placed the PAPR on the mannequin and took protection factor measurements with the N95-plus-PAPR combination, at 25 L/min and 40 L/min, with the PAPR operational and then deactivated.</p>\n<p>Results: The N95 significantly increased the PAPR's protection factor, even with the PAPR deactivated. The effect was multiplicative, not merely additive.</p>\n<p>Conclusions: <strong>An N95 decreases the concentration of airborne particles inspired by the wearer of a PAPR.</strong></p>\n</blockquote>\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/19025703/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/19025703/</a></p>\n"
},
{
"answer_id": 31862,
"author": "zombiefeeder",
"author_id": 26205,
"author_profile": "https://health.stackexchange.com/users/26205",
"pm_score": 2,
"selected": false,
"text": "<p>Just to add a component not otherwise mentioned: The Powered Air Purifying Respirator (PAPR) only filters air coming <em>into</em> the PAPR, i.e., the wearer is protected at an N95 level assuming an N95 filter is being used.</p>\n<p>However, the exhaled air of the wearer is <em>not</em> filtered. So if the PAPR wearer unknowingly has COVID, there is <em>some small</em> potential for contaminated air to be exhaled into the airspace, thus potentially infecting others (patients).</p>\n"
}
] | 2020/04/10 | [
"https://health.stackexchange.com/questions/23148",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/-1/"
] |
23,149 | <p>Popular understanding of how viruses work split immunity into four categories:</p>
<ol>
<li>Virus doesn't affect humans at all</li>
<li>No immunity - will get worst possible infection, seems to be the case with COVID-19</li>
<li>Partial immunity - you get sick, but it won't kill you - happens with flu mutations</li>
<li>Full immunity - very hard to get sick - measles is an example</li>
</ol>
<p>For #2 and #3 we could expect to find antibodies in the bloodstream proving that this person has partial or full immunity. But is it possible for some people to be resistant to a virus without having the corresponding antibodies in their bloodstream? And if so, how could their immunity be proven?</p>
| [
{
"answer_id": 23155,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Antibody production is part of the adaptive immune response but the first line of protection against viruses and bacteria is the innate immune response which is cell based, and involves the release of cytokines, interferons, as well as direct cellular attack of infected cells.</p>\n<p>Interestingly a recent study showed that some younger patients with milder symptoms had very low to neglible neutralizing antibody production after confirmed Covid-19 suggesting that their innate immunity was primarily responsible for fighting the virus.</p>\n<blockquote>\n<p>Huang said 10 of the patients in the study had an antibody presence so low it could not even be detected in the laboratory.</p>\n<p>These patients experienced typical Covid-19 symptoms including fever, chill and a cough, but might have beaten back the virus with other parts of the immune system such as T-cells or cytokines.</p>\n</blockquote>\n<p><a href=\"https://www.scmp.com/news/china/science/article/3078840/coronavirus-low-antibody-levels-raise-questions-about\" rel=\"nofollow noreferrer\">https://www.scmp.com/news/china/science/article/3078840/coronavirus-low-antibody-levels-raise-questions-about</a></p>\n"
},
{
"answer_id": 23167,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 0,
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"text": "<p>The answer is yes, there are \"general features\" of\nthe immune system and basically of our genome that combat many different pathogens, but also there are very specialized ones, only useful against a few. To make the matter more complicated, recent research has found that the immune system \"cross-learns\" from infections (and possibly from vaccines as well).</p>\n\n<p>First on \"purely genetic\" defences, some alleles confer enhanced resistance to some viruses. Quoting a <a href=\"https://doi.org/10.1038/nri2174\" rel=\"nofollow noreferrer\">2007 review</a></p>\n\n<blockquote>\n <p>Some proteins that are required for\n surviving viral infection are used to combat many other\n microorganisms as well. In mammals, for example, myeloid\n differentiation primary-response gene 88 (MyD88), a\n Toll-like receptor (TLR) adaptor molecule, is required for\n effective resistance to herpesviruses, Toxoplasma gondii\n and other organisms that have few obvious features in\n common. By contrast, some defences that evolved recently\n are matched against specific microorganisms and may\n operate only within a single host species. For example, the\n Ly49H receptor expressed by mouse natural killer (NK)\n cells seems to recognize only mouse cytomegalovirus\n (MCMV), and does so only in some strains of mice, as the\n receptor-encoding gene has been deleted in other strains.\n More tentative defences are also apparent. For example,\n <strong>mutational abrogation of the human CC-chemokine\n receptor 5 (<a href=\"https://en.wikipedia.org/wiki/CCR5\" rel=\"nofollow noreferrer\">CCR5</a>) protein offers strong protection against\n infection with HIV, but the most common protective allele\n has not been driven to fixation in humans.</strong> And it is likely\n that many other potential resistance mechanisms remain\n to be exploited in mammals.</p>\n \n <p>Some protective antiviral systems are cell autonomous,\n whereas others depend on multiple specialized cell types\n that interact both with the infected cells within the host\n and also with one another. In mammals, the response to\n viral infection overlaps substantially with the response\n to bacteria, using some of the same sensing, signalling and\n effector mechanisms. In insects, there is a greater reliance\n on cell-autonomous defence, and new advances must be\n made in defining the pathways that are involved. [...]</p>\n \n <p>Resistance to viral infection comes at a definite cost.\n In mammals, the cellular systems that confer protection\n against viruses are also capable of causing autoimmunity. This may be seen as a reflection of three facts. First, viruses\n have imposed a need to distinguish between host nucleic\n acid and foreign nucleic acid — a challenge that has been\n met by mammals in the large part, but not completely.\n Second, viruses certainly contributed to the evolution of\n adaptive immunity, upon which autoimmunity is predicated.\n And third, some of the elements of innate immunity\n that support autoimmune disease (among them the\n |IFNs and cells that produce them) evolved largely to\n combat viruses.</p>\n</blockquote>\n\n<p>Beyond this \"fixed\"/innate defense system, there's another more <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5087274/\" rel=\"nofollow noreferrer\">recently discovered</a> one that can be considered \"intermediate\" (i.e. between innate and the classical def of \"adaptive immunity\"):</p>\n\n<blockquote>\n <p>Protection against reinfection has been reported not only in plants and invertebrates that do not have adaptive immunity (4), but also in mammals, with old and <strong>new studies demonstrating cross-protection between infections with different pathogens</strong> (5). These studies have led to the hypothesis that innate immunity can be influenced by previous encounters with pathogens or their products, and this property has been termed <em>trained immunity</em> or <em>innate immune memory</em>.</p>\n</blockquote>\n\n<p>(In fact this discovery has led some to <a href=\"https://hal.archives-ouvertes.fr/hal-01964547/file/Pradeu-DuPasquier_Immunological%20memory_Online%20version.pdf\" rel=\"nofollow noreferrer\">propose</a> a reconsideration of the immune system dichotomy.)</p>\n\n<p>Also, you assume (in your #2) that COVID-19 outcomes are always better with more immune response, but that <a href=\"https://www.nature.com/articles/d41586-020-01056-7\" rel=\"nofollow noreferrer\">might not actually be the case</a> (harking back to a hypothesis about the 1918 flu deadliness):</p>\n\n<blockquote>\n <p>Some of the earliest analyses of coronavirus patients in China suggested that it might not be only the virus that ravages the lungs and kills; rather, an overactive immune response might also make people severely ill or cause death. Some people who were critically ill with COVID-19 had high blood levels of proteins called cytokines, some of which can ramp up immune responses. [...]</p>\n \n <p>A combination of damage from both a virus and the immune response to it is not uncommon, says Rafi Ahmed, a viral immunologist at Emory University in Atlanta, Georgia. The effects of 'hit-and-run' viruses such as norovirus, which make people sick almost immediately after infection, are more probably due to the virus itself, he says. By contrast, people infected with viruses such as coronavirus do not show symptoms until several days after infection. By then, collateral damage from the immune response often contributes to the illness.</p>\n</blockquote>\n\n<p>Based on the convergence of epidemiological data and animal research, the auto-immune response is <a href=\"https://www.nature.com/articles/445267a\" rel=\"nofollow noreferrer\">suspected</a> to have been a (probably more significant) factor in 1918:</p>\n\n<blockquote>\n <p>unlike contemporary influenza strains, which typically affect the very young and the elderly most severely, the 1918 influenza pandemic was mostly fatal in young adults, who generally possess more robust immune systems.</p>\n \n <p>The work of Kobasa et al. substantiates the findings of Kash et al., who showed in mice that the 1918 virus triggered a vigorous innate immune response that was linked to fatalities. Although the mechanisms of tissue destruction were not addressed in either study, the work clearly demonstrates the vital function of early innate immune defences in controlling the virus. It seems that the pandemic 1918 virus had a genetic composition and rapid replication kinetics that may have resulted in an excessively vigorous innate immune and inflammatory response that contributed to severe tissue damage, disease and death.</p>\n</blockquote>\n"
},
{
"answer_id": 23172,
"author": "huangy",
"author_id": 19209,
"author_profile": "https://health.stackexchange.com/users/19209",
"pm_score": 1,
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"text": "<p>The immune response to viruses involves multiple branches of the immune system. There are the innate and adaptive branches, and within the adaptive response, there are cell-mediated and antibody-mediated components. Different pathogens activate slightly different versions of the immune response. For example, cell-mediated immunity appears to be particularly important for protection against varicella zoster virus (VZV), and antibody titer is not necessarily reflective of immune status. In studies of the VZV vaccines, <a href=\"https://academic.oup.com/jid/article/200/7/1068/903990\" rel=\"nofollow noreferrer\">CD4+ T cells targeted to VZV are measured</a> in addition to antibody titers.</p>\n\n<p>A couple additional caveats about relying on antibody titers to determine protective immunity--</p>\n\n<p>Detection limits: It's important to consider the detection limit of the test being used. Undetectable antibody and absent antibody are not necessarily the same.</p>\n\n<p>Antibody target: Many antibodies may be generated to a virus, but only a subset of these will be effective at mounting an effective immune response to the virus. Detection of an antibody does not equate protective immunity.</p>\n"
}
] | 2020/04/10 | [
"https://health.stackexchange.com/questions/23149",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,157 | <p>I heard that NYC hospitals are seeing an increased cases of myocardial infarction with higher mortality than normal during this COVID-19 pandemic. What the connection is between COVID-19 and cardiovascular disease?</p>
| [
{
"answer_id": 23158,
"author": "D.Tan",
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"pm_score": 4,
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"text": "<p>Cardiovascular disease is known to worsen during infections such as influenza through two proposed mechanisms:</p>\n<ul>\n<li>cytokines from the resulting inflammation cause weaken atherosclerotic plaques and cause plaque rupture/thrombosis</li>\n<li>stress from illness can precipitate decompensated heart failure in predisposed patients</li>\n</ul>\n<p>Two studies from Wuhan have looked into this so far. One cohort study of 416 patients found that 19.7% of COVID-19 patients developed myocardial infarction during their hospitalization and had higher rates of mortality (51.2% MI vs 4.5% no MI)[2]. Another cohort study of 187 patients found that 27.8% of their patients developed MI with a similar mortality rate (59.6% MI vs 8.9% no MI). Patients from both studies who developed MIs seem to be older and have preexisting hypertension, diabetes and coronary artery disease.</p>\n<p>From these studies, the current data support the idea that getting COVID-19 increases the risk of having an MI, especially in those with risk factors.</p>\n<p>Update: The <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidance-management-patients.html\" rel=\"nofollow noreferrer\">CDC</a> states that patients with COVID-19 can also develop a hypercoagulable state, leading to thrombotic complications such as an MI. Unfortunately, the pathogenesis of COVID-19-related hypercoagulability is unknown.</p>\n<p>Source:</p>\n<ol>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763844\" rel=\"nofollow noreferrer\">JAMA Cardiology: Association of Coronavirus Disease 2019 (COVID-19) With Myocardial Injury and Mortality</a></p>\n</li>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763524\" rel=\"nofollow noreferrer\">JAMA Cardiology: Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China</a></p>\n</li>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763845\" rel=\"nofollow noreferrer\">JAMA Cardiology: Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)</a></p>\n</li>\n</ol>\n"
},
{
"answer_id": 23190,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 2,
"selected": false,
"text": "<p>A <a href=\"https://jamanetwork.com/journals/jama/fullarticle/2763485\" rel=\"nofollow noreferrer\">case series in Seattle published in JAMA on March 17, 2020</a> describes a potential cardiomyopathy associated with coronavirus in critically-ill patients. Current thinking includes a potential direct cardiac effect of the COVID-19 viral infection, rather than atherosclerotic or ischemic disease per se.</p>\n\n<p>The authors noted:</p>\n\n<blockquote>\n <p>It is unclear whether the high rate of cardiomyopathy in this case\n series reflects a direct cardiac complication of SARS-CoV-2 infection\n or resulted from overwhelming critical illness. Others have described\n cardiomyopathy in COVID-19, and further research may better\n characterize this risk</p>\n</blockquote>\n\n<p>They go on to cite two other reports on potential COVID-19 related cardiomyopathy and cardiac impacts.</p>\n\n<p>Mullen B. COVID-19 clinical guidance for the cardiovascular care team. Published online March 6, 2020. Accessed March 16, 2020. <a href=\"https://www.acc.org/~/media/665AFA1E710B4B3293138D14BE8D1213.pdf\" rel=\"nofollow noreferrer\">https://www.acc.org/~/media/665AFA1E710B4B3293138D14BE8D1213.pdf</a></p>\n\n<p>Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020. doi:10.1038/s41569-020-0360-5PubMedGoogle Scholar</p>\n"
}
] | 2020/04/10 | [
"https://health.stackexchange.com/questions/23157",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/13163/"
] |
23,166 | <p>Maurice Hillman developed a vaccine for the 1957 flu pandemic that was ready within five months (<a href="https://www.history.com/.amp/news/1957-flu-pandemic-vaccine-hilleman" rel="noreferrer">1</a>).</p>
<p>One commonly hears that it will take at least 12-18 months in total to deploy a vaccine against SARS-CoV-2.</p>
<p>As I understand, most of that time is taken up by clinical trials, which are claimed to be absolutely necessary.</p>
<p>Is this because candidates for the new vaccine are inherently more dangerous/less clear to be efficient than candidates for the vaccine against the 1957 flu? Or is this mostly because of higher risk aversion/regulatory burden compared to that time?</p>
| [
{
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"text": "<p>From the very article you've linked:</p>\n<blockquote>\n<p>Making a vaccine for a new flu strain is very different from making a vaccine for something completely new like COVID-19, the novel coronavirus that emerged in 2019. Doctors and scientists first developed viable flu vaccines in the 1940s, so they were not starting from scratch when they went to work on the 1957 flu vaccine. Still, Hilleman bypassed regulatory agencies in his efforts to push the vaccine forward because he worried those agencies would slow the process down.</p>\n</blockquote>\n<p>And an apt analogy from <a href=\"https://www.theatlantic.com/health/archive/2020/02/covid-vaccine/607000/\" rel=\"nofollow noreferrer\">The Atlantic</a> on testing:</p>\n<blockquote>\n<p>Like other drugs, vaccines require a long testing process to see whether they indeed protect people from disease, and do so safely. What this company—and others—has done is copy a bit of the virus’s RNA that one day could prove to work as a vaccine. It’s a promising first step, but to call it a discovery is like announcing a new surgery after sharpening a scalpel.</p>\n<p>Though genetic sequencing is now extremely fast, making vaccines is as much art as science. It involves finding a viral sequence that will reliably cause a protective immune-system memory but not trigger an acute inflammatory response that would itself cause symptoms. (While the influenza vaccine cannot cause the flu, the CDC warns that it can cause “flu-like symptoms.”) Hitting this sweet spot requires testing, first in lab models and animals, and eventually in people. One does not simply ship a billion viral gene fragments around the world to be injected into everyone at the moment of discovery.</p>\n</blockquote>\n<p>And since SARS is the closest relevant relative of Covid-19 (same source):</p>\n<blockquote>\n<p>During the SARS outbreak in 2003, researchers moved from obtaining the genomic sequence of the virus and into a phase 1 clinical trial of a vaccine in 20 months. Fauci wrote that his team has since compressed that timeline to just over three months for other viruses, and for the new coronavirus, “they hope to move even faster.”</p>\n<p>[...] Overall, if all pieces fell into place, Hatchett guesses it would be 12 to 18 months before an initial product could be deemed safe and effective. That timeline represents “a vast acceleration compared with the history of vaccine development,” he told me. But it’s also unprecedentedly ambitious. “Even to propose such a timeline at this point must be regarded as hugely aspirational,” he added.</p>\n<p>Fauci’s initial optimism seemed to wane, too. Last week he said that the process of vaccine development was proving “very difficult and very frustrating.” For all the advances in basic science, the process cannot proceed to an actual vaccine without extensive clinical testing, which requires manufacturing many vaccines and meticulously monitoring outcomes in people. [...]</p>\n<p>“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak. The real problem is that preparedness for this outbreak should have been happening for the past decade, ever since SARS. <strong>“Had we not set the SARS-vaccine-research program aside, we would have had a lot more of this foundational work that we could apply to this new, closely related virus,” he said. But, as with Ebola, government funding and pharmaceutical-industry development evaporated once the sense of emergency lifted. “Some very early research ended up sitting on a shelf because that outbreak ended before a vaccine needed to be aggressively developed.”</strong></p>\n</blockquote>\n<p>Some experts have <a href=\"https://www.nature.com/articles/d41586-020-00798-8\" rel=\"nofollow noreferrer\">expressed</a> skepticism that current single-focus on the spike protein of SARS-CoV-2 would suffice:</p>\n<blockquote>\n<p>The Moderna vaccine consists of an RNA molecule. Like many of the other SARS-CoV-2 vaccines in development, it is designed to train the immune system to make antibodies that recognize and block the spike protein that the virus uses to enter human cells.</p>\n<p>“I think it’s reasonable as a first pass, but we will learn that, perhaps, antibody responses to the spike exclusively may not be the whole story,” says [Michael] Diamond [--a viral immunologist at Washington University in St. Louis, Missouri]. A successful SARS-CoV-2 vaccine might need to prompt the body to generate antibodies that block other viral proteins, for instance, or make T cells that can recognize and kill infected cells.</p>\n</blockquote>\n<p>Also (same source):</p>\n<blockquote>\n<p>If humans do develop immunity, how long does it last?</p>\n<p>That’s another big unknown. <strong>Immunity is short-lived for the coronaviruses that cause common colds; even people who have high levels of antibodies against these viruses can still become infected</strong>, says Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City.</p>\n<p>The evidence is more equivocal for the two other coronaviruses that have triggered epidemics: those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Perlman says his team has found that <strong>after people recover from MERS, their antibodies against the virus drop precipitously</strong>. He also says that his team has gathered data — not yet published — showing that <strong>SARS antibodies are still present in the body 15 years after infection. But it’s not clear whether this immune response is enough to prevent reinfection.</strong> “We don’t have good evidence of long-lasting immunity, but we also don’t have really good data from both SARS and MERS,” Perlman adds.</p>\n</blockquote>\n<p>The same source discusses the risks of <a href=\"https://en.wikipedia.org/wiki/Antibody-dependent_enhancement\" rel=\"nofollow noreferrer\">"disease enhancement"</a> which are thought to be fairly low for SARS-CoV-2, but not inexistent. Actually Wikipedia has a somewhat deeper/different perspective on this:</p>\n<blockquote>\n<p>Non-human primates vaccinated with modified vaccinia Ankara (MVA) virus encoding full-length SARS-COV spike glycoprotein and challenged with the SARS-CoV virus had lower viral loads but suffered from acute lung injury due to antibody enhancement.[3] [...] Antibody-dependent enhancement as been observed in both severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) animal models allowing the respective viruses to enter cells expressing FcR including myeloid lineage cells.[5]</p>\n<p>Moreover, antibody-dependent enhancement of acute lung injury has been documented in both SARS and MERS. Rabbits intranasally infected with MERS-COV developed a pulmonary infection characterized by viremia and perivascular inflammation of the lung.[6] Interestingly, when challenged with MERS-COV a second time, rabbits were not protected from disease, despite having measurable antibody responses.[6] Moreover, the rabbits developed more severe lung disease on re-exposure to MERS-COV.[6] Similarly in SARS, mice vaccinated against SARS-COV had measurable antibody responses.[7] However, all mice within two days of challenge developed lung pathology.[7] The lack of protection from antibodies, and exacerbation of lung pathology has been a major challenge for coronavirus vaccine development and may similarly impact SARS-COV-2 vaccine research.</p>\n</blockquote>\n"
},
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"text": "<p>The 1957 influenza pandemic caused <a href=\"https://www.cdc.gov/flu/pandemic-resources/1957-1958-pandemic.html\" rel=\"nofollow noreferrer\">1.1 millions deaths worldwide</a>.</p>\n\n<p>According to History.com, the 1957 influenza vaccine was developed as <a href=\"https://www.history.com/news/1957-flu-pandemic-vaccine-hilleman\" rel=\"nofollow noreferrer\">the result of having serum from people over many past years with prior influenza infections</a>. Scientists were able to compare the 1957 flu virus against previous flu viruses and began working on a fundamentally different vaccine, but with the “head start” of flu vaccine development in general.</p>\n\n<p>According to History.com:</p>\n\n<blockquote>\n <p>Doctors and scientists first developed viable flu vaccines in the\n 1940s, so they were not starting from scratch when they went to work\n on the 1957 flu vaccine.</p>\n</blockquote>\n\n<p>Dr. Maurice Hilleman played an instrumental role in the vaccine development and production through Merck, where we worked. According to a <a href=\"https://www.inquirer.com/philly/health/maurice-hilleman-influenza-pandemic-vaccine-merck-20180125.html?outputType=amp\" rel=\"nofollow noreferrer\">profile of him written in 2018</a>, US pharmaceutical companies had produced a vaccine by June of 1957, and distributed 40 million doses by late fall.</p>\n\n<p>By comparison, for novel coronavirus causing COVID-19, vaccine development has evolved in the past 50 years to examine safety and efficacy more closely.</p>\n\n<p>However, <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMp2005630\" rel=\"nofollow noreferrer\">several challenges have been noted by scientists</a>:</p>\n\n<ul>\n<li>what to target with the vaccine. Scientists believe the spike protein is a good target, but whether to target the whole protein or just a piece is a challenge.</li>\n<li>prior experience with MeRS and SARS suggests the need for caution. This is because some types of immune response may actually worsen lung disease. This begets the need for animal models testing and safety monitoring — neither of which appeared to be part of the 1957 influenza vaccine development process.\n\n<ul>\n<li>“as with naturally acquired infection, the potential duration of immunity is unknown; similarly, whether single-dose vaccines will confer immunity is uncertain.” </li>\n</ul></li>\n</ul>\n\n<p>That said, extraordinary steps are being taken to accelerate coronavirus vaccine development. A <a href=\"https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/0/nejm.ahead-of-print/nejmp2005630/20200406/images/img_medium/nejmp2005630_f1.jpeg\" rel=\"nofollow noreferrer\">chart</a> from the NEJM article illustrates the “parallel track” acceleration, beginning manufacturing well before the vaccine is proven out in clinical trials.</p>\n\n<p></p>\n"
}
] | 2020/04/11 | [
"https://health.stackexchange.com/questions/23166",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19304/"
] |
23,182 | <p>I have heard of from reading numerous journal articles, and newspaper/TV reports:</p>
<ul>
<li>age > 70</li>
<li>age < 5</li>
<li>obesity</li>
<li>smoker cigarettes or pot</li>
<li>male</li>
<li>blood group not group O</li>
<li>poor socio economic status</li>
<li>crowded and multi-generational living</li>
<li><a href="https://medicalsciences.stackexchange.com/questions/23202">black</a>, hispanic </li>
<li>hypertension</li>
<li>cardio respiratory disease</li>
<li>diabetes 1+2</li>
<li>immunosuppression</li>
<li>cancer</li>
<li>religious beliefs</li>
</ul>
<p>Note that some of these are inextricably linked to each other.</p>
<p>Any others?</p>
| [
{
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"selected": false,
"text": "<p>From the very article you've linked:</p>\n<blockquote>\n<p>Making a vaccine for a new flu strain is very different from making a vaccine for something completely new like COVID-19, the novel coronavirus that emerged in 2019. Doctors and scientists first developed viable flu vaccines in the 1940s, so they were not starting from scratch when they went to work on the 1957 flu vaccine. Still, Hilleman bypassed regulatory agencies in his efforts to push the vaccine forward because he worried those agencies would slow the process down.</p>\n</blockquote>\n<p>And an apt analogy from <a href=\"https://www.theatlantic.com/health/archive/2020/02/covid-vaccine/607000/\" rel=\"nofollow noreferrer\">The Atlantic</a> on testing:</p>\n<blockquote>\n<p>Like other drugs, vaccines require a long testing process to see whether they indeed protect people from disease, and do so safely. What this company—and others—has done is copy a bit of the virus’s RNA that one day could prove to work as a vaccine. It’s a promising first step, but to call it a discovery is like announcing a new surgery after sharpening a scalpel.</p>\n<p>Though genetic sequencing is now extremely fast, making vaccines is as much art as science. It involves finding a viral sequence that will reliably cause a protective immune-system memory but not trigger an acute inflammatory response that would itself cause symptoms. (While the influenza vaccine cannot cause the flu, the CDC warns that it can cause “flu-like symptoms.”) Hitting this sweet spot requires testing, first in lab models and animals, and eventually in people. One does not simply ship a billion viral gene fragments around the world to be injected into everyone at the moment of discovery.</p>\n</blockquote>\n<p>And since SARS is the closest relevant relative of Covid-19 (same source):</p>\n<blockquote>\n<p>During the SARS outbreak in 2003, researchers moved from obtaining the genomic sequence of the virus and into a phase 1 clinical trial of a vaccine in 20 months. Fauci wrote that his team has since compressed that timeline to just over three months for other viruses, and for the new coronavirus, “they hope to move even faster.”</p>\n<p>[...] Overall, if all pieces fell into place, Hatchett guesses it would be 12 to 18 months before an initial product could be deemed safe and effective. That timeline represents “a vast acceleration compared with the history of vaccine development,” he told me. But it’s also unprecedentedly ambitious. “Even to propose such a timeline at this point must be regarded as hugely aspirational,” he added.</p>\n<p>Fauci’s initial optimism seemed to wane, too. Last week he said that the process of vaccine development was proving “very difficult and very frustrating.” For all the advances in basic science, the process cannot proceed to an actual vaccine without extensive clinical testing, which requires manufacturing many vaccines and meticulously monitoring outcomes in people. [...]</p>\n<p>“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak. The real problem is that preparedness for this outbreak should have been happening for the past decade, ever since SARS. <strong>“Had we not set the SARS-vaccine-research program aside, we would have had a lot more of this foundational work that we could apply to this new, closely related virus,” he said. But, as with Ebola, government funding and pharmaceutical-industry development evaporated once the sense of emergency lifted. “Some very early research ended up sitting on a shelf because that outbreak ended before a vaccine needed to be aggressively developed.”</strong></p>\n</blockquote>\n<p>Some experts have <a href=\"https://www.nature.com/articles/d41586-020-00798-8\" rel=\"nofollow noreferrer\">expressed</a> skepticism that current single-focus on the spike protein of SARS-CoV-2 would suffice:</p>\n<blockquote>\n<p>The Moderna vaccine consists of an RNA molecule. Like many of the other SARS-CoV-2 vaccines in development, it is designed to train the immune system to make antibodies that recognize and block the spike protein that the virus uses to enter human cells.</p>\n<p>“I think it’s reasonable as a first pass, but we will learn that, perhaps, antibody responses to the spike exclusively may not be the whole story,” says [Michael] Diamond [--a viral immunologist at Washington University in St. Louis, Missouri]. A successful SARS-CoV-2 vaccine might need to prompt the body to generate antibodies that block other viral proteins, for instance, or make T cells that can recognize and kill infected cells.</p>\n</blockquote>\n<p>Also (same source):</p>\n<blockquote>\n<p>If humans do develop immunity, how long does it last?</p>\n<p>That’s another big unknown. <strong>Immunity is short-lived for the coronaviruses that cause common colds; even people who have high levels of antibodies against these viruses can still become infected</strong>, says Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City.</p>\n<p>The evidence is more equivocal for the two other coronaviruses that have triggered epidemics: those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Perlman says his team has found that <strong>after people recover from MERS, their antibodies against the virus drop precipitously</strong>. He also says that his team has gathered data — not yet published — showing that <strong>SARS antibodies are still present in the body 15 years after infection. But it’s not clear whether this immune response is enough to prevent reinfection.</strong> “We don’t have good evidence of long-lasting immunity, but we also don’t have really good data from both SARS and MERS,” Perlman adds.</p>\n</blockquote>\n<p>The same source discusses the risks of <a href=\"https://en.wikipedia.org/wiki/Antibody-dependent_enhancement\" rel=\"nofollow noreferrer\">"disease enhancement"</a> which are thought to be fairly low for SARS-CoV-2, but not inexistent. Actually Wikipedia has a somewhat deeper/different perspective on this:</p>\n<blockquote>\n<p>Non-human primates vaccinated with modified vaccinia Ankara (MVA) virus encoding full-length SARS-COV spike glycoprotein and challenged with the SARS-CoV virus had lower viral loads but suffered from acute lung injury due to antibody enhancement.[3] [...] Antibody-dependent enhancement as been observed in both severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) animal models allowing the respective viruses to enter cells expressing FcR including myeloid lineage cells.[5]</p>\n<p>Moreover, antibody-dependent enhancement of acute lung injury has been documented in both SARS and MERS. Rabbits intranasally infected with MERS-COV developed a pulmonary infection characterized by viremia and perivascular inflammation of the lung.[6] Interestingly, when challenged with MERS-COV a second time, rabbits were not protected from disease, despite having measurable antibody responses.[6] Moreover, the rabbits developed more severe lung disease on re-exposure to MERS-COV.[6] Similarly in SARS, mice vaccinated against SARS-COV had measurable antibody responses.[7] However, all mice within two days of challenge developed lung pathology.[7] The lack of protection from antibodies, and exacerbation of lung pathology has been a major challenge for coronavirus vaccine development and may similarly impact SARS-COV-2 vaccine research.</p>\n</blockquote>\n"
