Category Archives: Health and Medicine

The Complex Problem of Microplastic Particle Pollution

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The importance of microplastic particles in the ecosystem, both as they might effect ecological systems and human health, is the subject of great deal of new research, and is one of more rapidly developing areas of of knowledge related to environmental concern. Once thought of as mainly a problem in the oceans (related to the now famous “Pacific Garbage Patch“) it is now understood that microplastic particles are also common in the terrestrial ecosystem and the part of the food chain we eat.

Microplastic fluxes and associated ecosystem feedbacks: Deposition and accumulation of microplastics can affect soil properties, with consequences for process rates and net primary production (NPP), causing feedbacks to the atmosphere, including greenhouse gases (GHGs). So far, nanoplastic has unknown consequences for this system. Fig 1 from “Microplastics in Terrestrial Ecosystems” Rillig and Lehmann 2020. Science. GRAPHIC: A. KITTERMAN/SCIENCE FROM M. C. RILLIG AND A. LEHMANN

Sources of microplastic particles include wearing down of tires, the use of synthetic textiles, road paint, the coatings and pain used on boats, and personal care products (roughly in that order) as well as “city dust,” a ‘generic name given to a group of nine sources” including the soles of footwear, synthetic cooking utensils, building paint, cleaning supplies, etc, all with small individual contributions but collectively about 24% of the microplastic particle pollution observed in the ocean. (See this.)

Estimated contribution of various sources to the microplastic particle pollution observed in the oceans. Source: Primary microplastics in the oceans, IUCN (see link in text).

The effects of microplastic particles may be more related to size and shape of the particles, rather than toxicity. (But all these factors matter.) Microplastic particles are mostly made of carbon. Normally carbon gets spread around the environment as part of the photosynthetic segment of the carbon cycle. Microplastic particles now exist in what has become known of as the “plastic cycle.” (See this and this.) Since the nature of microplastic routed carbon is different than “natural” carbon, direct and indirect effects on ecology can occur. Soil structure can be affected (including the spaces where air or water may be trapped in soil). Microplastics in soil can benefit plants, because soil density is lowered, so root growth is easier. However, where microplastics make up a large proporation of fill, plant growth is reduced (see this).

Note that the carbon in microplastic particles is fossil carbon, which prior to the manufacture of the plastic was mostly trapped in petroleum or coal, which in turn is mostly out of the short and medium term carbon cycle. Moving carbon from the long term cycle (which involves processes like continents being subjected into the mantle of the Earth, to be belched out later from volcanoes or added to spreading sea floors) into the short and medium term cycle (such as the cycle affected by human activity to cause global warming) may be important.

Microplastic particle contamination has been associated with changes in the immune system, the spread of antibiotic resistant bacteria (in part because bacterial microfilms that cover microplastic particles may favor, or at least contain, resistant forms), and microplastic particles have been found all over the place. Microplastic particles can be a vector moving chemicals between parts of the ecosystem.

Conceptual model of the plastic pollution cycle and the interactions between biogeochemistry, trophic transfer, and human health and exposure. Note that arrows and artwork are not to scale and are for descriptive purposes only. Expanded, adapted, and redrawn, in part, from Rochman et al. (2019) with permission. Fig 1 in Environ. Sci. Technol. 2019, 53, 13, 7177-7179

See “Microplastic in terrestrial ecosystems” for a fuller review of the effects of microplastic particles in soils and other parts of the ecosystem. It is pretty complex.

We may tend to think of microplastic particles as being a problem because we use plastic containers, which can break down into micro particles. That is true. For example, using polypropylene bottles in the preparation of infant formula releases microplastic particles into the formula itself. But a lot of microplastic particles are introduced directly into the environment because we make and use those small sized particles in a range of applications including agriculture and cosmetics. As a rule where the material being used is less solid, the degree to which it is soluble and thus the ease with which it enters the environment increases. This could allow regulations to be focuses more stridently and more quickly on areas of plastic use and production that have the most effect.

