Coronavirus

Capt. Factorial

This Is Why We Can't Have Nice Things
Staff member
I am just not sure I buy that given the high R0 (I've seen 5.4?) and the fact that the Wuhan outbreak and subsequent Italian outbreak have done far greater damage than anything CA experienced plus it would have spread throughout the US first if CA was the epicenter. Of course it is possible it mutated from whatever hit people in CA last year (and I've heard people go back as far as February of 19) but to me this seems like a lot of wishful thinking.
Wishful thinking might be part of it, but I have to admit that I have no way of explaining how a disease that

1) Is very contagious (high R0)
2) Is frequently asymptomatic
3) Asymptomatic people are contagious
4) Is rampant in a country from which 8,000 visitors a day come to the U.S.

could somehow just fail to get a foothold in the U.S. for months on end. This thing was going in Wuhan by November at least, and travel didn't get shut down until the end of January. That's maybe 2-3 months worth of travelers (so on the order of 500,000+ travelers!) and no foothold? I can't make that add up. So I'm inclined to believe that either some of those assumptions are wrong, or it has already been here.

If it's already here, then the question becomes why didn't we see it?

The antibody tests described in that ABC news article will basically tell us whether the better question is "Why wasn't it here?" or "It was here, why didn't we see it?"
 
Wishful thinking might be part of it, but I have to admit that I have no way of explaining how a disease that

1) Is very contagious (high R0)
2) Is frequently asymptomatic
3) Asymptomatic people are contagious
4) Is rampant in a country from which 8,000 visitors a day come to the U.S.

could somehow just fail to get a foothold in the U.S. for months on end. This thing was going in Wuhan by November at least, and travel didn't get shut down until the end of January. That's maybe 2-3 months worth of travelers (so on the order of 500,000+ travelers!) and no foothold? I can't make that add up. So I'm inclined to believe that either some of those assumptions are wrong, or it has already been here.

If it's already here, then the question becomes why didn't we see it?

The antibody tests described in that ABC news article will basically tell us whether the better question is "Why wasn't it here?" or "It was here, why didn't we see it?"
On the other hand, how could it have had the effect it had in China and then blown up in Europe approximately 2 weeks prior to it simultaneously striking the East and West coasts of the US in massive ways if it was sitting in California for 6 months to a year?

There is a lot of stuff that makes no sense to me about this all. Like how our Governor in Oregon was in a blinking contest between Portland and the rural parts of our state while CA and WA were in full crisis - and yet we have seen a linear rate of infection (no curve) with under 100 cases a day for the last 2 weeks. I don't even think we've hit 1500 in our state. And Portland which is pretty close quarters compared to many CA neighborhoods is not even our epicenter here, it's the outer suburbs.

It seems probable to me that there may be multiple components outside the virus itself, whether they are environmental or other comorbidity factors that dramatically effect the way the virus manifests itself in its hosts.

Or like in the movie Contagion, a large chunk of population is just naturally immune while the population that is vulnerable experiences sudden and rapid illness resulting in hospitalization or death but you have no way of finding out for sure so we hunker down and pray for a vaccine.
 
On the other hand, how could it have had the effect it had in China and then blown up in Europe approximately 2 weeks prior to it simultaneously striking the East and West coasts of the US in massive ways if it was sitting in California for 6 months to a year?

There is a lot of stuff that makes no sense to me about this all. Like how our Governor in Oregon was in a blinking contest between Portland and the rural parts of our state while CA and WA were in full crisis - and yet we have seen a linear rate of infection (no curve) with under 100 cases a day for the last 2 weeks. I don't even think we've hit 1500 in our state. And Portland which is pretty close quarters compared to many CA neighborhoods is not even our epicenter here, it's the outer suburbs.

It seems probable to me that there may be multiple components outside the virus itself, whether they are environmental or other comorbidity factors that dramatically effect the way the virus manifests itself in its hosts.

Or like in the movie Contagion, a large chunk of population is just naturally immune while the population that is vulnerable experiences sudden and rapid illness resulting in hospitalization or death but you have no way of finding out for sure so we hunker down and pray for a vaccine.
One study is type O blood is more resistant and type A is more susceptible. Something like 38% of the population is type O.

The Italy numbers are due to having a high number of the population over 60 years old and direct daily flights from Wuhan and a neighboring province that was cycling in workers for factories. Italy didn't shutdown the flights till March 1st.
 

