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Sat Apr 25, 2020, 05:11 AM

Asymptomatic Transmission, the Achilles' Heel of Current Strategies to Control Covid-19

Traditional infection-control and public health strategies rely heavily on early detection of disease to contain spread. When Covid-19 burst onto the global scene, public health officials initially deployed interventions that were used to control severe acute respiratory syndrome (SARS) in 2003, including symptom-based case detection and subsequent testing to guide isolation and quarantine. This initial approach was justified by the many similarities between SARS-CoV-1 and SARS-CoV-2, including high genetic relatedness, transmission primarily through respiratory droplets, and the frequency of lower respiratory symptoms (fever, cough, and shortness of breath) with both infections developing a median of 5 days after exposure. However, despite the deployment of similar control interventions, the trajectories of the two epidemics have veered in dramatically different directions. Within 8 months, SARS was controlled after SARS-CoV-1 had infected approximately 8100 persons in limited geographic areas. Within 5 months, SARS-CoV-2 has infected more than 2.6 million people and continues to spread rapidly around the world.

What explains these differences in transmission and spread? A key factor in the transmissibility of Covid-19 is the high level of SARS-CoV-2 shedding in the upper respiratory tract,1even among presymptomatic patients, which distinguishes it from SARS-CoV-1, where replication occurs mainly in the lower respiratory tract.2Viral loads with SARS-CoV-1, which are associated with symptom onset, peak a median of 5 days later than viral loads with SARS-CoV-2, which makes symptom-based detection of infection more effective in the case of SARS CoV-1.3With influenza, persons with asymptomatic disease generally have lower quantitative viral loads in secretions from the upper respiratory tract than from the lower respiratory tract and a shorter duration of viral shedding than persons with symptoms,4which decreases the risk of transmission from paucisymptomatic persons (i.e., those with few symptoms).
Arons et al. now report in theJournalan outbreak of Covid-19 in a skilled nursing facility in Washington State where a health care provider who was working while symptomatic tested positive for infection with SARS-CoV-2 on March 1, 2020.5Residents of the facility were then offered two facility-wide point-prevalence screenings for SARS-CoV-2 by real-time reverse-transcriptase polymerase chain reaction (rRT-PCR) of nasopharyngeal swabs on March 13 and March 1920, along with collection of information on symptoms the residents recalled having had over the preceding 14 days. Symptoms were classified into typical (fever, cough, and shortness of breath), atypical, and none. Among 76 residents in the point-prevalence surveys, 48 (63%) had positive rRT-PCR results, with 27 (56%) essentially asymptomatic, although symptoms subsequently developed in 24 of these residents (within a median of 4 days) and they were reclassified as presymptomatic. Quantitative SARS-CoV-2 viral loads were similarly high in the four symptom groups (residents with typical symptoms, those with atypical symptoms, those who were presymptomatic, and those who remained asymptomatic). It is notable that 17 of 24 specimens (71%) from presymptomatic persons had viable virus by culture 1 to 6 days before the development of symptoms. Finally, the mortality from Covid-19 in this facility was high; of 57 residents who tested positive, 15 (26%) died.

An important finding of this report is that more than half the residents of this skilled nursing facility (27 of 48) who had positive tests were asymptomatic at testing. Moreover, live coronavirus clearly sheds at high concentrations from the nasal cavity even before symptom development. Although the investigators were not able to retrospectively elucidate specific person-to-person transmission events and although symptom ascertainment may be unreliable in a group in which more than half the residents had cognitive impairment, these results indicate that asymptomatic persons are playing a major role in the transmission of SARS-CoV-2. Symptom-based screening alone failed to detect a high proportion of infectious cases and was not enough to control transmission in this setting. The high mortality (>25%) argues that we need to change our current approach for skilled nursing facilities in order to protect vulnerable, enclosed populations until other preventive measures, such as a vaccine or chemoprophylaxis, are available.

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Reply Asymptomatic Transmission, the Achilles' Heel of Current Strategies to Control Covid-19 (Original post)
SunSeeker Apr 2020 OP
Igel Apr 2020 #1
SunSeeker Apr 2020 #2

Response to SunSeeker (Original post)

Sat Apr 25, 2020, 10:08 AM

1. One class that my peers in college hated was syntax.

It wasn't "learn these theories" or "learn these facts."