The universe of polymer species from primary microplastics to functional polymers, where solidity decreases, and solubility increases from polymer pellets to dispersion aids. Fig one in “Microplastic regulation should be more precise to incentivize both innovation and environmental safety” Nature October 21 2020.

Microplastic particles can be taken in to cells by a process called “internalization” or “endocytosis” (synonyms) (see abstract below). There is evidence that “fresh” microplastic particles are not easily taken in but once exposed to the environment for a while, the surface of the microplastic particles changes, allowing internalization to happen more easily. The effects of the microplastic on the inside of the cell is understudied, but could in some cases be a problem. Microplastics may decrease cellular activity and increase reactive oxygen species, which in turn has potentially serious health effects.

Is this hopeless? Possibly. Can we stop using plastics? Maybe. Can the environment sequester microplastic particles (and thus carbon) naturally? Sometimes and maybe. Developing nations contribute hugely to plastic pollution due to a lack of solid waste infrastructure. Developed nations like the US have a great plastic waste infrastructure, but use so many plastics that the contribution from these countries is still huge (see this). We shed microplastic particles through many activities from feeding one’s baby to driving to the store to buy more forumla.

The fact that microplastic particles are something we ingest, breath in, our that our cells engulf is not itself a novelty. The gas and liquids we exist among are normally full of particles. Many of these particles are polymers, like plastic, but natural (pollen, skin cells, etc.). The problem with microplastic particles isn’t so much that they exist, but that they exist and are subtly, or sometimes dramatically, different than what is normally there, and what we thus normally adapt to. Also, microplastic particles may create a different distribution than what would normally occur (like the frequency in baby formula?). The challenge is to figure out where microplastic particles matter most, and then figure out ways of addressing those problems first and fast. This will also involve figuring out if the best solutions (which is a function of how well the solution works and how likely it is to get it to happen) is a change in specific policies or regulations, or changes in individual behavior. And, of course, we must be cognizant that changes to avoid or reduce microplastic particles do not result in some other negative effect.

This is just a rough, preliminary look at microplastic particles. I tried to include a wide selection of links to recent works, but I’m afraid many may be behind paywalls. But, you should be able to find a lot more by CLICKING HERE.

Additional Info and Resources:
Machado, Et Al. 2018. Impacts of microplastics on the soil biophysical environment. Environ. Sci Technol 52(17)

Abstract: oils are essential components of terrestrial ecosystems that experience strong pollution pressure. Microplastic contamination of soils is being increasingly documented, with potential consequences for soil biodiversity and function. Notwithstanding, data on effects of such contaminants on fundamental properties potentially impacting soil biota are lacking. The present study explores the potential of microplastics to disturb vital relationships between soil and water, as well as its consequences for soil structure and microbial function. During a 5-weeks garden experiment we exposed a loamy sand soil to environmentally relevant nominal concentrations (up to 2%) of four common microplastic types (polyacrylic fibers, polyamide beads, polyester fibers, and polyethylene fragments). Then, we measured bulk density, water holding capacity, hydraulic conductivity, soil aggregation, and microbial activity. Microplastics affected the bulk density, water holding capacity, and the functional relationship between the microbial activity and water stable aggregates. The effects are underestimated if idiosyncrasies of particle type and concentrations are neglected, suggesting that purely qualitative environmental microplastic data might be of limited value for the assessment of effects in soil. If extended to other soils and plastic types, the processes unravelled here suggest that microplastics are relevant long-term anthropogenic stressors and drivers of global change in terrestrial ecosystems.

Ramsperger et al. 2020 “Environmental exposure enhances the internalization of microplastic particles into cells” Science Advances 6(50)
Abstract: Microplastic particles ubiquitously found in the environment are ingested by a huge variety of organisms. Subsequently, microplastic particles can translocate from the gastrointestinal tract into the tissues likely by cellular internalization. The reason for cellular internalization is unknown, since this has only been shown for specifically surface-functionalized particles. We show that environmentally exposed microplastic particles were internalized significantly more often than pristine microplastic particles into macrophages. We identified biomolecules forming an eco-corona on the surface of microplastic particles, suggesting that environmental exposure promotes the cellular internalization of microplastics. Our findings further indicate that cellular internalization is a key route by which microplastic particles translocate into tissues, where they may cause toxicological effects that have implications for the environment and human health.