},
{
"answer_id": 23199,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 2,
"selected": true,
"text": "<p>The 1957 influenza pandemic caused <a href=\"https://www.cdc.gov/flu/pandemic-resources/1957-1958-pandemic.html\" rel=\"nofollow noreferrer\">1.1 millions deaths worldwide</a>.</p>\n\n<p>According to History.com, the 1957 influenza vaccine was developed as <a href=\"https://www.history.com/news/1957-flu-pandemic-vaccine-hilleman\" rel=\"nofollow noreferrer\">the result of having serum from people over many past years with prior influenza infections</a>. Scientists were able to compare the 1957 flu virus against previous flu viruses and began working on a fundamentally different vaccine, but with the “head start” of flu vaccine development in general.</p>\n\n<p>According to History.com:</p>\n\n<blockquote>\n <p>Doctors and scientists first developed viable flu vaccines in the\n 1940s, so they were not starting from scratch when they went to work\n on the 1957 flu vaccine.</p>\n</blockquote>\n\n<p>Dr. Maurice Hilleman played an instrumental role in the vaccine development and production through Merck, where we worked. According to a <a href=\"https://www.inquirer.com/philly/health/maurice-hilleman-influenza-pandemic-vaccine-merck-20180125.html?outputType=amp\" rel=\"nofollow noreferrer\">profile of him written in 2018</a>, US pharmaceutical companies had produced a vaccine by June of 1957, and distributed 40 million doses by late fall.</p>\n\n<p>By comparison, for novel coronavirus causing COVID-19, vaccine development has evolved in the past 50 years to examine safety and efficacy more closely.</p>\n\n<p>However, <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMp2005630\" rel=\"nofollow noreferrer\">several challenges have been noted by scientists</a>:</p>\n\n<ul>\n<li>what to target with the vaccine. Scientists believe the spike protein is a good target, but whether to target the whole protein or just a piece is a challenge.</li>\n<li>prior experience with MeRS and SARS suggests the need for caution. This is because some types of immune response may actually worsen lung disease. This begets the need for animal models testing and safety monitoring — neither of which appeared to be part of the 1957 influenza vaccine development process.\n\n<ul>\n<li>“as with naturally acquired infection, the potential duration of immunity is unknown; similarly, whether single-dose vaccines will confer immunity is uncertain.” </li>\n</ul></li>\n</ul>\n\n<p>That said, extraordinary steps are being taken to accelerate coronavirus vaccine development. A <a href=\"https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/0/nejm.ahead-of-print/nejmp2005630/20200406/images/img_medium/nejmp2005630_f1.jpeg\" rel=\"nofollow noreferrer\">chart</a> from the NEJM article illustrates the “parallel track” acceleration, beginning manufacturing well before the vaccine is proven out in clinical trials.</p>\n\n<p></p>\n"
}
] | 2020/04/12 | [
"https://health.stackexchange.com/questions/23182",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/3414/"
] |
23,187 | <p>Here's WebMD's info on the subject which seems to implicate the corrective medication specifically rather than hypertension!:</p>
<p><a href="https://www.webmd.com/lung/coronavirus-high-blood-pressure#1" rel="nofollow noreferrer">https://www.webmd.com/lung/coronavirus-high-blood-pressure#1</a></p>
<p>Should a COVID-19 infected person immediately stop taking the inhibitor?</p>
| [
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"selected": false,
"text": "<p>From the very article you've linked:</p>\n<blockquote>\n<p>Making a vaccine for a new flu strain is very different from making a vaccine for something completely new like COVID-19, the novel coronavirus that emerged in 2019. Doctors and scientists first developed viable flu vaccines in the 1940s, so they were not starting from scratch when they went to work on the 1957 flu vaccine. Still, Hilleman bypassed regulatory agencies in his efforts to push the vaccine forward because he worried those agencies would slow the process down.</p>\n</blockquote>\n<p>And an apt analogy from <a href=\"https://www.theatlantic.com/health/archive/2020/02/covid-vaccine/607000/\" rel=\"nofollow noreferrer\">The Atlantic</a> on testing:</p>\n<blockquote>\n<p>Like other drugs, vaccines require a long testing process to see whether they indeed protect people from disease, and do so safely. What this company—and others—has done is copy a bit of the virus’s RNA that one day could prove to work as a vaccine. It’s a promising first step, but to call it a discovery is like announcing a new surgery after sharpening a scalpel.</p>\n<p>Though genetic sequencing is now extremely fast, making vaccines is as much art as science. It involves finding a viral sequence that will reliably cause a protective immune-system memory but not trigger an acute inflammatory response that would itself cause symptoms. (While the influenza vaccine cannot cause the flu, the CDC warns that it can cause “flu-like symptoms.”) Hitting this sweet spot requires testing, first in lab models and animals, and eventually in people. One does not simply ship a billion viral gene fragments around the world to be injected into everyone at the moment of discovery.</p>\n</blockquote>\n<p>And since SARS is the closest relevant relative of Covid-19 (same source):</p>\n<blockquote>\n<p>During the SARS outbreak in 2003, researchers moved from obtaining the genomic sequence of the virus and into a phase 1 clinical trial of a vaccine in 20 months. Fauci wrote that his team has since compressed that timeline to just over three months for other viruses, and for the new coronavirus, “they hope to move even faster.”</p>\n<p>[...] Overall, if all pieces fell into place, Hatchett guesses it would be 12 to 18 months before an initial product could be deemed safe and effective. That timeline represents “a vast acceleration compared with the history of vaccine development,” he told me. But it’s also unprecedentedly ambitious. “Even to propose such a timeline at this point must be regarded as hugely aspirational,” he added.</p>\n<p>Fauci’s initial optimism seemed to wane, too. Last week he said that the process of vaccine development was proving “very difficult and very frustrating.” For all the advances in basic science, the process cannot proceed to an actual vaccine without extensive clinical testing, which requires manufacturing many vaccines and meticulously monitoring outcomes in people. [...]</p>\n<p>“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak. The real problem is that preparedness for this outbreak should have been happening for the past decade, ever since SARS. <strong>“Had we not set the SARS-vaccine-research program aside, we would have had a lot more of this foundational work that we could apply to this new, closely related virus,” he said. But, as with Ebola, government funding and pharmaceutical-industry development evaporated once the sense of emergency lifted. “Some very early research ended up sitting on a shelf because that outbreak ended before a vaccine needed to be aggressively developed.”</strong></p>\n</blockquote>\n<p>Some experts have <a href=\"https://www.nature.com/articles/d41586-020-00798-8\" rel=\"nofollow noreferrer\">expressed</a> skepticism that current single-focus on the spike protein of SARS-CoV-2 would suffice:</p>\n<blockquote>\n<p>The Moderna vaccine consists of an RNA molecule. Like many of the other SARS-CoV-2 vaccines in development, it is designed to train the immune system to make antibodies that recognize and block the spike protein that the virus uses to enter human cells.</p>\n<p>“I think it’s reasonable as a first pass, but we will learn that, perhaps, antibody responses to the spike exclusively may not be the whole story,” says [Michael] Diamond [--a viral immunologist at Washington University in St. Louis, Missouri]. A successful SARS-CoV-2 vaccine might need to prompt the body to generate antibodies that block other viral proteins, for instance, or make T cells that can recognize and kill infected cells.</p>\n</blockquote>\n<p>Also (same source):</p>\n<blockquote>\n<p>If humans do develop immunity, how long does it last?</p>\n<p>That’s another big unknown. <strong>Immunity is short-lived for the coronaviruses that cause common colds; even people who have high levels of antibodies against these viruses can still become infected</strong>, says Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City.</p>\n<p>The evidence is more equivocal for the two other coronaviruses that have triggered epidemics: those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Perlman says his team has found that <strong>after people recover from MERS, their antibodies against the virus drop precipitously</strong>. He also says that his team has gathered data — not yet published — showing that <strong>SARS antibodies are still present in the body 15 years after infection. But it’s not clear whether this immune response is enough to prevent reinfection.</strong> “We don’t have good evidence of long-lasting immunity, but we also don’t have really good data from both SARS and MERS,” Perlman adds.</p>\n</blockquote>\n<p>The same source discusses the risks of <a href=\"https://en.wikipedia.org/wiki/Antibody-dependent_enhancement\" rel=\"nofollow noreferrer\">"disease enhancement"</a> which are thought to be fairly low for SARS-CoV-2, but not inexistent. Actually Wikipedia has a somewhat deeper/different perspective on this:</p>\n<blockquote>\n<p>Non-human primates vaccinated with modified vaccinia Ankara (MVA) virus encoding full-length SARS-COV spike glycoprotein and challenged with the SARS-CoV virus had lower viral loads but suffered from acute lung injury due to antibody enhancement.[3] [...] Antibody-dependent enhancement as been observed in both severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) animal models allowing the respective viruses to enter cells expressing FcR including myeloid lineage cells.[5]</p>\n<p>Moreover, antibody-dependent enhancement of acute lung injury has been documented in both SARS and MERS. Rabbits intranasally infected with MERS-COV developed a pulmonary infection characterized by viremia and perivascular inflammation of the lung.[6] Interestingly, when challenged with MERS-COV a second time, rabbits were not protected from disease, despite having measurable antibody responses.[6] Moreover, the rabbits developed more severe lung disease on re-exposure to MERS-COV.[6] Similarly in SARS, mice vaccinated against SARS-COV had measurable antibody responses.[7] However, all mice within two days of challenge developed lung pathology.[7] The lack of protection from antibodies, and exacerbation of lung pathology has been a major challenge for coronavirus vaccine development and may similarly impact SARS-COV-2 vaccine research.</p>\n</blockquote>\n"
},
{
"answer_id": 23199,
"author": "Henry Wei",
"author_id": 17942,
"author_profile": "https://health.stackexchange.com/users/17942",
"pm_score": 2,
"selected": true,
"text": "<p>The 1957 influenza pandemic caused <a href=\"https://www.cdc.gov/flu/pandemic-resources/1957-1958-pandemic.html\" rel=\"nofollow noreferrer\">1.1 millions deaths worldwide</a>.</p>\n\n<p>According to History.com, the 1957 influenza vaccine was developed as <a href=\"https://www.history.com/news/1957-flu-pandemic-vaccine-hilleman\" rel=\"nofollow noreferrer\">the result of having serum from people over many past years with prior influenza infections</a>. Scientists were able to compare the 1957 flu virus against previous flu viruses and began working on a fundamentally different vaccine, but with the “head start” of flu vaccine development in general.</p>\n\n<p>According to History.com:</p>\n\n<blockquote>\n <p>Doctors and scientists first developed viable flu vaccines in the\n 1940s, so they were not starting from scratch when they went to work\n on the 1957 flu vaccine.</p>\n</blockquote>\n\n<p>Dr. Maurice Hilleman played an instrumental role in the vaccine development and production through Merck, where we worked. According to a <a href=\"https://www.inquirer.com/philly/health/maurice-hilleman-influenza-pandemic-vaccine-merck-20180125.html?outputType=amp\" rel=\"nofollow noreferrer\">profile of him written in 2018</a>, US pharmaceutical companies had produced a vaccine by June of 1957, and distributed 40 million doses by late fall.</p>\n\n<p>By comparison, for novel coronavirus causing COVID-19, vaccine development has evolved in the past 50 years to examine safety and efficacy more closely.</p>\n\n<p>However, <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMp2005630\" rel=\"nofollow noreferrer\">several challenges have been noted by scientists</a>:</p>\n\n<ul>\n<li>what to target with the vaccine. Scientists believe the spike protein is a good target, but whether to target the whole protein or just a piece is a challenge.</li>\n<li>prior experience with MeRS and SARS suggests the need for caution. This is because some types of immune response may actually worsen lung disease. This begets the need for animal models testing and safety monitoring — neither of which appeared to be part of the 1957 influenza vaccine development process.\n\n<ul>\n<li>“as with naturally acquired infection, the potential duration of immunity is unknown; similarly, whether single-dose vaccines will confer immunity is uncertain.” </li>\n</ul></li>\n</ul>\n\n<p>That said, extraordinary steps are being taken to accelerate coronavirus vaccine development. A <a href=\"https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/0/nejm.ahead-of-print/nejmp2005630/20200406/images/img_medium/nejmp2005630_f1.jpeg\" rel=\"nofollow noreferrer\">chart</a> from the NEJM article illustrates the “parallel track” acceleration, beginning manufacturing well before the vaccine is proven out in clinical trials.</p>\n\n<p></p>\n"
}
] | 2020/04/12 | [
"https://health.stackexchange.com/questions/23187",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/1268/"
] |
23,192 | <p>The Novel Coronavirus antibody test has been around since February 2020 when it was invented at a <a href="http://www.xinhuanet.com/english/2020-02/17/c_138791386.htm" rel="nofollow noreferrer">Chinese University</a>. It can measure both IgM to show infection in progress and IgG to indicate full immunity. It is disparaged because it is only <a href="https://www.azcentral.com/story/news/local/arizona-health/2020/04/11/arcpoint-labs-offers-public-coronavirus-test-antibody-detection/2943254001/" rel="nofollow noreferrer">94.4% accurate</a>.</p>
<p>The <em>Detroit News</em> however reports the "gold standard" PCR test is only <a href="https://www.detroitnews.com/story/news/nation/2020/04/12/coronavirus-tests-false-negatives-doctors-doubts/111540614/" rel="nofollow noreferrer">90% effective</a>. People walked around town with false negatives when they were really positive. So why only use PCR tests and never IgM / IgG tests?</p>
<p>I would feel more comfortable with both tests. First the daily 15 minute finger prick blood testto see if IgM develops followed by hospital / lab PCR test. Then after positive PCR self isolate. Then after negative PCR test continue to self isolate until daily 15 minute finger prick blood test shows IgG. I think it's too early in the war to disparage either test but would point out the 15 minute finger prick blood test is cheap and doesn't drain limited healthcare resources.</p>
<p>It would be interesting to run the same blood sample on all the IgM / IgG test devices and compare results. It would also be interesting to send swabs from same suspect to multiple PCR test labs see how they stack up. Ones that don't agree with the majority either have a better test or failed and could be subject to government oversight.</p>
<p>IgM results will show up (I think I read) whilst suspect is asymptomatic. If we want to win this war in three months instead of three years like the Spanish Flu, we need to pull out all the stops. But the question remains, <strong><em>why are IgM / IgG tests (antibody tests) frowned upon</em></strong>?</p>
| [
{
"answer_id": 23194,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>The antibody tests, at least in the USA, have only just received fast track approval so at least in the USA were not available in an FDA approved form until recently. The <a href=\"https://medicalsciences.stackexchange.com/questions/22998/are-false-positives-from-cellex-s-coronavirus-antibody-test-systemic\">Cellex</a> test has a sensitity of 93.8% and specificity of 95.6% when tested in China but may be better in the USA. So, the antibody tests are to demonstrate exposure, either in the past or current. The test itself only takes some minutes.</p>\n<p>A rt-PCR test checks for the presence of virus from a swab, preferentially in the nasopharynx but also anterior nasal, and oropharynx where the rates of detection are likely to be lower. This demonstrates current infection. A positive antibody test may be followed by a rt-PCR test to see if the positive antibody test actually indicates current infection.</p>\n<p>However, there has been a world wide shortage of testing equipment so inadequate testing has been performed. The <a href=\"https://www.molecular.abbott/int/en/products/instrumentation/m2000-realtime-system\" rel=\"nofollow noreferrer\">Abbott M2000</a> system is supposed to be able to perform millions of tests but the test kits that go with them are in short supply</p>\n<blockquote>\n<p>Abbott’s machines, a model called the m2000, should have been capable of running about a million Covid-19 tests in the last three weeks, Deborah Birx, a member of the White House’s coronavirus task force, said at a briefing in Washington Wednesday night. But they have run less than 10% of that amount.</p>\n<p>“It’s a very high throughput machine, we have a million tests out there,” Birx said. “They’re not running. We’ve only run 88,000 tests in three weeks off of those machines, with a million test kits.”</p>\n<p>U.S. attempts to contain the coronavirus have been stymied by repeated problems and failures with diagnostic tests, which are necessary to identify patients and isolate them, or to help protect health workers treating them. Heath workers and officials around the U.S. have cited long delays in getting results and limited availability of tests from multiple different sources.</p>\n</blockquote>\n<p>In an ideal world the tests would be run as per their clinical indication. The reality is different due to supply constraints.</p>\n<p><a href=\"https://www.bloomberg.com/news/articles/2020-04-09/abbott-tests-to-detect-covid-19-are-falling-short-birx\" rel=\"nofollow noreferrer\">https://www.bloomberg.com/news/articles/2020-04-09/abbott-tests-to-detect-covid-19-are-falling-short-birx</a></p>\n"
},
{
"answer_id": 23273,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>The source you linked to says</p>\n<blockquote>\n<p>In a clinical evaluation, Zhejiang Orient Gene Biotech reported the tests to be 61.8% to 94.4% sensitive, depending on the type of antibody that shows up in the test results. [...] For IgM antibodies, Zhejiang Orient Gene Biotech reported an overall sensitivity of 61.8%, meaning that it may only accurately report a positive prior case of COVID-19 61.8% of the time. For IgG antibodies, Zhejiang Orient Gene Biotech reported an overall sensitivity of 94.4%, meaning that these tests should accurately report a positive case of COVID-19 most of the time.</p>\n</blockquote>\n<p>If it were 94.4% (all the time) as you claimed in your post, it would be a different matter.</p>\n<p>Furthermore, per <a href=\"https://www.rawstory.com/2020/04/the-fda-lets-pretty-much-anyone-sell-a-covid-19-antibody-test-and-a-lot-of-them-are-shoddy-cnn/\" rel=\"nofollow noreferrer\">recent news</a>, the antibodies tests are "disparaged" in the US because the FDA let anyone make them and didn't request data from the manufacturers as a prerequisite for approving them:</p>\n<blockquote>\n<p>On CNN Tuesday, senior medical correspondent Elizabeth Cohen warned that many of the antibody tests on the market for COVID-19 — the tests that show whether you are immune to the virus — are barely tested under the Food and Drug Administration’s new standards, and possibly ineffective. [...]</p>\n<p>“The problem is, the FDA lowered the standards last month, and basically pretty much anyone can sell an antibody test,” continued Cohen. “<strong>They don’t even have to show that it works. All they have to do is say, hey, FDA, I want to sell this test and I validated it here in my city where I am. That’s all they have to do. They don’t have to show their data.</strong>”</p>\n</blockquote>\n<p>And after the backlash, there's some sort of review <a href=\"https://edition.cnn.com/2020/04/14/health/fda-reverses-antibody-tests/index.html\" rel=\"nofollow noreferrer\">announced</a>:</p>\n<blockquote>\n<p>[Scott Becker, CEO of the Association of Public Health Laboratories] said FDA Commissioner Stephen Hahn told him and members of his association that the National Cancer Institute (NCI) would start reviewing tests that are on the market to see if they obtain correct results. [...]</p>\n<p>The FDA did not respond to questions for this story, referring CNN to the NCI.</p>\n</blockquote>\n<p>A lot of the media has incorrectly headlined these news as the FDA tightening the (approval) standards, but that doesn't seem to be actually happening yet.</p>\n<p>The WHO has now gone to <a href=\"https://www.cnbc.com/2020/04/17/who-issues-warning-on-coronavirus-testing-theres-no-evidence-antibody-tests-show-immunity.html\" rel=\"nofollow noreferrer\">some length</a> to explain their skepticism of the (rushed) antibodies tests.</p>\n<blockquote>\n<p>“These antibody tests will be able to measure that level of serology presence, that level of antibodies, but that does not mean that somebody with antibodies” is immune, said Dr. Maria Van Kerkhove, head of WHO’s emerging diseases and zoonosis unit. [...]</p>\n<p>Dr. Mike Ryan, executive director of WHO’s emergencies program, said scientists are also still determining the length of protection antibodies might give a person who has been infected with the coronavirus.</p>\n<p>“Plus some of the tests have issues with sensitivity,” he added. “They may give a false negative result.”</p>\n<p>Earlier this week, WHO officials <a href=\"https://www.cnbc.com/2020/04/13/who-officials-say-its-unclear-whether-recovered-coronavirus-patients-are-immune-to-second-infection.html\" rel=\"nofollow noreferrer\">said</a> not all people who recover from the coronavirus have the antibodies to fight a second infection, raising concern that patients may not develop immunity after surviving Covid-19.</p>\n</blockquote>\n<p>And from that earlier coverage:</p>\n<blockquote>\n<p>A preliminary study of patients in Shanghai found that some patients had “no detectable antibody response” while others had a very high response, said Dr. Maria Van Kerkhove, WHO’s lead scientist on Covid-19. Whether the patients who had a strong antibody response were immune to a second infection is “a separate question,” she added. [...]</p>\n<p>Ryan said there are questions about whether the virus can reactivate after a patient recovers and tests negative for Covid-19.</p>\n</blockquote>\n<p>So it's not the case that all such tests are flawed but that governments seem to pin a lot of hopes on them in terms of reopening their countries etc., which may or may not turn out justified given the present level of knowledge.</p>\n"
},
{
"answer_id": 23469,
"author": "cbeleites unhappy with SX",
"author_id": 11479,
"author_profile": "https://health.stackexchange.com/users/11479",
"pm_score": 3,
"selected": true,
"text": "<p>Summary: they are not yet sufficiently well validated (and many are not working sufficiently well) to be used for mass testing.</p>\n\n<p>For mass tests, </p>\n\n<ul>\n<li>of the kind you describe, we need high sensitivity very early into the disease</li>\n<li>of any kind, we need false positive rate (1 - specificity) to be well below the prevalence of SARS-CoV-2 positive people, otherwise we'll mostly find false positives the positive predcitive value (i.e. probability that you are really positive given that the test said so) would be too low to be of practical use: we'd want this to eventually conclude who is immune.</li>\n</ul>\n\n<p>See also: <a href=\"https://medicalsciences.stackexchange.com/q/21318/11479\">Why are people with COVID-19 symptoms being denied tests in the US?</a></p>\n\n<hr>\n\n<blockquote>\n <p>It would be interesting to run the same blood sample on all the IgM / IgG test devices and compare results</p>\n</blockquote>\n\n<p>This is what \n<a href=\"https://covidtestingproject.org/\" rel=\"nofollow noreferrer\">https://covidtestingproject.org/</a> does, comparing 10 commercially available rapid antibody tests for SARS-CoV-2 and 2 ELISA tests: an in-house one of the group and a commercial one.</p>\n\n<p><a href=\"https://www.dropbox.com/s/cd1628cau09288a/SARS-CoV-2_Serology_Manuscript.pdf\" rel=\"nofollow noreferrer\">Manuscript (pre peer-review)</a></p>\n\n<blockquote>\n <p>I would feel more comfortable with both tests. First the daily 15 minute finger prick blood testto see if IgM develops followed by hospital / lab PCR test. Then after positive PCR self isolate. Then after negative PCR test continue to self isolate until daily 15 minute finger prick blood test shows IgG. </p>\n</blockquote>\n\n<p>Unfortunately, the covid testing project data shows IGM (like IGG) not being very sensitive at the onset of symptoms: IGM sensitivity reaches 60 - 85 % (point estimates for the various tests) around day 11 - 15 after onset of symptoms for all but one test that never gets above 38 % sensitivity. </p>\n\n<p><strong>So the antibody tests including IGM kick in basically only after PCR testing for current infection is done: PCR for virus RNA and antibody testing are thus for different time windows.</strong></p>\n\n<p>The scenario that you could do a rapid test to check whether you can safely visit the grandparents or other vulnerable persons is thus not going to work with these rapid tests.</p>\n\n<p>A glance at the individual test results suggests:</p>\n\n<ul>\n<li><p>that (as one may expect) there is a trade-off between sensitivity and specificity, at least to some extent.<br>\nThis may not be a big problem, since we could choose more sensitive or more specific antibody tests according to the purpose of testing. (E.g. for a Corona-Antibody Passport, a highly specific test would be appropriate. For epidemiologic studies one may choose a different trade-off, but <a href=\"https://statmodeling.stat.columbia.edu/2020/04/19/fatal-flaws-in-stanford-study-of-coronavirus-prevalence/\" rel=\"nofollow noreferrer\">one would still need a sensible relationship between expected prevalence and specificity</a>.) </p></li>\n<li><p>high correlation between the misclassified cases, i.e. the false negative and false positive samples tend to be the same across the tests.<br>\nThis has the important consequence that the possibility to improve overall accuracy by combining tests from different manufacturers is limited.</p></li>\n</ul>\n\n<p>One important concern with the antibody tests is whether they show cross-sensitivity to the corona viruses that circulate since years and cause only normal harmless colds (I did not find studies on antibody prevalence for those). Unfortunately, the data so far includes only 4 such samples (of which some show low non-zero scores for some of the tests). Even for a test that correctly recognizes all four of them as negative for SARS-CoV-2 antibodies, the 95 % credible interval for specificity in this subgroup is only \"better than 55 %\". In other words, we cannot really rely [yet] on the tests in this particular respect.<br>\nAlso, since local prevalence of such corona virus strains may vary, it is not clear whether a test specificity can be directly used for populations on other continents.</p>\n"
},
{
"answer_id": 23623,
"author": "Marcus D",
"author_id": 19626,
"author_profile": "https://health.stackexchange.com/users/19626",
"pm_score": 1,
"selected": false,
"text": "<p>There is a group of research organisations that call themselves the <a href=\"https://covidtestingproject.org/\" rel=\"nofollow noreferrer\">Covid-19 testing project</a>, that has (and are) producing comparisons of various antibody tests.</p>\n\n<p>It sounds like because the FDA relaxed their rules on <a href=\"https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-serological-test-validation-and-education-efforts\" rel=\"nofollow noreferrer\">marketing Covid-19 tests</a> without the normal rigour that would insist in mid April 2020, but have since <a href=\"https://www.fda.gov/news-events/fda-voices/insight-fdas-revised-policy-antibody-tests-prioritizing-access-and-accuracy\" rel=\"nofollow noreferrer\">back tracked</a> on this slightly in early May, allowing 10 days to produce the evidence of clinical correctness, before the FDA pulling the test off the market.</p>\n\n<p>Looking at data in the covid testing project (link above) it shows the date of onset of symptoms will (obviously) give different levels of antibody detection. It is really only until >20 days that this seems to settle down. But even then with the 12 tests that were compared, there were a surprising variation in the false negatives between tests. False positives were not looked at in this analysis.</p>\n\n<p>So to answer the question more directly, it seems that because may tests have come out that have had poor clinical testing, this has caused a general negative impression of antibody tests for Covid-19.</p>\n"
}
] | 2020/04/12 | [
"https://health.stackexchange.com/questions/23192",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17751/"
] |
23,200 | <p>Given that as of this point of time no specific treatment exists for COVID-19 patients, why are governments primarily spending their testing capacity on those admitted to hospitals or otherwise in critical condition? In theory, anyone showcasing any of the COVID-19 symptoms could be presumed to actually have the disease, but doctors and policy makers seem to think otherwise. </p>
<p>I do understand why testing would be beneficial for asymptomatic/lightly symptomatic patients - knowing they're infected will help them socially isolate for others. But once a patient is in a hospital with breathing difficulties... what good does a test do?</p>
| [
{
"answer_id": 23201,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>The care for a COVID-19 patient is totally different from that of a patient with other forms of pneumonia. A COVID-19 patient is highly contagious, and is able to aerosolize large amounts of potentially lethal virions into the environment infecting other hospital patients and staff. This happens particularly in intubation. These patients need to be treated in rooms quarantined from other patients, or, shared only with other COVID-19 patients.</p>\n\n<p>The care of a COVID-19 patient also involves the use of PPE. There is a huge shortage of PPE in a large numbers of countries especially in epicentres where people have been resorting to wearing trash bags to help protect them from infection. PPE has traditionally been disposable between patients but the shortage of PPE has meant that it has been reserved just for use when working with patients with known COVID-19, and been reused.</p>\n\n<p>These are three nurses from Northwick Park, London, a centre of clinical excellence.</p>\n\n<p><img src=\"https://video-images.vice.com/test-uploads/articles/5e8f02279a053c009d7a87b5/lede/1586434223278-ETpjugsXgAUl_og.jpeg\" alt=\"\"></p>\n\n<p>wearing trash bags as protection, and using surgical masks instead of N95 masks. All three nurses subsequently contracted COVID-19.</p>\n\n<p>Early in the disease in some countries medical staff had to be stood down for self isolation when they had unprotected contact with COVID-19 patients. And estimates range from 20-80% of COVID-19 patients are asymptomatic which means testing needs to be done.</p>\n\n<p><a href=\"https://www.vice.com/en_us/article/dygbdz/these-nurses-had-to-wear-trash-bags-as-ppe-now-they-have-coronavirus\" rel=\"nofollow noreferrer\">https://www.vice.com/en_us/article/dygbdz/these-nurses-had-to-wear-trash-bags-as-ppe-now-they-have-coronavirus</a></p>\n"
