Here is what my local paper’s headline said: “Socializing is a must for many on the 4th.”
Digging in we find that “For some, it was a time to throw caution to the wind and reclaim normalcy as they headed to a lake cabins, parks and backyard barbecues…Across the state, Minnesotans are making their own decisions while health care and government officials hold their breath…”
The quest for normalcy is powerful enough to make people dishonest with themselves, so you get sentences of this form: “I heard the Virus did/didn’t really do this/that/other thing, so I guess it is OK if I whatever-whevever [fill in idiotic decision here].”
Let me tell you what normal is. You go a week without a funeral. Several weeks. Maybe months, or a year. Normal is not when one of your relatives, friends, work associates, one of the kids in your child’s class, or the parent of one of the kids, or the old person that lives two doors down but you never talk to much but they just took her away in the ambulance, or a checkout person who’s name you never knew, or two of the nurses at the hospital your kid was born in, etc. etc. … normal is not when one of those people dies on average about every 14 day or so (but sometimes with longer gaps, sometimes in clusters) at the peak of Your Local Epidemic.
If you want to achieve normalcy during the 365 days between moments of must, when you must do the thing that is least recommended by people who must be much smarter than you are, then you must not. This applies to gatherings on the fourth, it will apply to all the holidays throughout much of the year. Next winter holidays, like Christmas and New years, or before that, Halloween which seems to have become the local Spring Break party holiday among America’s 20-somethings, or the most traveled day of the year, Thanksgiving, if you must seek normalcy the grim reaper must seek your family and fiends.
And eventually, not your parents, cousins, children, or neighbors. But you. Ask not for whom the germ theory tolls.
It celebrates one date in a series of dates at the end of the Civil War when African Americans who were slaves gained their freedom in either legal or pragmatic terms.
That freedom did not, of course, end racial violence. One example of racial violence was the Tulsa Massacre, in Tulsa, Oklahoma. You can go read about it. Nobody really knows how bad it was. Thousands of African American people were burned out of their homes, interned, wounded or killed. Whites died as well. That happened at the end of May, 1921.
We are having a pandemic and there are concerns that large indoor gatherings would spread the infection.
We are having a revolution in which Americans are being forced to come to terms with deeply ingraned, systemic, and systematic racism that involves the widespread incarceration and murder of African Americans, many men. The number of African Americans incarcerated and killed each year in America exceeds that which occurred at the Tulsa Massacre, or approximately so, by my estimation.
So, naturally, Donald Trump is planning a huge indoor rally in Tulsa, Oklahoma, on Juneteenth.
The White House has issued a statement that Trump’s choice of Juneteenth for this rally is entirely a coincidence. They also issued a statement that Trump chose Juneteenth because African Americans are very “near and dear” to his heart.
Three thoughts come to mind.
1) People who reject science, and are willing to embrace Trump’s anti-science yammering, are walking into a death trap. Have a nice death trap. Shame on you for the people you will secondarily infect. Do not come near me or my family after this rally.
2) With enough people in a large venue inside, breathing, Trump will have maximal chance of being infected with the virus and getting COVID-19. This rally could kill him. It would be the end of a long national nightmare. We can only hope this is a suicide rally for Trump, because he is killing us and that has to top.
3) It would be funny if very few people showed up at the rally. It is possible. Such things have happened before.
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 particulartype 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!
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.
The scientific jury is not unanimous on this issue, but it looks like wearing a surgical mask matters enough to recommend their use under certain conditions, and their use, or the use of a more effective respirator, is recommended under certain conditions. In my experience, face masks are routinely distributed patients arriving in urgent care centers and similar when influenza is cranked up in the community.
Washing your hands a lot AND using a face mask seems to reduce transmission within a household where there is a sick person. This practice probably works, and is standard and recommended, for health care workers. People wandering around on the landscape who don’t have the flu or other virus probably don’t get real protection from wearing a surgical mask, but sick people probably transmit less, if for no other reason than it reduces the amount of nose/mouth-to-hand transfer of viral kooties.
