Tag Archives: Covid-19

Opening the schools, Plan B

This should really be Plan A but no school district is going to adopt this plan until after just the right cute little kid or beloved teacher dies of Covid-19 on a news day with few other distractions. This plan pertains to High Schools only. Perhaps later we can extend a version of this to other grades.

Here’s the plan.

1) Admit there is a deadly pandemic and that we need to not feed the virus. Also recognize that a realistic estimate of when a vaccine starts to be available is during the school year after the upcoming one, and that it will take a year or so to fully deploy it in the US. The plan for starting school should not be, as it is now, “we’ll do this for the first week then… who knows?” The plan should be one that will flexible but outlined for a two or three year time range, because that is the time range over which this pandemic is going to play out.

2) Change the requirements for graduating from high school. Henceforth, students must meet the core* class requirements, and do not need to meet total credit requirements. All students who have met these requirements are graduated instantly. That would instantly reduce the number of students in the schools by a few percent.

4) Add one year to the high school plan. Call it “Covid-Extention-Year.” (Why? See below.)

3) Identify (mainly) Seniors and Juniors who have only a few core class requirements to finish. Spread those required classes over the next two years (some Seniors will thus be extending their school time into CEY). Many students in most schools will in this manner only have one class at a time, at most, with many semesters/quarters not having to attend school at all.

4) Restrict all other teaching to core requirements only. So, no electives. All teachers are switched to core requirements, all students are taking core requirements.

Suddenly, 3-4% of students would be gone. Within one semester, another 10-15% of students would be graduated, while another 20% of students would be committed to attending school for only one or two classes over about a year and a half. These first four changes simply thin out the herd gracefully and without killing anyone, as opposed to the current approach, which will thin out the herd the hard way.

5) Do as much distance learning as possible, but if classes are required…

6) Revise the one room schoolhouse model.

  • Students stay in one room.
  • Passing time and bathroom access is set up to minimize hallway contact.
  • Teachers move from room to room (teaching core classes only) and wear hazmat
  • Very few students in each room so when an infection pops up the total number of students removed from school is small. They can come back in a few weeks.
  • Since teachers are suited up they do not have to be quarantined when a student in their room tests positive.

It is essential to keep the teaching staff intact. There will be more needed than usual because several will be out sick for more time than usual. Classes, both distant and in person, should have smaller class size (for most classes, some distant learning classes may not need that). The one room schoolhouse method not only reduces infection, but serves another goal: Relationship building will be easier and more solid in mostly distance learning settings.

*Many schools use the term “core” to refer to a specific subset of academics. What I mean here is different, and includes more. Think of it this way: Look at a set of class records for a sample of seniors. Consider the total number of classes, and the types of classes, that make those students viable HS graduates, and cut out everything else. In other words, pare down. Most students manage to get what we think of as a full on high school degree with a few classes extra. Some students do everything in three years, and earn a year of college. This does not mean removing art or music. It means paring down the individual student’s total work, and probably, the full range of options.

By reducing the number of students and keeping the number of teachers the same, and simplifying the offerings, it is easier to have smaller one-room learning units. While distance learning is ongoing the one-room learning units are not necessary, but they are ready to go when the students and teachers are called back into the classroom. This might be after a vaccine is available, but is still being deployed, and the virus is in smaller numbers but still a threat, which one might estimate to be some time during the 2021-2022 school year.

Understating Airborne Covid-19

My title is slightly misleading but meant to tell you what this essay is about. I want to talk about recent reports that SARS-CoV-2, the virus that causes Covid-19, is airborne.

The concept of airborne in thinking about pathogens is probably the single most misunderstood thing in epidemiology, not by epidemiologists but by regular people. It is also probably the most evocative, and stupifying. Recently, the word “airborne” has been used in discussions of Covid-19, and this led to many extreme reactions. Like this:

Input: Bla bla bla Covid-19 bla bla bla airborne.

Output: All the credible experts have agreed that Covid is airbone! it is no longer spread by contact, but now it is airborne! The Fauci mutation probably made it airborne! And so on!

SARS-CoV-2 is spread by shedding from an infected person’s respiratory system and getting into a new host’s respiratory system via droplets of mucus that go from hand to hand, hand to mouth, mouth to hand, mouth or nose to surface, surface to hand then hand to mouth, etc. Human upper respiratory bodily fluids (snot, etc.) get on stuff and then people touch stuff and then it get into their respiratory system. This is how most cold and flu infections are passed on, generally. That is not airborne spread.

Among all the many viruses that give us colds or the flu — the many strains of influenza, rhinovirus, coronaviruses other than SARS-CoV-2, etc. — this is how infection happens.

Again, this is not airborne spread. It might be airborne in your head, because you imagine someone sneezing, into the air, droplets of virus-containing spittle and snot flying around in the air, and since that stuff flies through the air it must therefore airborne. But that is not what airborne means, and the distinction is important.

There is probably a certain amount of true airborne transmission in any of the above mentioned categories of virus, including the flu and more common colds. But it is rare enough that these diseases are not said to be airborne.

So what is airborne then, if it is not simply flying snot particles?

Airborne spread requires several things to be true often enough that an observable number of cases were spread in this way. First, the virus must be aerosolized. This means that the virus is embedded in a very small gobs of snot, perhaps near 5 microns, droplets that are small enough to be suspended in the air. Larger drops will fall out of the air, these smaller drops will float in the air like they were part of the air. They act like a gas in the air.