It was structured as given a few facts, what's a good theory to handle them?

Now, here are more facts, more data. Does our theory work? Can it be saved reasonably? What handles the facts? Got a new or revised theory that works now? Wonderful.

Here are more data. How does your wonderful theory work? Can you save it? Fix it? Replace it? Got a brand new wonderful theory? Stupendous.

Here are more data. (Surprise, it's the midterm!) Fix your theory. (Yes, it's your midterm grade.)

There was protest, and he read them the opening paragraph of the syllabus: It was to teach them how to take data and develop conceptual structures for understanding them and making testable predictions. So this entire theorize/find data/theorize cycle continued through the rest of the fall semester. Before the final it was pure rebellion. Students, almost all the undergrads, demanded that the final *not* be like the midterm. Just test them over what was taught. The professor guaranteed that's what the final would be. He would test them just over what was taught.

Students were mostly shell-shocked when they walked in. "Here's a 1 page summary of where our theory stood last day of class. #1. Here are data. Fix the theory. #2. Okay, here are *more* data--revise your theory or say why you don't need to." Etc. (Most of the grad students smiled. Some laughed--schadenfreude.)

They said he lied. He said he didn't. He wasn't there to teach them data. He wasn't there to teach them a theory.

He was there to teach them how to think, produce testable hypotheses, test hypotheses, revise hypotheses, and decide when to chuck hypotheses and start over. He'd trashed theories that handled any data and weren't falsifiable; he trashed theories that got ever more elaborate and complicated, with exceptions and all kinds of tricks to handle additional data; he trashed theories that simply said the data must be wrong or there must be other data that makes it all okay.

Next term there was one class of 20 or 25 instead of two classes of 60. With 20% of the students he could finally really get down to brass tacks--no headwinds, he could teach.

Relevance? In February and March people devised a hypothesis on how to stop this plague in the US. It was elevated to the status of absolute truth.

People now know about the prevalence of asymptomatic (and presymptomatic) transmission of the SARS-CoV-2 virus. It pretty much either required herculean efforts and conditions that the US would not have accepted in mid *January* or it demolishes the hypothesis that was formed a couple of months ago.

People now hold two incompatible, self-contradictory views: Look how it spreads! From elsewhere, we know it was circulating in January. And, even though it spreads this way and makes these containment methods impossible, we are sufficiently faithful to our catechism (because we need to believe) that had the US done these things in mid-late February we would be safe now--and not only would none of us be sick, but somehow the rest of the world would have been safe.

Given new data, they can't go back and figure out that their hypothesis even needs fixing, much less bring themselves to fix it.

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Response to Igel (Reply #1)

Sat Apr 25, 2020, 12:51 PM

2. If we had done what South Korea did in late January/early February, we would have it under control.

South Korea didn't pretend this was not happening for two months like Trump did. They immediately started mass producing tests as soon as the WHO made the test (developed by Germany) available to the world for replication. They were thus able to use testing to determine where outbreak hot spots were and do targeted quarantines and contact tracing. We never did any of that. That is why they never had to shut down their economy and we did. Shutting down our economy was the only way we could flatten the infection curve and keep our hospitals from being overwhelmed. We could not do it like South Korea was doing it because Trump had completely botched the testing roll out.

And now here we are, with trolls on the internet supporting Republicans' insistence that we reopen immediately. Yet we still don't have widespread testing. No home tests. No drive thru testing at Wal-Mart and Target. We are still only testing the very sick. We still don't even have enough PPE. Trump wasted the month we were on lockdown not ramping up what we needed in order to open back up.

I have not seen anyone argue that had the US done these things in mid-late February we would be "safe" now--nor has anyone said "none of us would be sick" or that "the rest of the world would have been safe." This virus is a horrific danger to the world. But had we followed South Korea's example, we would have just a tiny fraction of the 50,000 US deaths we have right now, and we would not have destroyed our economy. The world looks to the US to deal with pandemics, we failed the world, and ourselves.

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