Most of the research on this topic was done during either the H1N1 or SARS hyperawareness period, as expected, but I’ve not seen anything contradictory since. Here are some examples:
” Face masks and hand hygiene combined may reduce the rate of ILI and confirmed influenza in community settings. These non-pharmaceutical measures should be recommended in crowded settings at the start of an influenza pandemic.” (Aiello et al 2012)
“This is the first RCT on mask use to be conducted and provides data to inform pandemic planning. We found compliance to be low, but compliance is affected by perception of risk. In a pandemic, we would expect compliance to improve. In compliant users, masks were highly efficacious. A larger study is required to enumerate the difference in efficacy (if any) between surgical and non-fit tested P2 masks.” (MacIntyre et al, 2008)
“Hand hygiene with or without facemasks seemed to reduce influenza transmission, but the differences compared with the control group were not significant. In 154 households in which interventions were implemented within 36 hours of symptom onset in the index patient, transmission of RT-PCRâ€“confirmed infection seemed reduced, an effect attributable to fewer infections among participants using facemasks plus hand hygiene (adjusted odds ratio, 0.33 [95% CI, 0.13 to 0.87]). Adherence to interventions varied.” (Cowling et al. 2009)
The CDC is not sure if asymptomatic non healthcare workers get much benefit, but they don’t say not to do it. They do say to get your vaccinations, and if you get sick, get medical attention which might include an anti-viral. Health care workers are told (by CDC) to always have a mask or respirator if they are within 6 feet of a sneezy coughy diseased person.
We had a bit of a conondrum when a legit looking analysis appeared in the Daily Mail. I normally won’t even look at the Daily Mail since it is a rag of teh worst kind. But, commenter Joseph M., a long time trusted friend and VSP (very smart person), and a scientist, dug in a bit farther, and he makes a convincing argument that this is worth posting.
The following are Joseph M.’s notes and comments on it, and some graphics:
Professor Mark Handley, absolutely checks out – he’s much more than legit. As are every one of the other sources.
So I said I’d check out this article and I did just that, vetting it thoroughly. (Several hours of investigative journalism on a work of (initially) questionable journalism.) It’s the real deal, all right – it’s just a bit unfortunate that the journalistically despised tabloid The Daily Mail got the story instead of a respected London newspaper like The Guardian or The Observer. But WTF – that’s just the way this particular cookie crumbled, and one has to give credit where credit is due. I think they scored a scoop, and that were it published in one of the aforementioned establishment papers, world news media would have picked it up and run with it. (Maybe they did, but I didn’t see anything. As I may have told you, my friend Allan sent me the link – and I blew him off because of the tabloid source.)
The inconvenient truth is this: All the experts cited and interviewed in the article are at the top of their respective professional games. No slouches, these guys. The only question is, how much credence do we want to give to a computer scientist – are doctors not echoing his projection because they’re inherently more conservative, or because they have legitimate reasons to question his methodology – or are they falling back on a lame argument from [their medical] authority? I just don’t know, but I also know – we both know – that government reassurances and Anthony Faucci’s public cautiousness notwithstanding, the numbers we’re seeing exploding all over the map seem consistent with Handley’s argument. (Of course, were this my field of expertise and I had the patience to plug in all the numbers, I’d create my own graphs just for the sake of comparison. For whereas this was an off-the-cuff tweet by a concerned professor who discovered an alarming pattern – not a formal paper with any stated methodology – it looks like simple Algebra 101 to me – just numbers of cases as a function of time for each country … and compare the slopes, allowing for the slight offsets in commencement of infection …)
Mark Handley, the guy who created and tweeted the attention-grabbing graph, is Professor of Networked Systems, University College London; a member of The Royal Academy, and (a quick web search confirms) highly regarded by the epidemiologists and infectious disease people with whom he consults. He’s a computer network nerd – what can I say?
We are, after all, dealing with nothing if not network theory – and obviously his kind are crucial to epidemiological modeling; as we both realize, they work closely with I.D. specialists everywhere.
There’s also a prominent Chinese computer scientist and systems engineer, “Eric” Feiqi Deng, Professor and Director of the Systems Engineering Institute, School of Automation Science and Engineering (South China University of Technology, Guangzhou) – who sounded alarms early on and also tweeted graphs, like the simulation of Covid-19 transmission scenarios I sent you a day ago (and am re-attaching) – I can’t remember if you (or I) already uploaded it.
