Monday, February 20, 2012

You are what you're infected with?

Rats infected with the parasite Toxoplasma gondii do crazy things.  They find the scent of cat urine sexy and attractive, they don't run from the actual beasts; they are more active in running wheels, which might indicate that the parasite induces increased activity which may more readily attract a cat's attention. When an infected rat is eaten by a cat, the T. gondii is passed on in the cat's feces to infect again.  T. gondii can only reproduce inside the cat.  Great survival strategy on the part of the parasite, this trick of making the rat no longer fear cats -- now that's really building a better mouse-trap! Did this strategy evolve by adaptive selection, or is it just something that happened?

Czech biologist, Jaroslav Flegr, thinks T. gondii infections do much the same to humans -- his story is told in the March 2012 Atlantic Monthly.  Toxoplasmosis, the infection caused by T. gondii, infects a significant segment of the world's population -- perhaps 20% of Americans, but 55% of French people are infected, probably because the French diet includes more rare or raw meat than the American diet.  The usual mode of transmission is from a member of the cat family to another warm-blooded animal via ingestion of feces from an infected cat, but raw or rare meat can be another source.  It can also be transmitted from mother to fetus, and can result in serious complications in an infected fetus, including stillbirth.  This is why pregnant women are told to avoid litter boxes.

Infection has long been supposed to cause mild flu-like symptoms in otherwise healthy individuals, but then it was assumed that the parasite lay dormant in cysts sequestered away inside brain cells.  People with weakened immunity were at greater risk, however; in the days before antiretroviral drugs for treating HIV, toxoplasmosis infections are thought to have caused much of the dementia in patients with end-stage AIDS.

But maybe the parasite actually does more damage than has been thought.
...if Flegr is right, the “latent” parasite may be quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents. And that’s not all. He also believes that the organism contributes to car crashes, suicides, and mental disorders such as schizophrenia. When you add up all the different ways it can harm us, says Flegr, “Toxoplasma might even kill as many people as malaria, or at least a million people a year.” 
Flegr's hypothesis comes directly from his own experience.  He wondered for years why he was willing to take risks that others wouldn't, like crossing a street in the middle of traffic, or speaking out against communism in Communist Czechoslovakia.  Entirely by fluke, he was tested for T. gondii by someone in his institution looking for infected people to study a diagnostic kit they were developing, and he was discovered to be positive. To him, this explained his bizarre risk-taking behavior.

He reasons that T. gondii is not the only parasite that affects behavior.  The rabies virus incites fury in infected animals, ensuring that they bite others, and thus pass on the infection.  Ants infected with parasitic Cordyceps fungi do all kinds of bizarre, self-destructive things, including climbing onto a blade of grass and then clamping on with their mandibles. Soon the fungus consumes the ant's brain, and fungal fruiting bodies sprout from the ant's head (as in the video) and burst, releasing spores into the air, to settle and find a home in another unsuspecting, soon to be robotic ant. Apparently the Cordyceps fungi release chemicals that change an ant's pheromone reception, which alters their sense of navigation. Is this coincidence, not specific enough to have evolved per se?  Or is it a specific adaptation?



Another example of zombie ants involves infection by the lancet liver fluke, Dicrocoelium dendriticum.  When infected, the ant again climbs onto a blade of grass where it clamps on, there to be eaten by a grazing sheep or cow.  The ant does this only in the evening, when the air cools, and if it survives the night uneaten, it climbs down and behaves normally again until the following evening, when the fluke regains control. Again, this is remarkable, but it is it specific enough and frequent enough to be a Darwinian adaptation?  And what's in it for the poor manipulated ant? 

Things that seem (to human observers) so bizarre probably would be expected to have a balance, or else the victim species would have evolved resistance.  So many questions are raised by these examples.  And there are many more like them. 