Rilling and Lehman. 2020. Microplastic in terrestrial ecosystem. Science.


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Everything is as expected, even the Covid-19 pandemic

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When I was in graduate school, four things happened at almost the same time (probably within a three year time frame, but who’s counting?) 1) The publication of The Coming Plague: Newly Emerging Diseases in a World Out of Balance by Laurie Garrett (well, and my reading of the book); 2) the cultural phenomenon of “hot zone” movies and books, of which the most memorable is probably Outbreak starting Dustin Hoffman; and 3) the realization that a good part of the archaeology I was doing in the Congo was of villages that had been abandoned because a plague of some kind came along and killed enough people that everyone moved elsewhere, which is apparently a tradition in that area; and 4) the Zaire Ebola outbreak in Kikwit. Since I had been working in the area, I got involved, in a minor way, with some of the Ebola research, and I produced evidence for a model for the virus jumping from fuit bats to humans that turned out to be exactly what had happened about ten years later when the West African Ebola epidemic occurred. Continue reading Everything is as expected, even the Covid-19 pandemic


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Covidpocalypse Now: an update

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Most of the Covid news is about vaccines.

A second vaccine has passed the final non-red tape hurdle in the US, and will likely be authorized by the end of the week. Six million doses will be distributed, probably over the weekend or early in the week, to over 3,000 locations.

There is argument and discussion going on as to the lower age limit on the vaccines. So far everything seems authorized for 18 year olds and older. It will probably be a serious mistake if that isn’t adjusted very soon. Now, the kids who transmit the disease that kill grandma are anonymous. Once they are the main carriers, they will not be, and a spotty subgroup of an entire generation will be scarred. At least, we’ll be given by fate the name for that generation. The Marys (for Typhoid Mary).

Let’s talk about Pregnant and lactating women for a minute. There have been no systematic trials pertaining to pregnant women, so the FDA advice is vague. They say, “you decide.” The following are supportable facts:

1) There is evidence, subject to revision because it is not the focus of any systematic experimental study, that pregnant women are somewhat protected from getting Covid-19, but not to anywhere near the degree that they can flout caution.

2) There is evidence, again subject to revision, that when pregnant women do get Covid-19, they have a number of worse outcomes than other people of similar age. They may get sicker, and there is a possible risk of preterm birth.

3) Non-live vaccines are generally considered safe for pregnant women.

To manufacturers and health care providers, this may be more a mater of blame and liability than anything else. Of all the people who get the vaccine, some are going to get sick or die randomly even if the vaccine never causes an actual problem, and someone is going to sue somebody over something. The chance of such a suit winning probably goes up if the plaintiff is a pregnant woman or her survivors, or if a baby is born with a problem etc. etc. So, by saying “you decide” we just get on with it, is probably the thinking.

VERY IMPORTANT: We humans have a lot of misconceptions about immunity and pregnancy. A common falsehood is that immunity of the mother is passed on to the offspring. This is not true. Also, an in utero fetus does not get vaccinated when the mother gets vaccinated. A lot of people believe these things happen but they do not.

What does happen is that the mother’s immune products, if she’s got them, circulate in the fetus, and may even be found in the newborn for a while. But an infant does not have much of a functioning adaptive immune system, so there can be no development of long term immunity, and the magical immunity stuff we have spent so much time talking about can’t be passed on.

During lactation, some of this humeral immunity of the mother will be shared with the offspring via breast feeding. This, of course, is also temporary.

It has been a while since I’ve done a literature search on this, but last time I looked there were no studies that really examined how effective any of this passive immunity is. Our cultural love of breastfeeding, and rhetoric from pro-breast feeding organizations, have led many people to believe that mother to infant immunity (i.e. through breastfeeding and esp the passing on of colostrum) is powerful and highly effective. We don’t really know this.