Of course, there’s been a veritable deluge of similar computer simulations and graphs – nothing new here – except for the interesting part, namely that ”we must flatten the curve” – terminology I’ve heard Trump administration people, CDC officials, and even reporters frequently use – is quickly becoming the newest American meme. [My physician friend Allan Wang (who himself has a deep understanding of infectious disease dynamics) forwarded me Deng’s tweeted (or published?) graph – and I’m unable to locate it online for context or proper citation. Don’t ask me why, but Deng took a helluva lot of international (and ad-hominem) heat for circulating this (I’m also guilty of dissing him in some emails, and I can’t even recall why!), and if I remember correctly he was slammed by (among other people) Harvard Chan School of Public Health epidemiologists – presumably for scaring the shit out of people when the graph went viral and for not being a biologist or physician.
The stink this raised lingeref for quite a few days – Deng was even interviewed in some newspaper articles – and now [this, alas, has become my constant refrain] I can’t even reconstruct what I read. Maybe my mention of the brouhaha will ring a bell with you?. Even without any context – the discussion (journal paper or tweet this was certainly part of), Deng’s graph is self-explanatory. – it’s essentially an elaborated version of the colored graph you posted on your Facebook page, or that article w/animated graph by the New Zealander that I posted there. (Frankly, this total immersion in Covid-19, compelling as it is, has me flailing around w/respect to my real obligations. What to do? The situation isn’t merely fluid or extremely dynamic – it might conceivably blow up into the worst domestic disaster we’ve ever seen – and no doubt the most unnecessary one, n the sense that, well, if only cooler heads were around to prevail … Did you read the anecdotes I posted on your blog about the violently irrational blowback I got from my brothers – all because of coronavirus?!)
Handley’s blunt tweet that “Everyone else will be Italy in 9-14 days time” was seconded by John K. Crane MD, PhD, Professor of Medicine, and Adjunct Professor of Microbiology and Immunology and of Pharmacology and Toxicology at the Jacobs School of Medicine and Biomedical Sciences, University of Buffalo – some obscure city in an obscure state I never heard of. http://medicine.buffalo.edu/content/medicine/faculty/profile.html?ubit=jcrane
So in other words this Daily Mail article (despite its clickbait bold black headline and equally bold bullet points underneath) – with its most compelling content consisting of unedited tweets (!) – is not conventional journalism, to say the least Still, it is solidly reported and chock full of valuable resources (compelling color photos; American news videos). I highly recommend that at the minimum we post the graph and its legend, and maybe include one or two screen captures from the more substantive tweets, with a link to the actual article.
The extensive Twitter commentary is informative, especially the tweets from Dr. Nick Christakis (see below). Your perhaps skeptical readers (perhaps pacified with a line or two from one of us to soften them up) will just have “get over” their reflexive revulsion from seeing The Daily Mail masthead. This is most certainly not the typical sensationalized puff piece on the latest shenanigans of some obscure fourth cousin to the Queen.
To sum up, Mark Handley’s alarming numerical projections are consistent with all the data we’ve seen – and (sadly) with the high likelihood that our government – this particular administration – will continue to drop the ball in some fashion or another and make things much worse, even dire. (DJT has some pretty-fucking-scary emergency powers at his disposal, and we both know how and why he’ll be inclined – and by whom prodded – to deploy them.)
Handley’s graph shows that rates of increase in 8 of the 9 countries he examined follow the same slope, albeit with a predictable time lag correlated with the date of the respective initial outbreaks. (The graph is pretty ‘busy” and somewhat hard to read (precisely because eight of the plotted countries follow identical, overlapping trajectories), but per the black color coding it seems that the single low-slope country is Japan, – which as we know caught’ Covid-19 from Chinese travelers early on, and so is probably starting to flatten out.)