But in any case, parasite-induced behavior changes are not unprecedented.  Could T. gondii really do the same?
In the Soviet-stunted economy, animal studies were way beyond Flegr’s research budget. But fortunately for him, 30 to 40 percent of Czechs had the latent form of the disease, so plenty of students were available “to serve as very cheap experimental animals.” He began by giving them and their parasite-free peers standardized personality tests—an inexpensive, if somewhat crude, method of measuring differences between the groups. In addition, he used a computer-based test to assess the reaction times of participants, who were instructed to press a button as soon as a white square popped up anywhere against the dark background of the monitor.
The subjects who tested positive for the parasite had significantly delayed reaction times. Flegr was especially surprised to learn, though, that the protozoan appeared to cause many sex-specific changes in personality. Compared with uninfected men, males who had the parasite were more introverted, suspicious, oblivious to other people’s opinions of them, and inclined to disregard rules. Infected women, on the other hand, presented in exactly the opposite way: they were more outgoing, trusting, image-conscious, and rule-abiding than uninfected women.
Flegr confirmed these surprising findings with further research, finding that infected men were suspicious, sloppy dressers, and introverted, while infected women were well-dressed and gregarious.  Reaction times of infected people were considerably slower than uninfected, and he found that they were 2 1/2 times more likely to be in traffic accidents -- this statistic has been replicated in other countries.  Flegr says that the personality changes are generally subtle, only detectable on a statistical basis.  But, it turns out that a fairly substantial percentage of people diagnosed with schizophrenia are T. gondii positive. 



What's the mechanism? 
Many schizophrenia patients show shrinkage in parts of their cerebral cortex, and Flegr thinks the protozoan may be to blame for that. He hands me a recently published paper on the topic that he co-authored with colleagues at Charles University, including a psychiatrist named Jiri Horacek. Twelve of 44 schizophrenia patients who underwent MRI scans, the team found, had reduced gray matter in the brain—and the decrease occurred almost exclusively in those who tested positive for T. gondii.
That's not clearly a mechanism, however, as the shrinkage could be entirely unrelated to schizophrenia.  Indeed, since only 1/4 of the patients tested showed reduced gray matter.  Anything more convincing?

Apparently, sequencing of the T. gondii genome suggests that it has 2 genes that can make the infected animal increase production of dopamine, and elevated dopamine levels are a mark of schizophrenia. Infection also, apparently, increases the infected animal's gregariousness, and in humans, increases sociability -- even infection with the influenza virus.  Infection can, apparently, even increase a person's (or a rat's) sex drive, and because many of these infections can be transmitted sexually, this improves their chances of being passed on.  This relates to any kind of infection that has been tested, not just T. gondii.

As it turns out, schizophrenia has been associated with a number of infections ("maternal rubella (German measles), influenza, Varicella zoster (chicken pox), Herpes (HSV-2), common cold infection with fever, or poliovirus infection while in childhood or adulthood, coxsackie virus infection (in neonates) or Lyme disease (vectored by the Ixodes tick and Borrelia Burgdorferri) or Toxoplasmosis" -- from a 2011 paper by C.J. Carter), and in fact, while genomewide association studies haven't found genes with major effects, or reliably replicated what they have found, for schizophrenia, itself, they have found 600 genes with small effect, many associated with inflammatory response, others implicated in the life cycle of the associated pathogens.  The same paper suggests that:
Schizophrenia may thus be a “pathogenetic” autoimmune disorder, caused by pathogens, genes, and the immune system acting together, and perhaps preventable by pathogen elimination, or curable by the removal of culpable antibodies and antigens.
That is, the authors suggest that the susceptibility genes code for proteins that are homologous to the pathogen's proteins, and that the latter might be intermingling or replacing endogenous proteins, and they are different enough to disrupt normal function, and lead to disease.
Pathogens' proteins may act as dummy ligands, decoy receptors, or via interactome interference. Many such proteins are immunogenic suggesting that antibody mediated knockdown of multiple schizophrenia gene products could contribute to the disease, explaining the immune activation in the brain and lymphocytes in schizophrenia, and the preponderance of immune-related gene variants in the schizophrenia genome. 
Further,
All of the pathogens implicated in schizophrenia express proteins with homology to multiple schizophrenia susceptibility gene products. The profile of each individual pathogen is again specific for different types of gene product, but all target key members of the schizophrenia network including dopamine, serotonin and glutamate receptors as well as neuregulin and growth-related or DISC1 related pathways.
So, the idea is that our genomes, our particular DNA variants, determine which human/viral matches we carry, and thus which pathogens we're susceptible to damage from.  So, in that sense, Carter, and others, suggest, schizophrenia and other behavioral disorders may be 'genetic', but environmental exposures, our vaccination history and so on determine the pathogens we might be infected with, and our immune system determines how we respond.

To be sure, these are statistical findings and there are so many genes associated with schizophrenia -- or perhaps more accurately so many genes not clearly but weakly, possibly, maybe, but not replicably associated, that it is possible one could almost always find some potential association with these pathways.  That makes it hard to evaluate the infectious scenario.