Doses:

In the US right now 2.9 million Pfizer doses (with second doses already accounted for) have been shipped. Moderna will ship over 5 million doses right away. According to Health and Human Services (a Trump Crime Family Joint) there will be enough doses to vaccinate everybody in the US by the end of June 2021. We await the replacement of the Deplorables with Biden appointees to confirm (or deny) that.

Can you pass Covid-19 on if you are vaccinated?

Nobody knows yet, but there is not really a useful “yes” or “no” answer to this. Here’s the story: What matters is the R0 value of the disease, right? How many people will get infected down the road if a particular individual is infected. More realistically, sort of, imagine a population of 1 million people, and 1,000 people freshly infected show up and there are no precautions taken. If that disease is Covid and the 1 million are not vaccinated, the next “generation” of infection will see more than 1,000 people infected, and the next generation, more than that, etc. as a wave of the disease spreads across the populations. SO, maybe, 1,000 gets you 1800, and that gets you 2500, and that gets you 4,800, and so on.

If most everybody is vaccinated, the whole point is that the chance of the virus being able to reproduce in you at all is lower, the time frame and intensity of that reproduction is shorted or lowered. Maybe to zero, but even if not, the R0 value is significantly lowered.

So, in the above scenario, with the population mainly vaccinated, 1,000 infected people gets you maybe 100 (max, that would b a lot) which gets you 10, which gets you zero, and Bob’s your uncle.


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Covid-19 Update: Vaccines, Airborne, Seasonality, Irony

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A tale of two vaccines

Two vaccines are racing to the finish line. We can’t say which one will arrive first, because they each have a different finish line.

The good vaccine, the one likely to be safe (though not necessarily without some side effects) and effective (though you may need two doses, which is normal for vaccines so don’t panic about that) had this deadline: When it is ready, as in, finished with Phase 3 trials. My money is still on the Oxford Jenner vaccine. If that is the first one ready, don’t expect to see it in the US because a) Jared Kushner does not have any ownership in it and b) Jared’s F-I-L is the corrupt leader of the formerly Democratic Republic of the United States. We’ll get it after Joe and Kamala, if they are not killed by Putin, are in the White House.

What? You think we are going to let you have a vaccine that I don’t make money off of? Nope, not going to happen as long as the Trump Crime Family is in charge!
The bad vaccine is whatever vaccine the Trump Crime Family has decided they can sell us. The deadline for that is November 3rd, but really, earlier, because of early voting. FDA Commissioner Stephen Hahn, a member of the Trump Crime Family has started to say, “Oh, no, if we approve a vaccine early, and that is possible, then it will be a great vaccine, a really great vaccine, don’t worry, we are not going to play political games here. Nope. No October Surprise from the FDA, no sir.” Meanwhile all of the senior actual scientists in the government that have anything to do with this have warned Hahn, uselessly, that he should not do this, because they expect him to do this.

I’m fine with this. The fake vaccine might actually work. It will be distributed among Republicans first, and they will blindly take it because they are morons and the head of the Trump Crime Family will order them to do it. If the vaccine turns out to be dangerous, it will be they that suffer, deservedly for the adults (sorry, kids, your parents are dangerous assholes) and it will be they that later sue (if they live) Hahn and Trump over the damage done. If, on the other hand, the fake vaccine is actually a good vaccine, an emergency use authorization by Hahn will certainly speed up data collection, owing to the additional rats, er, lab rats.

See “Here’s how the U.S. could release a COVID-19 vaccine before the election—and why that scares some

The Second Coming

Never mind what you may have heard about Covid-19’s virus not being seasonal. The assertions that it is not were falsehoods, mostly generated by the press misunderstanding what this all means, spread by people who, amazingly, are not actual epidemiologists, on Facebook. OK, admittedly, I am not actually an epidemiologist either, though back in Grad school when I discovered it exists, I almost jumped ship. And, I do play one in the classroom in the class I co-teach on immunology and epidemiology. Point is, I know a little better than the average person when I’m about to say something stupid. Usually, I then shut up. But not always, so beware.