The droplets also have to be small enough to get into the parts of the respiratory system that the virus targets, which for SARS-CoV-2 is not too much of a limiting factor since it likes to inhabit the upper respiratory tract. But, since it also can invade the lungs, there would be the possibility that airborne transmission would be more associated with a more serious infection, if and when it happens.

Airborne spread also requires that the virus can live in the air long enough to get to its target. The longer the virus can live in the air, the worse of a problem it is because it can travel farther, through ventilation systems, down hallways, etc. There is no evidence that SARS-CoV-2 does that like, say measles, the king of airborne infection does it. Whatever environmental conditions are experienced by this suspended droplet have to NOT kill the virus. IV light kills SARS-CoV-2, so it is not going to get far during the day, outside, when the sun is out. SARS-CoV-2 might like certain humidity levels. None of this is really known for SARS-CoV-2, but it is a virus of type that we generally know about. Other forms of coronavirus are known to survive a while in the air, so that may pertain here. Be cautious in reacting to what you hear though. Detecting a virus some distance away from a sneeze does not mean that the virus is viable or capable of infection

Also, the virus has to be out there in the air in sufficient numbers to actually cause an infection. One would think that it only takes one single virus to infect someone, but generally it takes a much larger number. There seems to be a threshold for most viruses. The body dispenses of the first N viruses, then after that it gets harder, and eventually the system is overwhelmed. Maybe. The point is, virus experts will tell you that is has to be a large number for most viruses, and this is certainly true for SARS-CoV-2.

Truly aerosolized, viable, in sufficient numbers.

Finally, note that if SARS-CoV-2 was mainly airborne, we would know it by now. You can look at it, epidemiologically, and say, no, the main form of transmission is not airborne. That does not mean that there is not an airborne component, but it means that airborne is not the major way of spread. That has not changed.

What does the new research tell us?

Well, by the standards of peer reviewed scientific research, pretty much nothing, because that research is still in its infancy. But here is what happened. Several cases of infection have been reported that can be best explained by airborne infection. How many? So few that some would interpret that as potentially useless data. These may be cases that are simply misreported. Somebody licked someone else’s tongue and refuses to admit it. Does that really happen? Well, ask any expert on the epidemiology of sexually transmitted diseases about it. Of course it can. Most rare cases can be explained away or ignored.

But in this case, a large number of experts have settled on a provisional consensus: They see enough cases of possible airborne transmission of SARS-CoV-2 to ask the overarching institutional authorities like the CDC to seriously consider it and look into it. Yeah, that is it. Important, concerning, should shape policy modestly for now, requires more consideration. The smart money is on SARS-CoV-2 being transmittable via aerosol, though that will probably not be the main modality of transmission in most settings. That is my bet. Airborne transmission can happen, and will happen in some cases. More on that below. But, this is provisional.

What this does not mean.

This does not mean that there is a new mutation. Repeat: this is not a new mutation. This has been there all along, and the fact that it has not been obvious since the beginning means, as stated, this is not the new mode of transmission. This does not mean that the virus has changed. Probably.

This also has no impact on mask wearing. Airborne transmission will go right around the masks most people wear, but we already know that if airborne transmission is happening, it is not the main way the virus is spread. This is NOT AN ARGUMENT TO NOT WEAR MASKS so don’t go making that argument or you are a full-on jerk. Ignorant jerk. I know you won’t, but if you see that argument being made by others, that is what you are seeing. That argument is so stupid, you can expect Trump to make it soon.

What this might mean.

This is the important part of all this, worthy of careful consideration. Assume that normal near-distance non airborne transmission is the normal and most common form of transmission by a large margin. We assume that if people are kept a minimum of 6 feet away from each other (or 10 if you like) and do not share objects with their hands and faces, i.e, social distancing, that transmission will be minimized. This works for social gatherings, according to some, especially if masks are worn.

However, over longer term, while people are avoiding infecting each other by keeping their mucus to themselves, a low level background transmission via the air could be happening at a small level.

It would be rare. Say one hour of exposure within a single medium size room with modest air circulation has a one in a thousand chance of one infected person giving the disease to one other person in the room. (I am totally making up all these numbers, but just bear with me.)

But now, we take that room and put between zero and three infected people in it, and 30 target non infected people. But we put then in that room for 8 hours, and do that for 185 days. This configuration of people might sound familiar to you.

This is a classroom full of students social distancing. But wait, you say, if they are social distancing, they can’t fit 30 people in the room. But you would be wrong in some cases. Elementary schools with the pod system have four classes of 30 (including teachers) in the room. They will get their social distancing by spreading out into larger rooms in closed high schools or other places (gyms, etc.), so the main class of about 30 is still in one room. Maybe not. The point is, in the worst case scenario, we divide 1,000 by 8 (hours) then again by 185 (days) to get a baseline on transmission probability (though the math is slightly more complex than that) to arrive at this conclusion: Transmission within the classroom where there are one or two virus shedding individuals on any given day is nearly inevitable if there is a low probability of airborne transmission. Most classrooms may have zero infected people most of the time, but in a given school there would be several classes. In a given school system, maybe dozens and dozens.

If the air circulation does not remove the viruses, maybe they are being spread across the school. Students passing in halls, or any classes where the kids are reshuffled add to the dynamic, families with multiple kids (or both kids and staff) in the same school, etc. add to the dynamic.

You can do a similar calculation for restaurants and bars. Regular inside dining and bar hopping even with social distancing and mask wearing is probably not recommended if there is a low level of airborne transmission. More limitations on how retail shopping happens may be recommended. Certainly, unnecessary retail shopping maybe an unnecessary danger.

