parasites-microbiome   117

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Friends with malefit. The effects of keeping dogs and cats, sustaining animal-related injuries and Toxoplasma infection on health and quality of life | bioRxiv
The main problem of many studies was the autoselection – participants were informed about the aims of the study during recruitment and later likely described their health and wellbeing according to their personal beliefs and wishes, not according to their real status. To avoid this source of bias, we did not mention pets during participant recruitment and hid the pet-related questions among many hundreds of questions in an 80-minute Internet questionnaire. Results of our study performed on a sample of on 10,858 subjects showed that liking cats and dogs has a weak positive association with quality of life. However, keeping pets, especially cats, and even more being injured by pets, were strongly negatively associated with many facets of quality of life. Our data also confirmed that infection by the cat parasite Toxoplasma had a very strong negative effect on quality of life, especially on mental health. However, the infection was not responsible for the observed negative effects of keeping pets, as these effects were much stronger in 1,527 Toxoplasma-free subjects than in the whole population. Any cross-sectional study cannot discriminate between a cause and an effect. However, because of the large and still growing popularity of keeping pets, the existence and nature of the reverse pet phenomenon deserve the outmost attention.
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12 weeks ago by nhaliday
Braves | West Hunter
If  Amerindians had a lot fewer serious infectious diseases than Old Worlders, something else had to limit population – and it wasn’t the Pill.

Surely there was more death by violence. In principle they could have sat down and quietly starved to death, but I doubt it. Better to burn out than fade away.
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may 2019 by nhaliday
WHO | Priority environment and health risks

Environmental factors are a root cause of a significant disease burden, particularly in developing countries. An estimated 25% of death and disease globally, and nearly 35% in regions such as sub-Saharan Africa, is linked to environmental hazards. Some key areas of risk include the following:

- Unsafe water, poor sanitation and hygiene kill an estimated 1.7 million people annually, particularly as a result of diarrhoeal disease.
- Indoor smoke from solid fuels kills an estimated 1.6 million people annually due to respiratory diseases.
- Malaria kills over 1.2 million people annually, mostly African children under the age of five. Poorly designed irrigation and water systems, inadequate housing, poor waste disposal and water storage, deforestation and loss of biodiversity, all may be contributing factors to the most common vector-borne diseases including malaria, dengue and leishmaniasis.
- Urban air pollution generated by vehicles, industries and energy production kills approximately 800 000 people annually.
- Unintentional acute poisonings kill 355 000 people globally each year. In developing countries, where two-thirds of these deaths occur, such poisonings are associated strongly with excessive exposure to, and inappropriate use of, toxic chemicals and pesticides present in occupational and/or domestic environments.
- Climate change impacts including more extreme weather events, changed patterns of disease and effects on agricultural production, are estimated to cause over 150 000 deaths annually.

Note the high point at human origin (Africa, Middle East) and Asia. Low points in New World and Europe/Russia. Probably key factor in explaining human psychological variation (Haidt axes, individualism-collectivism, kinship structure, etc.). E.g., compare Islam/Judaism (circumcision, food preparation/hygiene rules) and Christianity (orthodoxy more than orthopraxy, no arbitrary practices for group-marking).

I wonder if the dietary and hygiene laws of Christianity get up-regulated in higher parasite load places (the US South, Middle Eastern Christianity, etc.)?

Also the reason for this variation probably basically boils down how long local microbes have had time to adapt to the human immune system.

obv. correlation:

Tropical disease:
Tropical diseases are diseases that are prevalent in or unique to tropical and subtropical regions.[1] The diseases are less prevalent in temperate climates, due in part to the occurrence of a cold season, which controls the insect population by forcing hibernation. However, many were present in northern Europe and northern America in the 17th and 18th centuries before modern understanding of disease causation. The initial impetus for tropical medicine was to protect the health of colonialists, notably in India under the British Raj.[2] Insects such as mosquitoes and flies are by far the most common disease carrier, or vector. These insects may carry a parasite, bacterium or virus that is infectious to humans and animals. Most often disease is transmitted by an insect "bite", which causes transmission of the infectious agent through subcutaneous blood exchange. Vaccines are not available for most of the diseases listed here, and many do not have cures.

cf. Galton:
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july 2018 by nhaliday
Existential Risks: Analyzing Human Extinction Scenarios
Would you endorse choosing policy to max the expected duration of civilization, at least as a good first approximation?
Can anyone suggest a different first approximation that would get more votes?
How useful would it be to agree on a relatively-simple first-approximation observable-after-the-fact metric for what we want from the future universe, such as total life years experienced, or civilization duration?

We're Underestimating the Risk of Human Extinction:
An Oxford philosopher argues that we are not adequately accounting for technology's risks—but his solution to the problem is not for Luddites.

Anderson: You have argued that we underrate existential risks because of a particular kind of bias called observation selection effect. Can you explain a bit more about that?

