It’s rather peculiar to dismiss our knowledge of how other diseases act and think we should be starting from ground zero here. There’s no reason to think asymptomatic people are quietly getting permanent neurological damage.
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Correct, it does not include the past week. However, I don’t think that would alter the story. There was not a spike in deaths that I’m aware of. Number of deaths has continued to trend down. For me, one of the most frustrating things surrounding COVID is uncertainty surrounding data. I view the CDC as a reasonable source. Perfect? Nope. I’m 100% open to suggestions as to a more reliable data set.
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Yes, I neglected to include babies. In my mind babies and children represent distinct groups Maybe they shouldn’t. Here’s how the data looks on babies under 1 year from 2/1/2020 through 6/20/2020: 6,504 total deaths - 9 from COVID, 59 from pneumonia, 14 from influenza.
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Again, data is murky. If there’s a golden standard we should I use, I’d love to have access to it. Are some places undercounting COVID deaths? Certainly possible. Are some places overcounting? Also possible. People will have to set their own confidence intervals and assume the data is accurate to within band they deem reasonable. 10%? 20%? I’d say that’s defensible. I personally don’t think the numbers are skewed by > 50% or anything near that magnitude. I don’t find the suggestion that a child could have died from COVID and it completely escaped the doctors and coroner very likely to be true. Given the current climate, I’d venture to say that 99+% of kids that have died with respiratory symptoms have been tested for COVID.
Nor is there any reason to think they don’t, especially given that some people who do show symptoms do get permanent damage.
It could eventually turn us all into lizard people. We just have no way of knowing.
You gonna eat that fly?
~VOW 
Go ahead, I don’t like wings.
[quote=“mhendo, post:238, topic:913281”]But I also think it’s important not to just soak up and throw around terms like “super spreaders” without looking at what the epidemiologists have to say.[/quote] (sorry, not sure what happened with the quote thingy)
It stands to reason that if we’re referring to really young people who are less likely than their adult counterparts to get the disease, they are naturally less likely to spread it as well.
And yet, the outbreaks are clearly happening at an accelerated rate, and the population that seems to be coming down with COVID-19 is much younger than before. They may not be school-aged children, but they are part of a demographic that is younger and considered to be in the lower-risk category.
So what gives? Maybe it’s the fact that even if a particular group is comparatively more immune and less infectious, if said group gets infected in sufficient enough numbers, you can throw “low risk” out the door. The sheer volume of the patients makes this age group a risk. This is what I am referring to when I refer to vectors.
From the above article:
“We know why the overall death count is much higher than normal. There are various reasons why there’s a gap between that figure (O) and the normal average (n) plus the covid-19 (c) count (O > n + c). There could be an undercount for covid-19 because there haven’t been enough tests conducted and many people who died from covid-19 were given a different cause of death. It could be that the data collection is just delayed. Or it could be that some people/agencies are assigning the wrong cause of death in order to keep the covid-19 death count lower. In reality, it’s probably a combination of those factors, but the degree to which it is one or another is not clear at all at this point.”
While I do agree that students are less likely to transmit the disease, the thing that the pediatrics people miss is that a lot of the research cited is preliminary, and opening the schools does miss an important item, how the contacts multiply and make the situation worse even if the kids transmit the disease less.
In one study, published last week in the journal Science, a team analyzed data from two cities in China — Wuhan, where the virus first emerged, and Shanghai — and found that children were about a third as susceptible to coronavirus infection as adults were. But when schools were open, they found, children had about three times as many contacts as adults, and three times as many opportunities to become infected, essentially evening out their risk.
Based on their data, the researchers estimated that closing schools is not enough on its own to stop an outbreak, but it can reduce the surge by about 40 to 60 percent and slow the epidemic’s course.
“My simulation shows that yes, if you reopen the schools, you’ll see a big increase in the reproduction number, which is exactly what you don’t want,” said Marco Ajelli, a mathematical epidemiologist who did the work while at the Bruno Kessler Foundation in Trento, Italy.
It was for this and other studies that the ones in the study I previously cited concluded that there is still a lot of uncertainty.
Here’s a child who won’t be in anybody’s mortality figures, because she survived. I’m sure she and her family really wish she hadn’t caught it, though.
More than 145 children are believed to have it in New York City and at least about 50 more in New York state. Three have died. In recent days, medical centers in 14 other states have reported similar cases. Scientists still believe most children and young people experience only mild illness or none at all if they become infected with the coronavirus. But they’re concerned about the critical nature of the inflammatory syndrome cases, which seem to be appearing in children weeks after a wave of infections in their communities.
Note the date of the story is May 17. Not sure what’s happened since. Story implies up to a two-month lag between an initially asymptomatic case and the onset of severe and possibly fatal symptoms. – here’s a more recent article, which found an increasing number of cases (the study ran from mid-March to mid-May and nearly all the cases were hospitalized after April 16).