The article is 50% wheat, 50% chaff. For example, there’s the stark Daily Mail headline “America will be in lockdown like Italy in less than two weeks” and similar (but remarkably restrained) editorializing … What I therefore attempted was to “migrate” the good parts to a Word document as a preparatory step for GLB / FB posting. But it was just too cumbersome – my draft Word “repository’ wound up being over 20 pages long! This is largely because of the massive number of follow-up tweets from very relevant players – especially Nicholas Christakis https://eeb.yale.edu/people/faculty-affiliated/nicholas-christakis and Jason Van Schoor, an anesthetist and clinical fellow at University College London https://twitter.com/jasonvanschoor?lang=en , evidently highly respected,* who at the end of this long Daily Mail article relays powerfully disturbing real-time reporting from his medical friends on the front lines in Lombardy. We’ve all see news videos to the same effect.
[ * https://virginia.sportswar.com/mid/13441707/board/general/ ? “I do not know van Schoor but he has had a Twitter account since 2012, has more than 8,000 followers which include some people in health care I know and respect. He was quoted today in an article by UK’s 3rd largest newspaper, the Daily Mail (link below). The fact that others are picking it up too does not make it sketchy.”]
COVID-19 can be spread before it causes symptoms, when it produces symptoms like those of the common cold, and as many as 12 days after recovery…
…Researchers at Johns Hopkins found a median incubation period for COVID-19 of 5.1 days—similar to that of severe acute respiratory syndrome (SARS).
… novel coronavirus quickly begins producing high viral loads, sheds efficiently, and grows well in the upper respiratory tract (nose, mouth, nasal cavity, and throat).
“Shedding of viral RNA from sputum outlasted the end of symptoms,” the authors wrote. “These findings suggest adjustments of current case definitions and re-evaluation of the prospects of outbreak containment.”
… “In SARS, it took 7 to 10 days after onset until peak RNA concentrations (of up to 5×105 copies per swab) were reached In the present study, peak concentrations were reached before day 5, and were more than 1,000 times higher.”
Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, which publishes CIDRAP News, said that the results challenge the World Health Organization’s assertion that COVID-19 can be contained.
The findings confirm that COVID-19 is spread simply through breathing, even without coughing, he said. They also challenge the idea that contact with contaminated surfaces is a primary means of spread, Osterholm said.
“Don’t forget about hand washing, but at the same time we’ve got to get people to understand that if you don’t want to get infected, you can’t be in crowds,” he said. “Social distancing is the most effective tool we have right now.”
…researchers estimated the median incubation period at 5.1 days (95% confidence interval [CI], 4.5 to 5.8 days). They found that 97.5% of patients who have symptoms do so within 11.5 days of infection (CI, 8.2 to 15.6 days).
After the recommended 14-day quarantine or active monitoring period, “it is highly unlikely that further symptomatic infections would be undetected among high-risk persons. However, substantial uncertainty remains in the classification of persons as being at ‘high,’ ‘medium,’ or ‘low’ risk for being symptomatic, and this method does not consider the role of asymptomatic infection.”
“The current recommendation of 14 days for active monitoring or quarantine is reasonable, although with that period some cases would be missed over the long-term.”
I’m not really going to live blog this virus, but I wanted to get a few thoughts down, and expect to be interrupted by a scheduled event in a few minutes. So, I’ll come back with more later. Perhaps this post will become a regularly updated/edited thing, we’ll see.
Call it 2019-nCoV (pronounced “Encovee”? — rhymes with anchovy –) because if you call it “coronavirus” you will have to spend time in the obligitory sidetrack: “Don’t panic about this virus, there are many kinds of coronaviruses, most of them are harmless, the common cold is a coronavirus.” That is much like saying “don’t panic about this serial killer that just started operating in your neighborhood, they are just humans, and most humans are totally harmless.”
Speaking of coronaviruses, yes, they are common, and this is likely to cause some, maybe much, variation in immunological response to Encovee, since there could be some cross effects of immunity from previous forms of the virus.
It is being noted by many that the flu is a much more common and deadly disease. Let’s talk about that for a second. Yes, it is, but most influenza viruses are moving across an experienced landscape of hosts that have a combination of prior immunity and vaccination. Encovee is treading on immunologically virgin ground. This likely means it will spread fast, almost with impunity. After that, maybe it will become just another one of the coronaviruses.
We really have no idea whatsoever what the rate of illness or mortality is. We can talk about this later, but this is a very complex and generally poorly understood thing. What we do know is that most people who get Encovee don’t die from it. We have no idea how many people are infected but show no symptoms, or the ratio of people who get a little sick vs. very sick, or, really, the ratio of those who get it and die. Graphs of the rate of its spread show an alarming verticality, but with mortality being a low almost flat line, at a very low percentage.