},
{
"answer_id": 23212,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": true,
"text": "<p>This q is based on fairly incorrect premises e.g.</p>\n<blockquote>\n<p>why are governments primarily spending their testing capacity on those admitted to hospitals or otherwise in critical condition?</p>\n<p>[...]</p>\n<p>once a patient is in a hospital with breathing difficulties... what good does a test do?</p>\n</blockquote>\n<p>There seems to be a conflation here that "admitted to hospitals" is (nearly) always "in critical condition" and likewise that "with breathing difficulties" somehow also equates "in critical condition" <em>and</em> a Covid-19 diagnosis.</p>\n<p>Besides HCW safety, addressed in Dr. Chiu's answer, there's an obvious reason to test someone with "breathing difficulties" (for Covid-19) to establish a differential diagnosis. I think first a diagnosis of what the breathing difficulties actually are is done, e.g. is it pneumonia? Second, the guidelines for further diagnosing the serious cases of pneumonia generally recommend establishing the actual pathogen, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473649/\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<blockquote>\n<p>Optimal treatment of lung infections relies on rapid and accurate detection of the offending pathogen. Delay in diagnosis can lead to increased morbidity and mortality.</p>\n</blockquote>\n<p>See also <a href=\"https://medicalsciences.stackexchange.com/questions/22913/use-of-antibiotics-with-chest-infections\">Use of antibiotics with chest infections</a> for a bit more detailed discussion on this.</p>\n<p>Additionally, early in the epidemic, <a href=\"https://journals.sagepub.com/doi/pdf/10.1177/0846537120913033\" rel=\"nofollow noreferrer\">evidence from China (Mar 4)</a> was that [their] virus tests were actually rather insensitive, i.e. they could only detect high viral loads:</p>\n<blockquote>\n<p>In the initial screening, computed tomography (CT) examination is needed for the auxiliary diagnosis. The diagnosis is\nthen confirmed by the positive results of the nucleic acid amplification test (NAAT) of the respiratory tract or blood specimens\nusing reverse transcription real-time fluorescence polymerase\nchain reaction (RT-PCR). However, this diagnosis method is\nhighly limited: (1) <strong>When the viral load is low, the detection rate\nis low, leading to false-negative results.</strong> (2) Only a positive\ndiagnosis can be made, but the severity of COVID-19 and its\nprogression cannot be judged (in contrast, CT imaging can\nreveal disease progression). (3) The supply of the reagents\ncannot keep up with the demand, and the quality of new products of major companies awaits to be studied and improved. (4)\nIt takes 1 day or longer to obtain the results after sampling. For\nthese reasons, <strong>Chinese researchers strongly recommend CT\nimaging as the main basis for the diagnosis of COVID-19 in\nthe current situation</strong>.</p>\n</blockquote>\n<p>So in such circumstances (low-sensitivity tests) the virus tests probably aren't even very useful for the mild cases, so "saving" [such insensitive] tests for these mild case is basically completely pointless.</p>\n<p>(See also related q here on that latter issue: <a href=\"https://medicalsciences.stackexchange.com/questions/23126/why-were-so-many-covid-19-negative-tests-among-close-contacts-of-the-early-chine\">Why were so many Covid-19 negative tests among close contacts of the early Chinese cases?</a> )</p>\n"
}
] | 2020/04/13 | [
"https://health.stackexchange.com/questions/23200",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,206 | <p>Several countries around the world have instituted extremely harsh lockdowns: France, Spain, Italy, New Zealand, Argentina. However for some reason all of those countries keep getting new infections 2+ weeks after the lockdowns have started, which suggests gaps in their enforcement or coverage. Has there been any research done in these countries to try and understand where these cases are coming from? Some ideas:</p>
<ol>
<li>It's all from essential workers and their families</li>
<li>It's from neighbors hanging out with each other - either voluntarily or involuntarily (elevators, stairs, common areas)</li>
<li>It's from supermarkets, hospitals and pharmacies</li>
<li>It's from people who are outside the "system", such as the homeless</li>
</ol>
<p>Seems like contact tracing/interviews should give a straightforward enough answer, so did any government try to investigate?</p>
| [
{
"answer_id": 23207,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>Very partial answer, from the South Korean <a href=\"https://www.ijidonline.com/article/S1201-9712(20)30150-8/fulltext\" rel=\"nofollow noreferrer\">experience</a>:</p>\n<blockquote>\n<p>The rapid spread of COVID-19 in South Korea has been attributed to one case linked to a superspreading event that has led to more than 3900 secondary cases stemming from church services in the city of Daegu (Kuhn, 2020; Ryall, 2020). This has led to sustained transmission chains of COVID-19, with 55% of the cases associated with the church cluster in Daegu (Bostock, 2020).</p>\n<p>Moreover, three other clusters have been reported, including one set in Chundo Daenam hospital in Chungdo-gun, Gyeongsanggbuk-do (118 cases), one set in the gym in Cheonan, Chungcheongnam-do (92 cases), and one Pilgrimage to Israel cluster in Gyeongsanggbuk-do (49 cases). These few clusters have become the primary driving force of the infection.</p>\n</blockquote>\n<p>The paper has more details on each cluster.</p>\n<p>Similar patterns of large gatherings followed by spreading in families have been reported elsewhere, <a href=\"https://www.theguardian.com/world/2020/apr/09/the-cluster-effect-how-social-gatherings-were-rocket-fuel-for-coronavirus\" rel=\"nofollow noreferrer\">e.g.</a> France and Italy. But most such studies published insofar focus on the early days of the pandemic, before the lockdowns were imposed.</p>\n<p>Alas, for a more topical answer, it depends what one means by "hardcore" lockdowns. There is one such <a href=\"https://www.theguardian.com/world/2020/mar/31/virologists-to-turn-germany-worst-hit-district-into-coronavirus-laboratory\" rel=\"nofollow noreferrer\">study</a> being conducted in the German hotspot in Heinsberg. Insofar there have been only press interviews with the investigators, <a href=\"https://www.businessinsider.com/death-rate-german-laboratory-city-5x-less-than-national-average-2020-4\" rel=\"nofollow noreferrer\">like</a></p>\n<blockquote>\n<p>Instead, claims Streeck, his study found that: "There is no significant risk of catching the disease when you go shopping. Severe outbreaks of the infection were always a result of people being closer together over a longer period of time."</p>\n</blockquote>\n<p>And as a reminder for what "hardcore" lockdowns actually <a href=\"https://mainichi.jp/english/articles/20200408/p2g/00m/0in/071000c\" rel=\"nofollow noreferrer\">means</a>:</p>\n<blockquote>\n<p>During the height of the lockdown, Wuhan residents were completely barred from stepping outside of their home, not even allowed to go grocery shopping and they were consequently completely reliant on designated neighborhood committees who delivered daily necessities to them.</p>\n</blockquote>\n<p>Basically more or less home arrest for almost everyone.</p>\n"
},
{
"answer_id": 23217,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 1,
"selected": false,
"text": "<p>New Zealand is undertaking rigorous contact tracing and so far only 2% of cases have been deemed community transmission meaning no known contact.</p>\n\n<p>Cases have been increasing because they include disease developing in those returning to the country during the lockdown period and placed into self isolation. As the numbers of people returning to New Zealand fall so do these new imported cases.</p>\n\n<p>These new cases are still within the numbers predicted by modelling.</p>\n\n<p><img src=\"https://www.health.govt.nz/sites/default/files/images/our-work/diseases-conditions/covid19/covid-epidemiccurve-newcases-13april.png\" alt=\"\"></p>\n\n<p>NZ moved to level 4 lockdown 25 March which means stay at home unless essential service.</p>\n\n<p>The other source are 4-5 larger clusters where one person has spread the disease to a number of others, and then these others have brought the disease back home. This also includes rest homes for the elderly and dementia units where either a visitor or staff before the lockdown had infected a resident, and the disease is still slowly spreading through these communities. At present we have a total of 16 clusters of 10 or more people infected.</p>\n\n<p>We are still testing below capacity but increasing testing has failed to find more cases in the community that were not related to a known cluster.</p>\n\n<p><a href=\"https://www.health.govt.nz/our-work/diseases-and-conditions/covid-19-novel-coronavirus/covid-19-current-situation/covid-19-current-cases\" rel=\"nofollow noreferrer\">https://www.health.govt.nz/our-work/diseases-and-conditions/covid-19-novel-coronavirus/covid-19-current-situation/covid-19-current-cases</a></p>\n"
}
] | 2020/04/13 | [
"https://health.stackexchange.com/questions/23206",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,210 | <p>Many hospitals have cancelled or postponed elective procedures due to the current COVID-19 pandemic. What kinds of considerations are ethics committees making when deciding to reopen elective procedures or keep it closed?</p>
<p>example of banned elective procedures:</p>
<p><a href="https://www.news9.com/story/41997738/ou-med-postpones-elective-surgeries-preparing-for-covid19-patient-surge" rel="nofollow noreferrer">https://www.news9.com/story/41997738/ou-med-postpones-elective-surgeries-preparing-for-covid19-patient-surge</a></p>
| [
{
"answer_id": 23211,
"author": "Thomas",
"author_id": 19070,
"author_profile": "https://health.stackexchange.com/users/19070",
"pm_score": 1,
"selected": false,
"text": "<p>There is most probably no hard rule that will fit (almost) every hospital, because it depends on a variety of factors. Central hospitals with a lot types of surgery will have a bigger pressure to work on elective surgery. Also, the categories elective versus non-elective can be misleading: On a very strict level elective surgery would include every type of surgery not immediately designed to save a life, while on a more relaxed level it could include only those operations where patients are able to stay at home versus where they would have to stay in hospital waiting on surgery (see also Wikipedia: <a href=\"https://en.wikipedia.org/wiki/Elective_surgery\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Elective_surgery</a>, where there is also a term called 'semi-elective surgery').</p>\n\n<p>With regards to the 'pressure' mentioned above, this could come from a variety of sources as well, such as the community, politics or financial reasons (some surgeries yield a lot more money than others). Of course, health of patients may be a factor: What at the moment may be a purely elective surgery down the road may become an emergency, that not only will have to be operated on, but also diminishes chances of a positive outcome somewhat. </p>\n\n<p>Coming back to a (kind of) ruling when to re-open elective surgeries, most of these will have to be decided on a case-by-case basis, however, for some categories of surgery there is a practically non-existent danger of becoming emergencies, even if quite some time passes, e. g.: arthroscopy. On the other hand any currently elective heart surgery may have the patient deteriorate over time.</p>\n\n<p>For some types of surgery intensive care monitoring is required, which in times of COVID-19 may be of severely limited availability as well.</p>\n\n<p>In closing I believe the re-opening of elective surgery will be gradual and consider more eminently endangered categories of currently elective surgery first.</p>\n"
},
{
"answer_id": 23244,
"author": "Zac",
"author_id": 19234,
"author_profile": "https://health.stackexchange.com/users/19234",
"pm_score": 3,
"selected": true,
"text": "<p>A lot of hospitals are not currently performing elective surgeries because:</p>\n\n<ol>\n<li>Operating rooms and PACUs (post-anesthesia care units) have been converted to take care of patients with COVID</li>\n<li>Staffing shortages due to reassignments to COVID-related units</li>\n<li>Shortages of PPE (e.g. gowns) that are needed to perform surgery</li>\n<li>Unnecessary risk of coronavirus transmission to staff and patients performing/receiving these procedures and surgeries</li>\n</ol>\n\n<p>You can review these considerations in <a href=\"https://www.facs.org/covid-19/clinical-guidance/patient-guide\" rel=\"nofollow noreferrer\">recent guidance by the American College of Surgeons</a> in the section titled \"Why are surgeries being postponed?\".</p>\n\n<p>Hospitals make a <a href=\"https://www.healthleadersmedia.com/clinical-care/ahrq-surgical-admissions-bring-48-hospital-revenue\" rel=\"nofollow noreferrer\">substantial amount of their revenue</a> from procedures and surgeries, and they have a financial incentive to perform them. They will decide to perform them based on the availability of 1-3 (space, staff, equipment) and their own balancing of the risk of virus transmission (some may prioritize revenue, others may prioritize safety).</p>\n"
}
] | 2020/04/13 | [
"https://health.stackexchange.com/questions/23210",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/13163/"
] |
23,221 | <p>Prominent politicians in the USA have been calling for the use of both Chloroquine and Hydroxychloroquine in the management of Covid-19.</p>
<blockquote>
<p>Day after day, the salesman turned president has encouraged coronavirus patients to try hydroxychloroquine with all of the enthusiasm of a real estate developer. The passing reference he makes to the possible dangers is usually overwhelmed by the full-throated endorsement. “What do you have to lose?” he asked five times on Sunday.</p>
</blockquote>
<p>The USA trade advisor Dr Peter Navarro also claims special expertise</p>
<blockquote>
<p>Navarro told CNN that studies including one published in the last few days involving Wuhan, China prove hydroxychloroquine can help coronavirus patients recover. Navarro said the Wuhan study was one of the first randomized in a control group.</p>
<p>The trade adviser also claimed his PhD in economics qualified him to have such debates with health experts like Fauci.</p>
<p>“Doctors disagree about things all the time,” he said. “My qualifications in terms of looking at the science is that I’m a social scientist. I have a PhD, and I understand how to read statistical studies.”</p>
</blockquote>
<p>Although generally safe when used in the treatment of malaria and rheumatoid arthritis, sle, these conditions are dramatically different from the scenario of sick hypoxic covid-19 patients who may also be suffering from myocardial injury from the virus.</p>
<p>What are the early trials telling us?</p>
<p><a href="https://www.nytimes.com/2020/04/06/us/politics/coronavirus-trump-malaria-drug.html" rel="nofollow noreferrer">https://www.nytimes.com/2020/04/06/us/politics/coronavirus-trump-malaria-drug.html</a></p>
<p><a href="https://www.theguardian.com/us-news/2020/apr/06/peter-navarro-fauci-hydroxychloroquine" rel="nofollow noreferrer">https://www.theguardian.com/us-news/2020/apr/06/peter-navarro-fauci-hydroxychloroquine</a></p>
| [
{
"answer_id": 23229,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>And June news: that large study <a href=\"https://www.bbc.com/news/health-52929916\" rel=\"nofollow noreferrer\">was withdrawn</a>. And there are some <a href=\"https://www.theguardian.com/world/2020/jun/03/covid-19-surgisphere-who-world-health-organization-hydroxychloroquine\" rel=\"nofollow noreferrer\">real questions</a> if their data was real! </p>\n\n<p>May <a href=\"https://finance.yahoo.com/news/hydroxychloroquine-shows-no-coronavirus-benefit-raises-death-risk-144240073.html\" rel=\"nofollow noreferrer\">23 news (AFP)</a> of a large study found no benefits and an increased risk of dying from treatment of Covid-19 with hydroxychloroquine and chloroquine:</p>\n\n<blockquote>\n <p>A study of nearly 100,000 coronavirus patients has shown no benefit in treating them with anti-viral drugs hydroxychloroquine and chloroquine and even increased the likelihood of them dying in hospital.</p>\n \n <p>Chloroquine is an anti-malarial. Both drugs can produce potentially serious side effects, particularly heart arrhythmia. </p>\n \n <p>And neither drug benefitted patients hospitalised with COVID-19, according to a study published on Friday in The Lancet. </p>\n \n <p>Looking at the records of 96,000 patients across hundreds of hospitals, they found that administering the drugs actually increased the risk of dying.</p>\n \n <p>They compared outcomes from four groups: those treated with hydroxychloroquine alone, with chloroquine alone, and then two groups given the respective drugs in combination with antibiotics. </p>\n \n <p>There was also a control group of patients not given these treatments. </p>\n \n <p>At the end of the study period around nine per cent of those in the control group had died. </p>\n \n <p>Of those treated with hydroxychloroquine or chloroquine alone, 18 per cent and 16.4 per cent respectively had died. </p>\n \n <p>And those given each drug in combination with antibiotics were even more likely to die: 22.8 per cent with chloroquine and 23.8 per cent with hydroxychloroquine. </p>\n \n <p>The authors estimated that the drugs put patients at up to 45 per cent higher risk of dying from COVID-19 compared with underlying health issues. </p>\n</blockquote>\n\n<p>Some additional expert commentary on this study on <a href=\"https://www.statnews.com/2020/05/22/what-a-big-new-study-on-malaria-drugs-as-covid-19-treatments-tells-us-and-what-it-doesnt/\" rel=\"nofollow noreferrer\">Stat news</a>.</p>\n\n<blockquote>\n <p>The study is the largest observational study so far on the use of chloroquine and hydroxychloroquine to treat Covid-19; it combined data from 15,000 Covid-19 patients at 671 hospitals on six continents who were treated with the drugs. Those patients were compared to 81,000 patients who had Covid-19 but did not receive the drugs.</p>\n \n <p>Other observational studies have made comparisons in smaller populations. A study of 368 U.S. veterans also showed that the drugs might be potentially harmful. But two different studies each including 1,400 patients treated in New York during the Covid-19 pandemic showed no impact on mortality at all. [...]</p>\n \n <p>Adding more patients helps. But the problem is that, while researchers can control for risk factors that they know about, they can’t rule out that patients getting chloroquine and hydroxychloroquine are dying for reasons they don’t understand that have nothing to do with the drugs.</p>\n \n <p>Still, the results don’t bode well for the malaria drugs as Covid-19 treatments. After controlling for risks such as weight, heart disease, and lung disease, the mortality rate in the control group was 9%. For those who received hydroxychloroquine, it was 18%; when an antibiotic was added, it was more than 20%. That’s not what would be expected if the drugs were highly effective treatments.</p>\n</blockquote>\n\n<p>(And thankfully, this latter piece of news has a <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31180-6/fulltext\" rel=\"nofollow noreferrer\">link to the actual study</a>.)</p>\n\n<hr>\n\n<p>Old (April) answer below</p>\n\n<p>This is a pretty partial answer since several studies (including <a href=\"https://www.nih.gov/news-events/news-releases/nih-clinical-trial-hydroxychloroquine-potential-therapy-covid-19-begins\" rel=\"nofollow noreferrer\">a NIH one</a>) are ongoing on CQ and HCQ (I'm assuming you'll accept answers about the latter too, as related enough).</p>\n\n<p>The NYT and various medical blogs have reported <a href=\"https://www.medrxiv.org/content/10.1101/2020.04.07.20056424v1.full.pdf\" rel=\"nofollow noreferrer\">on a draft paper</a> of Brazilian researchers highlighting that they stopped one (high-dose) arm of their trial. Quoting from the conclusions:</p>\n\n<blockquote>\n <p>CQ, despite being a safe drug used for more than 70 years for malaria,\n might be toxic in the dosages recommended by Chinese authorities (high dosage 10g, for 10\n days). Our study raises enough red flags to stop the use of such dosage (12g of CQ in total [...]</p>\n</blockquote>\n\n<p>As for safety details:</p>\n\n<blockquote>\n <p>One patient developed severe rhabdomyolysis, and causality could be attributed to the virus\n or to CQ, which is already known to cause myolysis. Regarding cardiotoxicity and\n QTc over time, the variation in the QTc as compared to the baseline ECG increased more on\n days 2 and 3 in the high dose CQ arm, with both arms (low and high CQ) showing more\n similar QTc variations in the last three days of follow-up. Two patients in the high\n dose CQ arm evolved with ventricular tachycardia before death. This severe type of arrythmia is usually facilitated when QTc is prolonged.</p>\n</blockquote>\n\n<p>And they did a Kaplan-Meier analysis too:</p>\n\n<blockquote>\n <p><a href=\"https://i.stack.imgur.com/pz1wz.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/pz1wz.png\" alt=\"enter image description here\"></a></p>\n \n <p>Time (in days) from randomization to death, in patients treated with each\n chloroquine dosage. The gray band represents the upper and lower limits of the confidence\n interval for lethality in hospitalized patients not receiving CQ obtained by the meta-analysis\n of the studies by Zhou et al. (Lancet, 2020) and Chen et al. (BMJ, 2020) (167/990 = 16.9%;\n 95% CI 14.5-19.2). </p>\n</blockquote>\n\n<p>In term of efficacy (which I won't detail here) they've concluded that (up to day 6):</p>\n\n<blockquote>\n <p>Major presented outcomes were not different between the arms.</p>\n</blockquote>\n\n<p>It might also be useful to quote a bit more from their related-research section:</p>\n\n<blockquote>\n <p>Before the CloroCovid-19 trial began, to our knowledge, there were no published reports of\n robust clinical studies on the safety and/or efficacy of chloroquine (CQ) and/or\n hydroxychloroquine (HCQ) for the treatment of COVID-19 during the recent 2020 pandemic.\n [...] We found three non-randomized studies with limited sample\n sizes in which (1) HCQ use led to a decrease in SARS-Cov-2 detected in respiratory\n secretions five days after treatment, together with azithromycin (France, 36 patients); (2)\n HCQ use shortened time to clinical recovery (China, 62 patients); and (3) CQ was superior to\n control treatment in inhibiting the exacerbation of pneumonia, improving lung imaging\n findings, and promoting virus-negative conversion and shortening the disease course (China,\n 100 patients). We found no published studies comparing different dosages of CQ/HCQ and\n their thorough safety assessment. </p>\n</blockquote>\n\n<p>There's also a <a href=\"https://www.cmaj.ca/content/cmaj/early/2020/04/08/cmaj.200528.full.pdf\" rel=\"nofollow noreferrer\">CMAJ review</a> posted a few days before that Brazilian paper came out. It mentions the same studies from China and France, as far as I can tell, and discusses the safety concerns from the general knowledge/perspective of CQ use in malaria etc.</p>\n\n<p>Of the Chinese studies, the <a href=\"https://www.medrxiv.org/content/10.1101/2020.03.22.20040758v3.full.pdf\" rel=\"nofollow noreferrer\">Wuhan one</a> reported as adverse events (on 31 HCQ-treated patients) only</p>\n\n<blockquote>\n <p>2 patients with mild adverse reactions in the HCQ treatment group [...] one patient developed a rash, and one patient experienced a headache</p>\n</blockquote>\n\n<p>but this was with</p>\n\n<blockquote>\n <p>5-day HCQ (400 mg/d) treatment</p>\n</blockquote>\n\n<p>There's a much shorter <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/32074550\" rel=\"nofollow noreferrer\">\"Breakthrough\"</a> (yeah, that's a word from its title) paper on the Chinese studies, which alas covers a lot more of them, but it's pretty contrieved in just annoucing:</p>\n\n<blockquote>\n <p>A number of subsequent clinical trials [ChiCTR ids list] have\n been quickly conducted in China to test the efficacy\n and safety of chloroquine or hydroxychloroquine in the\n treatment of COVID-19 associated pneumonia in more\n than 10 hospitals in Wuhan, Jingzhou, Guangzhou,\n Beijing, Shanghai, Chongqing, and Ningbo</p>\n \n <p>Thus far,\n results from more than <strong>100 patients</strong> have demonstrated\n that chloroquine phosphate is superior to the control\n treatment in inhibiting the exacerbation of pneumonia,\n improving lung imaging findings, promoting a virus negative\n conversion, and shortening the disease\n course according to the news briefing. <strong>Severe adverse\n reactions to chloroquine phosphate were not noted in\n the aforementioned patients.</strong></p>\n</blockquote>\n\n<p>More annoyingly, it says absolutely nothing about dosage.</p>\n\n<p>And as far as I can tell the <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102549/\" rel=\"nofollow noreferrer\">French study</a> does not mention any adverse reactions either. The dose administered was 600mg/day.</p>\n\n<p>On the other hand, a <a href=\"https://www.bmj.com/content/369/bmj.m1335.full\" rel=\"nofollow noreferrer\">BMJ news/review</a> (Apr 1) of this French paper says:</p>\n\n<blockquote>\n <p>Although Raoult reported the results as positive, he excluded from the analysis six patients in the hydroxychloroquine arm because they had not remained in the study for six days. The reasons for non-completion were that one patient died, three were transferred to the intensive care unit (ICU), and two withdrew. None of the 16 patients in the control group died, withdrew, or needed care in an ICU. [...]</p>\n \n <p>Eight days after his initial study, Raoult posted the results of an uncontrolled observational study of 80 patients. In that study one patient died and one remained in the ICU at the time of the report, putting the case fatality rate at 1.3% or 2.5%, depending on the outcome of the ICU patient. This compares with case fatality rates in Germany and the US of 0.9% and 1.8%, respectively.</p>\n \n <p>Raoult did not respond to requests for an interview by <em>The BMJ</em>.</p>\n</blockquote>\n\n<p>Another BMJ <a href=\"https://www.bmj.com/content/369/bmj.m1432\" rel=\"nofollow noreferrer\">editorial</a> published a week later is also quite critical of the CQ studies published thus far.</p>\n\n<p>Apparently the protest/questions directed at the French paper have resulted in a <a href=\"https://www.isac.world/news-and-publications/official-isac-statement\" rel=\"nofollow noreferrer\">official reaction</a> from the journal board (this was mentioned in \"quick reactions\" the later BMJ piece)</p>\n\n<blockquote>\n <p>Official Statement from International Society of Antimicrobial Chemotherapy (ISAC)</p>\n \n <p>Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial (Gautret P et al. PMID 32205204)</p>\n \n <p>ISAC shares the concerns regarding the above article published recently in the International Journal of Antimicrobial Agents (IJAA). <strong>The ISAC Board believes the article does not meet the Society’s expected standard, especially relating to the lack of better explanations of the inclusion criteria and the triage of patients to ensure patient safety.</strong></p>\n \n <p>Despite some suggestions online as to the reliability of the article's peer review process, the process did adhere to the industry's peer review rules. Given his role as Editor in Chief of this journal, Jean-Marc Rolain had no involvement in the peer review of the manuscript and has no access to information regarding its peer review. Full responsibility for the manuscript's peer review process was delegated to an Associate Editor.</p>\n \n <p>Although ISAC recognises it is important to help the scientific community by publishing new data fast, this cannot be at the cost of reducing scientific scrutiny and best practices. Both Editors in Chief of our journals (IJAA and Journal of Global Antimicrobial Resistance) are in full agreement.</p>\n \n <p>Andreas Voss\n ISAC President</p>\n \n <p>April 3rd-2020</p>\n</blockquote>\n\n<p><em>The Lancet</em> <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30817-5/fulltext\" rel=\"nofollow noreferrer\">noted (on Apr 11)</a> that contra France (and US/FDA), based on current data, the European Medicines Agency is not convinced CQ/HCQ has any role in treating Covid-19.</p>\n\n<p>See also, <a href=\"https://annals.org/aim/fullarticle/2764587/annals-call-covid-19-chloroquine-answer\" rel=\"nofollow noreferrer\">podcast discussion</a> on Annals of Internal Medicine and <em>Science Translational Medicine</em> <a href=\"https://blogs.sciencemag.org/pipeline/archives/2020/03/29/more-on-cloroquine-azithromycin-and-on-dr-raoult\" rel=\"nofollow noreferrer\">blog</a> critical of the 2nd (draft) French study. The latter piece notes that at one point:</p>\n\n<blockquote>\n <p>Raoult and several of his co-authors were banned from publishing in any ASM (American Society for Microbiology) journals for a year.</p>\n</blockquote>\n\n<hr>\n\n<p>A more recent <a href=\"https://www.medrxiv.org/content/10.1101/2020.04.10.20060699v1.full.pdf\" rel=\"nofollow noreferrer\">French study</a> (not from the Raoult group) found that HCQ wasn't effective (or more precisely that the effect wasn't statistically significant--although just a preprint it was also <a href=\"https://edition.cnn.com/2020/04/15/health/new-french-study-hydroxychloroquine/index.html\" rel=\"nofollow noreferrer\">covered by CNN</a> on April 15). The study also found some patients had to discontinue HCQ due to ECG changes:</p>\n\n<blockquote>\n <p>This study included 181 patients with SARS-CoV-2 pneumonia; 84 received HCQ within\n 48 hours of admission (HCQ group) and 97 did not (no-HCQ group). Initial severity was well\n balanced between the groups. In the weighted analysis, 20.2% patients in the HCQ group\n were transferred to the ICU or died within 7 days vs 22.1% in the no-HCQ group (16 vs 21\n events, relative risk [RR] 0.91, 95% CI 0.47–1.80). In the HCQ group, 2.8% of the patients\n died within 7 days vs 4.6% in the no-HCQ group (3 vs 4 events, RR 0.61, 95% CI 0.13–2.89),\n and 27.4% and 24.1%, respectively, developed acute respiratory distress syndrome within 7\n days (24 vs 23 events, RR 1.14, 95% CI 0.65–2.00). <strong>Eight patients receiving HCQ (9.5%)\n experienced electrocardiogram modifications requiring HCQ discontinuation.</strong></p>\n \n <p>Interpretation: These results do not support the use of HCQ in patients hospitalised for documented SARSCoV-2-positive hypoxic pneumonia. </p>\n</blockquote>\n\n<p>(The HCQ dose was 600 mg daily.)</p>\n"
},
{