Anyway, for all the various scientific reasons, it might be seasonal. Consider group of immunologists and epidemiologist siting around having a beer, and someone asks the question, “Is Covid-19 seasonal?” you’d get a lot of hemming and hawing. Then, the inquisitor says, “OK, fine. Each of you take this slip of paper and pencil, and write down “yes” if you think it will turn out to be seasonal, and “no” if you don’t think so. Don’t share your work. If you all turn out to say the same answer, then the beer is free for the rest of the night.”

I strongly suspect they would all write down a non-committal but educated “yes.”

The thing is, an outbreak has its own momentum. Some of the worse influenza outbreaks violated the seasonal pattern we know influenza has. All the Covid-19 outbreaks we have been having have masked any possible obvious seasonality for Covid, though one study that looked at underlying factors linked to seasonality concluded that there is a pretty good chance Covid-19 is seasonal.

On top of that, we have another (not unrelated) set of seasonal factors. No matter what you do to mitigate against spread of the disease in a school, going back to school, even in some sort of limited “hybrid” pattern, WILL result in increased spread. This is not an uncertainty. And, we are starting that now, and as you probably know, it is happening. Between back to school and climate related seasonal effects, we are looking at a long hard winter.

Related: COVID-19 rising in 26 states as US hits 6 million cases

Covid-19 is probably not mainly airborne.

But it is totally airborne as well.

I think it is funny (as in “funny, holy crap, how stupid can people be????”) that once news came out that Covid-19 is very likely airbonre, that many people actually then asserted that it was NOT spread hand to object to hand. It still is folks! KEEP WASHING YOUR DAMN HANDS PEOPLE. Jeesh.

But anyway, the evidence of airborne transmission builds and our understanding of that phenomenon deepens.

COVID-19 patients in earlier stages exhaled millions of SARS-CoV-2 per hour

Exhaled breath samples had the highest positive rate (26.9%, n=52), followed by surface swabs (5.4%, n=242), and air samples (3.8%, n=26). COVID-19 patients recruited in Beijing exhaled millions of SARS-CoV-2 RNA copies into the air per hour. Exhaled breath emission may play an important role in the COVID-19 transmission.

For refernece, this is the very rough not yet accepted article that started this whole thing: Outbreak of COVID-19 in a nursing home associated with aerosol transmission as a result of inadequate ventilation

See this for a very current summary on the airborne situation.

Or, maybe you are just on your own

The latest plan from the Trump administration, other than faking a new vaccine to make money somehow, is the do nothing and wait for herd immunity to “kick in.”

New Trump pandemic adviser pushes controversial ‘herd immunity’ strategy, worrying public health officials

One of President Trump’s top medical advisers is urging the White House to embrace a controversial “herd immunity” strategy to combat the pandemic, which would entail allowing the coronavirus to spread through most of the population to quickly build resistance to the virus, while taking steps to protect those in nursing homes and other vulnerable populations, according to five people familiar with the discussions.

The administration has already begun to implement some policies along these lines, according to current and former officials as well as experts, particularly with regard to testing.

The approach’s chief proponent is Scott Atlas, a neuroradiologist and fellow at Stanford’s conservative Hoover Institution, who joined the White House in August as a pandemic adviser. …

Irony

Yes, I am aware that the picture at the top of the post is an example of irony. That is why it is there.


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Teachers: This one neat trick could save your life

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This is for all teachers, but only some of you will be able to do this. Depends on your topic. This may pertain mostly to biology teachers, maybe stats or math, but by extension, any science or empirical topic including history.

Never mind that the first thing bio students to know is about Hydrogen bonds, or that the first thing stats students need to know is basic probability theory. You already probably do some sort of introduction thing that gets the students oriented to your subject, with a “get to know you” component, etc.