Bostrom: The idea of an observation selection effect is maybe best explained by first considering the simpler concept of a selection effect. Let's say you're trying to estimate how large the largest fish in a given pond is, and you use a net to catch a hundred fish and the biggest fish you find is three inches long. You might be tempted to infer that the biggest fish in this pond is not much bigger than three inches, because you've caught a hundred of them and none of them are bigger than three inches. But if it turns out that your net could only catch fish up to a certain length, then the measuring instrument that you used would introduce a selection effect: it would only select from a subset of the domain you were trying to sample.

Now that's a kind of standard fact of statistics, and there are methods for trying to correct for it and you obviously have to take that into account when considering the fish distribution in your pond. An observation selection effect is a selection effect introduced not by limitations in our measurement instrument, but rather by the fact that all observations require the existence of an observer. This becomes important, for instance, in evolutionary biology. For instance, we know that intelligent life evolved on Earth. Naively, one might think that this piece of evidence suggests that life is likely to evolve on most Earth-like planets. But that would be to overlook an observation selection effect. For no matter how small the proportion of all Earth-like planets that evolve intelligent life, we will find ourselves on a planet that did. Our data point-that intelligent life arose on our planet-is predicted equally well by the hypothesis that intelligent life is very improbable even on Earth-like planets as by the hypothesis that intelligent life is highly probable on Earth-like planets. When it comes to human extinction and existential risk, there are certain controversial ways that observation selection effects might be relevant.
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march 2018 by nhaliday
Plague of Frogs | West Hunter
For a few years the herpetologists were concerned yet happy. Concerned, because many frog populations were crashing and some were going extinct. Happy, because confused puppies in Washington were giving them money, something that hardly ever happens to frogmen. The theory was that amphibians were ‘canaries in a coal mine’, uniquely sensitive to environmental degradation.


It took some time for herpetologists to admit that this chytrid fungus is the main culprit – some are still resisting. First, it was a lot like how doctors resisted Semmelweiss’ discoveries about the cause of puerperal fever – since doctors were the main method of transmission. How did this fungus get to the cloud forests of Costa Rica? On the boots of herpetologists, of course.

The second problem is Occam’s butterknife: even though this chytrid fungus is the main culprit, it’s just got to be more complicated than that. Even if it isn’t. People in the life sciences – biology and medicine – routinely reject simple hypotheses that do a good job of explaining the data for more complex hypotheses that don’t. College taught them to think – unwisely.
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february 2018 by nhaliday
Why Sex? And why only in Pairs? - Marginal REVOLUTION
The core conclusion is that mutations continue to rise with the number of sex-participating partners, but in simple Red Queen models the limiting features of the genotypes is the same whether there are two, three, or more partners.

Men Are Animals:
I agree with all the comments citing motility/sessility.
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january 2018 by nhaliday
The Evil Dead | West Hunter
Someone asked me to go over a chapter he wrote, about the impact of certain customs on human health. One of them was the health advantages of quick burial: the problem is, usually there aren’t any.   People seem to think that the organisms causing decomposition are pathogenic, but they’re not.  People killed by trauma (earthquakes,  floods, bullets) are dead enough, but not a threat.  Sometimes, the body of someone that died of an infectious disease is contagious – smallpox scabs have been known to remain infectious for a long, long time – but most causative agents are unable to survive for long after the host’s death. Now if you’re dissecting someone,  especially if they’re fresh, you probably don’t want to nick yourself with the scalpel – but if you just walk past the corpse and refrain from playing with it, you’re usually OK.
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november 2017 by nhaliday
Bouncing Off the Bottom | West Hunter
Actually going extinct would seem to be a bad thing, but a close call can, in principle, be a good thing.

Pathogens can be a heavy burden on a species, worse than a 50-lb sack of cement. Lifting that burden can have a big effect: we know that many species flourish madly once they escape their typical parasites. That’s often the case with invasive species. It’s also a major strategy in agriculture: crops often do best in a country far away from their place of origin – where the climate is familiar, but most parasites have been left behind. For example, rubber trees originated in South America, but they’re a lot easier to grow in Liberia or Malaysia.

Consider a situation with a really burdensome pathogen – one that specializes in and depends on a single host species. That pathogen has to find new host individuals every so often in order to survive, and in order for that to happen, the host population has to exceed a certain number, usually called the critical community size. That size depends on the parasite’s persistence and mode of propagation: it can vary over a huge range. CCS is something like a quarter of a million for measles, ~300 for chickenpox, surely smaller than that for Epstein-Barr.

A brush with extinction- say from an asteroid strike – might well take a species below the CCS for a number of its pathogens. If those pathogens were limited to that species, they’d go extinct: no more burden. That alone might be enough to generate a rapid recovery from the population bottleneck. Or a single, highly virulent pathogen might cause a population crash that resulted in the extinction of several of that species’s major pathogens – quite possibly including the virulent pathogen itself. It’s a bottleneck in time, rather than one in space as you often see in colonization.

