Listen: I’m a dog person. I don’t have much justification for this belief, except to say that I’ve thought for some time that many cats have a frankly nefarious vibe. Didn’t have much justification for this belief, until a few weeks ago, that is. My degree has given me many things, most of them not that great, and now it’s given me a valid reason not to like cats. Enter, Toxoplasma gondii.
T. gondii is an intracellular parasite that infects all warm-blooded animals. Its host of choice in terms of reproduction (known as its ‘definitive host’), however, is the members of the Felidae family; tigers, lions, leopards, panthers and yes, domestic cats. Cats become infected by eating an infected rodent or bird. The virus then reproduces inside the cat’s small intestine, ends up in its litter box, and promptly infects whichever human is unfortunate enough to be tasked with changing it. Many infections come from cat-to-human transmission, and humans can also become infected by eating undercooked contaminated meat or shellfish.
Amongst humans, T. gondii is one of the most common parasites; up to 50% of people globally have been estimated to be infected. Fortunately, infection with T. gondii is basically harmless. It causes a parasitic disease, toxoplasmosis, but it’s largely asymptomatic in adults – only when transmitted congenitally is it thought to have serious effects.
Or so we thought.
A 2007 study in the Schizophrenia Bulletin (can you see where this is going?), however, indicated otherwise. The researchers compared infected adults (those with antibodies to T. gondii and hence assumed to have a latent infection) with uninfected adults and found a whole legion of significant psychological differences between the two groups. The infected adults were more expedient, more suspicious, more jealous, more dogmatic – or the men were, at least, but that’s a conversation for another day. They scored more poorly in tests that measure psychomotor activity; when the researchers accordingly analysed seroprevalence data surrounding motor vehicle accidents, they determined that infected individuals had over twice the risk of causing a traffic accident. T. gondii infection has been consistently linked to schizophrenia.
As with everything else in biology, the actions of Toxoplasma gondii can be understood as having been optimised to result in the creation of more Toxoplasma gondii. In order to make more T. gondii, it wants to get back into its definitive host. Although our chances of being eaten by a cat are fairly remote now, this wasn’t necessarily the case for our primate ancestors; monkeys and apes are fairly often eaten by large felines. If, as a parasite, you wanted to lead to the demise of your dead-end host and get back into a more useful one, it wouldn’t be a bad idea to affect their brain chemistry in a way that alters their psychomotor activity. If your brain chemical of choice was dopamine and if that also leads to schizophrenia, well, that’s not your problem, is it?
There’s something deeply unsettling about the idea that our brain chemistry could be manipulated by a parasite. Perhaps it shouldn’t be; we participate enthusiastically in the nature vs. nurture debate, after all, and this isn’t so different. Attributing our actions to a parasite isn’t any more fatalistic than attributing them to our genes or our parents. And yet, the idea of an external agent having the ability to change the way we behave, the way we think and feel and perceive the world – that’s straight out of about five different horror movies.
We likely needn’t worry, anyhow. Later studies have shown that the association between T. gondii and schizophrenia may not be as strong as initially thought. Researchers have indicated that it might double your risk. That sounds alarming, but it’s doubling from a very small risk to what is effectively still a very small risk, and is similar to other schizophrenia risk factors that we don’t worry about, such as living in a city. It’s non-negligible, though, and that’s enough justification for me. Nefarious vibe indeed.