Capt. Factorial

This Is Why We Can't Have Nice Things
Staff member
On the other hand, how could it have had the effect it had in China and then blown up in Europe approximately 2 weeks prior to it simultaneously striking the East and West coasts of the US in massive ways if it was sitting in California for 6 months to a year?

There is a lot of stuff that makes no sense to me about this all. Like how our Governor in Oregon was in a blinking contest between Portland and the rural parts of our state while CA and WA were in full crisis - and yet we have seen a linear rate of infection (no curve) with under 100 cases a day for the last 2 weeks. I don't even think we've hit 1500 in our state. And Portland which is pretty close quarters compared to many CA neighborhoods is not even our epicenter here, it's the outer suburbs.

It seems probable to me that there may be multiple components outside the virus itself, whether they are environmental or other comorbidity factors that dramatically effect the way the virus manifests itself in its hosts.

Or like in the movie Contagion, a large chunk of population is just naturally immune while the population that is vulnerable experiences sudden and rapid illness resulting in hospitalization or death but you have no way of finding out for sure so we hunker down and pray for a vaccine.
Yeah, it's a puzzle. I'd actually say that Portland not being a current hot spot does seem to argue that perhaps the virus has already come through Portland once before.

I'll throw out another wild guess:

Right now best evidence (and yes, I know a lot is anecdotal and the earliest studies are imperfect due to, I don't know, being thrown together on a moment's notice during a pandemic) suggests that (hydroxy)chloroquine + zinc + azithromycin can sometimes be effective at treating COVID-19. The azithromycin part is initially odd, as it's an antibiotic, but speaks to the fact that secondary infections are a big deal in COVID-19.

So let's assume that for whatever reason, people with COVID-19 are especially susceptible to secondary bacterial infections and see where that gets us.

Let's further assume there was a West coast coronavirus bloom in, say, December. It manifests as an influenza-like-illness, and those who get sick enough to go see the doctor (but not sick enough to need a ventilator, obviously) are told: "You've probably got the flu, go home and rest up." They go home, fight off a nasty bug, and most recover without hospitalization. There are no tests for coronavirus. Nobody knows they have it, and the assumption going around is that it's not in the U.S. anyway. (Some are hospitalized, some die, but influenza kills enough in season that it goes unnoticed as an additional phenomenon.)

Then we have the cruise ship outbreak and the Washington state nursing home outbreak, and there's a rush for testing. Tests are deployed and sure enough, we start finding coronavirus. The more testing ramps up, the more cases we find (of course). But now, when somebody is sick enough to go see the doctor they get a coronavirus test. If they're positive, the doctor says, "Whoa, you've got COVID-19, we can't send you home, we'd better put you in the hospital." And what's a petri dish of secondary infections? The hospital.

What if - and I stress this is just speculation - what if the way we are treating patients now that we *know* they have a disease more deadly than the flu (instead of assuming they just have the flu) is actually unintentionally causing a spike in the death rate? At the very least, assuming the coronavirus has been in the U.S. for a while, this could explain why there wasn't an obvious concomitant jump in mortality until we started testing.

Now, there are a LOT of assumptions here. But I don't know of any data that is problematic for those assumptions. If it turns out that presence of coronavirus antibodies on the West coast is very low, then it certainly doesn't support that wild guess, and leans more towards the idea that it just wasn't here.

It's certainly possible that early waves were less deadly, and there was a mutation that made it worse. But I still don't see how that is able to translate into Portland currently being spared relative to the suburbs without also proposing a previous wave to hit Portland and provide some immunity.
 

VF21

#KingsFansForever
Staff member
Wishful thinking might be part of it, but I have to admit that I have no way of explaining how a disease that

1) Is very contagious (high R0)
2) Is frequently asymptomatic
3) Asymptomatic people are contagious
4) Is rampant in a country from which 8,000 visitors a day come to the U.S.

could somehow just fail to get a foothold in the U.S. for months on end. This thing was going in Wuhan by November at least, and travel didn't get shut down until the end of January. That's maybe 2-3 months worth of travelers (so on the order of 500,000+ travelers!) and no foothold? I can't make that add up. So I'm inclined to believe that either some of those assumptions are wrong, or it has already been here.

If it's already here, then the question becomes why didn't we see it?

The antibody tests described in that ABC news article will basically tell us whether the better question is "Why wasn't it here?" or "It was here, why didn't we see it?"
Just a guess but possibly because until things blew up in China, nobody was paying attention. I was sick in January with what I know now are all the classic symptoms of COVID-19. I was pretty sick for about two weeks before I recovered. I didn't go to the doctor because I was sure it was a variety of the flu. Other people in my community also got sick; most recovered. A couple of them passed but they had pre-existing illnesses/conditions that were most likely contributory factors including COPD, emphysema, etc.