The final meaning of it all: When it comes to basic day to day life, under the current conditions of caution and distancing, this airborne problem would not have that much of an effect because it has to be rare. We know it is rare (if it is real) because if it was common we would see it. But, under school or large workplace reopening conditions, or reopening of indoor dining and shopping, etc., it may be a factor that causes two really bad problems.

1) More outbreaks, and some insidious ones. The school children, some getting very sick and maybe dying, others never becoming ill, passing the disease on to their families. Ignoring the airborne problem may involve asking our children to kill their grandparents, then live with that for the rest of their lives. You might get sick because you needed to shop for a new comic book or try out the headphones at the electronic store instead of ordering on line.

2) Not discussed anywhere else as far as I know, but I would think obvious: if we set up a situation where the rare airborne transmission has a better chance of actually transmitting the disease, we may also be setting up a positive selective environment for that. In other words, we may help make SARS-CoV-2 more airborne by giving it this chance. That is pure speculation on my part, but speculation based on some damn powerful theory (Darwinian evolution). It is not a chance I’d like to take.

How The Pandemic Ends

The gold standard, the ones to beat, the top dog, brain trust magnate, 800 pound gorilla, paragon, cream of the crop, and the one head and shoulders above all others, in the matter of a Covid-19 vaccine, is Oxford.

The group at Oxford already made a Coronavirus vaccine, for MERS, but it never underwent final testing and deployment. Not enough people were getting sick from MERS, and it was under control.

This group is optimistic about having a vaccine in September of this year. Give them a month leeway, a few months for emergency intensified field testing, and some extra time to ramp up production and negotiate liability issues, and we could have a world wide vaccination program well under way by the end of January.

Between now and, say, August 15th, the medicos will have developed and deployed a half dozen nursing, ER, and IC procedures that drop the death rate of the most severely ill well below its near 90% level, to maybe half, and various treatments, therapies, and all will drop the number who go from diagnosed to severe down by a double digit percent.

Although natural herd immunity would take multiple waves and years, a certain reduction of infection rate happens at any percentage. New normal practices will have adapted to slow the disease. By mid September there will be parts of the US, and various smaller sized countries, where COVID-19 will become rare or nearly non existent, even as new hotspots emerge. But even those hotspots will be dealt with better than the US addressed this disaster in the early week.

But the flareups will be severe, and in most cases, caused by politically driven Republican strategies cheered on by Trump and sullenly overseen by Pence. The carnage will continue to be so bad, and the response to it by Trump and his gang of Republicans so inept and inextricably linked to nefarious side bets and deals, that there is a non-zero chance his administration will not still be in place on election day, November 3rd. Either way, Trump will be voted out of office on November 3rd, and probably dragged from the White House and impaled with a broom stick well before inauguration day by angry tourists and DC residents after he attempts to annul the election results. There is a non-zero chance that the 46th President of the United States will be Speaker Pelozi, for the several days between Trump and Pence’s awkward and painful departure (captured on hundreds of cell phones) and the inauguration of President Joe Biden.

There will be no Biden Inaugural Ball and his Inauguration speech will be on Zoom, But his first act will be to sign the 2021 Rapid Immunization Order, speeding up the delivery of the vaccine already developed by Oxford and manufactured everywhere but the United States even as Jared Kushner tries to get his vaccine (which is fatal to 1 in 200 who are injected with it, and does not actually protect against COVID-19) to be the legally required stick.

But I digress.

Schools will not reopen in the Fall, but by Spring it will be possible to have limited activities, as vaccination spreads faster than COVID-19 itself ever did. Kids who come from anti-Vax families will be shunned, and hate their parents forever, because they won’t be allowed to go to the 2021 proms and graduation ceremonies, which will be endlessly televised and smeared across social media until we are giddily sick of them.

By the end of 2021, the virus will be history (except in the Congo, where all diseases go to retire securely), social distancing will be a fond memory (for everyone with sensory processing disorder), and our new society, led by science and reason, will begin the process of building windmills instead of tilting at them.

Problems conceptualizing Covid

The Covid-19 pandemic is serious, scary, real, and kills. And there is a fair amount we don’t know about it.

There I said it. You don’t have to worry about me thinking Covid-19 isn’t serious. That happens to me a lot. Someone says “OMG, the COVID-19 is just like a grizzly bear eating your face off!” and I point out that a virus and a face-eating grizzly bear present distinctly different problems. Then the person gets all pissy and mad because I did not share their specific horror. Generally, I prefer it if people do not shove their fears in my face at the expense of reason. We have real fears, we don’t need to add on the ones that are bogus, unsupported, panicked, or untethered from reality.

You might say, jeezh, Greg, what harm does it do if people don’t understand every little thing about COVID-19 and, in their conceptualizing this disease, stray away from actual science and reality and stuff? Most of the time it probably does’t matter. But people make decisions on the basis of what they think they know. If you think the SARS-CoV2 virus doesn’t really live on surfaces, you won’t be careful about door knobs and push plates in heavily used public places, and you may thus contribute to the spread of this disease. If you think COVID-19 can be spread by eating food from a can, you might waste your energy, my energy, everybody’s energy, by campaigning against canned food. And so on.

So what kinds of things are people getting wrong? Here’s a sampling.

COVID-19 is caused by a virus. Most life lessons about pathogens are not transferable across types of pathogens. A coronavirus can’t be compared usefully to malaria or sleeping sickness because those are single celled eukaryotes. COVID-19 can’t be compared to bacterial infections. All these different kinds of pathogens have different effects, do different things, act in different ways, and need to be dealt with using specific actions (or avoiding specific actions).