One clear point, though, is that even when what we are is genetic, the genes need not be those we were born with.  Bacteria, and hence their genes are vital to our survival and that appears just to be for starters.  When parasites affect our gene expression or function, their genomes become part of ours.  And from a biological point of view, our genetic battle for persistence -- for staying alive -- may have more to do with microbial challenges than with wearing out, which is basically what many GWAS targets are about (cancer, diabetes, etc.)

Even more important, perhaps, and a hint that we need to pay more attention to, is that many GWA kinds of studies are finding genes in immune-related systems, or those related to 'inflammation' for what appeared to be totally non-infectious and non-behavioral diseases, even including diabetes, intestinal disorders, retinal disorders of the eye, and many others.  These would be genetic in the sense that genetic susceptibility is involved, but not in the sense of intrinsically harmful genetic variants.

Is this behavioral parasite work definitive?  Do we now know that schizophrenia, and other disorders, are infectious in origin?  No.  Many questions have yet to be answered.  Maternal or early childhood exposure seem to be associated with risk, but why does schizophrenia have such a relatively late age of onset, given early age of exposure?  And why so stereotypically in late adolescence?  And so on.

But, it's intriguing that many GWAS have found an albeit small proportion of risk of many diseases explained by immune genes.

46 comments:

  1. This is awesome food for thought Anne. Thank you!

    To brainstorm on your last question about adult onset of symptoms rather than in children who are infected ... what if it's to do with the differences in male/female phenotypes which wouldn't develop until adulthood is reached?

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    1. This is definitely food for thought. I'm not sure what I think of it yet, because there are a lot of unanswered questions. Another one that I don't know the answer to, but someone surely does, is whether all the other parasites that have been associated with schizophrenia also have genes homologous to human genes, and if not dopamine, what?

      And, all these observational studies certainly can't answer the question. And, if T. gondii is in fact causative, it won't explain all schizophrenia, as the disease, like all other complex diseases, will surely turn out to have multiple causes.

      The brain is still developing during adolescence, so it's certainly plausible that some developmental stage has to be reached, and then interact with whatever the parasite is doing, to trigger disease. But of course that's not even a guess about mechanism. It wouldn't be the first instance of a disease, even a clearly genetic one, having a delayed age of onset.

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    2. This really shatters the foundation of the 'great man's' hubris in such a hilarious way. To think that humankind, with all our philosophical pomposity-we are so vulnerable that, that which defines us-our brainy magnificence-could so swiftly be hijacked by such a thing as T. gondii.
      Sometimes I wonder, who's behind the wheel?...

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    3. Well, the great conundrum of life, so very hard to grasp, is that there is nobody behind the wheel....and there isn't any wheel!

      Yet, it seems, we really aren't so vulnerable. After all, every one of us here today is the descendant of 3.8 billion years of entirely successful ancestors (whatever their infection status)!

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    4. Or.... maybe it's a parasite behind the wheel!

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    5. I think my initial reaction was a bit excited, fevered, impulsive...last night I was listening to WTF-Marc Maron's podcast- and he was talking about this. Of course he went off on a hot-headed rant about this parasite, while positing the possibility-because he airs the podcast from his "cat ranch"- that toxoplasmosis may be the cause of his volatility, and other glitches.
      Then I see this this morning; impetuous paranoia ensues.
      Well, after reading the research article, the calm of reasonability set it in.
      Do you guys know what that whole increased intelligence in women with latent toxoplasmosis is about?, or did I read that wrong?...those journals, replete with analytical jargon is sometimes daunting for the average dolt,

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    6. Calms of reasonability are to be encouraged. Perhaps not T. gondii's forte, however... As for increased intelligence in women with latent toxoplasmosis, the one Flegr paper I've read on the subject is less than convincing. The number of women with latent infection isn't clear, but it's got to be small, and it's not clear whether he controlled for obvious possible confounders like age, socieoeconomic strata and so on. And, it looks to me as though the difference in intelligence, however they measured it, is trivial. So, not something I'd write home about.