As of last night, here is what WHO was saying:
WHO’s risk assessment of the new #coronavirus (2019-nCoV) situation has not changed: ?very high in #China?? ?high at the regional level ?moderate at the global level
Their most recent situation report (of Jan 25) shows 1,320 confirmed cases, with most from China, HOng Kong, Macau, and Taipei. There were 23 confirmed cases outside of that area, 21 of which had history travelling to Wuhan, the Chinese epicenter. The others appear to be human to human contact within a family or similar.
Of a subset of 1287 cawses, 237 are counted as severe. There had been 41 deaths.
Note that all the scary numbers and charts you’ve seen, if you’ve seen them, are projections based on various models.
Projecting a disease outbreak at the beginning is like taking a bead on a certain direction and walking that way, and seeing where you get, but with this caveat: At the start of your journey, your compass sucks, and you don’t know how badly it works. Slowly over time, it improves, and it is hard at first to tell how much it improves. Eventually it starts to become a pretty good, but still limited, tool. Put another way, we can model the course (spread, magnitude) of a disease outbreak very very accurately — after it has happened.
Suman Seth is associate professor in the Department of Science and Technology Studies, at Cornell. He is an historian of science, and studies medicine, race, and colonialism (and dabbles as well in quantum theory). In his new book, Difference and Disease: Medicine, Race, and the Eighteenth-Century British Empire, Seth takes on a fascinating subject that all of us who have worked in tropical regions but with a western (or northern) perspective have thought about, one way or another.
As Europeans, and Seth is concerned mainly with the British, explored and conquered, colonizing and creating the empire on which the sun could never set no matter how hard it tried, they got sick. They also observed other people getting sick. And, they encountered a wide range of physiological or biosocial phenomena that were unfamiliar and often linked (in real or in the head) to disease. A key cultural imperative of British Colonials as to racialize their explanations for things, including disease. The science available through the 18th and 19th century was inadequate to address questions that kept rising. Like, why did a Brit get sick on his first visit to a plantation in Jamaica, but on return a few years later, did not get as sick? If you have a model where people of different races have specific diseases and immunities in their very nature, how do you explain that sort of phenomenon? How might the widely held, or at least somewhat widely held, concept of polygenism, have explained things? This is an early version of the multi-regional hypothesis, but more extreme, in which god created each type of human independently where we find them, and we are all different species. (Agassiz, with his advanced but highly imperfect geological understanding, thought the earth was totally frozen over with each ice age, and repopulated with these polygenetic populations of not just humans, but all the organisms, after each thaw).
Seth weaves together considerations of slavery and abolition, colonialism, race, geography, gender, and illness. This is an academic book, but at the same time, something of a page turner. Anyone interested in disease, colonial history, and race, will want to re-excavate the British colonial world, looking at disease, illness, and racial thinking, with Suman Seth as your guide. I highly recommend this book.
Here are some theories of what this red line is caused by. The last one is the correct one, but I include the first two because they are examples of wrongness, and we are all about that on the Internet, aren’t we?
The first explanation, historically, is that the red substance found in damp places, which today include the inside of your toilet or other places in your bathroom or kitchen, but in those days (before porcelain toilets) included other human-made as well as natural locations, is that this is the blood of Christ. This wass especially thought to be true when this red substances was found on bread, and especially when the bread was the Eucharist, the piece of bread that Catholics believe is the actual body of Jesus Christ, which you then eat. Blood coming out of anything linked to Christ, especially the actual body of Christ in the form of a wafer of bread, is about as intense as it gets if you are a Medieval Christian.
The second explanation, the one I see all the time today, is that there is something wrong with the water supply. We often see the red film or line forming in toilet bowls, or behind the fixture on your sink, or in showers or tubs, blamed on the poor quality of the city water supply, and often, this theory links the red substance to iron in the water causing rust.
The red substance of which we speak here is not rust, and it is not blood of any kind. It is Prodigiosin, a red pigment. When you see this red pigment, you are actually looking at a very likely thriving and living colony of the bacterium Serratia marcescens.