COVID-19 is caused by a particular type of virus. There are many kinds of viruses, and the different kinds have distinctly different biologies. Comparing the behavior of SARS-CoV2, the virus that causes COVID-19, to the influenza virus, is like comparing the behavior of eels to eagles. How they reproduce inside a cell, how they avoid a body’s immune response, how much they mutate, and how a vaccine might work for each type of virus, are really very different, in fact, astonishingly different. Comparisons are not helpful at all.

Immunity is a tricky concept to understand. I wrote about it here. I think immunity (to a pathogen) is often viewed as an absolute, and as a somewhat magical thing. If I’m immune to a particular pathogen, that pathogen can not infect me, right? If I’m walking down the street, and a pathogen is coming the other way and I’m immune to it, it crosses the street to not get anywhere near me, right?

No. If I’m what we call “immune” to a pathogen, that means that the pathogen still goes inside me. It starts to do whatever that pathogen normally does in a human body. It is, in fact, infecting me. Then, because I’m “immune” a particular part of my immune system quickly responds to that pathogen’s presence, because I’ve acquired an immunity to it either by prior infection or by vaccination. Other parts of my immune system also work against a pathogen whether I was previously vaccinated or exposed or not.

The acquired immunity that comes with vaccination or prior exposure causes my body to respond more quickly. The best kind of immunity is where my body responds well within the time period where the pathogen hasn’t made me sick yet, attacks the pathogen, and kicks the crap out of it before it can do anything. I don’t get “sick” from the pathogen not because it did not infect me — it did infect me — but because the illness that pathogen typically causes never got of the ground. The natural biological course of the pathogen did not advance sufficiently to either make me feel bad or to be passed on to another person. Or, in a less ideal immunity, common with many pathogens, I do actually get somewhat sick, and maybe I can even pass the disease on, but acquired immunity makes me much less sick and much less contagious.

And as noted, a person who is “not immune” is typically a little immune anyway. That is because the immune system has several parts that try to stop a pathogen, and because the above mentioned acquired immunity is still an immunity before it is trained up in your body. It just takes longer.

The difference between a typical “non-immune” person and a typical “immune” person, as the term is usually applied, is this and only this: For the immune person, the adaptive immune system (only one part of the immune system) acts faster because it is trained by prior infection or a vaccine (which simulates a prior infection) so the body is prepared.

Indeed, a normal immune response to a pathogen is often to get sick and seem not very immune at all. Little kids get colds all the time, and they can last a long time. It seems like from a certain young age until a few years later, still at a young age, a kid is sick all the time. Adults go around bragging about how they haven’t lost a day of work in 20 years. (Not all adults, but some.) This is largely because kids don’t have a very strong immunity to the handful of different viruses that give us regular colds. But over time, a human will typically develop a stronger and stronger immunity. All these humans are immune to those viruses to some degree, just not perfectly and totally immune.

With COVID-19, we hear stories of “reinfection” and this has led many people to believe that humans do not develop an immunity. The numbers of possible re-infections is very very small compared to the number of people infected, and it is highly likely that those instances are bad reports, or individuals who never really got rid of the disease to begin with. Of the remaining, much smaller number of individuals, re-infections may have happened because that person’s immune system just didn’t produce a strong immunity in that person. A very small number of possible re-infections is expected for any disease and isn’t alarming.

Usually, an exposure to a pathogen that we can develop an immunity to results in an immunity that lasts for a while. Usually, years.Sometimes enough years that it seems like a life long immunity, or close to it. In other cases, you get a modest immunity that gets better with more exposure. Remember, SARS-CoV2 is a particular virus, and should not be compared willy nilly to other viruses. HIV gets around the human immune system, but it is a very different virus. Not a valid comparison at all.

Sometimes our immunity does not help us much with a later infection, or so it seems. You get a Yellow Fever shot and later they tell you you need another one. Or, the flu shot from last year isn’t helpful this year. This might be a linguistic matter. We call the pathogen by a certain name, but underlying that name is a wide range of different species or strains of that pathogen. We use the word “flu” for “influenza” but there are many different major types of influenza. If influenza was a “canid” then there would be foxes, wolves, coyotes, and domestic dogs. All in the same family but not really the same.

Alternatively, later infection could be the result of a particular strain mutating enough to side step our immunity, somewhat. Or, it could be that our immunity wore off.

A common misconception about mutations is that they make a pathogen worse. Well, they can, but they usually don’t. We hear “COVID has had 29 mutations! Aieeeee!!!” I assure you that SARS-CoV2 has had many many more mutations than that. If you get COVID-19, the SARS-CoV2 inside you probably mutates hundreds or thousands of times as it replicates using your cellular machinery, as viruses do. But, the vast majority of mutations cause a viral strain to become broken, or to not change at all. A small number may make the virus a little better at what it does, or a little less good at what it does. From our point of view as the host of the virus, a small number of mutations might make it harder to pass it on, or easier to pass it on, or liable to make a person a little more sick or a little less sick. That any one of these mutations occurs in your body does not mean that that mutation will now be part of the general population of SARS-CoV2 viruses. The vast majority of mutations that both happen in an infected individual and that do not produce a dead-end variant will not be passed on to the next person. You will just sneeze them out and they will be killed by ultraviolet light, hand sanitizer, or the main thing that kills most individual virus particles: Time.