I live in an area that is geographically perfect for social distancing anyway, especially during the winter. Now, with the weather warming up, and people venturing out of their homes into the sunlight, I'm curious to see if it rears its head up here (again?).
 
Interesting thoughts there Capt. I really am beyond puzzled how Portland hasn't at least experienced they same level of cases as Sacramento. Air quality is a little higher here, but so is urban density (by quite a bit). And population sizes are fairly similar.

We are very white, particularly among over 50s. But CA definitely took it seriously about a week before we did.
 
Yeah, it's a puzzle. I'd actually say that Portland not being a current hot spot does seem to argue that perhaps the virus has already come through Portland once before.

I'll throw out another wild guess:

Right now best evidence (and yes, I know a lot is anecdotal and the earliest studies are imperfect due to, I don't know, being thrown together on a moment's notice during a pandemic) suggests that (hydroxy)chloroquine + zinc + azithromycin can sometimes be effective at treating COVID-19. The azithromycin part is initially odd, as it's an antibiotic, but speaks to the fact that secondary infections are a big deal in COVID-19.

So let's assume that for whatever reason, people with COVID-19 are especially susceptible to secondary bacterial infections and see where that gets us.

Let's further assume there was a West coast coronavirus bloom in, say, December. It manifests as an influenza-like-illness, and those who get sick enough to go see the doctor (but not sick enough to need a ventilator, obviously) are told: "You've probably got the flu, go home and rest up." They go home, fight off a nasty bug, and most recover without hospitalization. There are no tests for coronavirus. Nobody knows they have it, and the assumption going around is that it's not in the U.S. anyway. (Some are hospitalized, some die, but influenza kills enough in season that it goes unnoticed as an additional phenomenon.)

Then we have the cruise ship outbreak and the Washington state nursing home outbreak, and there's a rush for testing. Tests are deployed and sure enough, we start finding coronavirus. The more testing ramps up, the more cases we find (of course). But now, when somebody is sick enough to go see the doctor they get a coronavirus test. If they're positive, the doctor says, "Whoa, you've got COVID-19, we can't send you home, we'd better put you in the hospital." And what's a petri dish of secondary infections? The hospital.

What if - and I stress this is just speculation - what if the way we are treating patients now that we *know* they have a disease more deadly than the flu (instead of assuming they just have the flu) is actually unintentionally causing a spike in the death rate? At the very least, assuming the coronavirus has been in the U.S. for a while, this could explain why there wasn't an obvious concomitant jump in mortality until we started testing.

Now, there are a LOT of assumptions here. But I don't know of any data that is problematic for those assumptions. If it turns out that presence of coronavirus antibodies on the West coast is very low, then it certainly doesn't support that wild guess, and leans more towards the idea that it just wasn't here.

It's certainly possible that early waves were less deadly, and there was a mutation that made it worse. But I still don't see how that is able to translate into Portland currently being spared relative to the suburbs without also proposing a previous wave to hit Portland and provide some immunity.
To add on, I know someone who died the Friday before Kobe in January. He was over 60 and pre-existing conditions. He was in the hospital for 2 weeks and eventually a respirator. Probably did die from COVID19 before tests were available.

NY is reporting that 80% of people who go on respirators die. They are trying to not use them anymore. They think either the respirator is doing more damage and stress or enhancing the illness. So if it comes out that a respirator is not the correct treatment, will they change the numbers? Does that meant it was medical malpractice or COVID-19 that killed them?

My office had at least 25% sick over the winter with the COVID 19 symptoms. It's an office of 70 people.
 
I came down with something the week after thanksgiving (very early December). Between thanksgiving get together with family from several states and a large 3 day antique show in downtown Columbus starting on Black Friday.

I was at home with pretty much what’s out there now. Went to my doctor twice and urgent care twice. Lost over 10 pounds and had that dry cough for over a month.

My doctor had told me it was a viral thing and was happy it stayed out of my lungs. He also said more than half of his patients were coming in for the same thing. I have O positive for what ever that means.

I have no idea if here in Ohio we had a higher than average death rate during that time? But with how many folks are dying in New York City at this point that is a horse of a different color.

More than likely a slightly different strain that’s more aggressive.
 