"answer_id": 23233,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>We now have some data from randomized studies that provide some indications of safety considerations when using Hydroxychloroquine/Chloroquine in the management of Covid-19. The first study (non-peer reviewed) from Renmin Hospital of Wuhan University</p>\n\n<blockquote>\n <p>Main methods: From February 4 to February 28, 2020, 62 patients suffering from COVID-19 were diagnosed and admitted to Renmin Hospital of Wuhan University. All participants were randomized in a parallel-group trial, 31 patients were assigned to receive an additional 5-day HCQ (400 mg/d) treatment, Time to clinical recovery (TTCR), clinical characteristics, and radiological results were assessed at baseline and 5 days after treatment to evaluate the effect of HCQ</p>\n</blockquote>\n\n<p>So, these were 62 patients half of whom were only given 5 days of 400 mg of Hydroxychloroquine, which is a standard dose used in the management of rheumatic disease at approximately 5 mg/Kg, 400 mg/d (200 mg/bid) between days 1 and 5.</p>\n\n<p>It's important to note the inclusion criteria here in particular</p>\n\n<blockquote>\n <ol start=\"4\">\n <li>SaO2/SPO2 ratio > 93% or PaO2/FIO2 ratio > 300 mmHg under the condition in the hospital room (mild illness); </li>\n </ol>\n</blockquote>\n\n<p>So, these were mildly affected patients who would have been expected to have a good outcome. Average age was 44.7 years (sd 15.3 years) with approximately even split in gender, so again a group expected to do well. Excluded were:</p>\n\n<blockquote>\n <ol>\n <li>Severe and critical illness patients </li>\n </ol>\n</blockquote>\n\n<p>among other criteria.</p>\n\n<p>Although this was an efficacy study, there were minor side effects noted in the treatment arm</p>\n\n<blockquote>\n <p>Notably, a total of 4 of the 62 patients progressed to severe illness, all of which occurred in the control\n group not receiving HCQ treatment. For adverse effects, it should be noted that there were two patients\n with mild adverse reactions in the HCQ treatment group, one patient developed a rash, and one patient\n experienced a headache, none severe side effects appeared among them. </p>\n</blockquote>\n\n<p>The next large study we have is from Brazilian Hospital <em>Hospital e Pronto-Socorro Delphina Rinaldi Abdel Aziz</em> and is a</p>\n\n<blockquote>\n <p>double-blinded, randomized clinical trial addressing different dosages of Chloroquine for the treatment of severe patients with COVID-19 in the absence of a control group using placebo. </p>\n</blockquote>\n\n<p>The inclusion criteria included</p>\n\n<blockquote>\n <p>Hospitalized patients aged 18 years or older at the time of inclusion, with respiratory rate\n higher than 24 rpm AND/OR heart rate higher than 125 bpm (in the absence of fever)\n AND/OR peripheral oxygen saturation lower than 90% in ambient air AND/OR shock\n (defined as mean arterial pressure lower than 65 mmHg, with the need for vasopressors\n medicines or oliguria or a lower level of consciousness) were included.</p>\n</blockquote>\n\n<p>So, these were very sick patients. Their age was slightly higher at average of 51.1 years (sd 13.9) </p>\n\n<p>Annoyingly there is no placebo controlled arm due to \"ethical\" considerations, and we note that this study is very different from the Wuhan study in that it looks at <strong>severe</strong> patients.</p>\n\n<p>The high dose arm intended to give 12 g of Chloroquine over 12 days (Wuhan used 2 g over 5 days), and their low dose arm used 2.7 g over 5 days. Both arms also used ceftriaxone and azithromycin as well, and their preliminary data used 81 patients from a predefined population size of 440.</p>\n\n<p>Given the toxicity of hydroxychloroquine/chloroquine at high dose with Qtc prolongation, and theoretically compounded with the co-administration of azithromycin, not unexpectedly Qtc prolongation was observed:</p>\n\n<blockquote>\n <p>Regarding cardiotoxicity and\n QTc over time, the variation in the QTc as compared to the baseline ECG increased more on\n days 2 and 3 in the high dose CQ arm, with both arms (low and high CQ) showing more\n similar QTc variations in the last three days of follow-up (Figure 2). Two patients in the high\n dose CQ arm evolved with ventricular tachycardia before death. This severe type of arrythmia\n is usually facilitated when QTc is prolonged. </p>\n</blockquote>\n\n<p>There was also evidence of myocardial injury in both arms</p>\n\n<blockquote>\n <p>Occurrence of myocarditis (defined as CKMB higher than 2x the upper normal\n limit), which may be a final complication of severe sepsis or a lesion triggered by the virus\n itself, was seen in 2/24 (8.3%) patients (1 patient/arm). No echocardiogram was performed. </p>\n</blockquote>\n\n<p>By day 6, 4 of the low dose arm had died, and 7 of the high dose arm. Ventricular tachycardia was observed in 2 of the high dose arm deaths at total dose of 7.2 g of Chloroquine. However, more patients with heart disease were randomized to the high dose arm, and there were 5 people over age 75 in the high dose arm, and none in the low dose.</p>\n\n<p>Given the appearance of a cardiotoxicity signal as well as excess deaths, enrollment in the high dose arm was ceased and all patients were moved to the low dose arm. However, there is no comparator arm going forwards.</p>\n\n<p>Their table 3 also has a mistake in that they state 4/41 died in the High Dose arm, and 7/40 in the low dose which is not what the conclusions state.</p>\n\n<p><strong>Update: 16 April 2020</strong></p>\n\n<p>A review has just been pre-published looking at the safety of Hydroxychloroqine in combination with other drugs that points to the possible lethality of combination of hydroxychloroquine with azithromycin.</p>\n\n<blockquote>\n <p>Results: Overall, 956,374 and 310,350 users of hydroxychloroquine and sulfasalazine, and 323,122 and 351,956 users of hydroxychloroquine-azithromycin and hydroxychloroquine-amoxicillin were included. No excess risk of SAEs was identified when 30-day hydroxychloroquine and sulfasalazine use were compared. SCCS confirmed these findings. However, <strong>when azithromycin was added to hydroxychloroquine, we observed an increased risk of 30-day cardiovascular mortality (CalHR2.19 [1.22-3.94]), chest pain/angina (CalHR 1.15 [95% CI 1.05-1.26]), and heart failure (CalHR 1.22 [95% CI 1.02-1.45])</strong> Conclusions: Short-term hydroxychloroquine treatment is safe, but addition of azithromycin may induce heart failure and cardiovascular mortality, potentially due to synergistic effects on QT length. We call for caution if such combination is to be used in the management of Covid-19.</p>\n</blockquote>\n\n<p><strong>Update: 22 April 2020</strong> </p>\n\n<p>A VA review looked at 386 VA patients treated with Hydroxychloroquine with or without Azithromycin vs with neither until 11th April 2020</p>\n\n<blockquote>\n <p>performed a retrospective analysis of data from patients hospitalized with confirmed SARS-CoV-2 infection in all United States Veterans Health Administration medical centers until April 11, 2020. Patients were categorized based on their exposure to hydroxychloroquine alone (HC) or with azithromycin (HC+AZ) as treatments in addition to standard supportive management for Covid-19. The two primary outcomes were death and the need for mechanical ventilation.</p>\n</blockquote>\n\n<p>And there appeared to be worse outcomes for those on HC</p>\n\n<blockquote>\n <p>RESULTS: A total of 368 patients were evaluated (HC, n=97; HC+AZ, n=113; no HC, n=158). Rates of death in the HC, HC+AZ, and no HC groups were 27.8%, 22.1%, 11.4%, respectively</p>\n</blockquote>\n\n<p>A weakness of the study was that it was retrospective review of outcomes.</p>\n\n<p>Safety of hydroxychloroquine, alone and in combination with azithromycin, in light of rapid wide-spread use for COVID-19: a multinational, network cohort and self-controlled case series study\n<a href=\"https://www.medrxiv.org/content/10.1101/2020.04.08.20054551v1\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.08.20054551v1</a></p>\n\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.03.22.20040758v3.full.pdf\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.03.22.20040758v3.full.pdf</a></p>\n\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.04.07.20056424v1.full.pdf\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.07.20056424v1.full.pdf</a></p>\n\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.04.16.20065920v1\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.16.20065920v1</a></p>\n"
}
] | 2020/04/14 | [
"https://health.stackexchange.com/questions/23221",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/3414/"
] |
23,225 | <p>I'm a lay person.</p>
<p>When somebody has ARDS, when is non-mechanical ventilation used, vs mechanical ventilation? </p>
<p>(I'm talking no intubation, no sedation)</p>
<p>From what I understand, mechanical ventilation involves air being forced in, rather than breathed in naturally.</p>
<p><strong>Added elaboration</strong></p>
<p>This is not answered here <a href="https://medicalsciences.stackexchange.com/questions/22905">When can mechanical ventilation be performed without intubation?</a>
That question is asking about an A and a B, where A is with intubation and B is not.</p>
<p>But my question is asking about an A and a B, where both A and B are without intubation. But A is non-mechanical ventilation and B is mechanical ventilation.</p>
| [
{
"answer_id": 23230,
"author": "Purab Patel",
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"text": "<p>Obviously depends on the exact case at hand, but from what I know, non mechanical ventilation (ie. Venti mask, etc.) Is only used for very mild ARDS where there is fairly good oxygenation and the patient is hemodynamically stable (good blood pressure and heart rate), able to keep their airway open, no copious secretions, etc. (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=22020236\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed?term=22020236</a>). In moderate or severe ARDS, intubation is usually used (most cases end up requiring at least some form of ventilation). </p>\n\n<p>Yes, you are absolutely correct. Mechanical ventilation is when there is pressure forcing air in, while non mechanical is not forcing any air in and rather providing more oxygen flow. </p>\n"
},
{
"answer_id": 23231,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>To clarify there are different types of ventilation where ventilation means to assist the delivery of oxygen to a patient.</p>\n\n<h2>Non-invasive Ventilation (NIV)</h2>\n\n<ul>\n<li><p>Without significantly increasing pressure in the airways</p>\n\n<ul>\n<li><p>Masks</p></li>\n<li><p>high flow nasal cannula </p></li>\n</ul></li>\n<li><p>Positive airways pressure </p>\n\n<ul>\n<li><p>CPAP</p></li>\n<li><p>BPAP</p></li>\n</ul></li>\n<li><p>Negative Pressure Ventilation</p>\n\n<ul>\n<li>Iron lungs</li>\n</ul></li>\n</ul>\n\n<h2>Invasive Ventilation</h2>\n\n<ul>\n<li>intubation or tracheostomy delivered</li>\n</ul>\n\n<p>It sounds like you're asking when treating a case of ARDS when does one switch from using a mask/cannula to using CPAP/BPAP.</p>\n\n<p><img src=\"https://www.uptodate.com/contents/images/PULM/108315/Helmetinterface.jpg\" alt=\"\"></p>\n\n<blockquote>\n <p>Several types of helmets are commercially available in Europe, each with different features. There are no helmets commercially available for use with NIV in the US, but one helmet is approved for use in bariatric chambers to protect against excessively high oxygen tensions. This graphic shows a representative image of helmet interface used to deliver noninvasive ventilation. Shown are ventilation ports for the administration and removal of gas flow and a rubber seal at the neck, while others have additional optional features including ports for the introduction of catheters and under-arm straps for extra security to ensure a tight seal.</p>\n</blockquote>\n\n<p>ARDS is by definition a severe illness and it's usually only at the very early stages that a patient can be managed using NIV positive airways pressure ventilation. </p>\n\n<blockquote>\n <p>Noninvasive ventilation (NIV; ie, ventilation via a mask or nasal prongs with breaths delivered by a NIV device) may be reserved for the <strong>occasional patient with mild ARDS who is hemodynamically stable, is easily oxygenated, does not need immediate intubation, and has no contraindications to its use.</strong> This approach is based upon our experience and conflicting data regarding the benefit of NIV (eg, prevention of intubation, improved mortality) in this population. Importantly, when NIV is implemented, frequent evaluation is necessary and clinicians should have a low threshold for intubation.</p>\n</blockquote>\n\n<p>However, there are risks from such an approach</p>\n\n<blockquote>\n <p>In contrast, a study of patients with hypoxemic respiratory failure, many of whom had ARDS, reported increased mortality in association with NIV when compared with patients treated with high flow nasal cannula (HFNC)</p>\n</blockquote>\n\n<p>So, at least some studies suggest that switching from masks/cannula to using positive airways pressure could increase mortality. Whereas other studies suggest using a helmet may reduce the mortality and increase the number of days free of intubation.</p>\n\n<p><a href=\"https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome\" rel=\"nofollow noreferrer\">https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome</a></p>\n"
},
{
"answer_id": 23234,
"author": "barlop",
"author_id": 19340,
"author_profile": "https://health.stackexchange.com/users/19340",
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"text": "<p>note- I won't accept my own answer, as discussion with others here has helped contribute to it.</p>\n\n<p>I'm a lay person.</p>\n\n<p>Having discussed this with people, I now see there is some confusion in the question, which if cleared up, would make for a clearer question. To address the confusion, the question asks.</p>\n\n<blockquote>\n <p>\"When somebody has ARDS, when is non-mechanical ventilation used, vs\n mechanical ventilation? (I'm talking no intubation, no sedation)\"</p>\n</blockquote>\n\n<p>One person I spoke to has said</p>\n\n<p>All ventilators are mechanical. And when people say mechanical, hands-free is meant - not manual. Machine operated. And a ventilator would be forcing air in at set intervals. (Note- there are CPAP machines that give a continuous supply of air, but they are not ventilators. <a href=\"https://geekymedics.com/cpap-vs-niv-bipap\" rel=\"nofollow noreferrer\">https://geekymedics.com/cpap-vs-niv-bipap</a> ) </p>\n\n<p>Masks being fed a steady air supply wouldn't be ventilators. </p>\n\n<p>HFNC - not a ventilator. (it doesn't force air in at set intervals). </p>\n\n<p>NRB - not a ventilator</p>\n\n<p>NIV e.g.(NIPPV/NPPV or NPV) - are ventilators </p>\n\n<p>BVM <a href=\"https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html\" rel=\"nofollow noreferrer\">https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html</a> wouldn't be considered a ventilator 'cos it's hand operated.</p>\n\n<p>Also, regarding the term \"mechanical ventilator\" I think it's not really used much as the qualifier doesn't add anything, as when somebody says ventilator, they mean that hands free machine device forcing air in in a timed manner, it's a machine, hands free, not manual. The term \"mechanical ventilator\" gets 523K results on google. The term \"mechanical ventilation\" gets 6.6 million results. </p>\n\n<p>The term ventilation is not particular to medicine and means supplying air to some enclosed space. Medicine does have non-mechanical ventilation. A Bag Valve Mask <a href=\"https://en.wikipedia.org/wiki/Bag_valve_mask\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Bag_valve_mask</a> would be a form of manual ventilation. And as that link mentions, you also have \"mouth to mouth ventilation\", whicj would also be manual. </p>\n\n<p>In terms of English, machines that don't force air e.g. HFNC would not be ventilation devices 'cos it helps get oxygen in, rather than helps with breathing(getting air in/out). </p>\n\n<p>A BPAP or CPAP machine for sleep apnea machine that does a bit of the work of breathing, could perhaps be a ventiation device. But not a ventilator. A ventilator is capable of handling a person's breathing completely. Like a sleep apnea BPAP machine but with more power.</p>\n\n<p>Specific to medicine, is the term \"mechanical ventilation\", a form of respiratory therapy, with ventilators. <a href=\"https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/\" rel=\"nofollow noreferrer\">https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/</a> And when they speak of non-invasive ventilation, they talk of non-invasive ventilators.</p>\n\n<p>So the question could be split into the question about mechanical ventilators, and a question of, when somebody has ARDS, when are they moved from HFNC or NRB, to NPPV and eventually perhaps to an (invasive) ventilator(i.e. ventilator with intubation). </p>\n"
}
] | 2020/04/14 | [
"https://health.stackexchange.com/questions/23225",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19340/"
] |
23,246 | <p>According to research research conducted in Wuhan and published on April 9 in following article,
<a href="https://www.kidney-international.org/article/S0085-2538(20)30369-0/fulltext" rel="nofollow noreferrer">https://www.kidney-international.org/article/S0085-2538(20)30369-0/fulltext</a>, out of 26 autopsies conducted on people who died of Covid-19, nine of which had acute kidney injury, seven were found to have clusters of coronavirus particles with distinctive spikes in the tubular epithelium and podocytes on electron microscopy. In addition, immunostaining with SARS-CoV nucleoprotein antibody was shown to be positive in tubules.
Other case reports indicating extra-pulmonary involvement have surfaced including hepatitis, myocarditis along with arrhythmias, and thromboses. I have not seen any histopathology reports indicating direct viral infection of other organ systems besides lung and kidney, but the above would seem to suggest that there should be a viremic phase associated with this illness.
Have there been any studies of blood viral loads or qualitative pcr measurements taken of hospitalized patients with this illness?</p>
| [
{
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"text": "<p>Obviously depends on the exact case at hand, but from what I know, non mechanical ventilation (ie. Venti mask, etc.) Is only used for very mild ARDS where there is fairly good oxygenation and the patient is hemodynamically stable (good blood pressure and heart rate), able to keep their airway open, no copious secretions, etc. (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=22020236\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed?term=22020236</a>). In moderate or severe ARDS, intubation is usually used (most cases end up requiring at least some form of ventilation). </p>\n\n<p>Yes, you are absolutely correct. Mechanical ventilation is when there is pressure forcing air in, while non mechanical is not forcing any air in and rather providing more oxygen flow. </p>\n"
},
{
"answer_id": 23231,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>To clarify there are different types of ventilation where ventilation means to assist the delivery of oxygen to a patient.</p>\n\n<h2>Non-invasive Ventilation (NIV)</h2>\n\n<ul>\n<li><p>Without significantly increasing pressure in the airways</p>\n\n<ul>\n<li><p>Masks</p></li>\n<li><p>high flow nasal cannula </p></li>\n</ul></li>\n<li><p>Positive airways pressure </p>\n\n<ul>\n<li><p>CPAP</p></li>\n<li><p>BPAP</p></li>\n</ul></li>\n<li><p>Negative Pressure Ventilation</p>\n\n<ul>\n<li>Iron lungs</li>\n</ul></li>\n</ul>\n\n<h2>Invasive Ventilation</h2>\n\n<ul>\n<li>intubation or tracheostomy delivered</li>\n</ul>\n\n<p>It sounds like you're asking when treating a case of ARDS when does one switch from using a mask/cannula to using CPAP/BPAP.</p>\n\n<p><img src=\"https://www.uptodate.com/contents/images/PULM/108315/Helmetinterface.jpg\" alt=\"\"></p>\n\n<blockquote>\n <p>Several types of helmets are commercially available in Europe, each with different features. There are no helmets commercially available for use with NIV in the US, but one helmet is approved for use in bariatric chambers to protect against excessively high oxygen tensions. This graphic shows a representative image of helmet interface used to deliver noninvasive ventilation. Shown are ventilation ports for the administration and removal of gas flow and a rubber seal at the neck, while others have additional optional features including ports for the introduction of catheters and under-arm straps for extra security to ensure a tight seal.</p>\n</blockquote>\n\n<p>ARDS is by definition a severe illness and it's usually only at the very early stages that a patient can be managed using NIV positive airways pressure ventilation. </p>\n\n<blockquote>\n <p>Noninvasive ventilation (NIV; ie, ventilation via a mask or nasal prongs with breaths delivered by a NIV device) may be reserved for the <strong>occasional patient with mild ARDS who is hemodynamically stable, is easily oxygenated, does not need immediate intubation, and has no contraindications to its use.</strong> This approach is based upon our experience and conflicting data regarding the benefit of NIV (eg, prevention of intubation, improved mortality) in this population. Importantly, when NIV is implemented, frequent evaluation is necessary and clinicians should have a low threshold for intubation.</p>\n</blockquote>\n\n<p>However, there are risks from such an approach</p>\n\n<blockquote>\n <p>In contrast, a study of patients with hypoxemic respiratory failure, many of whom had ARDS, reported increased mortality in association with NIV when compared with patients treated with high flow nasal cannula (HFNC)</p>\n</blockquote>\n\n<p>So, at least some studies suggest that switching from masks/cannula to using positive airways pressure could increase mortality. Whereas other studies suggest using a helmet may reduce the mortality and increase the number of days free of intubation.</p>\n\n<p><a href=\"https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome\" rel=\"nofollow noreferrer\">https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome</a></p>\n"
},
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"pm_score": 0,
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"text": "<p>note- I won't accept my own answer, as discussion with others here has helped contribute to it.</p>\n\n<p>I'm a lay person.</p>\n\n<p>Having discussed this with people, I now see there is some confusion in the question, which if cleared up, would make for a clearer question. To address the confusion, the question asks.</p>\n\n<blockquote>\n <p>\"When somebody has ARDS, when is non-mechanical ventilation used, vs\n mechanical ventilation? (I'm talking no intubation, no sedation)\"</p>\n</blockquote>\n\n<p>One person I spoke to has said</p>\n\n<p>All ventilators are mechanical. And when people say mechanical, hands-free is meant - not manual. Machine operated. And a ventilator would be forcing air in at set intervals. (Note- there are CPAP machines that give a continuous supply of air, but they are not ventilators. <a href=\"https://geekymedics.com/cpap-vs-niv-bipap\" rel=\"nofollow noreferrer\">https://geekymedics.com/cpap-vs-niv-bipap</a> ) </p>\n\n<p>Masks being fed a steady air supply wouldn't be ventilators. </p>\n\n<p>HFNC - not a ventilator. (it doesn't force air in at set intervals). </p>\n\n<p>NRB - not a ventilator</p>\n\n<p>NIV e.g.(NIPPV/NPPV or NPV) - are ventilators </p>\n\n<p>BVM <a href=\"https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html\" rel=\"nofollow noreferrer\">https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html</a> wouldn't be considered a ventilator 'cos it's hand operated.</p>\n\n<p>Also, regarding the term \"mechanical ventilator\" I think it's not really used much as the qualifier doesn't add anything, as when somebody says ventilator, they mean that hands free machine device forcing air in in a timed manner, it's a machine, hands free, not manual. The term \"mechanical ventilator\" gets 523K results on google. The term \"mechanical ventilation\" gets 6.6 million results. </p>\n\n<p>The term ventilation is not particular to medicine and means supplying air to some enclosed space. Medicine does have non-mechanical ventilation. A Bag Valve Mask <a href=\"https://en.wikipedia.org/wiki/Bag_valve_mask\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Bag_valve_mask</a> would be a form of manual ventilation. And as that link mentions, you also have \"mouth to mouth ventilation\", whicj would also be manual. </p>\n\n<p>In terms of English, machines that don't force air e.g. HFNC would not be ventilation devices 'cos it helps get oxygen in, rather than helps with breathing(getting air in/out). </p>\n\n<p>A BPAP or CPAP machine for sleep apnea machine that does a bit of the work of breathing, could perhaps be a ventiation device. But not a ventilator. A ventilator is capable of handling a person's breathing completely. Like a sleep apnea BPAP machine but with more power.</p>\n\n<p>Specific to medicine, is the term \"mechanical ventilation\", a form of respiratory therapy, with ventilators. <a href=\"https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/\" rel=\"nofollow noreferrer\">https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/</a> And when they speak of non-invasive ventilation, they talk of non-invasive ventilators.</p>\n\n<p>So the question could be split into the question about mechanical ventilators, and a question of, when somebody has ARDS, when are they moved from HFNC or NRB, to NPPV and eventually perhaps to an (invasive) ventilator(i.e. ventilator with intubation). </p>\n"
}
] | 2020/04/15 | [
"https://health.stackexchange.com/questions/23246",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19072/"
] |
23,289 | <p>There have been a number of well recognised super spreader events such as <a href="https://www.aljazeera.com/news/2020/03/31-south-korea-sudden-spike-coronavirus-cases-200303065953841.html" rel="nofollow noreferrer">Patient 31</a> in South Korea where a member of the church called Shincheonji was thought to have spread the disease to 30-40 others in a church meeting.</p>
<p>Does the evidence now point to the virus also being spread from the Huanan market as well as a super-spreader event rather than created there amongst the bats and other animals?</p>
| [
{
"answer_id": 23230,
"author": "Purab Patel",
"author_id": 19343,
"author_profile": "https://health.stackexchange.com/users/19343",
"pm_score": 2,
"selected": false,
"text": "<p>Obviously depends on the exact case at hand, but from what I know, non mechanical ventilation (ie. Venti mask, etc.) Is only used for very mild ARDS where there is fairly good oxygenation and the patient is hemodynamically stable (good blood pressure and heart rate), able to keep their airway open, no copious secretions, etc. (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=22020236\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed?term=22020236</a>). In moderate or severe ARDS, intubation is usually used (most cases end up requiring at least some form of ventilation). </p>\n\n<p>Yes, you are absolutely correct. Mechanical ventilation is when there is pressure forcing air in, while non mechanical is not forcing any air in and rather providing more oxygen flow. </p>\n"
},
{
"answer_id": 23231,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>To clarify there are different types of ventilation where ventilation means to assist the delivery of oxygen to a patient.</p>\n\n<h2>Non-invasive Ventilation (NIV)</h2>\n\n<ul>\n<li><p>Without significantly increasing pressure in the airways</p>\n\n<ul>\n<li><p>Masks</p></li>\n<li><p>high flow nasal cannula </p></li>\n</ul></li>\n<li><p>Positive airways pressure </p>\n\n<ul>\n<li><p>CPAP</p></li>\n<li><p>BPAP</p></li>\n</ul></li>\n<li><p>Negative Pressure Ventilation</p>\n\n<ul>\n<li>Iron lungs</li>\n</ul></li>\n</ul>\n\n<h2>Invasive Ventilation</h2>\n\n<ul>\n<li>intubation or tracheostomy delivered</li>\n</ul>\n\n<p>It sounds like you're asking when treating a case of ARDS when does one switch from using a mask/cannula to using CPAP/BPAP.</p>\n\n<p><img src=\"https://www.uptodate.com/contents/images/PULM/108315/Helmetinterface.jpg\" alt=\"\"></p>\n\n<blockquote>\n <p>Several types of helmets are commercially available in Europe, each with different features. There are no helmets commercially available for use with NIV in the US, but one helmet is approved for use in bariatric chambers to protect against excessively high oxygen tensions. This graphic shows a representative image of helmet interface used to deliver noninvasive ventilation. Shown are ventilation ports for the administration and removal of gas flow and a rubber seal at the neck, while others have additional optional features including ports for the introduction of catheters and under-arm straps for extra security to ensure a tight seal.</p>\n</blockquote>\n\n<p>ARDS is by definition a severe illness and it's usually only at the very early stages that a patient can be managed using NIV positive airways pressure ventilation. </p>\n\n<blockquote>\n <p>Noninvasive ventilation (NIV; ie, ventilation via a mask or nasal prongs with breaths delivered by a NIV device) may be reserved for the <strong>occasional patient with mild ARDS who is hemodynamically stable, is easily oxygenated, does not need immediate intubation, and has no contraindications to its use.</strong> This approach is based upon our experience and conflicting data regarding the benefit of NIV (eg, prevention of intubation, improved mortality) in this population. Importantly, when NIV is implemented, frequent evaluation is necessary and clinicians should have a low threshold for intubation.</p>\n</blockquote>\n\n<p>However, there are risks from such an approach</p>\n\n<blockquote>\n <p>In contrast, a study of patients with hypoxemic respiratory failure, many of whom had ARDS, reported increased mortality in association with NIV when compared with patients treated with high flow nasal cannula (HFNC)</p>\n</blockquote>\n\n<p>So, at least some studies suggest that switching from masks/cannula to using positive airways pressure could increase mortality. Whereas other studies suggest using a helmet may reduce the mortality and increase the number of days free of intubation.</p>\n\n<p><a href=\"https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome\" rel=\"nofollow noreferrer\">https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome</a></p>\n"
},
{
"answer_id": 23234,
"author": "barlop",
"author_id": 19340,
"author_profile": "https://health.stackexchange.com/users/19340",
"pm_score": 0,
"selected": false,
"text": "<p>note- I won't accept my own answer, as discussion with others here has helped contribute to it.</p>\n\n<p>I'm a lay person.</p>\n\n<p>Having discussed this with people, I now see there is some confusion in the question, which if cleared up, would make for a clearer question. To address the confusion, the question asks.</p>\n\n<blockquote>\n <p>\"When somebody has ARDS, when is non-mechanical ventilation used, vs\n mechanical ventilation? (I'm talking no intubation, no sedation)\"</p>\n</blockquote>\n\n<p>One person I spoke to has said</p>\n\n<p>All ventilators are mechanical. And when people say mechanical, hands-free is meant - not manual. Machine operated. And a ventilator would be forcing air in at set intervals. (Note- there are CPAP machines that give a continuous supply of air, but they are not ventilators. <a href=\"https://geekymedics.com/cpap-vs-niv-bipap\" rel=\"nofollow noreferrer\">https://geekymedics.com/cpap-vs-niv-bipap</a> ) </p>\n\n<p>Masks being fed a steady air supply wouldn't be ventilators. </p>\n\n<p>HFNC - not a ventilator. (it doesn't force air in at set intervals). </p>\n\n<p>NRB - not a ventilator</p>\n\n<p>NIV e.g.(NIPPV/NPPV or NPV) - are ventilators </p>\n\n<p>BVM <a href=\"https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html\" rel=\"nofollow noreferrer\">https://www.redcross.org/store/disposable-bvm-bag-valve-mask-adult-size/760002.html</a> wouldn't be considered a ventilator 'cos it's hand operated.</p>\n\n<p>Also, regarding the term \"mechanical ventilator\" I think it's not really used much as the qualifier doesn't add anything, as when somebody says ventilator, they mean that hands free machine device forcing air in in a timed manner, it's a machine, hands free, not manual. The term \"mechanical ventilator\" gets 523K results on google. The term \"mechanical ventilation\" gets 6.6 million results. </p>\n\n<p>The term ventilation is not particular to medicine and means supplying air to some enclosed space. Medicine does have non-mechanical ventilation. A Bag Valve Mask <a href=\"https://en.wikipedia.org/wiki/Bag_valve_mask\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Bag_valve_mask</a> would be a form of manual ventilation. And as that link mentions, you also have \"mouth to mouth ventilation\", whicj would also be manual. </p>\n\n<p>In terms of English, machines that don't force air e.g. HFNC would not be ventilation devices 'cos it helps get oxygen in, rather than helps with breathing(getting air in/out). </p>\n\n<p>A BPAP or CPAP machine for sleep apnea machine that does a bit of the work of breathing, could perhaps be a ventiation device. But not a ventilator. A ventilator is capable of handling a person's breathing completely. Like a sleep apnea BPAP machine but with more power.</p>\n\n<p>Specific to medicine, is the term \"mechanical ventilation\", a form of respiratory therapy, with ventilators. <a href=\"https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/\" rel=\"nofollow noreferrer\">https://www.resmed.co.uk/healthcare-professional/respiratory-care/respiratory-therapy/</a> And when they speak of non-invasive ventilation, they talk of non-invasive ventilators.</p>\n\n<p>So the question could be split into the question about mechanical ventilators, and a question of, when somebody has ARDS, when are they moved from HFNC or NRB, to NPPV and eventually perhaps to an (invasive) ventilator(i.e. ventilator with intubation). </p>\n"
}
] | 2020/04/18 | [
"https://health.stackexchange.com/questions/23289",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/3414/"
] |
23,320 | <p>There are 2 contradicting messages out there that mandate this question:</p>
<ol>
<li><p>"It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes."
Refer <a href="https://www.cdc.gov/coronavirus/2019-ncov/prevent-getting-sick/how-covid-spreads.htm" rel="nofollow noreferrer">CDC page1</a>.</p></li>
<li><p>"Currently, there is no evidence to support transmission of COVID-19 associated with food. Based on information about this novel coronavirus thus far, it seems unlikely that COVID-19 can be transmitted through food – additional investigation is needed."
Refer <a href="https://www.cdc.gov/coronavirus/2019-ncov/faq.html#How-COVID-19-Spreads" rel="nofollow noreferrer">CDC page2</a>.</p></li>
</ol>
<p>So, my question now:
As per #1, it <em>could</em> spread when we touch an infected surface and touch our mouth.