From the above article:
“We know why the overall death count is much higher than normal. There are various reasons why there’s a gap between that figure (O) and the normal average (n) plus the covid-19 © count (O > n + c). There could be an undercount for covid-19 because there haven’t been enough tests conducted and many people who died from covid-19 were given a different cause of death. It could be that the data collection is just delayed. Or it could be that some people/agencies are assigning the wrong cause of death in order to keep the covid-19 death count lower. In reality, it’s probably a combination of those factors, but the degree to which it is one or another is not clear at all at this point.”
This seems to have been mostly debunked, at least the sky-high discrepancy in the Howard Dean post quoted in the article. Slightly confusing Twitter thread here, and less detailed news article here. Covid deaths probably are being undercounted, but not by anywhere near that much.
You mean in the middle ages?
One of the problems here is that symptoms can be incredibly diverse, and as some of the articles above cited note, respiratory symptoms are the most common but not the only ones. If a kid presents with neurological symptoms but no cough, e.g., are they still going to be tested for COVID? Would they have been back in March?
It’s not just that it doesn’t include the past week. The data can be much further behind; previous analyses of data completeness suggest that provisional counts are at least 75% complete within eight weeks of when the death occurred, but that still leaves a good chunk of deaths not correctly included even two months later. CDC thinks data timeliness has improved, but also notes that COVID deaths always require and influenza/pneumonia death are more likely to require manual coding, rather than automated processing. Non-standard or atypical presentations are particularly likely to be delayed, so there can be biases in the data that have material effects on fast-moving stories. There’s not a good way around this; you’re not going to find more reliable data, but I think it important to acknowledge the imperfections and uncertainties in the data, not just blithely state the provisional numbers as established fact. Just last week, New Jersey added more than 1800 deaths to their state’s count, increasing the toll by more than 14%, the majority just from a review of already-completed death certificates.
There are occasional case reports of people developing shingles without a history of chickenpox. Asymptomatic chlamydia can still cause long-term reproductive challenges such as tubal infertility. Congenital cytomegalovirus, even when asymptomatic at birth, is associated with increased risk of delayed-onset hearing loss, and there is some evidence of below-average intelligence and difficulties in language processing and verbal development.
There may be other long-term effects besides the neurological, of course. For example, one study out of China (not kids, however) showed that asymptomatic patients still showed lung lesions (“ground glass opacity”) on chest CT scans. Most will probably resolve on their own, but the inflammation that caused GGO is implicated in other lung disease such as COPD.
[addition due to character limits]
One thing to consider is what is the definition of asymptomatic? If the kid never has a fever, never has a cough, never shows any obvious definite symptoms at all, but was tired and cranky for a day or two, were they actually asymptomatic or merely paucisymptomatic? How clearly delineated and serious must the complaint be before it qualifies as an actual symptom?
A practical definition of “asymptomatic” is “Felt good enough to continue going about their normal daily activities and was never tested because there was no trigger for a test. But a later antibody tests shows they’d had COVID at some point in the past.”
So the point is that they passed through their period of contagiousness, however long and however intense that was, none the wiser that they were actively spreading disease towards whoever they encountered. Some of whom are likely to have caught it
And that, in addition to the point made in GIGOBuster’s cite about schools, is the real meat here. Whether we’re talking about schools specifically or any other sustained group interaction.
Practically asymptomatic cases exist. If any decent fraction of those folks are engaged in normal high-encounter-density life, eg. as school kids, high school students, college students, party-hearty 20-somethings, factory workers, in-office workers, they will be having close encounters at a monstrous rate compared to e.g. semi-retired folks like me who spend only 30 minutes per week in public and get within 6 feet of just 1 person per a week and then only briefly while outdoors and both masked.
It’s number of people infected times severity/contagiability per infected person times number of people encountered divided by effectiveness of both parties’ protective measures that determines spread.
Me wearing an N95 perfectly might reduce threats to me by WAG 80%. But if I’m mostly hanging around e.g. college kids who’re multiplying their individual threats by WAG 100x by their normal social behavior, the net effect is my risk is up 20x.
That’s a losing game when the whole society plays it. Which IMO it seems to be doing.
How about HPV?
Nice Latin! I hope you were there to trot that out when Republicans manufactured the notion of Obamacare “death panels”. 
I thought about that as I posted, actually. I’m not sure “makes you more susceptible to cancer in 30 years” is quite the same but certainly something to worry about.
Any distinction you draw is arbitrary. There’s literally dozens of viruses that in the early stages are non-lethal, mild and/or asymptomatic yet can have long term life altering impacts. Hepatitis, Polio, Zika, HIV, West Nile, Herpes, Shingles, Epstein-Barr and hundreds more that we don’t yet fully understand. Some doctors believe that a significant number of cancers are precipitated by yet unknown RNA viruses.
Just an FYI, cervical cancer is a disease of relatively young women . . .30s, early 40s. It doesn’t take 30 years for HPV to kill you.