Warhawk

The cake is a lie.
Staff member
NY is reporting that 80% of people who go on respirators die. They are trying to not use them anymore. They think either the respirator is doing more damage and stress or enhancing the illness. So if it comes out that a respirator is not the correct treatment, will they change the numbers? Does that meant it was medical malpractice or COVID-19 that killed them?
To be fair, only the "worst case" patients go on respirators to begin with. That's like saying 80% of those with stage 4 cancer die, but overall the cancer mortality rate is much less. While there may be something to respirators not being the best course of treatment, I wouldn't point at them being a cause for concern quite yet until more studies are done.
 
Have been talking to a few friends with minor symptoms like asthma or bronchitis and it seems at least their doctors have put them on a 7 day self quarantine. It may be a little overboard but why not be save until we have better ways to test folks remotely at our doctors office.
 

Warhawk

The cake is a lie.
Staff member
Interesting.

https://slate.com/technology/2020/04/coronavirus-circulating-california-2019-bunk.html

Let’s start with the facts. I reached out to Stanford Medicine to try to understand the goals of its antibody test, and how it relates to Hanson’s fall 2019 theory. The short answer on the latter is that it doesn’t. “Our research does not suggest that the virus was here that early,” says Lisa Kim of Stanford’s media relations team.

Neither does anyone else’s, it appears. “There is zero probability [SARS-CoV-2] was circulating in fall 2019,” tweeted Trevor Bedford, a computational biologist at Fred Hutchinson Cancer Research Center who has been tracking SARS-CoV-2’s genetic code as it has spread. Allison Black, a genomic epidemiologist working in Bedford’s lab, says this is apparent from researchers’ data. As the virus spreads, it also mutates, much like the way words change in a game of Telephone. By sequencing the virus’s genome from different individual samples, researchers can track strains of the coronavirus back to its origins. They have been continually updating their findings on Nextstrain. (In case you’re wondering, the strains have nothing to do with severity of illness. They’re simply a way to track the virus’s mutations over time.)

Richard Neher, an evolutionary biologist at the University of Basel in Switzerland, told the Scientist that Nextstrain researchers’ work has tracked the virus back to a single source “somewhere between mid-November and early December,” which then spread in China. The earliest cases in the U.S. appeared in January 2020, according to Nextstrain’s sequencing work. Washington state, where the first known COVID-19 case in the U.S. was identified, has at least six strains. A similar analysis of California’s coronavirus cases—which has yet to be peer-reviewed—identified at least eight strains in the state, suggesting transmission from Washington state, New York, Europe, and China.

If genomics aren’t your thing, consider this: If the virus had arrived earlier, we would have known. Humans have no natural immunity to this new virus, which is why it’s spreading quickly, infecting millions and killing tens of thousands. That’s evident in what’s going on in New York right now, says Black. “If it had arrived in fall of 2019, and we were all living our lives as normal, we would’ve had New York back in fall of 2019,” she says. There’s no reason why this virus would have spread undetected for months before wreaking the havoc it has.
 
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Yeah, it's a puzzle. I'd actually say that Portland not being a current hot spot does seem to argue that perhaps the virus has already come through Portland once before.

I'll throw out another wild guess:

Right now best evidence (and yes, I know a lot is anecdotal and the earliest studies are imperfect due to, I don't know, being thrown together on a moment's notice during a pandemic) suggests that (hydroxy)chloroquine + zinc + azithromycin can sometimes be effective at treating COVID-19. The azithromycin part is initially odd, as it's an antibiotic, but speaks to the fact that secondary infections are a big deal in COVID-19.

So let's assume that for whatever reason, people with COVID-19 are especially susceptible to secondary bacterial infections and see where that gets us.

Let's further assume there was a West coast coronavirus bloom in, say, December. It manifests as an influenza-like-illness, and those who get sick enough to go see the doctor (but not sick enough to need a ventilator, obviously) are told: "You've probably got the flu, go home and rest up." They go home, fight off a nasty bug, and most recover without hospitalization. There are no tests for coronavirus. Nobody knows they have it, and the assumption going around is that it's not in the U.S. anyway. (Some are hospitalized, some die, but influenza kills enough in season that it goes unnoticed as an additional phenomenon.)

Then we have the cruise ship outbreak and the Washington state nursing home outbreak, and there's a rush for testing. Tests are deployed and sure enough, we start finding coronavirus. The more testing ramps up, the more cases we find (of course). But now, when somebody is sick enough to go see the doctor they get a coronavirus test. If they're positive, the doctor says, "Whoa, you've got COVID-19, we can't send you home, we'd better put you in the hospital." And what's a petri dish of secondary infections? The hospital.