But as per #2, <em>there is no evidence</em> that touching infected food and eating it (food touching our mouth) will cause it. </p>
<p>Why is it that in #1 they seem to be more sure that it will transmit and in #2 they seem to look for evidence ?</p>
| [
{
"answer_id": 23324,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>I think what they are intended to convey is that they feel that the cooking process will destroy any virus found in food so cooked food should not be a source of infection. Of course that is subject to more data.</p>\n\n<p>However, it is clearly a different proposition if the person preparing the food is infected and contaminates the food after it is cooked. In which case it just it becomes another surface that can transmit the virus.</p>\n\n<p>Although it is currently a matter before the police the thought is that an infected member of crew on board the Ruby Princess was handling food and that's how they managed to infect so many passengers.</p>\n\n<p><a href=\"https://www.rnz.co.nz/news/world/414144/covid-19-waiter-or-food-handler-obvious-point-of-transmission-on-ruby-princess\" rel=\"nofollow noreferrer\">https://www.rnz.co.nz/news/world/414144/covid-19-waiter-or-food-handler-obvious-point-of-transmission-on-ruby-princess</a></p>\n"
},
{
"answer_id": 23338,
"author": "cpcodes",
"author_id": 19137,
"author_profile": "https://health.stackexchange.com/users/19137",
"pm_score": 1,
"selected": false,
"text": "<p>The short answer is that no one is entirely sure right now (more studies, yadda yadda yadda). But, the consensus seems to be that, with proper precautions, yes, it is safe.</p>\n\n<p>The short of it is that yes, food is a surface like any other. However, hot food likely inactivates the virus, but even cold food should be safe to eat because your mouth and stomach are environments that are inhospitable to most viruses. So, what goes into your mouth will likely not infect you, but you should wash your hands after handling your meal and not touch your face while eating to minimize spread from the food to mucous membranes, open wounds, etc (basically, treating your food as you would any other potentially compromised surface, other than putting it in your mouth - please don't do that with most other surfaces).</p>\n\n<p>While the mouth is a mucous membrane, the exposure from mildly contaminated food should be low enough that your body's normal response will be adequate to prevent infection. Note the \"mildly\", though. Proper food handling techniques should ensure this, but food prepared under questionable conditions would be bets avoided (and not just because of risk of COVID-19 infection).</p>\n\n<p>References:</p>\n\n<p><a href=\"https://www.forbes.com/sites/victoriaforster/2020/03/25/is-eating-takeout-food-safe-during-the-coronavirus-pandemic/#55c0ce912bd1\" rel=\"nofollow noreferrer\">https://www.forbes.com/sites/victoriaforster/2020/03/25/is-eating-takeout-food-safe-during-the-coronavirus-pandemic/#55c0ce912bd1</a></p>\n\n<p><a href=\"https://www.npr.org/sections/health-shots/2020/04/08/822903487/how-safe-is-it-to-eat-take-out\" rel=\"nofollow noreferrer\">https://www.npr.org/sections/health-shots/2020/04/08/822903487/how-safe-is-it-to-eat-take-out</a></p>\n\n<p><a href=\"http://needtoknow.nas.edu/id/infection/encountering-microbes/entering-the-human-host/\" rel=\"nofollow noreferrer\">http://needtoknow.nas.edu/id/infection/encountering-microbes/entering-the-human-host/</a></p>\n"
},
{
"answer_id": 23890,
"author": "Alex I",
"author_id": 2480,
"author_profile": "https://health.stackexchange.com/users/2480",
"pm_score": 3,
"selected": true,
"text": "<p>I would tend to think of coronavirus stability from a biophysics point of view. The virus is a small droplet of water inside a lipid membrane, with some proteins in the membrane and a bunch of proteins+RNA packed inside. It is very sensitive to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132493/\" rel=\"nofollow noreferrer\">Kampf 2020</a> (a) detergents - these dissolve the membrane and presumably cause the contents to spill out, (b) RNA damaging agents (such as UVC) - there is no nucleic acid repair machinery so even a single RNA break is likely to inactivate the virus, and (c) denaturing agents (such as heat) - if enough of the proteins are denatured it would stop being able to get into cells. Alcohol is both a detergent and a denaturing agent (over 60% conc). Note that dehydration does not affect the virus much either way: it is stable in water, but also stable if completely air-dried out: "able to retain viability for 3-5 days in dried form or 7 days in solution at room temperature" <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343644/\" rel=\"nofollow noreferrer\">Chan 2020</a> (probably because enough water is retained to allow it to rehydrate without damaging the structure). It would decay with time, very slowly (days to weeks) and it may also be eaten by bacteria or fungi (that eat anything organic) which may be a much faster process. A meta-analysis of 26 studies that measure inactivation under different conditions is in <a href=\"https://aem.asm.org/content/early/2020/07/13/AEM.01244-20.long\" rel=\"nofollow noreferrer\">Guillier 2020</a>.</p>\n<p>From that perspective, coronavirus in food would be expected to be quite stable at least over a few days to a week. It would only be inactivated by heat, or possibly lipid or protein digesting enzymes. How much heat is not clear, but there is no reason to think the coronavirus proteins are either especially thermally stable or unstable - so as a ballpark enough heat to cook meat, or boil an egg (both involve protein denaturation) would also be enough to denature most coronavirus proteins. A fridge, or especially freezer, would extend the half life considerably (weeks to months; "SARS-CoV-2 in solution ... remained viable for up to 14 days at 4°C" <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343644/\" rel=\"nofollow noreferrer\">Chan 2020</a>). There is very little specific evidence on the stability of any type of coronavirus <em>in food</em> (as opposed to on the surface of packaging, or in water), but what little exists points to persistence for several days, again with much longer times at lower temperatures (eg for MERS-CoV in milk, 37% viable after 72 h at 4°C; this and other studies are reviewed in <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417330/\" rel=\"nofollow noreferrer\">Olaimat 2020</a>).</p>\n<p>Note that cooked food which is contaminated after cooking would be just as problematic as raw food. It would have to be re-heated just before eating to be safe.</p>\n<p>Okay, assuming coronavirus is <em>stable</em> in food: is it possible to get infected by ingestion? Probably yes, or at least it cannot be ruled out: "SARS-CoV-2 spread from staff to food products or food surfaces is conceivable" <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289231/\" rel=\"nofollow noreferrer\">Ceylan 2020</a> and "SARS‐CoV‐2 may also have the potential for foodborne and waterborne transmission" <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7361302/\" rel=\"nofollow noreferrer\">Aboubakr 2020</a>. SARS-CoV-2 often manifests with GI symptoms first, and may infect the GI tract: "there is mounting evidence that SARS-CoV-2 infection also involves the GI tract" <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7184994/\" rel=\"nofollow noreferrer\">Ding 2020</a>; it is excreted in feces <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7130008/\" rel=\"nofollow noreferrer\">Yeo 2020</a> and is present in saliva <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/32298676/\" rel=\"nofollow noreferrer\">Azzi 2020</a>; and the oral route is the primary route for transmission of non-human coronaviruses such as MHV, BCoV, feline enteric coronavirus and others (also from Ding 2020). Even if the oral route is not very effective, it would be quite surprising if SARS-CoV-2 was completely non-infectious orally.</p>\n<p>P.S. Regarding the CDC pages you quote, pay close attention to the wording: "there is no evidence that X" doesn't mean that there is any evidence that X is <em>not true</em> either; it may mean simply that nobody has tried to do an experiment like that and so there is no (direct) evidence either way. Even so, it may be reasonable to think that X is likely to be true because of logic and indirect information (as here).</p>\n<p>P.P.S. Note that most things that inactivate the virus would cause an exponential decay in the amount of viable virus. So "stable for a week" doesn't mean there is 100% active virus at 6 days, and 0% and 8 days; it means that half of it would be inactivated in a week, half of the remainder in two weeks and so forth.</p>\n"
}
] | 2020/04/20 | [
"https://health.stackexchange.com/questions/23320",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19394/"
] |
23,321 | <p>I just heard a viral program on the bbc that corona isn't killed my sunlight. I thought all viruses and bacteria were attenuated an the sun, am i incorrect? </p>
| [
{
"answer_id": 23322,
"author": "Thomas",
"author_id": 19070,
"author_profile": "https://health.stackexchange.com/users/19070",
"pm_score": 2,
"selected": false,
"text": "<p>I'm a bit wary about the word \"all\" when it comes to medicine - what I've found with a quick Google search (GIYF):</p>\n\n<blockquote>\n <p>Under full-spectrum sunlight, all viruses investigated to date have\n been found to undergo endogenous inactivation. Among the viruses\n studied, human adenovirus (HAdV) and MS2 appear to be the most\n resistant whereas poliovirus and somatic phages are particularly\n sensitive. Even for the relatively resistant viruses, however,\n sunlight inactivation via endogenous mechanisms was found to be the\n main inactivation process in clear natural waters.\n Source: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064263/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064263/</a></p>\n</blockquote>\n\n<p>And then...\n\"Fact check: Sunlight does not kill the new coronavirus\"\n<a href=\"https://eu.usatoday.com/story/news/factcheck/2020/03/30/fact-check-sunlight-does-not-kill-new-coronavirus/2931170001/\" rel=\"nofollow noreferrer\">https://eu.usatoday.com/story/news/factcheck/2020/03/30/fact-check-sunlight-does-not-kill-new-coronavirus/2931170001/</a></p>\n\n<p>For SARS:</p>\n\n<blockquote>\n <p>RESULTS: The results showed that SARS coronavirus in the testing\n condition could survive in serum, 1:20 diluted sputum and feces for at\n least 96 h, whereas it could remain alive in urine for at least 72 h\n with a low level of infectivity. The survival abilities on the\n surfaces of eight different materials and in water were quite\n comparable, revealing reduction of infectivity after 72 to 96 h\n exposure. Viruses stayed stable at 4 degrees C, at room temperature\n (20 degrees C) and at 37 degrees C for at least 2 h without remarkable\n change in the infectious ability in cells, but were converted to be\n non-infectious after 90-, 60- and 30-min exposure at 56 degrees C, at\n 67 degrees C and at 75 degrees C, respectively. Irradiation of UV for\n 60 min on the virus in culture medium resulted in the destruction of\n viral infectivity at an undetectable level.\n Source: <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/14631830\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/14631830</a></p>\n</blockquote>\n"
},
{
"answer_id": 23325,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>We don't know yet whether sunlight will inactivate COVID-19.</p>\n\n<blockquote>\n <p>Sunlight contains three types of ultraviolet light — UVA, which tans your skin (and ages it) and can cause eye damage; UVB, which burns and also ages skin; and UVC, which is \"the most harmful one\" because it's quite good at destroying genetic material, explains Juan Leon, a virologist who focuses on environmental health at Emory University. Luckily, he notes, the sun's UVC rays don't reach us because they are filtered out by Earth's atmosphere.</p>\n</blockquote>\n\n<p>but data on SARS suggests it is not inactivated by sunlight</p>\n\n<blockquote>\n <p>\"Right now, there is no data on whether the UVA rays of the sun can inactivate this coronavirus,\" says Leon. However, research on SARS, another coronavirus closely related to the one causing the current pandemic, found that exposing that virus to UVA light for 15 minutes did nothing to reduce its infectivity, Leon says.</p>\n</blockquote>\n\n<p>duration didn't help</p>\n\n<blockquote>\n <p>We determined that greater than 15 min of UVC treatment inactivated the virus while <strong>UVA light had no effect on viability, regardless of duration of exposure.</strong> </p>\n</blockquote>\n\n<p>Inactivation of the coronavirus that induces severe acute respiratory syndrome, SARS-CoV\n<a href=\"https://www.sciencedirect.com/science/article/pii/S016609340400179X\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S016609340400179X</a></p>\n\n<p><a href=\"https://www.npr.org/sections/goatsandsoda/2020/04/17/836830157/coronavirus-faqs-can-sunlight-kill-the-virus-how-risky-is-an-elevator-ride\" rel=\"nofollow noreferrer\">https://www.npr.org/sections/goatsandsoda/2020/04/17/836830157/coronavirus-faqs-can-sunlight-kill-the-virus-how-risky-is-an-elevator-ride</a></p>\n"
}
] | 2020/04/20 | [
"https://health.stackexchange.com/questions/23321",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/14443/"
] |
23,323 | <p>Suppose a person with COVID-19 coughs into a bag. Let the bag sit in the sun for, say, 72 hours -- so as <a href="https://www.health.harvard.edu/diseases-and-conditions/coronavirus-resource-center" rel="nofollow noreferrer">to make the virus inactive</a>.</p>
<p>Could a healthy person breathe in the inactivated virus from the bag (perhaps done multiple times) to (eventually) trigger an antibody response to the virus?</p>
<p>Is this a known way to make <a href="https://www.vaccines.gov/basics/types" rel="nofollow noreferrer">inactivated vaccines</a>? Has it been studied, perhaps for other viruses?</p>
<p>Are there known reasons why this would not work?</p>
| [
{
"answer_id": 23326,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 5,
"selected": true,
"text": "<p>The only approved inhaled vaccine is the flu vaccine delivered intra-nasally. It uses a live attenuated virus. There are a whole list of people who should not receive it because it's a live virus, and it works better for children, but only is 40% effective for adults.</p>\n\n<p>The main issue is</p>\n\n<blockquote>\n <p>The intranasal LAIV, recommended for children above the age of 2 years, induces a broader immune response wherein protection <strong>is not antibody mediated</strong> and probably involves undefined multiple correlates of protection.</p>\n</blockquote>\n\n<p>and that's with a live virus.</p>\n\n<p>How well would a dead inhaled virus work? Well, we have some data from MERS that suggests that vaccination with whole dead virus can increase lung pathology when exposed to live virus.</p>\n\n<blockquote>\n <p>The implication of the current study is that application of an inactivated MERS-CoV vaccine for prevention of MERS in humans may carry a risk for lung immunopathology if subsequently exposed to MERS-CoV. The study also leads us to suggest that the extensive background of preclinical experience with inactivated SARS-CoV vaccines may be applicable to inactivated MERS-CoV vaccines.</p>\n</blockquote>\n\n<p>So, your cheap vaccine may increase your risk of death or disease when exposed to the live virus.</p>\n\n<p>Influenza Vaccination Strategies: Comparing Inactivated and Live Attenuated Influenza Vaccines\n<a href=\"https://www.cdc.gov/flu/prevent/nasalspray.htm\" rel=\"noreferrer\">https://www.cdc.gov/flu/prevent/nasalspray.htm</a></p>\n\n<p>Immunization with inactivated Middle East Respiratory Syndrome coronavirus vaccine leads to lung immunopathology on challenge with live virus\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027702/\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027702/</a></p>\n"
},
{
"answer_id": 24308,
"author": "chongman",
"author_id": 19917,
"author_profile": "https://health.stackexchange.com/users/19917",
"pm_score": 2,
"selected": false,
"text": "<p>It wouldn't be consistent. (as some of the commenters pointed out).</p>\n<p>Here are some numbers:</p>\n<ul>\n<li><p>The concentration of virus in sputum can vary by a factor of 10^5.\n(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224694/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224694/</a> for count of RNA in sputum)</p>\n</li>\n<li><p>Best guess is that 100-1000 RNA copies is a "quanta" in the Wills-Riley Model (<a href=\"http://tinyurl.com/covid-estimator\" rel=\"nofollow noreferrer\">http://tinyurl.com/covid-estimator</a>)</p>\n</li>\n<li><p>If it's known how many RNA copies is good to generate immune response but not disease, it's very hard to get the right level.</p>\n</li>\n<li><p>There will be variation in immune response / disease contracting.</p>\n</li>\n</ul>\n<p>But, this doesn't rule it out as possible. In fact, nothing can prove it's impossible except running every variation of what you're saying. To prove it's possible, you would need to run the controlled experiment.</p>\n<p>But that experiment would be considered unethical.</p>\n<p>You could try it in rats or mice first. But there is no good animal model for COVID19 right now (from what I read).</p>\n"
}
] | 2020/04/20 | [
"https://health.stackexchange.com/questions/23323",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17575/"
] |
23,328 | <p>Why are most people who contract COVID-19 asymptomatic?</p>
<p>Does it mean that they can fight COVID-19 and recover fast?</p>
<p>Does it mean they have a good immune system to fight coronavirus?</p>
| [
{
"answer_id": 23337,
"author": "Polydynamical",
"author_id": 19411,
"author_profile": "https://health.stackexchange.com/users/19411",
"pm_score": 3,
"selected": false,
"text": "<p>The reason why many people who contract COVID-19 are asymptomatic is simple. It is because your immune system can kill the pathogen before you show symptoms. In other words, your body overwhelms the virus before it takes over larger areas of your body.</p>\n\n<p>The answer to your second and third question is yes and no. Most people, that recover quickly without showing symptoms, signifies that they had a good immune system to fight it.</p>\n\n<p>This is the general response to any pathogen that enters your body and is not distinct to COVID-19. Your immune system immediately starts fighting the pathogen off. And if your body is able to find the antibody fast enough, the pathogen will be immobilized and will be restrained from infecting more cells.</p>\n\n<p>My source is these immune system videos:</p>\n\n<p>(1) <em><a href=\"https://www.youtube.com/watch?v=GIJK3dwCWCw\" rel=\"nofollow noreferrer\">Immune System, Part 1: Crash Course A&P #45</a></em></p>\n\n<p>(2) <em><a href=\"https://www.youtube.com/watch?v=2DFN4IBZ3rI\" rel=\"nofollow noreferrer\">Immune System, Part 2: Crash Course A&P #46</a></em></p>\n\n<p>(3) <em><a href=\"https://www.youtube.com/watch?v=rd2cf5hValM\" rel=\"nofollow noreferrer\">Immune System, Part 3: Crash Course A&P #47</a></em></p>\n"
},
{
"answer_id": 23343,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>At this point in time no one can say for sure why many people appear to have asymptomatic infection, and figures range from 20-80% though part of the problem appears to be from false positives in antibody tests. Nevertheless there have been large numbers picked up on rt-PCR who carry the virus but at the time do not show symptoms. Some, if not most, go on to develop symptoms so they are the pre-symptomatic.</p>\n\n<p>We know there's an age distribution so that those under the age of 5, and those over the age of 60 are more likely to have severe disease, and we know women have less severe disease than men.</p>\n\n<p>We also know that also the virus attacks cells via the ACE2 receptor, as one of its attack points, and these are more numerous in the young, and in women. So, one could posit that for any given dose or innoculm of virus, then the higher the dose relative to the number of ACE2 receptors, the worse the disease might be. So, this would explain why it's worse in very young children as they have a smaller body size and fewer cells relative to the inoculum, then as you get older you have the peak number, and then as you age the numbers drop off again so the dose becomes relatively higher.</p>\n\n<p>Then we now know the virus is mutating rapidly and this may explain why symptoms and disease severity may differ rapidly. And even in the same person you may have a number of different mutations present.</p>\n\n<p>And then there are the odd observations that some children have had asymptomatic viral pneumonia picked up on CT scan. So, they're developing lower respiratory tract disease without fever. Fever, muscle aches and pains are often on account of cytokines released during the innate immune response which appears to be highly variable in this disease. Many people who have died go on to develop a highly active innate immune response called a cytokine storm which causes death.</p>\n\n<p>In all the immune response appears to be highly variable, and there are host factors including co-morbities, that influence the disease response as well as mutations in the virus itself.</p>\n\n<p><a href=\"http://publichealth.lacounty.gov/phcommon/public/media/mediapubhpdetail.cfm?prid=2328\" rel=\"noreferrer\">http://publichealth.lacounty.gov/phcommon/public/media/mediapubhpdetail.cfm?prid=2328</a></p>\n\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1\" rel=\"noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1</a></p>\n"
},
{
"answer_id": 23411,
"author": "Twinkle Sheen",
"author_id": 17055,
"author_profile": "https://health.stackexchange.com/users/17055",
"pm_score": 1,
"selected": false,
"text": "<p>Recent studies have reported that about 80% of people infected with SARS-CoV2 are asymptomatic, it means they are \"silent carriers\". These patients show no or very mild symptoms. As it is known that viruses need to get into living cells to divide and survive.\nSame applies with SARS-CoV2, this virus attaches its spike protein present on the outer shell with the human cell's protein receptor, called <a href=\"https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2\" rel=\"nofollow noreferrer\">Angiotensin converting enzyme 2</a> (ACE2). These ACE2 receptors are normally found in the lungs, kidneys, heart and gut.\nAfter getting infected with this virus, it take incubation period of about 14 days for symptoms to arise. Having healthy immune system during this incubation period can reduce the viral load and thus prevent it from entering the lungs.</p>\n\n<p>Our immune system provides us two lines of defense.\nFirst one is <a href=\"https://en.wikipedia.org/wiki/Innate_immune_system\" rel=\"nofollow noreferrer\">innate component</a> including physical barriers such as skin and mucosal membranes, variety of proteins and some of the white blood cells for attacking foreign material. This immune response is non-specific and works fast. The second one is <a href=\"https://en.wikipedia.org/wiki/Innate_immune_system\" rel=\"nofollow noreferrer\">adaptive component</a>. This works slowly but is specific for particular infection and holds memory of infection.</p>\n\n<p>Specific genetic variations in humans might also play role in determining the intensity of sickness. By producing fast adaptive immune response, the body may recognize virus early and work against it. General health also determines the immune response.</p>\n\n<p>If SARS-CoV-2 virus still survives during this entry to the body, it makes entry into lungs via mucosal respiratory tract. There it binds to ACE2 receptors and replicates further, which triggers immune response. The amount of virus which one gets into lungs also determines severity of sickness. </p>\n\n<p>In many patients, the immune response is intense which results in \"cytokine storm\". Cytokines are proteins that act as signals to generate immune response. This can lead to excessive inflammation which can cause organ damage and can be fatal.</p>\n\n<p>(Via:<br>\n<a href=\"https://www.youtube.com/watch?v=UGxgNebx1pg&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=58&t=0s\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=UGxgNebx1pg&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=58&t=0s</a></p>\n\n<p><a href=\"https://www.youtube.com/watch?v=AToF8O5T86s&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=25&t=396s\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=AToF8O5T86s&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=25&t=396s</a></p>\n\n<p><a href=\"https://www.youtube.com/watch?v=qqZYEgREuZ8&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=49&t=274s\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=qqZYEgREuZ8&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=49&t=274s</a></p>\n\n<p><a href=\"https://www.youtube.com/watch?v=1vZDVbqRhyM&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=27&t=0s\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=1vZDVbqRhyM&list=PLQ_IRFkDInv-NvRRUN0aqe51sMs188k8z&index=27&t=0s</a>)</p>\n"
},
{
"answer_id": 25505,
"author": "Peter Bernhard",
"author_id": 21148,
"author_profile": "https://health.stackexchange.com/users/21148",
"pm_score": -1,
"selected": false,
"text": "<p>According to my google searching there is no authority on physiological or immunological reasons for asymptomatic infection with CoV-19, so general principles should apply.</p>\n<p>Individuals may differ in their immune system, but also may differ in their coping with a loss of normal cell function.</p>\n<p>Refering to the immune system:</p>\n<p>People differ genetically in their MHC, major histocompatibility complex. T-cells that kill infected cells to prevent further - symptomatic - spreading are being activated by a signal that is a combination of the specific viral antigen and the individual's specific MHC. That might explain why all - other factors equal - people will have different affinity of their killer t-cells. These t-cells also (as T4-Helper-cells) activate antibody production by B cells which should lead to indivually different patterns of antibody production.</p>\n<p>Compare e.g. <a href=\"https://link.springer.com/chapter/10.1007/978-0-387-39241-7_10\" rel=\"nofollow noreferrer\">https://link.springer.com/chapter/10.1007/978-0-387-39241-7_10</a>\n"By predicting the immunodominant peptides from various common viruses we found that different MHC alleles are expected to provide quite different levels of protection."</p>\n<p>Refering to the functions of normal body cells killed by virus:\nCoV-19 specifically attacks ACE2-cells which not only produce surfactant that enhances breathing but, functioning as stem cells, renew normal lung pneumocytes I. It seems evident that with age and existing diseases people differ in their coping with a loss of a certain amount of this functionality. What's more, infection might be stopped before CoV-19 enters the blood systems and affects different functionality of ACE2-cells that are part not of the lung but of the blood vessel epithelia. There again, people might differ in preexisting diseases.</p>\n<p>Some hint from a beginner's standpoint: any reaction of the immune system, be it innate or adapative, litterally needs at least some infection of cell, thus replication of the virus, thus infectivity, of the virus, to start up the defence mechanisms - as the infection of some cell triggers the defence. Thus, symptomless transmission, surprisingly, appears as the rule, not the exception! You'd need some level of neutralizing antibodies present in your blood,in your lung epithelia, e.g. some recent preinfection leading to antibodies present, to possibly fend off the infection of cells and the "incubative", symptomless infectivity.</p>\n"
}
] | 2020/04/21 | [
"https://health.stackexchange.com/questions/23328",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19399/"
] |
23,345 | <p>Toward the end of the widely read Medium article <a href="https://medium.com/@tomaspueyo/coronavirus-the-hammer-and-the-dance-be9337092b56" rel="nofollow noreferrer">The Hammer and the Dance</a>, the author talks about "the ROI [return on investment] of social distancing". He provides a chart and a table showing the costs and benefits of various social distancing measures, such as banning gatherings of a certain size, closing restaurants, closing schools, etc. But he notes that these illustrations are fake and "all the data is made up" because "nobody has done enough research about this or put together all these measures in a way that can compare them."</p>
<p>Is that really true? It would seem strange if these social distancing techniques are (to epidemiologists) apparently a go-to tool for epidemic suppression, and yet there is no real research on their effectiveness.</p>
<p>What I'm specifically curious about is if there are data or models that try to measure the effects of individual social distancing measures. This could be either for diseases in general, for specific classes of diseases (e.g., viruses spread via respiratory droplets), or for specific diseases (e.g., influenza). Obviously there won't be info for this specific virus due to its novelty but is there anything that would serve as a reasonable starting point?</p>
<p>I'm curious because most places around the world that have implemented some sort of lockdown appear to have taken a "do it all" approach, activating as many kinds of social distancing as they can. This makes sense as an initial emergency response to hit the brakes as hard as possible. However, as different jurisdictions consider lifting some of these restrictions, I don't see a lot in the press about decisions being made based on their relative efficacy. The discussion I see is mostly about things like increasing testing and monitoring the curve of cases to see when it's okay to lift restrictions, but not about how to decide which restrictions to lift. There are some general statements like "large sports events probably won't come back for a long time" but even those aren't really explained. I haven't seen anything like "banning gatherings of more than 10 people will slow the spread X% relative to banning gatherings of more than 50 people" or "reopening schools will be less damaging than reopening restaurants". Is there anything like that?</p>
| [
{
"answer_id": 23346,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Modelling has certainly been done but they operate under assumptions that may not be true.</p>\n\n<p>For example the one done for Singapore:</p>\n\n<blockquote>\n <p><strong>Findings</strong>\n For the baseline scenario, when R0 was 1·5, the median cumulative number of infections at day 80 was 279 000 (IQR 245 000–320 000), corresponding to 7·4% (IQR 6·5–8·5) of the resident population of Singapore. The median number of infections increased with higher infectivity: 727 000 cases (670 000–776 000) when R0 was 2·0, corresponding to 19·3% (17·8–20·6) of the Singaporean population, and 1 207 000 cases (1 164 000–1 249 000) when R0 was 2·5, corresponding to 32% (30·9–33·1) of the Singaporean population. Compared with the baseline scenario, the combined intervention was the most effective, reducing the estimated median number of infections by 99·3% (IQR 92·6–99·9) when R0 was 1·5, by 93·0% (81·5–99·7) when R0 was 2·0, and by 78·2% (59·0 −94·4) when R0 was 2·5. Assuming increasing asymptomatic fractions up to 50·0%, up to 277 000 infections were estimated to occur at day 80 with the combined intervention relative to 1800 for the baseline at R0 of 1·5.</p>\n \n <p><strong>Interpretation</strong>\n Implementing the combined intervention of quarantining infected individuals and their family members, workplace distancing, and school closure once community transmission has been detected could substantially reduce the number of SARS-CoV-2 infections. We therefore recommend immediate deployment of this strategy if local secondary transmission is confirmed within Singapore. However, quarantine and workplace distancing should be prioritised over school closure because at this early stage, symptomatic children have higher withdrawal rates from school than do symptomatic adults from work. At higher asymptomatic proportions, intervention effectiveness might be substantially reduced requiring the need for effective case management and treatments, and preventive measures such as vaccines.</p>\n</blockquote>\n\n<p>but this model is based on an influenza model which is a droplet spread infection but there's increasing suspicion that SARS-CoV-2 can also spread by nuclear droplets (like measles and tuberculosis). And their value of R0 goes up to 2.5 but others are now saying that the true R0 is closer to 5.7. If these are the case, then the social distancing model falls apart as we can't get apart far enough.</p>\n\n<p>Interventions to mitigate early spread of SARS-CoV-2 in Singapore: a modelling study\n<a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30162-6/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30162-6/fulltext</a></p>\n\n<p>High Contagiousness and Rapid Spread of Severe Acute Respiratory Syndrome Coronavirus 2\n<a href=\"https://wwwnc.cdc.gov/eid/article/26/7/20-0282_article\" rel=\"nofollow noreferrer\">https://wwwnc.cdc.gov/eid/article/26/7/20-0282_article</a></p>\n"
},
{
"answer_id": 23379,
"author": "D.Tan",
"author_id": 13163,
"author_profile": "https://health.stackexchange.com/users/13163",
"pm_score": 1,
"selected": false,
"text": "<p>3Blue1Brown made a great video (<a href=\"https://www.youtube.com/watch?v=gxAaO2rsdIs\" rel=\"nofollow noreferrer\">Simulating an Epidemic</a>) showcasing the effects of tweaking various parameters on outbreaks using simulations.</p>\n\n<p><strong>Background</strong>:</p>\n\n<p>His simulation is based on the <a href=\"https://www.maa.org/press/periodicals/loci/joma/the-sir-model-for-spread-of-disease-the-differential-equation-model\" rel=\"nofollow noreferrer\">SIR model</a>, which categorizes a population into people <strong>S</strong>usceptible to the disease, people <strong>I</strong>nfected with the disease, and people <strong>R</strong>ecovered from the disease. For every unit of time a susceptible person spends within the infectious radius of an infected person, the suspectible person will have some probability of contracting the disease. After a certain number of time, an infected person will recover (or be removed) and will not be able to spread the disease.</p>\n\n<p><strong>Findings</strong>:\nThe 5 main takeaways from the video are</p>\n\n<ol>\n<li>The growth rate of new cases is sensitive to # of daily interactions, probability of infection (e.g. better hygiene) and duration of infection [4:41]</li>\n<li>Changes in how many people are tested (and quarantined) cause disproportionately large changes to the total number of people infected [9:06]</li>\n<li>Social distancing slows the spread of infection, but even small imperfections prolongs it [12:54]</li>\n<li>Reducing contact between communities, late in an outbreak, has a limited effect [14:00]</li>\n<li>Shared central locations (e.g. grocery store) dramatically speed up the spread [17:42]</li>\n</ol>\n\n<p><strong>Disclaimer</strong>:</p>\n\n<p>3Blue1Brown notes that his simulations are toy models and uses a small population-size, so his findings are not necessarily generalizable to real-world examples.</p>\n\n<p>Here is a fan-made interactive simulation based on the same video:\n<a href=\"https://prajwalsouza.github.io/Experiments/Epidemic-Simulation.html\" rel=\"nofollow noreferrer\">https://prajwalsouza.github.io/Experiments/Epidemic-Simulation.html</a> </p>\n"