We hear a lot now about rare and scary things. Twenty-three year olds dropping dead of a stroke, or other odd blood clotting things, and so on. Those may be real or they may not be real. If tens of millions of people get a disease, there will be situations where a cluster of individuals were going to also have some other thing happen to them medically, and they happen to have this thing occur while they have COVID-19. Coincidence. Or, a disease like this might really have some other effect that is very rare, but that thing is, well, very rare. After the discovery of some possible odd effects on blood clotting, people started to say things like “it kills young people in this strange way and we didn’t know it until now! Aieeeee!!!!” but at the same time, the death-over-age statistics did not change. We did not find 300,000 dead 23 year olds. The strange new thing remained rare, and enigmatic. Important, interesting, something we must find out about. But still very rare.

I’ll end here with a dirty little secret of the immune system: Of all the different biological systems that make up the typical animal (including humans) it is with the immune system that the gap between all that can be known and what we confidently know is largest and deepest. We know a lot, but we also don’t know a lot. And, it is so damn complicated that it is impossible to expect the average non-expert to not make the sorts of mistakes mentioned above. I can add this: I’m heavily revising what I cover in my course on the immune system, to help future generations of pandemic victims have an easier time parsing what is happening around them. Assuming I can get back into a classroom with them!

How To Think About Immunity to COVID-19

This is what immunity is not: You are an organism walking down the street, and you are immune to the rare virus squirrelpox. A squirrelpox virus is walking on the same sidewalk towards you. It sees you, and goes, “that one’s immune to me,” and quickly crosses the street, going nowhere near you. Beause you are immune.

This is what immunity often is: You have built up an immunity to a common cold virus. Somebody infected with that virus sneezes on you and now that virus is in you. It begins to reproduce and do its thing, and you develop cold symptoms. However, your adaptive immune system has seen this virus before, so it quickly mounts a defense, so even though you do get a cold, you fight it off quickly and in five days you feel fine.

Lots of times, though, immunity works like this: You have an immunity to a certain disease. Perhaps you had that disease earlier in your life and your adaptive immune system developed a strategy to attack this pathogen next time it comes around. Perhaps you got a vaccine that prompted your adaptive immune system to develop a strategy to attack this pathogen next time it comes around. The virus goes in you — the virus does in fact infect you, it does not “cross the street” to avoid you. But your body is so ready for it that the counter attack is fast and effective, and before you can either develop symptoms or start passing the disease on to someone else, your body’s immune system has literally killed it.

An acquired or induced immunity can be called “100%” and it can be “life long” but it is never able to actually keep the disease out, and it is likely that few, if any, adaptive immune system build-ups last for the entire life of a person who lives a long time. Some immunity does not stop you from getting sick but does cause you to get better faster, and some immunity doesn’t last that long.

Much of the misunderstanding about immunity comes from the fact that our understanding of immunity comes from two distinct diseases: Polio and influenza. Polio vaccine is famous because its invention and deployment was historic and significant. Polio vaccine confers a strong immunity, one that is seen as life long and complete. Even this is not so simple, but if you believe what I just said about polio vaccination and immunity you would be in the ballpark. Influenza immunity is often discussed because it is at the center of the anti-vax debate, everyone gets the flu now and then (or so it seems) and the so-called “flu vaccine” is supposedly only “60% effective” or thereabouts, and thus, being imperfect, is the focus of rage on the internet as though it was a candidate for office.

If polio is an outlaw gunslinger in the old west, and the polio vaccine is Marshal Dillon, then influenza is all the underground crime organizations imagined in fiction and the flu vaccine is a competent but underfunded police agency.

When we say that the influenza vaccine is 50% effective in a give year in the US, as an example, what that can mean is that there are five kinds of flu circulating at various proportions in the population, and there are three kinds of vaccine in the shot you get; maybe two of those vaccines are nearly 100% effective in immunizing a person against two of the circulating influenza viruses, one of the viruses is untouched by the vaccine but doesn’t get you that sick, and one of the vaccines is for a virus that never really showed up, and the leftover viruses are the ones doing most of the damage. Or something along those lines. The outcome is, across the population, that the average vaccinated person in the population under consideration would have their chance of getting the flu if exposed is half what it would have been were they not vaccinated. So, 50% effective that year. Some other year these parameters may be very different, and the “vaccine” (a mix of different vaccines in one shot) is different. And, each vaccine may itself have a higher or lower level of effectiveness.

And that is the simple version of the story.

Immunity is not a folk concept. It is a medical concept. The fact that many people believe that immunity is the inability of a disease to affect a person, which is 100% wrong in every way, is not relevant to anything but people’s misunderstanding of the concept.

When we hear that there is a certain possible reinfection rate of COVID-19 in China or Japan, this does not mean that people don’t get immunity once they have the disease, or that COVID-19 has special powers. One health expert misstated that since we don’t know for sure what acquired immunity to COVID-19 looks like, we can’t assume that it is long term. That is balderdash. It is very likely long term (if “long” is years) because that is what normally happens. This statement is like looking at the first new car off the line of a new make and model and saying, “since we’ve never actually seen one of the drive, we have to assume there is a good chance none of these cars will work.” There may be a few recalls in the future of this make and model car, but it will work.

We can assume normalcy, we can assume biology to do what biology does. Bill O’Reilly does not know how tides work, but someone else does. Normally, adaptive immunity occurs, and lasts for a good time. Normally, immunity to certain kinds of viruses can be less than 100%, so there is some getting sick, and normally, a subset of people don’t develop much of an immunity because their own immune system simply fails at that task. COVID-19 will ultimately be found to match normal biological expectations, though we don’t know the details yet, and we won’t for some time. The fact that normal biological expectations do not form the basis of folk thinking about this disease, or pathogens and immunity in general, does not make Covid-19 a preternatural force, or an unknowable thing.