What if - and I stress this is just speculation - what if the way we are treating patients now that we *know* they have a disease more deadly than the flu (instead of assuming they just have the flu) is actually unintentionally causing a spike in the death rate? At the very least, assuming the coronavirus has been in the U.S. for a while, this could explain why there wasn't an obvious concomitant jump in mortality until we started testing.

Now, there are a LOT of assumptions here. But I don't know of any data that is problematic for those assumptions. If it turns out that presence of coronavirus antibodies on the West coast is very low, then it certainly doesn't support that wild guess, and leans more towards the idea that it just wasn't here.

It's certainly possible that early waves were less deadly, and there was a mutation that made it worse. But I still don't see how that is able to translate into Portland currently being spared relative to the suburbs without also proposing a previous wave to hit Portland and provide some immunity.
The azithromycin is used for more of a synergistic effect rather than for its antibacterial profile. It’s actually a “weaker” antibiotic than what we normally use in the hospital. While it’s true you can get coinfection with bacterial infection ( we see a lot of this in flu patient) the coverage choice of antibiotic is usually a lot broader and stronger in the hospital since we assume they may catch a bacterial infection in the hospital. In fact, In chronic COPD patient, I tend to use azithromycin along with doxycycline since they both have a mild anti inflammatory properties.
 
Or it was here in a strain that wasn't as contagious and didn't mutate till January. The Chinese media is less trustworthy than ours so who knows what was happening in China in the fall. Some reports say it was around a year ago in China.
I think the gist of the article (third paragraph on) is that we have the genetic papertrail that disproves that hypothesis.
 
I caught the flu earlier this week and did a phone appointment with the doctor. He said since I didn't have breathing problems then I probably didn't have it and am not a candidate to get tested. It's unnerving because not everyone has the exact same symptoms when it comes to this virus so I'm stuck in this limbo where I don't know whether I have it or not. I don't think I do but I can't be sure so now I don't know if I should return to work or what.
Good luck with that. I think it's ridiculous that someone in your position cannot get tested. Everyone reacts as an individual. There's too much thought by the medical field that EVERYONE has to have the exact same symptoms and reactions. That's why vaccines don't work for everyone. This whole testing process has been a cluster**** since the beginning. You'd think it would have been solved by now. Maybe you should call back and tell them you're having breathing problems now. Whatever.
 
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VF21

#KingsFansForever
Staff member
Good luck with that. I think it's ridiculous that someone in your position cannot get tested. Everyone reacts as an individual. There's too much thought by the medical field that EVERYONE has to have the exact same symptoms and reactions. That's why vaccines don't work for everyone. This whole testing process has been a cluster**** since the beginning. You'd think it would have been solved by now. Maybe you should call back and tell them you're having breathing problems now. Whatever.
The post you're answering is almost a month old...
 
will do captain :). I read some favorable reviews on the 2 whiskeys and while I have not had this specific Oban, it’s my go to scotch.
I will provide my write up after I get past this raging headache
On a related note...I think there is a possibility my kids, and myself, find maybe 50% of the eggs I just hid
 
That Balcones looks quite woody...I expect a report!
ok here is my review...
-Balcones has a bite to it and you are right, had a woody flavor with a little fruit elements. My wife hated it. I like a bite to my whiskey, so I enjoyed it.
-the Shin was pretty smooth, but Smokey. Tasted like a scotch. My wife enjoyed that one, but the bar was low from the Balcones lol
-the Oban little bay was super smooth. I really like my scotch on the rocks and specifically after the ice has melted a bit. I really need to just start cutting my scotch with cold water. My wife is not a fan of scotch, but once she tried it when it was watered down she really enjoyed it

happy Easter everyone :)
 
-the Oban little bay was super smooth. I really like my scotch on the rocks and specifically after the ice has melted a bit. I really need to just start cutting my scotch with cold water. My wife is not a fan of scotch, but once she tried it when it was watered down she really enjoyed it

happy Easter everyone :)
This is how I drink and sounds up my alley. I get a little frustrated with those places that do "ROCK" instead of rocks because those giant cubes don't melt. they also don't seem to get my whiskey to it's preferred temp and I don't get to enjoy nibbling those seasoned ice cubes while waiting for round 2. or 3. or 4.

I am not a drunk I swear!

happy easter!!!
 
Just read where Karl-Anthony towns mother passed away from complications of Coronavirus.
Sadly many people are passing away due to this virus as most every day someone who is known has left us.