Such positive effects could last a long time – things need not go back to the old normal. The flea-unbitten species might be able to survive and prosper in ecological niches that it couldn’t before. You might see a range expansion. New evolutionary paths could open up. That brush with extinction could be the making of them.

When you add it all up, you begin to wonder if a population crash isn’t just what the doctor ordered. Sure, it wouldn’t be fun to be one of the billions of casualties, but just think how much better off the billions living after the bottleneck will be. Don’t be selfish.
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november 2017 by nhaliday
Darwinian medicine - Randolph Nesse
The Dawn of Darwinian Medicine:
TABLE 1 Examples of the use of the theory of natural selection to predict the existence of phenomena otherwise unsuspected
TABLE 2 A classification of phenomena associated with infectious disease
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november 2017 by nhaliday
Measles and immunological amnesia | West Hunter
A new paper in Science , by Michael Mina et al,  strongly suggests that measles messes up your immunological defenses for two or three years. This is the likely explanation for the fact that measles inoculation causes much greater decreases in child morbidity and mortality than you’d expect from preventing the deaths directly due to measles infection. The thought is that measles whacks the cells that carry immunological memory, leaving the kid ripe for reinfections.  I think there can be a similar effect with anti-cancer chemotherapy.

If correct, this means that measles is much nastier than previously thought. It must have played a significant role in the demographic collapse of long-isolated peoples (such as the Amerindians). Its advent may have played a role in the population decrease associated with the decline of the Classical world.  Even though it is relatively new (having split off from rinderpest a couple of thousand years ago) strong selection for resistance may have  favored some fairly expensive genetic defenses (something like sickle-cell) in Eurasian populations.

We already know of quite a few complex side effects of infectious disease, such the different kind of immunosuppression we see with AIDs, Burkitt’s lymphoma hitting kids with severe Epstein-Barr infections followed by malaria, acute dengue fever that requires a previous infection by a different strain of dengue, etc: there may well be other important interactions and side effects, news of which has not yet come to Harvard.
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october 2017 by nhaliday
UCR Computational Entomology Page
The Computational Entomology Lab at UCR has produced simple graphics to allow people to visually understand the importance and utility of avoiding the outdoors at dawn and dusk. Using sensors to detect insect flight, we have monitored several species West Nile vector mosquitoes for their entire lifespan, in order to produce daily activity plots. As shown below, these plots strongly confirm the CDC advice (this figure helps you understand how to interpret the plots). For example, assuming you get up after dawn, and you need to spend most of your day outdoors: if you can manage to go indoors an hour before sunset, and stay indoors until an hour after sunset, your chances of being bitten by a mosquito is about two hundred times less than if you had spend those two indoor hours taking a noontime siesta, but stayed outdoors to watch the sunset.

Pokémon Go and Exposure to Mosquito-Borne Diseases: How Not to Catch ‘Em All:
Vector-borne diseases - Dengue outbreak in Madeira Island:
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october 2017 by nhaliday
[1709.01149] Biotechnology and the lifetime of technical civilizations
The number of people able to end Earth's technical civilization has heretofore been small. Emerging dual-use technologies, such as biotechnology, may give similar power to thousands or millions of individuals. To quantitatively investigate the ramifications of such a marked shift on the survival of both terrestrial and extraterrestrial technical civilizations, this paper presents a two-parameter model for civilizational lifespans, i.e. the quantity L in Drake's equation for the number of communicating extraterrestrial civilizations. One parameter characterizes the population lethality of a civilization's biotechnology and the other characterizes the civilization's psychosociology. L is demonstrated to be less than the inverse of the product of these two parameters. Using empiric data from Pubmed to inform the biotechnology parameter, the model predicts human civilization's median survival time as decades to centuries, even with optimistic psychosociological parameter values, thereby positioning biotechnology as a proximate threat to human civilization. For an ensemble of civilizations having some median calculated survival time, the model predicts that, after 80 times that duration, only one in 1024 civilizations will survive -- a tempo and degree of winnowing compatible with Hanson's "Great Filter." Thus, assuming that civilizations universally develop advanced biotechnology, before they become vigorous interstellar colonizers, the model provides a resolution to the Fermi paradox.
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october 2017 by nhaliday
Post-Columbian Evolution – Holes | West Hunter
At this point, we have some decent examples of post-Columbian evolution, genetic changes in New World populations after 1492. There is evidence for selection for increased fertility in Quebec, along with increased mutational load due to relaxed selection. Something similar must have occurred in American colonial populations.

I think that the Amish are probably becoming plainer, thru the boiling-off process – which can’t be a common mechanism, because it requires very high fertility, enough to sustain a substantial defection rate.