Still, remain hiding in your house until the all clear.

There is another level of thinking about immunity that I won’t go into detail about right now, but I’ll mention. We often, rightly, think of immunity at the population level, even though it does, truly, work at the individual and molecular level. Assume a particular vaccine, or exposure, typically provides ~100%) immunity in individuals. If 10% of the population have that immunity at the start, the disease will act like nobody is immune, as far as we’d be able to see. Often, natural (genetic?) immunity at low levels exist in a population, and can only be discovered by intensive research over a long time. If, on the other hand, 90% of the people in a population are ~100% immune, the disease may be so unable to get a foothold that it is like it isn’t there. The point is, the appearance of a diseases behavior seems to range from 0% (there ain’t none) to 100% (it’s everywhere!) on the surface, but this outcome is a function of a much smaller range of actual immunity values, like the 10-90% just noted, or more likely, closer to 0-70%. Putting this another way, a population gets very close to “immune” at the population level as the proportion of individuals who can’t get and pass on the pathogen rises over about half. This is called herd immunity. It will take several cycles of COVID-19 infection to achieve natural herd immunity, most likely, unless a vaccine is found. But once that happens, the disease is likely to stay around at low levels then occasionally come back and be menacing, but not as bad as it is now, on occasion.

So, let’s get that vaccine going!

The Complete Scientific Guide to COVID-19

… will be written in about three years from now. Meanwhile …

We labor under a number of falsehoods about how science works. Even scientists do. There are considerable differences among the panoply of scientific disciplines, and these are important enough that I would never trust the practitioners of one scientific discipline to, say, review research procedures or grant proposals from another discipline, by default.

These differences are even more significant outside of science itself. A common example is this one. A lay person evaluating peer reviewed research claims that a certain scientific conclusion can not be supported because there have been no double blind studies. That person may be unaware of the fact that almost no science uses double blind studies. This is a methodology used only in some areas of research. A study of earthquake hazards, genetic phylogeny of chickadees, or how long a particular virus lingers on a surface will not have a double blind methodology.

In some fields of study, a single idea will often be represented by a single major publication (sometimes a book) and will not be seen elsewhere unless it is being criticized. This is not common in the true sciences, per se, but this does happen in the peer reviewed literature. In other fields of study, a single idea may be addressed in hundreds of peer reviewed papers. In some fields of study, if a published peer reviewed paper presents a conclusion that is thought to be wrong, because of some flaw, the scholars in that field are expected to learn of this problem and thereafter avoid citing that paper. In other fields, when this happens, the paper is withdrawn from the literature after the invocation of complex rituals that might or might not involve the sounding of trumpets.

There seems to be two falsehoods affecting some of our thinking about COVID-19. One is the idea that a “study” or “publication” about some detail of the disease tells us something that we can take as fact. Yes, Covid-19 stays on a certain kind of surface for N days, therefore we can’t do X! That sort of thing. However, this research is, firstly, not peer reviewed. There may very well be no peer reviewed papers on COVID-19 at this time. This Pandemic has lasted less time that the typical peer review process takes. Maybe there are a few out there, but mostly, we are dealing with non-reviewed work, or work in review. This is good work, and important work, but it is more like a set of “emergency results” that address specific pressing questions in a provisional way.

It has been important to decide which of a small number of broad categories COVID-19 can be placed in, and the work on persistence on various surfaces has provided that rough and ready guide. There are pathogens that can find their way out of an exam room, go 20 feet down the hall, and infect a person sitting in a different exam room. There are pathogens that are so unlikely to infect another person that you practically have to lick the inside of their mouth five times to catch the disease. COVID-19 is in the in between category, where it sheds into the air and hangs around on surfaces for long enough that surfaces are found to have the virus on them. Is COVID-19 more or less surface-contaminating than, say, norovirus? Rotavirus? Nobody knows, because the research to determine that, and the publication array that would be necessary to lead to policy and recommendations about that, will take time. Someday there will be a study that looks at how much of the virus persists for how long on various surfaces, integrated with the other important question of how can the virus on a given surface actually infect a human, in order to allow for a realistic and useful statement about how to go about keeping a home, and ICU, an examining room, or a school relatively safe. COVID-19 has the potential to be the most studied pathogen in recent history, but not today.

So, that is the first fallacy: that a handful of quick and dirty, rough and ready, studies designed to get a clue about this disease constitute a well tempered and developed peer reviewed literature from which we can glean an accurate characterization of most o fhte important details of this disease. Nope.

One cost of this fallacy is the second fallacy, that we can evaluate models of either COVID-19’s behavior, or the efficacy of our reaction to it, based on a solid knowledge of the disease. That is backwards. We will eventually be able to evaluate ideas like “curve flattening” by understanding a lot about COVID-19, but that will happen after we have actually seen what various curve flattening efforts have done. A recent proposal that certain areas of the world may have seen a prior passage of COVID-19, causing some local immunity. One well meaning expert (not an actual expert) on social media responded that given the way COVID-19 operates, this is simply impossible. But that is backwards. The way we will eventually be able to describe how COVID-19 actually works is by observing it, measuring it, developing good explanations for what we see, strengthening and tempering those explanations by further hypothesis testing, replication, critique in the formal peer review process as well as the less formal but sometimes more important conversations at the conference-bar setting, and time. Time to just think. Then, we will be able to say things like “X is pretty much impossible because this is how COVID-19 works.” Now, we have an expansive void where some good theory and data will eventually reside, and the job of the scientists focused on this problem is to carefully and thoughtfully fill that void with what they come to know. To get a sense of how this works, read up on the literature that came out of the 2013 Ebola epidemic. Many key known things about the pathogen and its effects were not nailed down until months or years after the last patient was identified. These things take time.