Replace that with this. The first thing the students should encounter in your classroom is some sort of topic appropriate, level and age appropriate, encounter with pandemic reality. Many of your students are not taking this pandemic seriously. They’ve been hanging round mask-less and in close quarters with their friends all summer, maybe practicing on a team, whatever. They are not going to properly manage their own viral shed or the possibility of someone else’s pathogenic effluence. They are going to be gobbing all over each other, their desks, and you.

Now is the time to use your mad teaching skills to push at least some of your students in the direction of being more careful, and possibly, slowing the spread of the Covid-19 causing disease.

I know, I know, you are saying “we are doing distance learning, this does not matter.” But it does matter. The back to school outbreak is going to happen whether or not you, or your school, is doing distance learning, and your small part of the learning community overlaps with the rest of it. And, you never know when your college, HS administration, or school district is going to send the students back into your room. This is your chance. Take it.

Can’t think of an example of a lesson that would smart up your students, to enhance the behavioral part of their innate immune system? Don’t give me that! Of course you can, you are a great teacher! In face, once you’ve thought about it, I want to hear your ideas. Let’s get moving on this!


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Before the Covid-19 Vaccine, This.

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Antibodies may precede vaccines in fighting Covid-19. Antibody treatments involve producing antibodies against a disease, either by harvesting them from previously infected individuals or, better, making them using some sort of scientific magic (aka technology that is hard to explain). An antibody treatment can fight an existing virus, and avoid infection short term. Eventually the antibodies go away, so this does not confer immediate immunity.

This is not an uncommon situations. Lots of diseases appeared out of nowhere, and were initially treated this way until other longer term solutions could be developed. But many of those diseases were rare to begin with and remained rare, so the antibody treatment was not scaled up. Just read all those books and stories about “emerging diseases” from back in the “Hot Zone” literature days and you’ll see these stories played out.

Anyway, here is what some experts say quoted in a recent Science coverage by Jon Cohen:

“If you were going to put your money down, you would bet that you get the answer with the monoclonal before you get the answer with a vaccine,” says Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases (NIAID).

and

“Antibodies have the potential to be an important bridge until the vaccine is available,” says Ajay Nirula, a vice president at Eli Lilly, one of several large companies investing in them. Likely to be more effective than remdesivir and dexamethasone, the repurposed drugs shown to help against COVID-19, antibodies could protect the highest risk health care workers from becoming infected while also lessening the severity of the disease in hospitalized patients. But producing monoclonals involves using bioreactors to grow lines of B cells that make the proteins, raising concerns they could be scarce and expensive. On 15 July, Lilly, AbCellera, AstraZeneca, GlaxoSmithKline, Genentech, and Amgen jointly asked the U.S. Department of Justice (DOJ) whether they could share information about manufacturing their monoclonals without violating antitrust laws “to expand and expedite production.”

Antibody expert Amy Jenkins (Pandemic Prevention Platform (P3) program at the Defense Advanced Research Projects Agency) suggests a N ovember-December time line for seeing this technology in the field is not unrealistic.


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Your Normal Fourth

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I read the news today, oh boy. To coin a phrase.

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.


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Trump, Tulsa, COVID-19’s Wet Dream, Just Desserts

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The 19th of June is Juneteenth.

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.


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Problems conceptualizing Covid

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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!


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How To Think About Immunity to COVID-19

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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!


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Lack of coronavirus COVID-19 in Subsaharan Africa?

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That there is no coronavirus COVID-19 reported in Subsaharan Africa is a huge concern.

Why?

1) It seems likely that this virus spread out of China in part by Chinese people working or visiting overseas.

2) China has had a long standing diplomatic and commercial presence in several areas of Subsaharan Africa including the Congo and Sudan, and some other places.

3) These are places where illness are only barely monitored and generally not well reported.

My guess is that coronavirus COVID-19 is in the Congo and Sudan and a few other places, and it is not being addressed.


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Should I wear a facemask to avoid the flu or some other nasty virus like Coronavirus COVIC-19?

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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-PCR–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.


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