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    7. Thank's Anne.
      I talked to my professor today (Prof. Holly Dunsworth) about it. She helped to clear that up for me.
      We talked about the effects that have been observed in women, and how, even though the data is incomplete, what has been suggested doesn't sound particularly negative...which lead me to think; it wasn't long ago advertisements boasted a little parasitic product for weight loss-YES, WE'VE DONE IT AGAIN. NOW FROM THE SAME COMPANY THAT BROUGHT YOU THE 100% ALL NATURAL, 100% ORGANIC, WEIGHT LOSS SOLUTION, COMES THE PRODUCT THAT all you LADIES HAVE BEEN WAITING FOR...THE GREGARIOUS PERSONALITY POTION-DONT BE A SOCIAL PARASITE, BE A SOCIALITE, EXPLOIT OUR PARASITE...

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    8. You have a very fine professor, Mark! If you are in the DNAnonymous class, I hope we'll see some of your contributions to the class blog.

      I hadn't heard about the parasite diet! I have long wondered, though, why no one has adapted the tapeworm to the diet industry. Just looking for the ad you refer to, I note that in fact parasites are indeed used as diet aids in some places. Roundworms and tapeworms. So I guess this means we really are their slaves -- they've manipulated us into feeding them _and_ giving them a nice warm place to live. :-)

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  2. This is a plausible guess, certainly, for example if in infected persons some newly switched-on genes interact with the parasite's genes, etc.

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  3. Also, I cross in front of traffic very purposefully because I believe pedestrians/cyclists should have the right of way at all times and it's my small little way of sticking it to the man every time. I especially cross in front of cars that I believe are driving too fast near my house so that maybe they'll drive slowlier next time they come around. How does a study like this account for that "risk-taking" phenotype when it's not that at all? Or is it?

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    1. Holly.....have you been tested for T. gondii? Oh, but you're a dog person, not a cat person. I guess this is just home-grown self-destructive behavior, then! :)

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    2. Actually, the behavioral changes Flegr is documenting are, he says, imperceptible on the individual level, and only show up when he is comparing large(ish) groups. It's not like the parasite makes people climb trees and clamp on, waiting to be eaten. Most of what he says are associated behaviors are within the 'normal' range -- sloppy dressing, designer dressing, crossing in front of cars driving too fast in the hopes they'll slow down. So, it's only in comparing infected with uninfected that anything will look unusual.

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    3. There's a cross-cultural study in I think Proc Royal Soc B from the mid-late 00s on T. gondii linking incidence of schizophrenia with prevalence of cat-companionship at the population level.

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    4. How many cats does a person have to have to go over the line from normal to not so normal.... And why are cat ladies only women??

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    5. Yes, but Beware! of the ecological fallacy! Correlation at the group level doesn't mean the same at the individual level. Statistically, one might find that wearing grey hair up in a bun at advanced ages, is associated with schizophrenia. That's if, statistically, little old widows are fond of cats.

      Is it the blueing that's responsible rather than the cats?

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    6. Hmmm...maybe this is worth a short story....

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    7. Also, I could have T. gondii. I have lived with cats twice (briefly) and spent a lot of time at a neighbor's house who had cats while I was young. So I could very well have T. gondii and the traits you listed seem to match me pretty well except the well-dressed part. And I've been gregarious my whole life, not just in adulthood. As long as they don't sprout out of my head, it's all good.

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    8. A little bit of T. gondii could be a good thing!

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    9. Kevin and I have decided that T. gondii makes me walk in front of traffic and my consciousness rationalizes the behavior, post-hoc, to fit a pleasing self-image.

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    10. If you're lucky, you have latent toxoplasmosis. According to this paper, the longer you have it, the more intelligent you get. Your rationals will only get even more embellished as you age. :)

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    11. Mark (the poster above) and I were just having a funny conversation about how someone could wrongly interpret this research as: You want to get smarter? You should sniff cat poop!

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    12. *rationales! Apparently I can't write html and spell at the same time.

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    13. Do you think you can get away with just sniffing it?

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    14. haha. I typed "eat" but thought, yes, sniffing could be enough ;). Also, my brain is itchy.

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    15. Maybe 'graze' -- works euphemistically and literally too...

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    16. That list in the paper you linked to... those bold words describe most women I know. Especially academics.

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    17. Most women you know are dung eaters? or 'just' sniffers? or 'grazers'?! You have a strange, if intelligent, circle of friends....

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    18. So, are all these women academics because they are infected? Infected because they are academics? Uninfected and still academics? It would sure help to know how they tested intelligence, and how the women in the study got smarter. Mark said above that these papers, replete with academic jargon, can be daunting. They can also be just plain not good.