I’m not an epidemiologist, but I play one in the classroom. Amanda and I teach a class on the immune system and epidemiology. Had I not gone into palaeoanthropology, I might have gone into this field. Excellent books on the topic include The Coming Plague: Newly Emerging Diseases in a World Out of Balance by Laurie Garrett (not current but mind-changing and foundational, includes some important forgotten history), Epidemics and Society: From the Black Death to the Present (Open Yale Courses) by Frank Snowden, and for a good textbook, Gordis Epidemiology.

COVID-19: Don’t Just Flatten The Curve, but also, do this….

Is Washington State leveling off?

Are mainly Republican states seeing the greatest increases in COVID-19 infections (outside of New York)?

Is the NOLA effect an explainer of the the distribution of COVID-19 outbreaks?

What is the difference between flattening the curve and pushing the curve, and why is the latter what we need to be doing?

These and other questions….

Washington State is especially interesting because until New York muscled it out of the way, it was a US epicenter of Covid-19 infection. Over the last several days, the percentage increase in cases in Washington look like this:

16
11
18
11
11
11
4

Before getting too excited about that “4” we must digress to examine the “ever trust the last datum rule” in epidemiology. If you have been following the progress of COVID-19, you’ll notice that on many day — most days, really — the current situation always looks a bit rosy because the exponential rise in new cases is less for the most recent reading than for the previous readings. This is almost always an artifact of the nature of the data. Ignore the last day.

Having said that, it remains true that over the last several days the state of Washington’s new case number has not gone up as a percent of total cases. Washington is still in trouble, but measures being taken there may be helping.

It has been suggested that Republcian run states are going to have disproportionately more trouble from COVID-19 than Blue states, because Democrats pay attention to science and Republicans spend their days punching hippies and making liberals cry. This characterization of Democrats vs. Republicans is pretty much unassailable, but the effect on COVID-19 right now is a bit more complicated. Population size and density and other factors probably matter more, and it is possible that all the different virus related factors come together in the New York City Metropolitan area (which, to the surprise of Federal health authorities, includes about 10-12 counties, not four as they have been saying) to make that a hot zone no matter what.

Otherwise, the data, as shown in the following graphic which has a smudge on each state with the most rapid recent increase in COVID-19 infection, speak for themselves.

Sometimes, when data speaks for itself, it mumbles.

Not shown on that graphic because things are happening too quickly is the sudden and dramatic increase in cases, and deaths, in Louisiana. It thought that COVID-19 was active in that state during Mardi Gras. Contagious carnivalians were literally parading around on floats throwing the virus (on beads and such) to innocent revelers. There might have been some other forms of exposure. Right now, this morning, it appears that Louisiana has the second highest infection rate in the US, second only to New York and Washington, but possibly rising at a meteoric rate soon so surpass everyone.

And, of course, all those people who went home after Mardi Gras took it with them. I want to see travel to and from NOLA and other carnival sites mapped against infection outbreaks. Globally; Mardi Gras is only one carnival of many.

Flattening the curve is a nice idea, but there are two problems with it. First, it is probably very difficult to do unless cases are truly isolated prior to multiple infections. The idea of flattening the curve is to reduce R-naught, the number of people, on average, that are infected per infected person. Social distancing can help, but the only way to make a huge difference is to identify ill individuals very early in the course of their infection, and take them totally away from society. Social distancing does not do that enough. One can somewhat attenuate the curve, but mere social distancing is not going to do what happened in South Korea, Singapore, and China.

Moving the curve is somewhat difference. This involves recognizing that a spike will happen (though maybe a lower one than otherwise), but one moves the spike about two to three weeks ahead in time. Why? Because a given region probably has about 1/10th (or maybe in better scenarios, 1/5th) of the ICU beds needed to save most lives of the critically ill.

Flattening the curve is, explicitly, making the maximum infection rate low enough to duck under the bare of ICU bed number. Like this:

If the curve flattens a bit but fails at this objective, it was not flattening the curve, but rather, failing and losing to the virus. Like this:

Pushing the curve to later, which would probably reduce the amplitude of the peak but mostly result in the same huge increase in number of cases, allows the build up of ICU bed number. Like this:

That is what we are doing in Minnesota. We expect thousands of people to require ICU beds, no matter what happens. We are partly locked down, and increasing the lockdown on Friday. We are building new ICU facilities, apparently, at a sufficient rate to handle the eventual need.

Communities that are just flattening the curve, and that expect it to work, may run into trouble if they are not building out infrastructure now. We can argue about what the best approach is, but trying different methods in different states or regions is a hell of a way to test a hypothesis.

I learned yesterday that about 15% of the ventilators used in the US are made in Minnesota. We have about 2% of the population. So we’re good.

COVID-19 Conversation: Updates and meanderings

Updates

Spain has had a major surge in Covid-19 numbers. India has more people locked down right now than any other country. Trump intends to “open up” the economy by Easter. Fortunately he is powerless to do so. The best available information suggests that Covid-19 is not mutating much, suggesting that once a vaccine is developed, it can work widely and be more effective.