HbS (sickle-cell) gene frequency has almost certainly decreased significantly among African-Americans – a simple model suggests by about half. There has probably been a decrease in other expensive malaria defenses.


In principle, if you had an immune gene that defended against an Old World pathogen that didn’t cross into America, Amerindians would have gradually accumulated nonfunctional variants, just from mutational pressure. the percentage of people with such mutations in any particular immune defense gene would not be very high (not in only 500 generations) but since there are many such genes, the fraction of Amerindians with at least one such hole in their immunological armor might have been significant. Probably this would have been more of a problem in the Caribbean islands, where the Taino seem to have just melted away… Presumably most such holes are gone now in surviving populations, but you might be able to identify them in pre-Columbian DNA.

I see where some Kraut is saying that we now know that human evolution is continuing. I think that’s been an obvious conclusion for almost 160 years.
Sarazzin acknowledges it.

interesting guy:
He became well-known worldwide after publishing a controversial book about Muslim immigrants in Germany in 2010.[3] In his book Deutschland schafft sich ab ("Germany abolishes itself"),[4] he denounces the failure of Germany's post-war immigration policy, sparking a nationwide controversy about the costs and benefits of multiculturalism.
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october 2017 by nhaliday
House O’Rats | West Hunter
Not content with our simple selection experiment, we also install complicated mazes with flaming hoops that the rats have to jump through in order to get extra food and mates: we want rats with different brains, and eventually we get them. They’re maze-bright and flaming-hoop-bright. We install treadmills and feed the rats according to their work output, and eventually they produce more work per amount of food eaten. They’ve maximized efficiency rather than surge power, which was more useful back when they were wild and free. Not only that, they eventually come to like being on the treadmill, almost as if it’s some sort of race.

There are other silos – one full of rice and another full of maize. They have different mazes and flaming hoops, built at different times: and there are still wild rats, too, although not as many as in the silos.

But no matter how much they change, they’re still just a bunch of rats.
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september 2017 by nhaliday
Of Mice and Men | West Hunter
It’s not always easy figuring out how a pathogen causes disease. There is an example in mice for which the solution was very difficult, so difficult that we would probably have failed to discover the cause of a similarly obscure infectious disease in humans.

Mycoplasma pulmonis causes a chronic obstructive lung disease in mice, but it wasn’t easy to show this. The disease was first described in 1915, and by 1940, people began to suspect Mycoplasma pulmonis might be the cause. But then again, maybe not. It was often found in mice that seemed healthy. Pure cultures of this organism did not consistently produce lung disease – which means that it didn’t satisfy Koch’s postulates, in particular postulate 1 (The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.) and postulate 3 (The cultured microorganism should cause disease when introduced into a healthy organism.).

Well, those postulates are not logic itself, but rather a useful heuristic. Koch knew that, even if lots of other people don’t.

This respiratory disease of mice is long-lasting, but slow to begin. It can take half a lifetime – a mouse lifetime, that is – and that made finding the cause harder. It required patience, which means I certainly couldn’t have done it.

Here’s how they solved it. You can raise germ-free mice. In the early 1970s, researchers injected various candidate pathogens into different groups of germ-free mice and waited to see which, if any, developed this chronic lung disease. It was Mycoplasma pulmonis , all right, but it had taken 60 years to find out.

It turned out that susceptibility differed between different mouse strains – genetic susceptibility was important. Co-infection with other pathogens affected the course of the disease. Microenvironmental details mattered – mainly ammonia in cages where the bedding wasn’t changed often enough. But it didn’t happen without that mycoplasma, which was a key causal link, something every engineer understands but many MDs don’t.

If there was a similarly obscure infectious disease of humans, say one that involved a fairly common bug found in both the just and the unjust, one that took decades for symptoms to manifest – would we have solved it? Probably not.

Cooties are everywhere.

gay germ search:
It’s hard to say, depends on how complicated the path of causation is. Assuming that I’m even right, of course. Some good autopsy studies might be fruitful – you’d look for microanatomical brain differences, as with nartcolepsy. Differences in gene expression, maybe. You could look for a pathogen – using the digital version of RDA (representational difference analysis), say on discordant twins. Do some old-fashioned epidemiology. Look for marker antibodies, signs of some sort of immunological event.

Do all of the above on gay rams – lots easier to get started, much less whining from those being vivisected.

Patrick Moore found the virus causing Kaposi’s sarcoma without any funding at all. I’m sure Peter Thiel could afford a serious try.
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september 2017 by nhaliday
Mechanisms of microbial traversal of the blood–brain barrier
A journey into the brain: insight into how bacterial pathogens cross blood–brain barriers:
How do extracellular pathogens cross the blood-brain barrier?:
Defense at the border: the blood–brain barrier versus bacterial foreigners:
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september 2017 by nhaliday

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