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  4. You probably have been infected by that parasite that makes little fungal fruiting bodies sprout on your head. This scares the drivers who see you recklessly crossing in front of them. They think you're an ET with tiny antennas to communicate with a lethal spacecraft over head, and they, unlike you, still have fear reactions, which is why they don't just run you over.

    Remember, I'd say, not to take any of these stories too seriously as specific adaptations or even as being more universal than they may be, no matter how interesting and potentially important they could turn out to be. Speculation should lead to systematic gathering of evidence, then increased acceptance--especially, I think, when current function comes to be equated with suggestions of adaptive reasons.

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    1. The great lesson that I took from Anne's post is not about adaptation but about human variation and what contributes to it.

      (Also, Ken, you have written half of an awesome children's book right there. I'm serious. Brain parasites sprouting out of kids' heads!)

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  5. aarrgghh re differences that are "generally subtle, only detectable on a statistical basis" and within the normal range of variation. And then so many only-weakly associated genes ... maybe we just don't understand enough of genomic variation, mechanisms. It is so hard to sort out what is well-supported in these kinds of things.

    Thanks for the well-written and interesting discussion of such a complicated topic!

    Based on my own anecdotal (bogus I know) evidence re schizophrenia -- first-born sons with domineering parents, usually the father. I know so many cases (and no cats).

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    1. Well, we do know that even strong selection can achieve results in a selected direction, even when many individually minor genetic effects are involved (that's how agricultural breeding works).

      Here, among others, the questions would be whether the effect actually makes a net difference in reproduction (in regard to the human, not the parasite or if in the latter also in the parasite), and how long and how systematic or intense this kind of thing has actually been.

      I'd be on the circumspect side about any evolutionary inferences, even if the causal effect is real and replicable. But given that things are within the normal range, after-the-fact identification is a minefield for error and prejudgment.

      These subtle biases are hard to show but studies looking for them can usually find them. I was just listening to a BBC Radio program about the serious crisis in the supposedly objective fingerprint-identification process that showed how even that can be deeply subjective and self-fulfilling (find matches if one wants to find them).

      Just because someone is a bit more susceptible to infection or, if infected, to certain manifestations, doesn't imply selection....though it could be of current practical value,or at least just interest.

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    2. Thanks, Hollis! And yes, to complicate it even further, there are sure to be many pathways to the same phenotype, as well as variation in the disease. This is true of every complex disease, of course, and is another reason it's so hard to sort out causation.

      By chance I was listening to a BBC radio interview yesterday with a British psychiatrist whose expertise is schizophrenia. He didn't mention infectious causation, but he did say that incidence of the disease in immigrants to Britain was 6 times higher than in their home countries, and that incidence increases with the size of the city. The bigger the city, the higher the rates of schizophrenia. How would you figure out what this means? Do bigger cities have more rats, and thus more infected cats? Or is there something about the stress of city life? What is it about immigration?

      Genetic determinists still wouldn't give up, given these statistics -- they'd say that some genetic predisposition to emigrate must also be related to risk. Geneticists sold on schizophrenia as a genetic disorder often say that prevalence is stable across societies and over time, so it must be genetic, not environmental. But this seems not to be true.

      This psychiatrist also said that cannabis is clearly a trigger for teens, but that it must interact with genetic predisposition.

      I think the upshot is, who knows? I haven't heard domineering fathers blamed, only 'refrigerator mothers', but that's an idea no longer in favor. Thankfully, for the mothers.

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  6. "But, genetics and genome mapping is what I do!" say the geneticists.

    In their defense, it is reasonable for them to be interested in the susceptibility variation aspect of the story. Genetics is what they do as they proclaim. They may not be able to do, say, microbiology.

    The problem comes in with the system we have, by which large funding goes to that argument even if there is evidence that the genetic variation, which surely will be there, is trivial compared to other sources of variation. Because the geneticists naturally look after their own, so to speak.

    So, I think one should say that the issue isn't whether genetic variation is involved but whether it's worth studying (i.e., investing limited research funds in). The geneticists could simply be told to use their high level of expertise to address more clearly important, more tractable genetic, problems.

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    1. Even if it turns out that some people are genetically more susceptible to disease via parasite infection, mediated by gene homologies, risk will still depend on environmental exposures, and so won't be predictable, no matter the genotype. The most straightforward prevention would be vaccination against parasites. Yes, alas, leaving geneticists out of the equation.

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  7. great discussions you guys, much appreciated.

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  8. ok, this brings to mind ancient Egypt where that society dietized cats so they were everywhere. Is that one of the causes of the downfall of that great civilization?