Things are bad in Iran. According to Arash Karami, “Iran’s confirmed corona cases is now 27,017 with 2,077 deaths. In the last 24 hours there have been 2,206 new cases and 143 deaths. In total 43 doctors and nurses have died from corona.”

Yesterday, March 24, is the day Trump told us we would have zero cases of Covid-19 in the US. The actual number was 53,478.

I hear chest freezers are flying off the shelves.

Covid-19 is Partisan in the US

Example of the effects of social distancing on a symptomatic indicator of Covid-19, suggesting it is working well at least in some place.
The default behavior of the Covid-19 virus has almost the same pattern of spread and increase everywhere — exponential increase with a fairly high exponent, for a virus.

How different societies or regions attempt to “flatten the curve” seems to result in very different specific outcomes, but in several areas there has been real success.

It is probably true in the US that the federal response has been pretty much perfect, from the point of view of the Virus. Trump is treating Covid-19 much like he treats Putin. “What can I do for you, sir?” But fortunately, locally, it does not work that way.

Broadly speaking (with too few exceptions) Republican executives are literally supporting the virus in this manner. They want it to spike. Democratic executives are ordering serious responses and it is working to varying degrees. In states with Republican governors, Democratic (usually) mayors are responding despite what the Governors are saying, and that is working locally.

So, yes, Covid-19 response is partisan, and one of the parties is acting like a Death Panel determining that the aged, infirmed, and the less privileged be sacrificed for the benefit of the economy. The other party is trying to help. Republicans vs. Democrats.

The response in Congress is also partisan, but the Republican response is so awful that Democrats are winning out of sheer shame on Republicans. Plus at the moment, more Republcian Senators are down with the virus than are Democrats, so that seems to shift the balance of power.

In my own neighborhood, I’ve seen the Deplorable Housewives of Minnesota (yes, that is a thing) congregating in groups at the grocery store and loudly yammering about Nancy Pelosi and how she hates America, spreading viruses onto each other as they wander like a pack of hapless Gollumoids through the produce section.

(In the past the Senate Republican leadership has always been against remote voting. Now that it is in McConnell’s interest to have remote voting, expect his situational ethics to resituate.)

Bad News

The mother of NBA player Karl-Anthony Towns is very ill with Covid-19, as of this writing. Amy Klobuchar’s husband is in the hospital on O2 and quite ill. Minnesota’s Lt. Governor’s brother has died of complications of Covid-19. A minor youth in Los Angeles has died. Prince Charles has been diagnosed positive. There is a long list of famous people from Jackson Brown to Natalie Horner to Prince Albert II diagnosed. Terrence McNally dies of Covid-19. These folks happen to be famous, and the tends of thousands of non-famous victims do not exist on a lower plane. But having famous names across the spectrum of how people know them and what people think of them is, perhaps, to this pandemic what a set of really bad hurricanes is to climate change, if you get my drift.

Watching an interview with a former official from the Louisiana Health Department last night, we got two reminders. One is that Mardi Gras happened at just the right time and place to be a major incubator of the disease, and probably accounts for a lot of sick people. The number of cases in NOLA has skyrocketed. The other reminder: Official Atlantic Hurricane season starts June 1st, but actual hurricanes or tropical storms can show up in May. Gulf Coast and Eastern Seaboard hospitals and communities night have an interesting year.

Here is an interesting history of the N95 mask. An outtake:

In the fall of 1910, a plague broke out across Manchuria… “It’s apocalyptic. … It kills 100% of those infected, no one survives… within 24 to 48 hours of the first symptoms,” …

What followed was a scientific arms race, to deduce what was causing the plague and stop it. “Both Russia and China want to prove themselves worthy and scientific enough, because that would lead to a claim of sovereignty,” …

The Chinese Imperial Court brought in a doctor named Lien-teh Wu to head its efforts. … after conducting an autopsy on one of the victims, Wu determined that the plague was not spread by fleas, as many suspected, but through the air.

Expanding upon the surgery masks he’d seen in the West, Wu developed a heartier mask from gauze and cotton, which wrapped securely around one’s face and added several layers of cloth to filter inhalations. His invention was a breakthrough, but some doctors still doubted its efficacy.

“There’s a famous incident. He’s confronted by a famous old hand in the region, a French doctor [Gérald Mesny] . . . and Wu explains … his theory that plague is pneumonic and airborne,…and the French guy humiliates him . . . and in very racist terms says, ‘What can we expect from a Chinaman?’ And to prove this point, [Mesny] goes and attends the sick in a plague hospital without wearing Wu’s mask, and he dies in two days with plague.”

On Twitter

One way schools could help with the Covid-19 response

Most schools have science classes. Among the science classes there are some that occasionally use nitrile or latex gloves (“surgical gloves”). While it may be perennial true that science classes are low on gloves, there is a good chance that there are a few unopened boxes in the cabinet somewhere.

Schools will not be using these gloves for the rest of the school year, because there is not going to be in class instruction for the rest of the school year.

So, figure out how to get these gloves to an appropriate medical facility.

If you are not a teacher you may not understand this part: The science teachers may have had to promise their first born to even get these gloves, and other important scientific equipment, in the first place. They may be unwilling to go up against the bursars to give these gloves up now and fight later. Indeed, it would be technically illegal for them to unilaterally root through the cabinets and gather these gloves together.

The word has to come from the top. Call your local school’s principals or superintendents. Or email them. Make the suggestion. They’ll make a call or send out an email and it will happen.

I mentioned above “unopened boxes.” I assume previously opened boxes are less of interest to medial facilities, but I might have that wrong. Anybody know?

Anyway, try it, it may help.