}
] | 2020/04/22 | [
"https://health.stackexchange.com/questions/23345",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17847/"
] |
23,367 | <p>I am not sure if this is the right question in this forum, but since it pertains to medical symptoms usually encountered in patients affected by COVID-19, I am asking this question here. </p>
<p>Why in COVID-19 do (some) patients have "dry cough" and not "wet cough" as a symptom. I ask this because pertussis disease generally called "whooping cough" has symptoms such as runny nose, sneezing etc. (opposite to that of COVID-19) and is contagious as well spread through respiratory droplets (same as that of COVID-19). Can we make suitable comparisons between the two to understand the differences in symptoms or they are entirely different cases?</p>
| [
{
"answer_id": 23368,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": true,
"text": "<p>I'm not sure "rather" is the right word here, but the early studies showed dry cough as a more frequent correlate of Covid-19 positive PCR tests compared to wet cough, <a href=\"https://www.webmd.com/lung/covid-19-symptoms#1\" rel=\"nofollow noreferrer\">according to WebMD</a>:</p>\n<blockquote>\n<p>Early studies have found that at least 60% of people with COVID-19 have a dry cough. About a third have a cough with mucus, called a “wet” or “productive” cough.</p>\n</blockquote>\n<p>(Someone can perhaps dig up those studies, WebMD doesn't link to them.)</p>\n<p>The Guardian likewise <a href=\"https://www.theguardian.com/world/2020/apr/17/what-is-coronavirus-what-are-its-symptoms-and-when-should-i-call-a-doctor\" rel=\"nofollow noreferrer\">noted</a></p>\n<blockquote>\n<p>According to the WHO, the <strong>most common symptoms</strong> of Covid-19 are fever, tiredness and a dry cough. Some patients may also have a runny nose, sore throat, nasal congestion and aches and pains or diarrhoea. Some people report losing their sense of taste and/or smell.</p>\n</blockquote>\n<p>(Emphasis mine.) That doesn't mean there aren't less common symptoms, although admittedly the mass media usually doesn't seem to mention those less common ones.</p>\n<p>Healthline posted <a href=\"https://www.healthline.com/health-news/5-covid-19-myths#Myth-1:-COVID-19-is-just-another-flu\" rel=\"nofollow noreferrer\">this interview</a> with an expert, which hopefully is correct with respect to the timing of the cough type relative to Covid-19 progression:</p>\n<blockquote>\n<p>Dr. Bruce E. Hirsch, attending physician and assistant professor in the Infectious Disease Division of Northwell Health in New York, said there is some overlap between COVID-19 and other diseases caused by viral infections.</p>\n<p>“Differences between coronavirus and influenza and more common viruses still in circulation are that we know that <strong>the coronavirus binds to receptors in the lower part of the airways, and that accounts for the fact that so frequently, but not always, dry cough</strong> along with fever and fatigue are three of the symptoms that are <strong>most commonly associated with COVID-19</strong>,” Hirsch told Healthline.</p>\n<p>While dry cough, fever, and fatigue can occur with other viral infections, he said muscle aches and pains are distinct signs of the flu, while the common cold may bring on with a runny nose, sore throat, or sneezing.</p>\n<p>“Having a runny nose is not expected with COVID-19 infection. Having muscle aches and pains is much more common with influenza. <strong>Having a productive cough, coughing up phlegm, can occur with COVID-19 infections, particularly late on, but it’s not typical with what the early course is,</strong>” said Hirsch.</p>\n</blockquote>\n<p>Although again, no detailed studies are liked/mentioned.</p>\n"
},
{
"answer_id": 23371,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<blockquote>\n <p>Ciliated epithelium lines the human respiratory tract from the posterior third of the nose to the bronchioles.</p>\n</blockquote>\n\n<p>But the major part of the lung involved is distal to the bronchioles so there's no mechanism to move fluid to the mouth at this level. Hence, the cough is dry.</p>\n\n<p><strong>Update 25 April 2020</strong></p>\n\n<p>It has been previously stated in the literature that it is the type 2 alveolar cells or pneumocytes that carry ACE2 allowing them to be infected. But we now have a paper that describes ACE2 expression by ciliated cells, with the highest concentration carried by nasal epithelial cells including ciliated and goblet cells. Those these levels of expression are not as high as in the aleolar cells but does explain why we get positive nasopharyngeal swabs</p>\n\n<blockquote>\n <p>In this study, we explored multiple scRNA-seq datasets generated within the HCA\n consortium, and found that SARS-CoV-2 entry receptor ACE2 is more highly expressed (and co-expressed with viral entry-associated protease TMPRSS2) in nasal epithelial cells, specifically goblet and ciliated cells. This finding implicates these cells as loci of original infection and possible reservoirs for dissemination within a given patient and from person\n to person.</p>\n</blockquote>\n\n<p><a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/ciliated-epithelium\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/topics/medicine-and-dentistry/ciliated-epithelium</a></p>\n\n<p><a href=\"https://arxiv.org/ftp/arxiv/papers/2003/2003.06122.pdf\" rel=\"nofollow noreferrer\">https://arxiv.org/ftp/arxiv/papers/2003/2003.06122.pdf</a></p>\n"
}
] | 2020/04/23 | [
"https://health.stackexchange.com/questions/23367",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19099/"
] |
23,370 | <p>In the public and scientific discourse, there seems to be establishing a consensus that -contrary to flu epidemics- the role of children and schools in the covid-19 epidemic is small. <strong>On what research does this consensus rely?</strong></p>
<p>I found a <a href="https://www.reuters.com/article/us-health-coronavirus-schools/school-closures-will-have-little-impact-on-covid-19-control-review-finds-idUSKBN21O32E?fbclid=IwAR2gqQsDBILK8TMrWZt6WFFIeT0qIrA9HWfrXa--zYZ51GJhwgvURInFI2w" rel="nofollow noreferrer">reference to a study</a> on the 2003 SARS outbreak (also a coronavirus) which couldn't find an impact of school closures on the evolution of that epidemic.</p>
<p>There are <a href="https://www.theguardian.com/world/2020/apr/21/boy-with-covid-19-did-not-transmit-disease-to-more-than-170-contacts?fbclid=IwAR1x-QmfKw_iEduJwD9IqPDs05SIvqWOjq59G5zYPHRY7eNCoWCbxgmnUxQ" rel="nofollow noreferrer">anecdotal stories</a> about children who are infected and do not transmit the disease very easily.</p>
<p>Children do not feature heavily in <a href="https://www.statista.com/statistics/1102730/south-korea-coronavirus-cases-by-age/?fbclid=IwAR2gqQsDBILK8TMrWZt6WFFIeT0qIrA9HWfrXa--zYZ51GJhwgvURInFI2w" rel="nofollow noreferrer">the age-breakdown of people having tested positive for covid-19</a> or who tested positive for antibodies.</p>
<p>I can imagine researchers are mostly emboldened from that age-breakdown that I just mentioned, but what about the countering hypotheses that...</p>
<p>"many children who are positive for either covid-19 or its antibodies test negative because their bodies so easily overcome the disease (yielding both low virus concentrations throughout all stages of the disease and yielding low antibody concentration afterwards -> low concentrations are difficult to detect in a test)"</p>
<p>"Children may overcome the disease relatively quickly and unharmed, but in a society where the schools are not closed they interact so intensely with a large number of people that -despite their fast recovery- they still contribute a great deal to the overall R0 of that epidemic."</p>
| [
{
"answer_id": 23382,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
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"text": "<p>In the scientific discourse around Covid-19, I haven't seen statements that \"the role of children and schools in the covid-19 epidemic is small\". What I've seen is statements that \"the role of children and schools <em>alone</em> in the Covid-19 epidemic is small\", that is, closing schools <em>alone</em> will have little impact on the spread of the disease.</p>\n\n<p>In order to keep person A from infecting person B, you need to break <em>all</em> possible transmission links between the two people. It's very rare for two people whose children attend the same school to have that as the only transmission route between them. Odds are, they'll also shop at the same stores, attend the same church, eat at the same restaurants, and so on, all of which also provide potential transmission routes.</p>\n\n<p>Unfortunately, the word \"alone\" tends to get dropped when moving from scientific discourse to public discourse, giving the impression that re-opening schools is a low-risk activity. In actual practice, schools are a highly effective transmission route for most diseases, especially those with airborne or aerosol transmission.</p>\n"
},
{
"answer_id": 23644,
"author": "Marcus D",
"author_id": 19626,
"author_profile": "https://health.stackexchange.com/users/19626",
"pm_score": 0,
"selected": false,
"text": "<p>There is a <a href=\"https://www.thelancet.com/journals/lanchi/article/PIIS2352-4642(20)30095-X/fulltext\" rel=\"nofollow noreferrer\">recent (April 2020) article from the Lancet</a> which reviews school closures data for both SARS and Covid-19. Partial summary is quoted here.</p>\n\n<blockquote>\n <p>Modelling studies of SARS produced conflicting results. Recent modelling studies of COVID-19 predict that school closures alone would prevent only 2–4% of deaths, much less than other social distancing interventions. </p>\n</blockquote>\n"
},
{
"answer_id": 24309,
"author": "chongman",
"author_id": 19917,
"author_profile": "https://health.stackexchange.com/users/19917",
"pm_score": 0,
"selected": false,
"text": "<p>This is what the AAP (pediatrics) also said about viral infection for young people.</p>\n<p><a href=\"https://services.aap.org/en/pages/2019-novel-coronavirus-covid-19-infections/clinical-guidance/covid-19-planning-considerations-return-to-in-person-education-in-schools/\" rel=\"nofollow noreferrer\">https://services.aap.org/en/pages/2019-novel-coronavirus-covid-19-infections/clinical-guidance/covid-19-planning-considerations-return-to-in-person-education-in-schools/</a></p>\n<blockquote>\n<p>In Pre-K, the relative impact of physical distancing among children is likely small based on current evidence and certainly difficult to implement. Therefore, Pre-K should focus on more effective risk mitigation strategies for this population.</p>\n</blockquote>\n<p>However, the middle school case in Israel (and some elementary school infections), gives pause.</p>\n<p><a href=\"https://www.thedailybeast.com/israeli-data-show-school-openings-were-a-disaster-that-wiped-out-lockdown-gains\" rel=\"nofollow noreferrer\">https://www.thedailybeast.com/israeli-data-show-school-openings-were-a-disaster-that-wiped-out-lockdown-gains</a>\n<a href=\"https://www.haaretz.com/us-news/.premium-america-wants-to-reopen-schools-here-s-how-to-learn-from-israel-s-mistakes-1.9006697\" rel=\"nofollow noreferrer\">https://www.haaretz.com/us-news/.premium-america-wants-to-reopen-schools-here-s-how-to-learn-from-israel-s-mistakes-1.9006697</a></p>\n<p>In my blog, I mostly cover the science communication and planning side: <a href=\"http://ppeoptionsforschools.wordpress.com\" rel=\"nofollow noreferrer\">http://ppeoptionsforschools.wordpress.com</a></p>\n<p>But I do point to some references.</p>\n<h2>Exposure Bias</h2>\n<p>One of the biggest problems with the K-5 kids is that there may be selection bias, something I call <code>exposure bias</code>. Adults have many more contacts a day (say 30-100) and with random different people. K-5 may only contact their family. And, their family may try to limit their exposure to other people to protect them.</p>\n<h2>Google comes up with a lot of reports</h2>\n<p><a href=\"https://www.google.com/search?q=prevalence+infection+young+children+covid+19+by+country\" rel=\"nofollow noreferrer\">https://www.google.com/search?q=prevalence+infection+young+children+covid+19+by+country</a></p>\n<p>The CDC says confirmed cases in kids is low:</p>\n<blockquote>\n<p>In the United States, 2% of confirmed cases of COVID-19 were among persons aged <18 years.4\nIn China, 2.2% of confirmed cases of COVID-19 were among persons aged <19 years old.1\nIn Italy, 1.2% of COVID-19 cases were among children aged <18 years.2\nIn Spain, 0.8% of confirmed cases of COVID-19 were among persons aged < 18 years.5</p>\n</blockquote>\n<p>(<a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/pediatric-hcp.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/hcp/pediatric-hcp.html</a>)</p>\n"
}
] | 2020/04/23 | [
"https://health.stackexchange.com/questions/23370",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17835/"
] |
23,387 | <p>Walking around town I see quite a few people wearing gloves in addition to a mask. But is this actually useful? COVID-19 does not transmit via the skin, so you don't need to protect your hands per se. And you can still touch your face even if you're wearing gloves. Is there any research showing that gloves help against respiratory diseases?</p>
| [
{
"answer_id": 23382,
"author": "Mark",
"author_id": 333,
"author_profile": "https://health.stackexchange.com/users/333",
"pm_score": 2,
"selected": false,
"text": "<p>In the scientific discourse around Covid-19, I haven't seen statements that \"the role of children and schools in the covid-19 epidemic is small\". What I've seen is statements that \"the role of children and schools <em>alone</em> in the Covid-19 epidemic is small\", that is, closing schools <em>alone</em> will have little impact on the spread of the disease.</p>\n\n<p>In order to keep person A from infecting person B, you need to break <em>all</em> possible transmission links between the two people. It's very rare for two people whose children attend the same school to have that as the only transmission route between them. Odds are, they'll also shop at the same stores, attend the same church, eat at the same restaurants, and so on, all of which also provide potential transmission routes.</p>\n\n<p>Unfortunately, the word \"alone\" tends to get dropped when moving from scientific discourse to public discourse, giving the impression that re-opening schools is a low-risk activity. In actual practice, schools are a highly effective transmission route for most diseases, especially those with airborne or aerosol transmission.</p>\n"
},
{
"answer_id": 23644,
"author": "Marcus D",
"author_id": 19626,
"author_profile": "https://health.stackexchange.com/users/19626",
"pm_score": 0,
"selected": false,
"text": "<p>There is a <a href=\"https://www.thelancet.com/journals/lanchi/article/PIIS2352-4642(20)30095-X/fulltext\" rel=\"nofollow noreferrer\">recent (April 2020) article from the Lancet</a> which reviews school closures data for both SARS and Covid-19. Partial summary is quoted here.</p>\n\n<blockquote>\n <p>Modelling studies of SARS produced conflicting results. Recent modelling studies of COVID-19 predict that school closures alone would prevent only 2–4% of deaths, much less than other social distancing interventions. </p>\n</blockquote>\n"
},
{
"answer_id": 24309,
"author": "chongman",
"author_id": 19917,
"author_profile": "https://health.stackexchange.com/users/19917",
"pm_score": 0,
"selected": false,
"text": "<p>This is what the AAP (pediatrics) also said about viral infection for young people.</p>\n<p><a href=\"https://services.aap.org/en/pages/2019-novel-coronavirus-covid-19-infections/clinical-guidance/covid-19-planning-considerations-return-to-in-person-education-in-schools/\" rel=\"nofollow noreferrer\">https://services.aap.org/en/pages/2019-novel-coronavirus-covid-19-infections/clinical-guidance/covid-19-planning-considerations-return-to-in-person-education-in-schools/</a></p>\n<blockquote>\n<p>In Pre-K, the relative impact of physical distancing among children is likely small based on current evidence and certainly difficult to implement. Therefore, Pre-K should focus on more effective risk mitigation strategies for this population.</p>\n</blockquote>\n<p>However, the middle school case in Israel (and some elementary school infections), gives pause.</p>\n<p><a href=\"https://www.thedailybeast.com/israeli-data-show-school-openings-were-a-disaster-that-wiped-out-lockdown-gains\" rel=\"nofollow noreferrer\">https://www.thedailybeast.com/israeli-data-show-school-openings-were-a-disaster-that-wiped-out-lockdown-gains</a>\n<a href=\"https://www.haaretz.com/us-news/.premium-america-wants-to-reopen-schools-here-s-how-to-learn-from-israel-s-mistakes-1.9006697\" rel=\"nofollow noreferrer\">https://www.haaretz.com/us-news/.premium-america-wants-to-reopen-schools-here-s-how-to-learn-from-israel-s-mistakes-1.9006697</a></p>\n<p>In my blog, I mostly cover the science communication and planning side: <a href=\"http://ppeoptionsforschools.wordpress.com\" rel=\"nofollow noreferrer\">http://ppeoptionsforschools.wordpress.com</a></p>\n<p>But I do point to some references.</p>\n<h2>Exposure Bias</h2>\n<p>One of the biggest problems with the K-5 kids is that there may be selection bias, something I call <code>exposure bias</code>. Adults have many more contacts a day (say 30-100) and with random different people. K-5 may only contact their family. And, their family may try to limit their exposure to other people to protect them.</p>\n<h2>Google comes up with a lot of reports</h2>\n<p><a href=\"https://www.google.com/search?q=prevalence+infection+young+children+covid+19+by+country\" rel=\"nofollow noreferrer\">https://www.google.com/search?q=prevalence+infection+young+children+covid+19+by+country</a></p>\n<p>The CDC says confirmed cases in kids is low:</p>\n<blockquote>\n<p>In the United States, 2% of confirmed cases of COVID-19 were among persons aged <18 years.4\nIn China, 2.2% of confirmed cases of COVID-19 were among persons aged <19 years old.1\nIn Italy, 1.2% of COVID-19 cases were among children aged <18 years.2\nIn Spain, 0.8% of confirmed cases of COVID-19 were among persons aged < 18 years.5</p>\n</blockquote>\n<p>(<a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/pediatric-hcp.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/hcp/pediatric-hcp.html</a>)</p>\n"
}
] | 2020/04/24 | [
"https://health.stackexchange.com/questions/23387",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/7314/"
] |
23,397 | <p>According to several sources, <a href="https://www.cnbc.com/2020/04/22/no-lockdown-in-sweden-but-stockholm-could-see-herd-immunity-in-weeks.html" rel="nofollow noreferrer">models estimate 20% of people in Stockholm are already immune to COVID-19</a> (2014-04-22). However, <a href="https://www.deutschlandfunk.de/covid-19-was-hilft-im-kampf-gegen-das-coronavirus.1939.de.html" rel="nofollow noreferrer">German virologists estimate</a> (2020-04-19) that to reach herd immunity in Germany without overwhelming the healthcare system would take around a year. Stockholm has not seen the overwhelming of the healthcare system that cities like Bergamo or New York City have seen. How could Stockholm be already close to herd immunity without overwhelming the healthcare system, when the situation is so different in Germany (estimated to take a year, higher number of intensive care units per capita than most other countries), Bergamo or New York (overwhelmed healthcare system)?</p>
<p>See also: <a href="https://www.bbc.com/news/world-europe-52395866" rel="nofollow noreferrer">Coronavirus: Has Sweden got it right?</a>, BBC News, 2020-04-25, which doesn't really answer this question specifically.</p>
| [
{
"answer_id": 23399,
"author": "Charles E. Grant",
"author_id": 18010,
"author_profile": "https://health.stackexchange.com/users/18010",
"pm_score": 3,
"selected": false,
"text": "<p>The level at which herd immunity is achieved varies with the communicability of the disease. <a href=\"https://en.wikipedia.org/wiki/Herd_immunity#Mechanics\" rel=\"noreferrer\">The standard rule of thumb is that the percentage of the population that has to be immune is p<sub>c</sub> = (1 - 1 / R<sub>0</sub>)</a>. The value of R<sub>0</sub> for SARS-CoV-2 is not known precisely, but is thought to be between 1.4 and 3.9. This means that herd immunity would be achieved at somewhere between 29%-74% of the population. So we don't actually know if Stockholm is near herd immunity or not. In fact, if you read the details of the article you link to, Tegnell, the Swedish chief epidemiologist, says that herd immunity is achievable in a \"few weeks time\". So the statement that Stockholm is close may depend on what your your definition of close is.</p>\n\n<p>The article you link to also points out that Swedens death toll is double that of nearby Denmark and Finland. <a href=\"https://www.theguardian.com/world/2020/mar/23/swedish-pm-warned-russian-roulette-covid-19-strategy-herd-immunity\" rel=\"noreferrer\">The Swedish policy is controversial and other virologists and epidemiologists fear they could rapidly move into an NYC/Italy/Spain style outbreak</a>.</p>\n\n<p>It may also be worth noting that German has 8 times the population of Sweden, so they'd probably have to move towards herd immunity at a lower rate than Sweden to avoid overtaxing the medical system.</p>\n"
},
{
"answer_id": 23409,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 2,
"selected": false,
"text": "<p>The BBC <a href=\"https://www.bbc.com/news/world-europe-52395866\" rel=\"nofollow noreferrer\">has</a> some clarifications now (Apr 25):</p>\n<blockquote>\n<p>A public health agency report this week suggested around a third of people <strong>in Stockholm will have been infected by the start of May</strong>.</p>\n<p>That was later <strong>revised down to 26% after the agency admitted a calculation error.</strong> But several high-profile scientists have offered even greater numbers.</p>\n<p>Prof Johan Giesecke, ex-chief scientist of the European Centre for Disease Prevention and Control (ECDC), believes at least half of all Stockholmers will have caught the virus by the end of the month.</p>\n<p>It could even be up to half the population of Sweden, suggests Stockholm University mathematician Tom Britton.</p>\n</blockquote>\n<p>So yeah, the [revised] official projection is 26% have been infected in Stockholm by May 1st or so. Whether that is or isn't "close to herd immunity" depends on additional assumptions as nicely explained in Charles' answer.</p>\n<p>I've managed to <a href=\"https://www.folkhalsomyndigheten.se/nyheter-och-press/nyhetsarkiv/2020/april/uppdaterad-modellering-av-spridningen-av-covid-19-i-stockholms-lan/\" rel=\"nofollow noreferrer\">find that report</a>, or at least an announcement thereof [with the correction] but it's in Swedish. Via Google translate, the most detail I could gather is:</p>\n<blockquote>\n<p>The model that has been used is adapted to the number of reported cases of covid-19 between 17 February and 10 April 2020, and to results from the survey conducted in Stockholm to measure the current occurrence of covid-19 in society.</p>\n</blockquote>\n<p>Which links to <a href=\"https://www.folkhalsomyndigheten.se/nyheter-och-press/nyhetsarkiv/2020/april/rapport-fran-undersokning-av-forekomsten-av-covid-19-i-region-stockholm/\" rel=\"nofollow noreferrer\">another page in Swedish</a> for the survey informing their model. It seems to me they've used random/stratified sampling for this survey; again via google translate:</p>\n<blockquote>\n<p>The survey included 738 invited participants aged 2 to 86 who performed self-sampling at home and reported any symptoms via a survey. The samples and survey responses were collected between March 26 and April 3.</p>\n<p>The report contains details on the conduct of the study as well as the results regarding the occurrence of covid-19 and the symptoms reported.</p>\n<p>Overall, <strong>2.5 percent of participants tested positive for the SARS-CoV-2 virus</strong>. All of them reported some form of symptoms. In this study, the number of positives was too low to calculate any statistically significant difference in symptoms between participants who were positive and negative, respectively.</p>\n<p>The symptoms could be very mild.</p>\n</blockquote>\n<p>Alas I couldn't find the actual model/publication that details the progression from that 2.5% positive tests in the start-of-April survey to 26% projected as infected by start of May. Perhaps someone who speaks Swedish has better luck in that regard (finding the actual model/publication).</p>\n<hr />\n<p>Related (as to why their health system wasn't overwhelmed): Sweden has increased its ICU capacity. It looks like if they had held it constant to the pre-Covid-19 level, their ICU capacity would have been overwhelmed already. Quoting an <a href=\"https://skeptics.stackexchange.com/a/47461/29579\">answer from Skeptics</a>, which does have links/references, but they are in Swedish:</p>\n<blockquote>\n<p>[...] According to Socialstyrelsen (the government agency in charge of the health care system), the intensive care capacity of regular hospitals has slightly more than doubled: <strong>From 526 places before the crisis to 1131 places as of April 24. Source: Socialstyrelsen. Of those places, 533 are currently used for patients with Covid-19.</strong></p>\n<p>Note that this does not include the capacity from military tent hospitals that are not yet in use. The number of ICU places with ventilators they will have is unclear, but appears to be around 50-100 in total according to media reports [...].</p>\n</blockquote>\n<hr />\n<p>Also (if the UK experience is any indicator), the ICUs not being overwhelmed might not be the "end of story". A lot of extra/unexplained deaths can happen without them ever going to the ICU, particularly among the elderly:</p>\n<p><a href=\"https://i.stack.imgur.com/35bkV.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/35bkV.png\" alt=\"enter image description here\" /></a></p>\n<p>According <a href=\"https://www.theguardian.com/world/2020/apr/05/sweden-prepares-to-tighten-coronavirus-measures-as-death-toll-climbs\" rel=\"nofollow noreferrer\">to the Guardian (Apr 5)</a>:</p>\n<blockquote>\n<p>One third of Stockholm’s nursing homes are affected [by Covid-19].</p>\n</blockquote>\n<p>Giesecke said in one of his interviews (I think in <a href=\"https://www.youtube.com/watch?v=bfN2JWifLCY&feature=youtu.be&t=811\" rel=\"nofollow noreferrer\">this one</a>, but I'm not going to re-watch it to find the exact timestamp) that Swedish nursing homes are (individually) larger than in neighboring countries, which he used to explain the larger death toll in them... meaning that the virus can spread in a larger population once someone in such a [larger] nursing home is infected.</p>\n"
}
] | 2020/04/24 | [
"https://health.stackexchange.com/questions/23397",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/5401/"
] |
23,432 | <p>COVID-19 pandemic started because <strong>1 person</strong> had the virus, and then it spread to a lot of others.</p>
<p>Now, let's say your country imposed quarantine and distancing, and you managed to halt the growth of the virus entirely.</p>
<p>Ok, great. But eventually you have to re-open the country again. And when you do, won't the virus just start spreading again?</p>
<p>I mean, it's not like the quarantine has killed the virus entirely. It still exists, it's just not spreading as quickly. So won't it just start spreading fast once you re-open the country?</p>
| [
{
"answer_id": 23434,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
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"text": "<p><a href=\"https://edition.cnn.com/2020/03/12/world/coronavirus-covid-19-update-intl-hnk/index.html\" rel=\"nofollow noreferrer\">China</a> and <a href=\"https://www.reuters.com/article/us-health-coronavirus-newzealand/new-zealand-orders-quarantine-for-returning-citizens-in-coronavirus-battle-idUSKCN21R0D4\" rel=\"nofollow noreferrer\">New Zealand</a> are quarantining all returning citizens for 14 days.</p>\n\n<p>That could be beefed up by antibody testing and rt-PCR if those become readily available.</p>\n\n<p>That should halt the importation of the virus. And continued social distancing may be necessary for a couple of years yet.</p>\n\n<p>NZ is on target to <strong>completely eliminate the virus</strong> with no new cases for some days now, current cases no longer considered infectious and the only risk being from imported cases.</p>\n\n<p><a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31097-7/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31097-7/fulltext</a></p>\n"
},
{
"answer_id": 23768,
"author": "Charles E. Grant",
"author_id": 18010,
"author_profile": "https://health.stackexchange.com/users/18010",
"pm_score": 2,
"selected": false,
"text": "<p>The virus has actually continued to spread during the lockdowns, just at a slower pace than if no lockdown had been imposed. See for example <a href=\"https://www.doh.wa.gov/Emergencies/NovelCoronavirusOutbreak2020COVID19/DataDashboard\" rel=\"nofollow noreferrer\">Washington state in the USA</a>.</p>\n\n<p>The hope is that the lockdowns have reduced the spread of infections to <a href=\"https://en.wikipedia.org/wiki/Exponential_growth\" rel=\"nofollow noreferrer\">linear or sub-linear rather than exponential growth</a>. Linear or sub-linear growth provides an opportunity for other measures to be effective, like wide spread testing followed by <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/php/open-america/contact-tracing-resources.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-ncov%2Fphp%2Fopen-america%2Fcontact-tracing.html\" rel=\"nofollow noreferrer\">contact tracing</a>. If test and trace works, this would allow quarantine of only those who actually have the virus, or are known to have been exposed, rather than asking that <em>everyone</em> stay in lockdown preemptively.</p>\n\n<p><a href=\"https://www.cnn.com/2020/04/16/world/coronavirus-response-lessons-learned-intl/index.html\" rel=\"nofollow noreferrer\">It is argued that extensive contact tracing followed by targeted quarantine is what has allowed Germany, Taiwan, and South Korea</a> to avoid the massive outbreaks seen in Italy, Spain, and the Americas. However, if the number of new infections was doubling every few days, no testing and tracing system would be able to keep up.</p>\n"
}
] | 2020/04/26 | [
"https://health.stackexchange.com/questions/23432",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19464/"
] |
23,445 | <p>I understand that Omega-3 oils have anti-inflammatory properties.</p>
<p>At high daily dose (say 5 grams) could they reduce the dangerous COVID-19 related pneumonia seen in some patients?</p>
<p>I guess one would have to be careful of bleeding problems if the dose is too high.</p>
| [
{
"answer_id": 23447,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 0,
"selected": false,
"text": "<p>Here is Oregon State, Linus Pauling Institute. Immunity In Brief. They begin with Omega 3 to help reduce inflammation. I don’t think they give a dose, I don’t remember. Personally I would follow the label directions which are going to tell you to consult your doctor before taking if you are on medications, (and I would say particularly for a dose of 5 grams. ). <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a> If you are 60 or over, or have some other problem, then I think it would be even more important to consult your doctor first. <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a></p>\n\n<p>Remember Vitamin E and A can give some “thinning” and so can many herbal products. And obviously one must take into account other OTC products like aspirin and other NSAIDs. </p>\n\n<p>This just addresses Immunity in Brief according to the above article and not whether this will help prevent pneumonia in association with COVID 19, since the FDA is very strict on supplements being touted for COVID19. </p>\n\n<p>Bottom line: consult your doctor first. They know your medical history.</p>\n\n<p>PS to be more specific the OSU article says, “EPA and DHA have an overall anti-inflammatory effect.” see the link. </p>\n"
},
{
"answer_id": 23451,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>A very recent Cochrane review of the use of Omega 3 in ARDS, not specifically from COVID-19, did not find any benefit using trials up to 2018.</p>\n\n<blockquote>\n <p><strong>Conclusions</strong>: This Cochrane meta-analysis of 10 studies of varying quality examined the effects of omega-3 fatty acids and antioxidants in adults with ARDS. This intervention may produce little or no difference in all-cause mortality between groups. We are uncertain whether immunonutrition with omega-3 fatty acids and antioxidants improves ventilator days, ICU length of stay, or oxygenation due to the very low quality of evidence.</p>\n</blockquote>\n\n<p>Immunonutrition for Adults With ARDS: Results From a Cochrane Systematic Review and Meta-Analysis\n<a href=\"https://pubmed.ncbi.nlm.nih.gov/31506339/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/31506339/</a></p>\n"
}
] | 2020/04/27 | [
"https://health.stackexchange.com/questions/23445",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/-1/"
] |
23,446 | <p>Right now (April 27), the JHU data on new COVID-19 cases in the US show a very distinct weekly rhythm; reports are lowest on the weekends and peak in mid-week. This isn't at all surprising — any number of social factors would contribute to lower reporting on weekends — but the fact that it's not flat across mid-week is a little surprising to me, and I've seen too many people (albeit few experts) taking weekend dips as signs that things are on the downswing. Has this variance been studied in other medical reporting and is it worth compensating for or smoothing in situations like this where decisions are (rightly or wrongly) sometimes being made on a literal day-by-day basis?</p>
| [
{
"answer_id": 23447,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 0,