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    1. If the symptoms of T. gondii infection here and now are mostly 'normal' traits like sloppy dressing, or designer dressing, car accidents, slow reaction time, cat obsessions, and only occasionally schizophrenia, I have no idea what the corollaries would have been in Egypt. Cat obsession was the norm, I have no idea about fastidiousness or sloppiness, or what the equivalent of car accidents would have been. Some schizophrenia, perhaps. But I'm thinking that there's nothing here that would bring down a civilization.

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  9. Jumping in here, seems some here think that just because you have a cat or may have been infected with T.gondi you will have these psychological issues. C.J. Carter's article indicates that a number of genetic criteria has to be met before manifestation of Schizophrenia occurs. In addition, it's not just T.gondi. "Schizophrenia has also been associated with prenatal complications including maternal rubella (German measles) [11], influenza [12, 13], Varicella zoster (chicken pox) [14], Herpes (HSV-2) [15], common cold infection with fever [16], or poliovirus infection [17] while in childhood or adulthood, coxsackie virus infection (in neonates [18]) or Lyme disease (vectored by the Ixodes tick and Borrelia Burgdorferri) or Toxoplasmosis have been reported as risk factors [19, 20] (see Table 1). The human endogenous retrovirus, HERV-W, has also been implicated in schizophrenia [21]. A number of schizophrenia-related genes are implicated in the life cycles of these pathogens, suggesting an interplay between genes and risk factors [22]."

    "...genes, risk factors, and immunity can be linked together forming a unifying pathway whose elements are interdependent. Dysfunction of this network which is conditional upon interactions between its three branches may be responsible for schizophrenia."

    Then on the other end of the microbe spectrum, we have the symbiotic organisms/immune system interaction which is disrupted through antibiotic use, poor nutrition, vaccinations(?), and now GMOs, pollutants/pesticides, etc, etc. The excluded parameters which may affect the "three branches" of this scenario are overwhelming to consider, especially when you realize that people are genetic individuals, reacting uniquely to each of the listed parameters, creating exceptions to every theory.

    Just as an example, my son got sent home from second grade with a good case of head lice. We checked everyone in the house, he was the only one infested! A few years later, he would get Lyme disease (age 10), he's now 17, and exhibiting some disconcerting psych symptoms and it wasn't until I read Flegr's article that I started wondering about the latent psych- effects of Lyme disease, which Carter has somewhat confirmed. But now what? Feeling lost and overwhelmed by the implications of this information.
    Can you imagine what insurance companies would do with this information? Now would be a great time for socialized health care.

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  10. True, this is a complex issue. My heart goes out to you as you try to make sense of your son's symptoms. And I hear you re. socialized health care!

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  11. Synchronicity. I was just talking to a healthcare provider who advised me to be careful with my cat's litter- to wear gloves when changing it or at least wash my hands well after. I now will wear gloves and, while at my local pharmacy, found myself gazing at a box of $15- disposal masks considering their purchase to further protect myself. How funny that the very next day I would find this on my Facebook feed!

    I actually wanted to comment on your query of "why are crazy cat people always female?" Not so! I know the stereotype is of the crazy cat lady but I've experienced only crazy cat MEN in reality. One neighbor, in West Philadelphia, we even had to call animal control on- a sweet, mild-mannered older man who was a slob as well as a cat hoarder. Which brings me to the paper's observation of male "sloppy dressers" claim for those with T.gondi; I, myself, wear designer clothes and am very image conscious however housework and I are not good friends. I wouldn't call myself a slob but...things tend to pile up at times. I also cross mid-block when cars are coming but I grew up in N.Y.C. Even still, I DO have a weakened immune system so would I be a candidate for testing and how does one get a toxoplasmosis test??

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    1. I think there is still a lot that's not known about toxoplasmosis, including how real the sex differences among infected people might be.

      As for getting tested, if you read the Atlantic article that was the motivation for this post, you will notice that the author pretty much figured she was infected, given her traits, and was a little disappointed not to have it. So, give some thought to whether you really want to know! Maybe it's more romantic to think you've got it! Especially since nothing can be done about it anyway. If you do want to proceed, though, I'd imagine your health care provider would know how you'd go about getting tested.

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    2. We're not physicians so can't help you on that (getting a test). As to the stereotype, the 'craziest' cat person we know is .... a couple. They have something like 80 cats in their ordinary sized house. Not a pretty sight and not good for the cats.

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