Serratia marcescens can be a human pathogen. It is responsible for a percent or two of the known hospital based bacterial infections that have become such a problem. It affects children more than adults, can cause urinary tract infections, and sometimes it exists as strains that are resistant to bacteria.
The military in the US and UK used Serratia marcescens as a “harmless” bacterium in germ warfare trials, between 1950 and 1980. This made sense because it was thought to not cause disease, but being red, was easy to find and spot in a culture to test the efficacy of germ warfare delivery devices. Serratia marcescens was, therefore, spread across the San Francisco Bay region once, and a large area of England. In the case of San Francisco, it may have caused a spike in certain illnesses, and may have killed at least one person. In any event, it turns out it is not harmless.
Serratia marcescens is not the blood of Christ, and it is also not from your water supply. It is fairly ubiquitous so it can come from the air, from your body, from wherever. It probably does NOT come from your water supply because living Serratia marcescens would be killed in routine water treatment.
So do get rid of it. Most people don’t need to worry. It is not that pathogenic. But children may be somewhat susceptible, and anyone immune compromised is at risk. Experts concerned with infectious disease don’t have this in their toilets at home.
Do not scrub the Serratia marcescens from your porcelain devices using a metal scrubber. That will ruin the porcelain finish and create crevices and scratches at the microscopic level. Bacterial such as Serratia marcescens love those crevices and scratches.
Do not put bleach in the back of your toilet system. That will ruin metal and rubber parts and cause leaks.
Do use a bleach based cleaner in the toilet bowl, on the sink in the shower, etc. to clean away this red stuff.
Clean it up where you see it, and do a general cleaning of the entire kitchen and bathroom — all of your kitchens and bathrooms and places this stuff is seen in your house — at about the same time. Maybe you’ll get all of it, or most of it, and it won’t come back or it will take a long time to reappear. If you clean a red spot here or there in your bathroom but not all of the at once, it will migrate back to where you removed it more quickly. If you wipe away the line around your toilet bowl but ignore the underside of the rim (that yucky area you can’t see without doing a Kavanaugh) it will come back.
But really, it is going to come back no matter what, eventually. Perhaps you should frequently use a brush without cleaning fluid, and occasionally a bleach-based substance on a brush, to clean these areas on a more regular basis than you are doing now. Chances are you see the red rim around your toilet water in the bathroom you hardly use, and do not see it in the toilet in the bathroom you usually use and thus clean regularly. What you should be doing is cleaning unused toilets in your house on a regular basis (weekly, bi-monthly, whatever) instead of ignoring them.
There is, of course, rust in some water, and that may be what you’ve got. But rust is not pink and does not form that line around the edge quite the same way. Medieval Catholics knew about rust, and thought this red stuff was blood. They just don’t look the same.
Serratia marcescens will, of course, coat the entire surface of the underwater part of your toilet but it tends to concentrate around the edge due to evaporation. It is also left behind when tiny puddles form, say, in the built-in soap dish in your shower or behind suction cups that are meant to hold stuff up in the shower, or behind the fixtures on your bathroom sink, etc.
I personally use one of these (though you might prefer this style) in the bathroom, and yes, I admit, I use this to clean both parts of the shower (down on the floor) and the bathroom (changing brushes, of course).
This post was originally published on December 3, 2012. Since it is now fairly old research, it may not be that important, but since I did go through the trouble of writing it, and people took the trouble to comment on it, I see no reason to delete the post.
Yet, hpph;r (move your fingers to the left one and type those letters to see what I said there) has determined this post to be a violation of norms. I changed the title of the post and replaced a few other words in it so their bothered bot will not be bothered, and reposted the post below. Note that I’ve added the earlier comments as screen grabs at the bottom of the post
A study has just come out in the Journal of when-mommy-and-daddy-really-love-each-other-and-want-to-show-it Research comparing various psychological and lifestyle measures of women who act in pornographic films with matched sets of women who do not.
There is a pretty clear association between negative attitudes towards pornography and negative assessments of the quality of life for actresses in the pornography genre. Studies have shown that those who regarded pornography as harmful to society also believed that those acting in the films must not like their work. Studies have also shown that people tend to believe that porn stars have serxual and physical abuse in their backgrounds at a higher rate than the general population. Conversely, people who have more positive attitudes towards pornography also seem to have a more positive attitude about porn actresses. As a whole, the research that involved asking people what they thought about pornography and those who participated on the stage in making it painted a picture that has become known as the “Damaged Goods Hypothesis.”