"selected": false,
"text": "<p>Here is Oregon State, Linus Pauling Institute. Immunity In Brief. They begin with Omega 3 to help reduce inflammation. I don’t think they give a dose, I don’t remember. Personally I would follow the label directions which are going to tell you to consult your doctor before taking if you are on medications, (and I would say particularly for a dose of 5 grams. ). <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a> If you are 60 or over, or have some other problem, then I think it would be even more important to consult your doctor first. <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a></p>\n\n<p>Remember Vitamin E and A can give some “thinning” and so can many herbal products. And obviously one must take into account other OTC products like aspirin and other NSAIDs. </p>\n\n<p>This just addresses Immunity in Brief according to the above article and not whether this will help prevent pneumonia in association with COVID 19, since the FDA is very strict on supplements being touted for COVID19. </p>\n\n<p>Bottom line: consult your doctor first. They know your medical history.</p>\n\n<p>PS to be more specific the OSU article says, “EPA and DHA have an overall anti-inflammatory effect.” see the link. </p>\n"
},
{
"answer_id": 23451,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>A very recent Cochrane review of the use of Omega 3 in ARDS, not specifically from COVID-19, did not find any benefit using trials up to 2018.</p>\n\n<blockquote>\n <p><strong>Conclusions</strong>: This Cochrane meta-analysis of 10 studies of varying quality examined the effects of omega-3 fatty acids and antioxidants in adults with ARDS. This intervention may produce little or no difference in all-cause mortality between groups. We are uncertain whether immunonutrition with omega-3 fatty acids and antioxidants improves ventilator days, ICU length of stay, or oxygenation due to the very low quality of evidence.</p>\n</blockquote>\n\n<p>Immunonutrition for Adults With ARDS: Results From a Cochrane Systematic Review and Meta-Analysis\n<a href=\"https://pubmed.ncbi.nlm.nih.gov/31506339/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/31506339/</a></p>\n"
}
] | 2020/04/27 | [
"https://health.stackexchange.com/questions/23446",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19472/"
] |
23,472 | <p>Just a basic medical science question. Is a vacutainer necessary for use in venous whole blood sample collection? Also is the needle with plastic holder required? Can we not draw blood using a sterile syringe and place it into containers? Convenience and efficiency aside, is it considered a requirement? In the Wikipedia <a href="https://en.m.wikipedia.org/wiki/Vacutainer" rel="nofollow noreferrer">article</a>, it says that the traditional method of drawing blood is with a syringe and needle. However, that doesn't explain the need for EDTA, citrate and heparin additives in the tubes. </p>
| [
{
"answer_id": 23447,
"author": "Gordon",
"author_id": 13819,
"author_profile": "https://health.stackexchange.com/users/13819",
"pm_score": 0,
"selected": false,
"text": "<p>Here is Oregon State, Linus Pauling Institute. Immunity In Brief. They begin with Omega 3 to help reduce inflammation. I don’t think they give a dose, I don’t remember. Personally I would follow the label directions which are going to tell you to consult your doctor before taking if you are on medications, (and I would say particularly for a dose of 5 grams. ). <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a> If you are 60 or over, or have some other problem, then I think it would be even more important to consult your doctor first. <a href=\"https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/health-disease/immunity-in-brief</a></p>\n\n<p>Remember Vitamin E and A can give some “thinning” and so can many herbal products. And obviously one must take into account other OTC products like aspirin and other NSAIDs. </p>\n\n<p>This just addresses Immunity in Brief according to the above article and not whether this will help prevent pneumonia in association with COVID 19, since the FDA is very strict on supplements being touted for COVID19. </p>\n\n<p>Bottom line: consult your doctor first. They know your medical history.</p>\n\n<p>PS to be more specific the OSU article says, “EPA and DHA have an overall anti-inflammatory effect.” see the link. </p>\n"
},
{
"answer_id": 23451,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>A very recent Cochrane review of the use of Omega 3 in ARDS, not specifically from COVID-19, did not find any benefit using trials up to 2018.</p>\n\n<blockquote>\n <p><strong>Conclusions</strong>: This Cochrane meta-analysis of 10 studies of varying quality examined the effects of omega-3 fatty acids and antioxidants in adults with ARDS. This intervention may produce little or no difference in all-cause mortality between groups. We are uncertain whether immunonutrition with omega-3 fatty acids and antioxidants improves ventilator days, ICU length of stay, or oxygenation due to the very low quality of evidence.</p>\n</blockquote>\n\n<p>Immunonutrition for Adults With ARDS: Results From a Cochrane Systematic Review and Meta-Analysis\n<a href=\"https://pubmed.ncbi.nlm.nih.gov/31506339/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/31506339/</a></p>\n"
}
] | 2020/05/01 | [
"https://health.stackexchange.com/questions/23472",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19498/"
] |
23,489 | <p>Due to the Covid-19 pandemic, we citizens are asked to wear masks in Germany. Early reports said that wearing a mask may not help to protect myself from other infected people, but it protects others from me (who might be infected). New reports say that the mask might actually also protect myself. After going outside with my mask, I am supposed to not touch the outside of the mask when taking it down, because it might contain the virus on the outside - since I might have been in an area with the virus flying around and I would not want to contaminate my hands when touching the outside of the mask once I am back at home.</p>
<p>This makes sense so far. BUT... let's assume, while being outside, I walk into a cloud of droplets originating from the sneeze of an infected person and my mask is now full of virus at the outside. I would assume that my clothes, like my shirt, are also full of virus. So I would think that now I have to take off all clothes, put them into the washing machine at once and go straight into the shower without touching my face. Anything else does not seem to make sense to me. However, I have not read anything like that anywhere. Am I missing something?</p>
| [
{
"answer_id": 23494,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 4,
"selected": true,
"text": "<p>There are a lot of inconsistencies in what we are being told.</p>\n<p>One is that masks don't protect you, and make it more likely that you will get infected because they irritate your face, and you'll be constantly touching the mask risking transfer from the mask to your mouth or eyes.</p>\n<blockquote>\n<p>People in some regions (eg, Thailand, China, and Japan) opted for makeshift alternatives or repeated usage of disposable surgical masks. Notably, improper use of face masks, such as not changing disposable masks, could jeopardise the protective effect and even increase the risk of infection.</p>\n</blockquote>\n<p>But SARS-CoV-2 is a respiratory pathogen, so if the virus is covering your mask, it's certainly better than breathing it in.</p>\n<p>And if the virus is on your mask, it's even more likely to be on your shoes and other clothing as it's primarily droplet spread and droplets fall by gravity so the highest concentration of virus increases towards the ground.</p>\n<p>And medical workers with full PPE include gowns, and shoe covers. If worn correctly, PPE when removed should not leave any virus on one's clothing worn inside the PPE.</p>\n<p>So the degree of protective measures you take depends on your risk. If you live in a region of high community transmission, then you should be looking at disinfecting the soles of your shoes, and changing footwear when you enter your house, as well as removing any outer protective clothing such as a raincoat. Ultimately your best protection from infection by fomites is handwashing before eating.</p>\n<p>If you're a medical worker that doesn't change out of full PPE at your hospital then recommendations from the AAFP recommend</p>\n<blockquote>\n<p><strong>When you arrive home</strong></p>\n<p>If you were unable to change clothes before leaving work, change in an isolated location (e.g., garage, mudroom, laundry room).</p>\n<p>Do not wear shoes from work into your home. Clean them, top and bottom, with disinfecting wipes.</p>\n<p>Wash clothes worn at work using your usual laundry detergent.</p>\n<p>Wash or safely discard dirty clothes bag.</p>\n<p>Wash hands after handling dirty clothes and shoes.</p>\n<p>Shower before interacting with your family.</p>\n<p>You may choose to isolate, if possible, from your family to limit their potential for exposure:</p>\n</blockquote>\n<p>Rational use of face masks in the COVID-19 pandemic\n<a href=\"https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30134-X/fulltext\" rel=\"noreferrer\">https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30134-X/fulltext</a></p>\n<p><a href=\"https://www.health.state.mn.us/facilities/patientsafety/infectioncontrol/ppe/comp/index.html\" rel=\"noreferrer\">https://www.health.state.mn.us/facilities/patientsafety/infectioncontrol/ppe/comp/index.html</a></p>\n<p><a href=\"https://www.aafp.org/journals/fpm/blogs/inpractice/entry/covid19_home.html\" rel=\"noreferrer\">https://www.aafp.org/journals/fpm/blogs/inpractice/entry/covid19_home.html</a></p>\n"
},
{
"answer_id": 23515,
"author": "gatorback",
"author_id": 7446,
"author_profile": "https://health.stackexchange.com/users/7446",
"pm_score": 0,
"selected": false,
"text": "<p>TL\\DR: a mask protect the public from you. It is not sufficient to protect your from the public \\ others. Do not think that wearing a mask provides protection from high risk areas \\ behaviors. Avoid Avoid Avoid infection opportunities.</p>\n\n<p>Surgeons wear a mask (covering nose / mouth) in the operating room to prevent the spread of pathogens from the Surgeon's mouth / nose to the patient's surgical site. </p>\n"
}
] | 2020/05/03 | [
"https://health.stackexchange.com/questions/23489",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19512/"
] |
23,495 | <p><strong>Something I never understood:</strong></p>
<ul>
<li>Does "asymptomatic" mean that someone will never show symptoms whether they catch the disease and therefore, can have without even realizing?</li>
<li>Does it mean that they won't show symptoms while they have the disease (during the incubation period) and therefore showing symptoms (after the incubation period)?</li>
<li>Or does it mean that they won't show symptoms while they have the disease (during the incubation period), but they never finish the incubation period getting the disease itself and, therefore, not realizing they had it?</li>
</ul>
| [
{
"answer_id": 23498,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Asymptomatic refers to a state of no symptoms at a particular time. One can be asymptomatic in the incubation period, and/or, in the period following the infection as shown by positive rtPCR which shows that an infection is present. It doesn't mean that they'll remain asymptomatic forever.</p>\n\n<p>Presymptomatic means during the incubation period for the virus and you have no symptoms. </p>\n\n<blockquote>\n <p>The antibody serosurveys getting underway in different parts of the country add further evidence that a good number – possibly anywhere from around 10 percent to 40 percent – of those infected might not experience symptoms.</p>\n</blockquote>\n\n<p>And in this context, it meant the person remained asymptomatic throughout the whole infection.</p>\n\n<p><a href=\"https://www.sciencealert.com/a-physician-answers-5-questions-about-asymptomatic-covid-19\" rel=\"nofollow noreferrer\">https://www.sciencealert.com/a-physician-answers-5-questions-about-asymptomatic-covid-19</a> </p>\n"
},
{
"answer_id": 23507,
"author": "Harper - Reinstate Monica",
"author_id": 14568,
"author_profile": "https://health.stackexchange.com/users/14568",
"pm_score": 3,
"selected": true,
"text": "<p>With a virus, there are 2 separate things that happen at different speeds, and not at the same time: </p>\n\n<ul>\n<li>Live virus comes in contact with your body, and starts replicating, and your body is emitting copies of the live virus in exhalation etc. <em>You are contagious and can spread it to other people at this point.</em> </li>\n<li>The virus starts damaging the body badly enough to do harm, or to provoke an immune system response that itself makes you feel ill. <em>You know you are sick at this point.</em> </li>\n</ul>\n\n<p>These things are separate, and can run on totally different timelines, or may not happen at all, depending on the virus and the person. <strong>When a person has the disease (#1) but does not feel the effects of illness (#2), that is called \"asymptomatic\"</strong>. You can be asymptomatic temporarily, which is what happens to almost everyone with COVID-19. Or, what happened for Typhoid Mary, you can be at #1 forever without any #2, so you never know you have it! That is called being a \"carrier\". </p>\n\n<p>On a well-behaved virus, the two will happen about the same time, so a person will feel ill and go into seclusion to protect themselves and others. </p>\n\n<p>On a more dangerous virus, the time lag between #1 and #2 is quite long, and/or some people experience mild #2 effects which they mistake for normal stress/tiredness/side effects of a drug they take for something else. Then, you have a perfect storm for a disease that spreads widely, because you have a lot of unwitting \"carriers\", at least temporarily. </p>\n"
}
] | 2020/05/03 | [
"https://health.stackexchange.com/questions/23495",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19519/"
] |
23,496 | <p>In <a href="https://www.sciencedirect.com/science/article/pii/S0924857920300996" rel="nofollow noreferrer">this publication</a>
36 patients, 16 in control group (31,25% were kids (!!!!) 10-16 y.o., 25% asymptomatic, 62,5% URTI and 12,5% LRTI), 14 in HCQ (14,3% were asymptomatic, 71,4% with URTI and 14,3% with LRTI), 6 in AZ+HHQ (66,67% had LRTI). </p>
<p>What was the reason to include kids in this trial?</p>
<p>What for they prescribed HCQ for asymptomatic cases and URTI? </p>
| [
{
"answer_id": 23499,
"author": "Bryan Krause",
"author_id": 8728,
"author_profile": "https://health.stackexchange.com/users/8728",
"pm_score": 2,
"selected": false,
"text": "<p>This study was pretty much worthless as anything but a case series, and has been criticized all over (see some references below, but these hardly even scratch the surface of the criticism...).</p>\n\n<p>They also excluded patients from the treatment group after the study started if they worsened (so the treatment group patients <em>couldn't</em> have suffered any negative consequences).</p>\n\n<p>It's really probably best to <a href=\"https://en.wikipedia.org/wiki/Flogging_a_dead_horse\" rel=\"nofollow noreferrer\">stop worrying about all the individual things wrong with this paper</a>, and have a broader discussion of how this sort of information got disseminated and into the eyes of the public without the caveats being sufficiently presented.</p>\n\n<hr>\n\n<p>Dahly, D., Gates, S., & Morris, T. (2020). Statistical review of hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label nonrandomized clinical trial. Preprint. Posted online, 23.</p>\n\n<p>Kim, A. H., Sparks, J. A., Liew, J. W., Putman, M. S., Berenbaum, F., Duarte-García, A., ... & Ugarte-Gil, M. F. (2020). A rush to judgment? Rapid reporting and dissemination of results and its consequences regarding the use of hydroxychloroquine for COVID-19. Annals of internal medicine.</p>\n\n<p>Batra, U., Sharma, M., & Redhu, P. (2020). Chloroquine and hydroxychloroquine: Clutching at straws in the time of COVID-19?. Cancer Research, Statistics, and Treatment, 3(5), 3.</p>\n"
},
{
"answer_id": 23500,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 2,
"selected": false,
"text": "<p>Apart from the fact that the study in question has been widely panned such that <a href=\"https://retractionwatch.com/2020/04/12/elsevier-investigating-hydroxychloroquine-covid-19-paper/\" rel=\"nofollow noreferrer\">Elsevier</a>, the publisher, is even investigating it, the answer to your questions are:</p>\n\n<p>A. The children were part of the control group to see how quickly the virus clearly naturally ( even though that is problematic since children respond differently to the virus than adults ). The study wasn't randomized so all the children were in the control group.</p>\n\n<p>B. They weren't prescribing HCQ for URTI and asymptomatic cases. They were prescribing HCQ to confirmed cases of COVID-19, some of whom had URTI symptoms, to see how quickly viral clearance was achieved.</p>\n"
}
] | 2020/05/03 | [
"https://health.stackexchange.com/questions/23496",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19518/"
] |
23,505 | <p>I found this link on the internet:</p>
<p><a href="https://www.bloomberg.com/news/articles/2020-04-13/who-says-70-vaccines-in-the-works-with-three-leading-candidates" rel="noreferrer">70 vaccines are getting ready for coronavirus: 3 very promising</a></p>
<p>Why is it that there will be vaccines before a cure? Shouldn't it be the other way around? What is the reason for the vaccine first then the cure?</p>
| [
{
"answer_id": 23508,
"author": "Kate Gregory",
"author_id": 400,
"author_profile": "https://health.stackexchange.com/users/400",
"pm_score": 7,
"selected": true,
"text": "<p>Your question contains a lot of misconceptions.</p>\n\n<ul>\n<li>A cure is definitely possible</li>\n<li>A cure could be found, proved, and proved safe, more quickly than a vaccine</li>\n<li>People and firms that could be working on cures are choosing to work on vaccines</li>\n</ul>\n\n<p>None of these are correct. Most virus-caused diseases have no cure: colds, Zika, Dengue, and so on. A tiny handful have treatments that can ease the course of the disease: you've heard of Tamiflu and so on. And some can be actually cured with medication. So the first assumption, that a cure exists to be found, is not a sure thing by any means, and is actually quite unlikely.</p>\n\n<p>Then there is the matter of side effects, unintended consequences, and so on. We are pretty familiar with vaccinations by now. We know how to test that a vaccine doesn't cause other problems. But a cure often can have really bad effects. A drug that is supposed to lower your [blood pressure, heart rate, blood sugar, whatever] or raise your [immune response, whatever] might raise or lower it too much. It might cure one thing but give you a stroke or a heart attack. The immunotherapy that cured my 3-months-to-live melanoma also wiped out my thyroid and nearly killed me with a skin reaction. [I am fine with that trade, but the point is treatments can and do kill people. We only use them if the curing outweighs what the side effects do.] Cures have to be tested to understand all of these possibilities. In most cases we want to know the long term reactions -- and that means giving the drug and monitoring and studying for months or more. Plus, we give treatments to sick people, but vaccines to healthy people, so the side effects are even more of a big deal for a treatment.</p>\n\n<p>And finally, the money and teams to work on a vaccine are entirely different than the money and teams who work on cures. So work is underway on cures too. It hasn't been set aside to focus on vaccines.</p>\n\n<p>What you're observing is that everyone predicts a vaccine will come more quickly. It's a better understood area (we have vaccines for tons of viruses, but cures for very few) with less concern about hurting or killing the people we give it to. It's most likely the vaccine teams will succeed before the cure teams do. But it's not because there isn't any work happening on possible cures.</p>\n"
},
{
"answer_id": 23510,
"author": "Charles E. Grant",
"author_id": 18010,
"author_profile": "https://health.stackexchange.com/users/18010",
"pm_score": 5,
"selected": false,
"text": "<p>Drugs are typically <a href=\"https://en.wikipedia.org/wiki/Small_molecule\" rel=\"noreferrer\">small molecules</a> that interfere with some chemical process in the disease causing microbe, and therein lies the rub. Bacteria, fungi, protozoa, worms, etc. are sustained by their own complex systems of chemical reactions, largely independent of chemical systems that sustain us. That makes it easier to find a chemical that attacks something in the microbe's chemistry, but doesn't affect our own chemistry (much). <a href=\"https://en.wikipedia.org/wiki/Penicillin\" rel=\"noreferrer\">Penicillin</a> for example, targets an enzyme bacteria use to maintain their cell walls. Our own cells don't have cell walls in the same way bacteria do, and we don't use that enzyme, so a drug that blocks that enzyme in bacteria may cripple the bacteria without having (much) of an effect on our own cells.</p>\n\n<p>Viruses on the other hand, are really just a bit of DNA or RNA wrapped in a coat of sugars, proteins, and fats. They don't have any life processes of their own. They simply piggy-back and subvert our own chemical systems. That means any drug that targets a chemical process used by the virus is likely to have bad side effects on the patient too. In some cases it is possible to create an <a href=\"https://en.wikipedia.org/wiki/Antiviral_drug#Transcription\" rel=\"noreferrer\">anti-viral</a> drug that attacks a protein unique (or mostly unique) to the virus. The problem is that this is a much narrower range of possible targets, and it tends to be specific to a single virus. Drugs like penicillin often work on whole families of bacteria. This is what makes finding a drug that \"cures\" viral diseases so hard.</p>\n\n<p>However, living creatures have had to defend themselves against viruses for billions of years, so we've evolved sophisticated internal defenses against them. Even <a href=\"https://en.wikipedia.org/wiki/CRISPR\" rel=\"noreferrer\">bacteria have a sort of immune system against viruses</a>. When you are infected with a virus your body begins a race to mount an effective immune response before the virus does severe or even fatal damage to your body. Vaccines allow your body to begin mounting an immune response before you are actually exposed to the virus. Then if you are eventually exposed your immune system is able to shut the virus down much more quickly. Getting a workable vaccine is still tricky though, because you have to find substances that starts an immune response specific to the target virus in most people, but that doesn't also kick the immune system into an over reaction that itself can be very dangerous.</p>\n"
},
{
"answer_id": 23514,
"author": "Graham Chiu",
"author_id": 3414,
"author_profile": "https://health.stackexchange.com/users/3414",
"pm_score": 3,
"selected": false,
"text": "<p>I don't believe we have the data to say that vaccines will be deployed earlier than an effective treatment.</p>\n\n<p>Vaccine technology is old technology and the go to for most infectious diseases as there is a desire to prevent preventable illness. However, HIV was discovered in 1984 but we still <a href=\"https://www.healthline.com/health/hiv-aids/vaccine-how-close-are-we\" rel=\"noreferrer\">don't have a vaccine against it</a> though we have effective treatments. Some of the problems with a vaccine for HIV is that it's not a respiratory virus, and it mutates rapidly.</p>\n\n<p>The SARS epidemic was in 2003 and we still also don't have a vaccine for that, and it's unclear if the new <a href=\"https://www.modernatx.com/modernas-work-potential-vaccine-against-covid-19\" rel=\"noreferrer\">mRNA vaccines for COVID-19</a> will be effective or not as there has not been one deployed successfully before.</p>\n\n<p>Most of our drugs used in treatment are small molecules but many of our modern biological drugs are synthetic humanised antibodies, and there is a lot of experience in developing such treatments in diseases such as Rheumatoid Arthritis, and Axial spondyloarthropathies.</p>\n\n<p>To develop such antibodies to fight COVID-19 an animal (mouse) can be infected with SARS-CoV-2 and the subsequent antibodies are screened for effectiveness. Those most promising are humanised and then further developed for testing. Celltrion are using antibodies taken from recovered Korean patients.</p>\n\n<blockquote>\n <p>Through a partnership with the Korea Centers for Disease Control and Prevention (KCDC), Celltrion initially identified and secured 300 different types of antibodies that bind to the SARS-CoV-2 antigen. These were then screened based on their ability to bind to the virus Spike (S) protein. Celltrion was then able to capture a total of 38 potent neutralising antibodies, of which, 14 were identified as most potent against SARS-CoV-2.</p>\n</blockquote>\n\n<p>...</p>\n\n<blockquote>\n <p>Ki-Sung Kwon, Head of R&D Unit at Celltrion said: “We are bringing our full resources and expertise to overcome this global health crisis and are glad to have identified these antibodies sooner than previously expected. These antibodies can recognise multiple epitopes, thus increasing the probability of neutralisation against viral mutations. Given the expedited development process of our antiviral antibody treatment, we anticipate moving to first-in-human clinical trials in July. We are also on track with the development of a ‘super antibody’ or ‘an antibody cocktail’ and the launch of a rapid diagnostic kit in the summer of this year.”</p>\n</blockquote>\n\n<p>These would be expected to work like naturally developed antibodies that develop during the adaptive immune response to fight the infection.</p>\n\n<p><a href=\"https://www.drugtargetreview.com/news/60206/celltrion-selects-14-lead-monoclonal-antibodies-for-covid-19-treatment/\" rel=\"noreferrer\">https://www.drugtargetreview.com/news/60206/celltrion-selects-14-lead-monoclonal-antibodies-for-covid-19-treatment/</a></p>\n"
}
] | 2020/05/04 | [
"https://health.stackexchange.com/questions/23505",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/-1/"
] |
23,511 | <p>Back in mid-April some commentary/news <a href="https://www.theatlantic.com/technology/archive/2020/04/us-coronavirus-outbreak-out-control-test-positivity-rate/610132/" rel="noreferrer">was</a> that the US was not doing enough testing as evidenced by the test positivity rate:</p>
<blockquote>
<p>America’s 20 percent positivity rate is disquieting. The U.S. did almost 25 times as many tests on April 15 as on March 15, yet both the daily positive rate and the overall positive rate went up in that month. [...] when tests are rationed so strictly, only people with severe symptoms make it into the testing pool, ensuring that the positivity rate will be extremely high. [...]</p>
<p>The test-positivity rate, then, is a decent (if unusual) proxy for the severity of an outbreak in an area. And it shows clearly that the U.S. still lags far behind other countries in the course of fighting its outbreak. South Korea—which discovered its first coronavirus case on the same day as the U.S.—has tested more than half a million people, or about 1 percent of its population, and discovered about 10,500 cases. The U.S. has now tested 3.2 million people, which is also about 1 percent of its population, but it has found more than 630,000 cases. So while the U.S. has a 20 percent positivity rate, South Korea’s is only about 2 percent—a full order of magnitude smaller.</p>
<p>South Korea is not alone in bringing its positivity rate down: America’s figure dwarfs that of almost every other developed country. Canada, Germany and Denmark have positivity rates from 6 to 8 percent. Australia and New Zealand have 2 percent positivity rates. Even Italy—which faced one of the world’s most ravaging outbreaks—has a 15 percent rate. [...] New York City’s positivity rate is an astonishing 55 percent.</p>
</blockquote>
<p>US officials actually acknowledge this problem and the WHO guidelines of bringing down the positivity rate under 10%; <a href="https://www.npr.org/sections/health-shots/2020/04/22/840526338/is-the-u-s-testing-enough-for-covid-19-as-debate-rages-on-heres-how-to-know" rel="noreferrer">April 22 news</a>:</p>
<blockquote>
<p>But how much testing is enough?</p>
<p>There's no exact number to aim for, but here's a guiding principle: You want a low percentage of your tests to come back positive, around 10% or even lower, says William Hanage, an epidemiologist at Harvard.</p>
<p>That 10% benchmark is based on recommendations from the World Health Organization. Why should positives be low? If a high percentage of tests come back positive, it's clear there's not enough testing to capture all of the infected people in the community. "The lower the percentage of tests you're doing that come back positive, the better," Hanage says.</p>
<p>Some countries that have done extensive testing have positive rates near this 10% benchmark, or lower. South Korea is "testing so many people that only 3% of them are positive," said Rochelle Walensky, an infectious disease specialist at Massachusetts General Hospital, during a livestream hosted by the medical journal JAMA.</p>
<p>But, so far the U.S. appears to fall short of this benchmark. Nationally, according to CDC data, about 18% of tests have been positive to date, and 21% were positive in the week ending April 11. [...]</p>
<p><strong>Admiral Brett Giroir, a member of President Trump's coronavirus task force, acknowledged the importance of this benchmark. "This is a good metric that you want to get about one positive for every 10 tests," he said during the White House coronavirus task force briefing</strong> Monday night [Apr 20?].</p>
</blockquote>
<p>So, question: What is the most recent data with for this test positivity rate in the US? And better still, is there an up-to-date graph over time for it (perhaps even a separate graph for each US state)?</p>
| [
{
"answer_id": 23513,
"author": "Graham Chiu",
"author_id": 3414,
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"text": "<p>From your link, <em>The Atlantic</em> has its data tracking project at <a href=\"https://covidtracking.com/data\" rel=\"nofollow noreferrer\">https://covidtracking.com/data</a></p>\n\n<p>If you go there you can drill down by state, the number of cumulative positive and negative results. They show the number of new daily tests and so you can extract the data you want from there about the positivity rates</p>\n\n<p>So, the cumulative data for <a href=\"https://covidtracking.com/data/state/alabama#historical\" rel=\"nofollow noreferrer\">Alabama</a> </p>\n"
},
{
"answer_id": 31875,
"author": "Michael Altfield",
"author_id": 19986,
"author_profile": "https://health.stackexchange.com/users/19986",
"pm_score": 2,
"selected": false,
"text": "<p>Many websites tracking COVID-19 source their data from John Hopkins. You can <a href=\"https://github.com/CSSEGISandData/COVID-19/tree/master/csse_covid_19_data\" rel=\"nofollow noreferrer\">explore the data here</a>:</p>\n<ul>\n<li><a href=\"https://github.com/CSSEGISandData/COVID-19/tree/master/csse_covid_19_data\" rel=\"nofollow noreferrer\">https://github.com/CSSEGISandData/COVID-19/tree/master/csse_covid_19_data</a></li>\n</ul>\n<h4>Our World In Data</h4>\n<p>My favorite site for viewing this data is Our World In Data. For example, you can see the number of positive test cases per capita (7-day rolling average) in the US here:</p>\n<ul>\n<li><a href=\"https://ourworldindata.org/explorers/coronavirus-data-explorer?facet=none&Metric=Confirmed+cases&Interval=7-day+rolling+average&Relative+to+Population=true&Color+by+test+positivity=false&country=%7EUSA\" rel=\"nofollow noreferrer\">https://ourworldindata.org/explorers/coronavirus-data-explorer?facet=none&Metric=Confirmed+cases&Interval=7-day+rolling+average&Relative+to+Population=true&Color+by+test+positivity=false&country=~USA</a></li>\n</ul>\n<p><a href=\"https://i.stack.imgur.com/O4BuQ.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/O4BuQ.png\" alt=\"Daily new confirmed COVID-19 cases per million people in Germany and the United States\" /></a></p>\n<h4>Coviz</h4>\n<p>I created a tool that takes this one step further: extrapolating the (cumulative) curve to predict future spread of the virus:</p>\n<ul>\n<li><a href=\"https://coviz.org/\" rel=\"nofollow noreferrer\">https://coviz.org/</a></li>\n</ul>\n<p><a href=\"https://i.stack.imgur.com/gBPeb.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gBPeb.png\" alt=\"COVID-19 cases per capita in the Germany with 2-degree polynomial extrapolation 1 month into the future\" /></a></p>\n"
}
] | 2020/05/04 | [
"https://health.stackexchange.com/questions/23511",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/10980/"
] |
23,521 | <p>Assuming the immune system is healthy,</p>
<p>How much SARS-CoV-2 virus (cause of COVID-19) is required to make a person sick?</p>
<p>This might also depend on time, if it was a high infectious dose but just some minutes, maybe not that bad outcomes.</p>
<p>Or if it's a very low infectious dose, but during a whole day, maybe a bad outcome.</p>
<p>In addition, Would it be possible that a person was exposed to SARS-CoV-2 virus, and so the virus got inside their system, and even still this person's immune system didn't let the virus to infect this person? </p>
<p>Note that it's not the case that this person will be totally asymptomatic, it's the case when the virus wasn't "strong enough" to infect this person even being inside their system.</p>
<ul>
<li>MID - minimum infectious dose defined as"the smallest quantity of infectious material that regularly produces infection"</li>
</ul>
| [
{
"answer_id": 23522,
"author": "I likeThatMeow",
"author_id": 17725,
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"text": "<ul>\n<li>From this link <a href=\"https://www.statnews.com/2020/04/14/how-much-of-the-coronavirus-does-it-take-to-make-you-sick/\" rel=\"nofollow noreferrer\">How much of the coronavirus does it take to make you sick?</a></li>\n</ul>\n<blockquote>\n<p>The amount of particles a person is exposed to can affect how <strong>likely</strong> they are to become infected and, once infected, how severe the symptoms become.</p>\n<p>A high infectious dose may lead to a higher viral load, which can impact the <em>severity</em> of COVID-19 symptoms.</p>\n<p>Viral load is a measure of virus particles. It is the amount of virus present once a person has been infected and the virus has had time to replicate in their cells. <em>With most viruses, higher viral loads are associated with worse outcomes.</em></p>\n<blockquote>\n<p>“The more viral particles that get into the lungs, the more damage to the lungs that is probably happening,” said W. David Hardy, a professor of infectious disease at Johns Hopkins University School of Medicine.</p>\n</blockquote>\n</blockquote>\n<ul>\n<li>From this link <a href=\"https://www.sciencealert.com/does-the-amount-of-covid-19-virus-you-are-exposed-to-determine-how-sick-you-ll-get\" rel=\"nofollow noreferrer\">Does The Amount of Coronavirus You're Exposed to Determine How Sick You'll Get?</a></li>\n</ul>\n<blockquote>\n<p>A report from China suggested that there is <a href=\"https://www.medrxiv.org/content/10.1101/2020.03.15.20036707v2.full.pdf\" rel=\"nofollow noreferrer\">no difference</a> between how much coronavirus a person is exposed to and how sick they get.</p>\n<p>But another report showed that <a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30232-2/fulltext\" rel=\"nofollow noreferrer\">patients with milder disease had lower levels of the virus.</a></p>\n</blockquote>\n"
},
{
"answer_id": 23553,
"author": "BobE",
"author_id": 11421,
"author_profile": "https://health.stackexchange.com/users/11421",
"pm_score": 1,
"selected": false,
"text": "<p>Disclaimer: I am not entirely satisfied with this answer in as much as the author fails to source the claim that 1000 viral particles may be the threshold for infection. However the author has significant expertise and more importantly (to me as a non-expert) has written a piece that is entirely readable and plausible. I offer it for your consideration:</p>\n\n<p>Dr Bromage <a href=\"https://erinbromage.wixsite.com/covid19/post/the-risks-know-them-avoid-them?fbclid=IwAR0ghyWnc-FT0UK1tdjioj8MFMfcfEK-_DOX58ID8c_-Ef89AqRKmH5uO4U\" rel=\"nofollow noreferrer\">The Risks - Know Them - Avoid Them</a> posits that 1000 viral particles are sufficient to produce an inflection. He then discusses the risks of encountering that threshold and how to minimize one's risk.</p>\n\n<p>Update: </p>\n\n<blockquote>\n <p>The minimum infectious dose of SARS-CoV-2, the virus that causes Covid-19, is unknown so far, but researchers suspect it is low. “The virus is spread through very, very casual interpersonal contact,” W. David Hardy, a professor of infectious disease at Johns Hopkins University School of Medicine, told STAT.\n Blockquote\n <a href=\"https://www.statnews.com/2020/04/14/how-much-of-the-coronavirus-does-it-take-to-make-you-sick/\" rel=\"nofollow noreferrer\">STAT</a></p>\n</blockquote>\n\n<p>For comparison purposes:</p>\n\n<blockquote>\n <p>... it takes just 18 particles of norovirus to cause an infection. This can lead to the classic clinical signs of vomiting and diarrhoea </p>\n</blockquote>\n\n<p><a href=\"https://www.sciencealert.com/does-the-amount-of-covid-19-virus-you-are-exposed-to-determine-how-sick-you-ll-get\" rel=\"nofollow noreferrer\">LINK, with citation to norovirus study for infectous dose</a></p>\n"
},
{
"answer_id": 24844,
"author": "Jay Parry",
"author_id": 20529,
"author_profile": "https://health.stackexchange.com/users/20529",
"pm_score": -1,
"selected": false,
"text": "<p>It seems we are looking at the kinetics of viral growth in the body, the time to release of the cell containing the replicated virus, the amount of virus released per cell and the rate of adsorption of the virus into the cell. I don't speak with authority regarding the biochemistry of this process, but I do remember quite a lot about chemical kinetics. If the rate of replication of the virus in the body is faster than the rate of adsoprtion through the ACE-2 enzyme then you can launch all the virus you want at the cell, it is replicating the virus faster than the virus can penetrate cells. Similarly the time to release the virus from the infected cell and the amount of virus released per cell all contribute to the effect of any viral infection. See this for example <a href=\"https://doi.org/10.1016/j.virol.2011.12.005\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.virol.2011.12.005</a>. This more recent article seemed to try to answer the question - but did not <a href=\"https://wwwnc.cdc.gov/eid/article/26/9/20-1495_article\" rel=\"nofollow noreferrer\">https://wwwnc.cdc.gov/eid/article/26/9/20-1495_article</a> So it depends.. I guess.</p>\n"
}
] | 2020/05/05 | [
"https://health.stackexchange.com/questions/23521",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/17725/"
] |
23,525 | <p>Has the viral load in individuals identified as carriers, without manifesting the disease itself been studied for how long they have a viral load present in their system, this is also relevant for influenza asymptomatic carriers.</p>
| [
{
"answer_id": 23522,
"author": "I likeThatMeow",
"author_id": 17725,
"author_profile": "https://health.stackexchange.com/users/17725",
"pm_score": 0,
"selected": false,
"text": "<ul>\n<li>From this link <a href=\"https://www.statnews.com/2020/04/14/how-much-of-the-coronavirus-does-it-take-to-make-you-sick/\" rel=\"nofollow noreferrer\">How much of the coronavirus does it take to make you sick?</a></li>\n</ul>\n<blockquote>\n<p>The amount of particles a person is exposed to can affect how <strong>likely</strong> they are to become infected and, once infected, how severe the symptoms become.</p>\n<p>A high infectious dose may lead to a higher viral load, which can impact the <em>severity</em> of COVID-19 symptoms.</p>\n<p>Viral load is a measure of virus particles. It is the amount of virus present once a person has been infected and the virus has had time to replicate in their cells. <em>With most viruses, higher viral loads are associated with worse outcomes.</em></p>\n<blockquote>\n<p>“The more viral particles that get into the lungs, the more damage to the lungs that is probably happening,” said W. David Hardy, a professor of infectious disease at Johns Hopkins University School of Medicine.</p>\n</blockquote>\n</blockquote>\n<ul>\n<li>From this link <a href=\"https://www.sciencealert.com/does-the-amount-of-covid-19-virus-you-are-exposed-to-determine-how-sick-you-ll-get\" rel=\"nofollow noreferrer\">Does The Amount of Coronavirus You're Exposed to Determine How Sick You'll Get?</a></li>\n</ul>\n<blockquote>\n<p>A report from China suggested that there is <a href=\"https://www.medrxiv.org/content/10.1101/2020.03.15.20036707v2.full.pdf\" rel=\"nofollow noreferrer\">no difference</a> between how much coronavirus a person is exposed to and how sick they get.</p>\n<p>But another report showed that <a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30232-2/fulltext\" rel=\"nofollow noreferrer\">patients with milder disease had lower levels of the virus.</a></p>\n</blockquote>\n"
},
{
"answer_id": 23553,
"author": "BobE",
"author_id": 11421,
"author_profile": "https://health.stackexchange.com/users/11421",
"pm_score": 1,
"selected": false,
"text": "<p>Disclaimer: I am not entirely satisfied with this answer in as much as the author fails to source the claim that 1000 viral particles may be the threshold for infection. However the author has significant expertise and more importantly (to me as a non-expert) has written a piece that is entirely readable and plausible. I offer it for your consideration:</p>\n\n<p>Dr Bromage <a href=\"https://erinbromage.wixsite.com/covid19/post/the-risks-know-them-avoid-them?fbclid=IwAR0ghyWnc-FT0UK1tdjioj8MFMfcfEK-_DOX58ID8c_-Ef89AqRKmH5uO4U\" rel=\"nofollow noreferrer\">The Risks - Know Them - Avoid Them</a> posits that 1000 viral particles are sufficient to produce an inflection. He then discusses the risks of encountering that threshold and how to minimize one's risk.</p>\n\n<p>Update: </p>\n\n<blockquote>\n <p>The minimum infectious dose of SARS-CoV-2, the virus that causes Covid-19, is unknown so far, but researchers suspect it is low. “The virus is spread through very, very casual interpersonal contact,” W. David Hardy, a professor of infectious disease at Johns Hopkins University School of Medicine, told STAT.\n Blockquote\n <a href=\"https://www.statnews.com/2020/04/14/how-much-of-the-coronavirus-does-it-take-to-make-you-sick/\" rel=\"nofollow noreferrer\">STAT</a></p>\n</blockquote>\n\n<p>For comparison purposes:</p>\n\n<blockquote>\n <p>... it takes just 18 particles of norovirus to cause an infection. This can lead to the classic clinical signs of vomiting and diarrhoea </p>\n</blockquote>\n\n<p><a href=\"https://www.sciencealert.com/does-the-amount-of-covid-19-virus-you-are-exposed-to-determine-how-sick-you-ll-get\" rel=\"nofollow noreferrer\">LINK, with citation to norovirus study for infectous dose</a></p>\n"
},
{
"answer_id": 24844,
"author": "Jay Parry",
"author_id": 20529,
"author_profile": "https://health.stackexchange.com/users/20529",
"pm_score": -1,
"selected": false,
"text": "<p>It seems we are looking at the kinetics of viral growth in the body, the time to release of the cell containing the replicated virus, the amount of virus released per cell and the rate of adsorption of the virus into the cell. I don't speak with authority regarding the biochemistry of this process, but I do remember quite a lot about chemical kinetics. If the rate of replication of the virus in the body is faster than the rate of adsoprtion through the ACE-2 enzyme then you can launch all the virus you want at the cell, it is replicating the virus faster than the virus can penetrate cells. Similarly the time to release the virus from the infected cell and the amount of virus released per cell all contribute to the effect of any viral infection. See this for example <a href=\"https://doi.org/10.1016/j.virol.2011.12.005\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.virol.2011.12.005</a>. This more recent article seemed to try to answer the question - but did not <a href=\"https://wwwnc.cdc.gov/eid/article/26/9/20-1495_article\" rel=\"nofollow noreferrer\">https://wwwnc.cdc.gov/eid/article/26/9/20-1495_article</a> So it depends.. I guess.</p>\n"
}
] | 2020/05/05 | [
"https://health.stackexchange.com/questions/23525",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19554/"
] |
23,565 | <p>Given controversy and confusion over aspects of COVID-19, particularly over comparisons and contrasts with the mortality risk of seasonal flu, this question seeks data and findings on the <strong>mortality risk (Infection Fatality Rate) of Covid-19</strong>.</p>
<p>The mortality risk, or Infection fatality rate (IFR), sometimes known as ‘mortality rate’, ‘death rate’, or 'lethality' represents the risk of dying after contracting the virus, and is calculated as the number of deaths divided by the number infections.</p>
<p>The mortality risk (IFR) of COVID-19 is often overlooked in mainstream news media, which tends to focus on the case fatality rate (number of deaths divided by the number of CASES), or falsely equate/conflate the two.</p>
<p>The case fatality rate is in itself not a valid indicator of the mortality risk of a virus as it does not account for unreported/asymptomatic cases and therefore the true number of infections, or estimates of them. Hence the interest in data/studies on the mortality risk.</p>
<p>Ref:<br />
<a href="https://medicalxpress.com/news/2020-05-team-covid-infection-fatality.html" rel="nofollow noreferrer">https://medicalxpress.com/news/2020-05-team-covid-infection-fatality.html</a><br />
<a href="http://jdmichel.blog.tdg.ch/archive/2020/03/24/covid-19-the-game-is-over-305275.html?fbclid=IwAR2xfWuLuVodAVLk8bZ9VzDTGsa_7CS0B0xmlZw6AqskRNRjjGLDAi4Mp2c" rel="nofollow noreferrer">http://jdmichel.blog.tdg.ch/archive/2020/03/24/covid-19-the-game-is-over-305275.html?fbclid=IwAR2xfWuLuVodAVLk8bZ9VzDTGsa_7CS0B0xmlZw6AqskRNRjjGLDAi4Mp2c</a></p>
<p><strong>Source / information criteria</strong>:</p>
<p>For the purposes of this question, all answers must come with specific, referenced data/findings based on (or at least explicitly indicating) the <strong>number of infections</strong> (either directly known through testing of the entire study population, as in confinement/isolation situations, or based on modeled/estimated/extrapolated number of infections), and the <strong>number of deaths</strong> in each case.</p>
<p>This question <strong>does not</strong> seek answers containing personal estimates from respondents, and sources providing guesses based on anecdotal evidence or impressions/experience <strong>do not</strong> meet the criteria for this question.</p>
<p>Information based entirely on the CASE fatality ratio (i.e which ignores the number of unreported infections/asymptomatic infections) is <strong>not</strong> of interest for the purposes of this question for the reasons mentioned.</p>
<p>To avoid statistical errors due to small sample sizes, please limit sources to only those findings which are based on populations/sample sizes (total number of infections, either estimated or known) <strong>greater than 500</strong>.</p>
<p>Other coronavirus strains already circulating among population before COVID-19 (eg. 229E, HKU1, NL63, OC43) are not of interest for the purposes of this question.</p>
<p>In the case of news articles, obviously references should be included in support of data/findings, or at least traceable from the article, otherwise the information is not useful.</p>
<p>Goes without saying that the ratio/risk presented in any given source does not, in itself, determine the quality of the answer, and all answers meeting the given criteria are encouraged, regardless how consistent or inconsistent the findings they contain may be with other findings.</p>
<p>Feel free to indicate the following data points if they are known when indicating any sources of information, as they are of obvious relevance for the mortality risk (IFR). In any case, I will read all posts and summarize the data under various headings as I have done in my own answer to the question, which I will update as answers come in.</p>
<ul>
<li>Average age of the people considered in the study, and age stratified mortality risk (mortality risk for different age groups) if known.</li>
<li>How much time has passed since all persons considered in the study became infected if known, as deaths can occur after data is collected.</li>
<li>Whether Outcome delay adjustments (adding a percentage increase of deaths due to possible deaths after releasing data) are included in the information, if known.</li>
<li>Possible underlying illnesses which can increase likelihood of death if known.</li>
<li>Other factors.</li>
</ul>
<p>Below I have provided an answer (now a wiki) where all the sources which I have found or have been provided here meeting the given criteria are summarized with the corresponding mortality risk.</p>
<p>Edit (in light of one answer below):</p>
<p>Please note, answers based on 'common sense', or which cite or are based on data pertaining to cases (rather than infections) <strong>do not</strong> meet the criteria for this question. For the sake of the clarity and relevance of the data found here, please take the necessary time to research and understand these terms and the criteria specified for the data provided here before posting any data / papers.</p>
| [
{
"answer_id": 23567,
"author": "Dale Newton",
"author_id": 19597,
"author_profile": "https://health.stackexchange.com/users/19597",
"pm_score": 2,
"selected": false,
"text": "<p>Below is a summary of all data and findings answering this question meeting the question criteria which I have found or which have been pointed out in answers to this question. The mortality risk given is that provided in the research paper cited, or, where no paper is cited (sources 6,7 and 9), the number of deaths divided by number of infections based on the raw data.</p>\n<ol>\n<li>'Estimates of the severity of coronavirus disease 2019: a model-based analysis'. Robert Verity, PhD et al.<br />\n<a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30243-7/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30243-7/fulltext</a></li>\n</ol>\n<p><strong>Mortality risk (overall) = 0.657%</strong></p>\n<p><strong>Mortality risk (age stratified):</strong><br />\n0–9 = 0.00161%<br />\n10–19 = 0.00695%<br />\n20–29 = 0.0309%<br />\n30–39 = 0.0844%<br />\n40–49 = 0.161%<br />\n50–59 = 0.595%<br />\n60–69 = 1.93%<br />\n70–79 = 4.28%<br />\n≥80 = 7.80%</p>\n<hr />\n<ol start=\"2\">\n<li>LA COUNTY PUBLIC HEALTH DEPARTMENT / UNIVERSITY OF SOUTHERN CALIFORNIA STUDY FINDINGS.<br />\n<a href=\"https://qz.com/1841445/covid-19-may-be-undercounted-50-fold-in-la-antibody-surveys-show/\" rel=\"nofollow noreferrer\">https://qz.com/1841445/covid-19-may-be-undercounted-50-fold-in-la-antibody-surveys-show/</a><br />\n<a href=\"https://reason.com/2020/04/20/l-a-county-antibody-tests-suggest-the-fatality-rate-for-covid-19-is-much-lower-than-people-feared/\" rel=\"nofollow noreferrer\">https://reason.com/2020/04/20/l-a-county-antibody-tests-suggest-the-fatality-rate-for-covid-19-is-much-lower-than-people-feared/</a><br />\nInfections (in US, extrapolated) = 221,00 to 442,000.<br />\nAge factors: Age adjusted estimate for entire US population.</li>\n</ol>\n<p><strong>Mortality risk (IFR) = 0.1% - 0.3%.</strong></p>\n<hr />\n<ol start=\"3\">\n<li>GANGELT, GERMANY STUDY.<br />\n<a href=\"https://www.land.nrw/sites/default/files/asset/document/zwischenergebnis_covid19_case_study_gangelt_0.pdf\" rel=\"nofollow noreferrer\">https://www.land.nrw/sites/default/files/asset/document/zwischenergebnis_covid19_case_study_gangelt_0.pdf</a><br />\n<a href=\"https://www.technologyreview.com/2020/04/09/999015/blood-tests-show-15-of-people-are-now-immune-to-covid-19-in-one-town-in-germany/?fbclid=IwAR1P-zqpfx6ATyVsGYa_9EHVgr3aY0ryKDh_uuC90xKtXMWXKR4fR4OMYKI\" rel=\"nofollow noreferrer\">https://www.technologyreview.com/2020/04/09/999015/blood-tests-show-15-of-people-are-now-immune-to-covid-19-in-one-town-in-germany/?fbclid=IwAR1P-zqpfx6ATyVsGYa_9EHVgr3aY0ryKDh_uuC90xKtXMWXKR4fR4OMYKI</a><br />\nAge factors: Age adjusted estimate for entire adult population of Gangelt.<br />\nInfections (approx.) = 2% of adult population of Gangelt.</li>\n</ol>\n<p><strong>Estimated mortality risk (IFR) = 0.37%</strong></p>\n<hr />\n<ol start=\"4\">\n<li>DIAMOND PRINCESS OUTBREAK.<br />\n<a href=\"https://www.statista.com/statistics/1099517/japan-coronavirus-patients-diamond-princess/\" rel=\"nofollow noreferrer\">https://www.statista.com/statistics/1099517/japan-coronavirus-patients-diamond-princess/</a><br />\nDate of last possible infection: March 1st, 2020<br />\nDeaths to date: 13\nDiamond Princess study #1 (Mortality risk):<br />\n'Estimating the infection and case fatality ratio for COVID-19 using age-adjusted data from the outbreak on the Diamond Princess cruise ship'. Timothy W Russell et al.<br />\n<a href=\"https://www.medrxiv.org/content/10.1101/2020.03.05.20031773v2\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.03.05.20031773v2</a><br />\nAverage age: Age adjusted estimate for entire population of China.<br />\nCI= 95%.</li>\n</ol>\n<p><strong>Estimated mortality risk (IFR) = 0.5%</strong></p>\n<p>Diamond Princess study #2 (infections estimate):<br />\n‘The contribution of asymptomatic SARS-CoV-2 infections to transmission -a model-based analysis of the Diamond Princess outbreak’. Jon C . Emery et al.<br />\n<a href=\"https://cmmid.github.io/topics/covid19/reportsEmery_Transmission%20from%20asymptomatic%20SARS-CoV-2.pdf\" rel=\"nofollow noreferrer\">https://cmmid.github.io/topics/covid19/reportsEmery_Transmission%20from%20asymptomatic%20SARS-CoV-2.pdf</a><br />\nAverage age = 65.<br />\nTotal estimated infections: 1,304 (1,198-1,416).</p>\n<p><strong>Mortality risk (IFR) based on mean infections estimate= 0.99%</strong></p>\n<hr />\n<ol start=\"5\">\n<li>MORTALITY RISK ESTIMATE FROM JEAN-DOMINQUE MICHEL.<br />\n<a href=\"https://phusis.ch/2020/03/25/covid-19-il-sagit-dune-epidemie-banale/\" rel=\"nofollow noreferrer\">https://phusis.ch/2020/03/25/covid-19-il-sagit-dune-epidemie-banale/</a><br />\nAge factors: Statistics cited for entire population of china as of time of publishing (25th March, 2020).</li>\n</ol>\n<p><strong>Mortality risk (IFR) =< 0.3%</strong></p>\n<hr />\n<ol start=\"6\">\n<li>STOCKHOLM STUDY.<br />\nInfections data: ‘Estimates of the peak-day and the number of infected individuals during the covid-19 outbreak in the Stockholm region, Sweden.<br />\nFebruary – April 2020’.<br />\n<a href=\"https://www.folkhalsomyndigheten.se/publicerat-material/publikationsarkiv/e/estimates-of-the-peak-day-and-the-number-of-infected-individuals-during-the-covid-19-outbreak-in-the-stockholm-region-sweden-february--april-2020/\" rel=\"nofollow noreferrer\">https://www.folkhalsomyndigheten.se/publicerat-material/publikationsarkiv/e/estimates-of-the-peak-day-and-the-number-of-infected-individuals-during-the-covid-19-outbreak-in-the-stockholm-region-sweden-february--april-2020/</a><br />\nType: Modelling based estimate.<br />\nCI: Unknown.<br />\nDeaths data: <a href=\"https://c19.se/en/Sweden/Stockholm\" rel=\"nofollow noreferrer\">https://c19.se/en/Sweden/Stockholm</a>.<br />\nAge factors: Age adjusted estimate for entire population of Stockholm.<br />\nNumber of infections as of April 8th, 2020 = 70,500<br />\nNumber of deaths as of May 1st, 2020 = 1,417.</li>\n</ol>\n<p><strong>Mortality risk (IFR)= 2%</strong></p>\n<hr />\n<ol start=\"7\">\n<li>USS THEODORE ROOSEVELT OUTBREAK.<br />\n<a href=\"https://navylive.dodlive.mil/2020/03/15/u-s-navy-covid-19-updates/\" rel=\"nofollow noreferrer\">https://navylive.dodlive.mil/2020/03/15/u-s-navy-covid-19-updates/</a><br />\nOutbreak arrival date: 24th March, 2020.<br />\nNumber of infections = 2,141<br />\nNumber of deaths = 1<br />\nAverage age = ?</li>\n</ol>\n<p><strong>Mortality risk (IFR) = 0.046%</strong></p>\n<hr />\n<ol start=\"8\">\n<li>DRAFT OF META-STUDY ESTIMATING IFR OF CORONAVIRUS.<br />\n'A systematic review and meta-analysis of published research data on COVID-19 infection-fatality rates', Gideon Meyerowitz-Katz et al.<br />\n<a href=\"https://www.medrxiv.org/content/10.1101/2020.05.03.20089854v1\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.05.03.20089854v1</a><br />\nAge factors: Meta-study based on studies with varying age groups/average ages. Average age of meta-study not indicated.</li>\n</ol>\n<p><strong>Estimated mortality risk = 0.75% (0.49-1.01%)</strong></p>\n<hr />\n<ol start=\"9\">\n<li>CHARLES DE GAULLE AIRCRAFT CARRIER OUTBREAK.<br />\n<a href=\"https://en.wikipedia.org/wiki/COVID-19_pandemic_on_Charles_de_Gaulle\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/COVID-19_pandemic_on_Charles_de_Gaulle</a><br />\nArrival date: April 10th.<br />\nAverage age = ?<br />\nNumber of infections = 1,046<br />\nDeaths: 0</li>\n</ol>\n<p><strong>Mortality risk (IFR) = 0%</strong></p>\n<hr />\n<ol start=\"10\">\n<li>Bulletin of the World Health Organization, 99 (1): 19 - 33F, Ioannidis, John P A. (2021). <em>Infection fatality rate of COVID-19 inferred from seroprevalence data.</em></li>\n</ol>\n<p><strong>Generalized Mortality Risk (IFR): 0.23%</strong></p>\n<hr />\n"
},
{
"answer_id": 23568,
"author": "Fizz",
"author_id": 10980,
"author_profile": "https://health.stackexchange.com/users/10980",
"pm_score": 3,
"selected": false,
"text": "<p>Well, there is one meta-analytical estimate of the IFR for Covid-19 out already albeint only as a <a href=\"https://www.medrxiv.org/content/10.1101/2020.05.03.20089854v1\" rel=\"noreferrer\">draft paper</a>:</p>\n\n<blockquote>\n <p>there were 13 estimates of IFR included in the final meta-analysis, from a wide range of countries, published between February and April 2020. The meta-analysis demonstrated a point-estimate of IFR of 0.75% (0.49-1.01%) with significant heterogeneity (p<0.001). Conclusion: Based on a systematic review and meta-analysis of published evidence on COVID-19 until the end of April, 2020, the IFR of the disease across populations is 0.75% (0.49-1.01%). However, due to very high heterogeneity in the meta-analysis, it is difficult to know if this represents the \"true\" point estimate. It is likely that different places will experience different IFRs. More research looking at age-stratified IFR is urgently needed to inform policy-making on this front.</p>\n</blockquote>\n\n<p>A couple of additional points from the paper:</p>\n\n<blockquote>\n <p>Analysing by country of origin did not appear to have a substantial effect on the findings, with both those studies from within and outside of China showing similar aggregate estimates [...] There was very significantly lower heterogeneity in studies published using Chinese data (I<sup>2</sup> = 0%, p>0.5)</p>\n</blockquote>\n\n<p>On the other hand, they found that IFR estimates (insofar) increased by month, in April in particular, although this refers to the date of publication of the study rather than the time interval spanned by the study's observations. (Personally, I find this a little intriguing, as during the H1N1/09 pandemic, I've <a href=\"https://medicalsciences.stackexchange.com/questions/21035/in-what-time-frame-exactly-was-the-2009-h1n1-fatality-rate-overestimated\">read</a>--albeit not in great detail-- that the CFR estimates mostly went down over time.)</p>\n\n<p><a href=\"https://i.stack.imgur.com/UwxPt.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/UwxPt.png\" alt=\"enter image description here\"></a></p>\n\n<p>There's a summary table with the exact findings of each of the 13 studies at the end of this meta-analysis. Alas it's in a somewhat too gaudy of a format to include here; that table spans 5 pages in the draft paper.</p>\n"
},
{
"answer_id": 23716,
"author": "Alex I",
"author_id": 2480,
"author_profile": "https://health.stackexchange.com/users/2480",
"pm_score": 1,
"selected": false,
"text": "<p><strong>Around 1 to 2%</strong>.</p>\n\n<p>While @Fizz and @Dale Newton have already provided a nice collection (with statistics even), I'd like to add one more, which is based on <strong>common sense as well as statistics</strong>.</p>\n\n<p>First off, the source should be such that it could reasonably be expected to report truthful data; that pretty much means democratic governments which are taking this seriously and not trying to minimize it for various reasons. Second, the number of infections (as the most likely source of error) should be estimated from as large a dataset as possible; so only data from countries that have a <em>very</em> large ratio of tests to positive results, and a rigorous test program. Third, the test should have a sensitivity and specificity which is well known.</p>\n\n<p>The one source that best meets these criteria is <strong>South Korea</strong>. <a href=\"https://www.statista.com/topics/6082/coronavirus-covid-19-in-south-korea/\" rel=\"nofollow noreferrer\">South Korea</a> has done 802k tests, found 11142 confirmed infections, and had 264 deaths (as of 2020-05-22), for a raw infection fatality rate of <strong>2.37%</strong>.</p>\n\n<p>Australia and New Zealand both provide approximate confirmation of the South Korea-based estimate. <a href=\"https://www.health.gov.au/sites/default/files/documents/2020/05/coronavirus-covid-19-at-a-glance-coronavirus-covid-19-at-a-glance-infographic_21.pdf\" rel=\"nofollow noreferrer\">Australia</a> has done 1192k tests, found 7106 confirmed infections, and had 102 deaths, for an IFR of <strong>1.43%</strong>. <a href=\"https://www.health.govt.nz/our-work/diseases-and-conditions/covid-19-novel-coronavirus/covid-19-current-situation/covid-19-current-cases\" rel=\"nofollow noreferrer\">New Zealand</a> has done 259k tests, found 1504 confirmed infections, and had 21 deaths, for an IFR of <strong>1.39%</strong>.</p>\n\n<p>In South Korea, the ratio of tests to confirmed infections at 72:1 is very high; Australia and New Zealand are even higher, but (perhaps) with less good tracing. The definition of \"confirmed\" is a positive PCR test, with a positive re-test. South Korea also has a <a href=\"https://www.businessinsider.com/south-korea-contact-tracing-helped-control-nightclub-outbreak-2020-5\" rel=\"nofollow noreferrer\">robust contact tracing program</a>, and surveilance for people presenting with symptoms which would be suspicious even if not linked to a known cluster. Recently, just one new case led to running 45k tests on possible contacts. Of course that doesn't mean they've caught <em>every single</em> infection, but they would not be far from it; it is reasonable to think they have found most of the infections, symptomatic or not. \"Most\" is a bit hard to quantify, but over 50% is virtually certain, and over 80% is quite likely.</p>\n\n<p>The 2.37% fatality rate is quite disturbingly high, and much higher than most other reports, but it does in my opinion come from the most trustworthy (and largest) dataset. There are a few things that may account for that: demographics (older population), most cases occured quite early in the timeline (less worldwide experience on effective treatment), or possibly a few large clusters that just happened to be in an older population; and yes, of course they missed some infections. Because of that I think it's reasonable to think a population-average infection fatality rate ought to be a bit lower; 1% to 2% is a good common-sense range. A somewhat earlier but more detailed South Korean report including demographics is here: <a href=\"https://www.medrxiv.org/content/10.1101/2020.03.15.20036368v1.full.pdf\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.03.15.20036368v1.full.pdf</a> (if anyone can find a more recent one, please add a link to it)</p>\n\n<p>I consider most of the sources collected in other answers as <strong>not credible</strong>, for various reasons. The Lancet article is based primarily on Chinese data. The LA County study was done by Eran Bendavid (who did the similarly flawed Santa Clara study which was thoroughly trashed by just about everyone <a href=\"https://www.mercurynews.com/2020/04/20/feud-over-stanford-coronavirus-study-the-authors-owe-us-all-an-apology/\" rel=\"nofollow noreferrer\">link</a> <a href=\"https://www.nationalgeographic.com/science/2020/05/why-unreliable-tests-are-flooding-the-coronavirus-conversation-cvd/\" rel=\"nofollow noreferrer\">link</a> and subsequently retracted), used an antibody test that may have a fairly high false positive rate (which itself is based on a <em>tiny</em> validation data set; 3 false positives out of 401 known negative samples) and found 35 positives out of 863 (also quite small sample). Common sense says that conclusions based on a whole country's worth of data and based on ultra-reliable PCR tests trumps conclusions based on a few hundred tests based on unreliable antibodies, any day. Similarly, all of the studies cited in Meyerowitz-Katz's meta-analysis linked above either (a) draw conclusions from a tiny number of cases/infections/tests, or (b) use completely unreliable methods to estimate the rate of infections, or both.</p>\n\n<p>I would give the whole-country data from South Korea (and other countries with thorough testing) a huge weight in any meta-analysis; data from large seroconversion studies a medium weight (but there aren't any of those yet); and small seroconversion studies (or studies that just estimate prevalence using models) essentially no weight. <strong>I think trying to claim we know a more precise rate than the 1-2% range I described, or that the rate is significantly less than 1% for an average population, is simply not supported by the data available now.</strong></p>\n\n<p><strong>NOTE</strong> This assumes a health care system which is not overwhelmed. For an example of what happens if the system is overwhelmed, see Italy: also from Statista, Lombardy had 228k tests, 86k reported infections, 15.8k deaths. The ratio of tests to positive results is less than 3:1; the infection fatality rate based on <em>known</em> infections is 18%. How many total infections were there that are not counted? Well, Italian data on seroconversion is pretty sparse, but at least <a href=\"https://www.medrxiv.org/content/10.1101/2020.05.11.20098442v1\" rel=\"nofollow noreferrer\">one source</a> says 4-11% (presumably: 400k to 1.1M infections in Lombardy, with very wide error bars). That gives an IFR of 2 to 5% (also with very wide error bars).</p>\n"
}
] | 2020/05/09 | [
"https://health.stackexchange.com/questions/23565",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19597/"
] |
23,575 | <p>Can every study that is focused on evaluating the effect of a drug in humans be regarded as a clinical trial study? For example: A study is conducted to find the effect of "Azadirachta indica" on hypertension in humans. Can this be called a clinical trial study?</p>
<p>I think the definition of clinical trial study is a study performed to check the effect of a drug or medicinal agent in humans.</p>
| [
{
"answer_id": 23576,
"author": "Franck Dernoncourt",
"author_id": 43,
"author_profile": "https://health.stackexchange.com/users/43",
"pm_score": 2,
"selected": false,
"text": "<p>From <a href=\"https://clinicaltrials.gov/ct2/about-studies/learn#WhatIs\" rel=\"nofollow noreferrer\">https://clinicaltrials.gov/ct2/about-studies/learn#WhatIs</a>:</p>\n\n<blockquote>\n <p>A clinical study involves research using human volunteers (also called participants) that is intended to add to medical knowledge. There are two main types of clinical studies: clinical trials (also called interventional studies) and observational studies. </p>\n</blockquote>\n\n<p>Note that unlike what the quote says, participants/subjects don't have to be human, e.g. see veterinary clinical trials.</p>\n"
},
{
"answer_id": 24938,
"author": "Blue Various",
"author_id": 16820,
"author_profile": "https://health.stackexchange.com/users/16820",
"pm_score": 0,
"selected": false,
"text": "<p>I think the term "clinical study" is broader in meaning than the term 'clinical trial'.</p>\n<p>I think a 'clinical trial' is a clinical study to obtain approval for an investigational drug or medical device, and the notion of the 'clinical study' includes studies that are not aimed at obtaining approval.</p>\n<p>So, 'the study to find the effect of "Azadirachta indica"' is a clinical study, but I think it is somewhat incongruous to call this a clinical trial. However, if the active ingredient is purified and then sought for approval as a drug, I think it would regarded as a clinical trial.</p>\n<p>The <a href=\"https://www.clinicaltrials.gov/ct2/about-studies/learn\" rel=\"nofollow noreferrer\">website</a> of ClinicalTrials.gov has following descriptions;</p>\n<blockquote>\n<p>There are two main types of clinical studies: clinical trials (also called interventional studies) and observational studies. ClinicalTrials.gov includes both interventional and observational studies.</p>\n</blockquote>\n<p>According to the description above, if it is an interventional study, it might be called a clinical trial.</p>\n"
}
] | 2020/05/10 | [
"https://health.stackexchange.com/questions/23575",
"https://health.stackexchange.com",
"https://health.stackexchange.com/users/19601/"
] |