The damaged goods hypothesis posits that female performers in the adult entertainment industry have higher rates of childhood serx abuse (CSA), psychological problems, and drug use compared to the typical woman.
OK, there is a report just out that suggests that we are playing too fast and loose with food additives and other chemicals, and that we might want to draw back on some of that. Fine. We should maybe.
But I’ve already seen this report misconstrued, with panic ensued. I’ve seen people suggest that we should no longer use microwaves for food. Or that we should not dishwash plastic or put plastic containers in the microwave. And some other stuff.
For both of those behaviors, the concern is the potentially harmful BPA getting out into our food. If you put BPA laced objects in the microwave of dishwasher, that could be a problem.
The thing is, if you’ve been paying attention to BPAs all along, then you probaby don’t have BPA laced water bottles or microwavable containers, so there is NOTHING TO SEE HERE. Typical “Tupperware” (never actually Tupperware) wares typically don’t have BPA. Most water bottles don’t either.
Here’s the thing. This report covers a LOT of things, not just BPAs, not just microwaving things or cleaning water bottles. And, the report is pretty easy to read and very clear. Well, the whole issue of what to do and not do is not necessarily clear, but you can easily figure out what they are getting at.
There are two sources. Read them, and then you’ll know what all the buzz is about. An overview from the American Association of Pediatrics is here. The policy statement itself is here.
There are items of concern here, but if you simply stop using plastic in the microwave and think you are done, chance are that a) you did something useless and b) you are missing something important.
Human brains, presumably mammal brains in general, do not have microbiomes. If they did, they would look like Donald Sutherland in that movie.
Also, a microbiome is not the same thing as an infection. A microbiome is a mutualistic (or similar) ecology of multi-celled organisms or part thereof (like, your gut or your eyeballs or something) and microbes, probably including multiple species or varieties. Brains do not have that. If there are microbes in the brain it is an infection.
There is some interesting research out there possibly linking infections and Alzheimers. It is unfortunately being couched in terms of microbiomes. Why? Mainly because science reporters are generally not scientists, so they don’t bump on errors like that? Maybe. But in this case, there seems to be an actual project that claims to be actually mapping out the brain’s microbiome, including “helpful” organisms.
The individual is a pig, and one of several where things didn’t go so well, but this is a fairly spectacular result.
This isn’t a lung developed from scratch, quite. A lung is taken from a donor pig. That pig, of course, loses its lung and presumably is converted to other uses such as ham. That lung is then sripped of cells and liquid tissues, leaving just the connected tissues that make up a sort of non-cellular skeleton.
This skeleton is then seeded with cells and growth factors and such, and the cells find their proper location and re-constitute a pig lung.
This is not an ideal scenario for a lung transplant in a human, but it is a step in the right direction. The way it would work for humans is probably like this: You get a pig lung and remove the cells and blood. You get some cells from the recipient and bio-engineer them. Perhaps you remove the genes that cause the recipient to have a bad lung to begin with. You further bio-engineer the lungs to properly divide and propagate and migrate, to move the correct locations with the pig-lung-skeleton. Then you stick that lung in the recipient and sis-bam-boom, new lung.
Lungs are complex organs to engineer: They contain multiple specialized cell types in extracellular matrix with a unique architecture that must maintain compliance during respiration. Nichols et al. tackled the challenges of vascular perfusion, recellularization, and engraftment of tissue-engineered lungs in a clinically relevant pig model. Nanoparticle and hydrogel delivery of growth factors promoted cell adhesion to whole decellularized pig lung scaffolds. Autologous cell–seeded bioengineered lungs showed vascular perfusion via collateral circulation within 2 weeks after transplantation. The transplanted bioengineered lungs became aerated and developed native lung-like microbiomes. One pig had no respiratory symptoms when euthanized a full 2 months after transplant. This work represents a considerable advance in the lung tissue engineering field and brings tissue-engineered lungs closer to the realm of clinical possibility.