Most behavior altering parasites are pretty specialized – they can only infect a few types of animals, or even just a few species. One, however, is a worldwide menace that can infect nearly any warm blooded animal. Toxoplasma gondii is a microscopic intracellular protozoan – a single celled organism that lives inside the cells of other animals. It’s target hosts are members of the family felidae, including domestic cats, which have the perfect gut biome in which the parasite can reproduce. Toxoplasma start out their life in the soil as oocysts – the zygotic form of a protozoan parasite. Eventually, they come in contact with a suitable host, ideally an animal frequently predated by cats, such as small birds or rodents. This infection has a primary stage in which the oocysts break open and release spores that infect cells in the intestines, and a secondary stage in which the more mature protozoans replicate and spread into neuronal cells, where they form tissue cysts [1]. Infected rats’ behavior is subtly changed to the benefit of the parasite in a few ways: they have reduce aversion to the smell of cats, and they forget fear more quickly than healthy rats do [2]. Toxoplasma also has an interesting feature that sets it apart from other parasites covered in this blog – it is able to affect humans. Most people with a T. gondii infection won’t notice the difference, since it’s mostly asymptomatic in immunocompetent adults. That doesn’t mean this protist doesn’t have any control over us, though. Latent Toxoplasmosis (the chronic form of the infection, once the parasitic cysts have made their way to the host’s brain) is associated with many other variables, ranging from increased warmness to strangers to higher risk of depression, schizophrenia, and OCD [3].
Some of the neurophysiological effects associated with Toxoplasma infection seem to explain this wide range of symptoms and behavioral changes. As with many behavior altering parasites, manipulation of neurotransmitters is the primary suspect for the mechanism T. gondii uses to change its hosts’ brains. The parasite seems to modify the host’s dopamine and serotonin circuits in some way, though the exact pathway isn’t fully understood. These two neurotransmitters are associated with the reward pathway, learning, and memory. Imbalances of dopamine and serotonin are associated with many common mental disorders, including all the ones associated with Toxoplasmosis. One study found that dopamine metabolites – the small molecules that result when dopamine is broken down in the body – were significantly higher in Toxoplasma positive mice. It was also found that important proteins that moderate serotonin levels were reduced in infected mice, meaning that serotonin levels were higher [2]. One theory suggests that the changes in neurotransmitter levels seen in chronic Toxoplasma infections are actually due to the host’s own body – the immune system produces enzymes that break down important amino-acids in the protozoan’s cells, but these enzymes (as well as the byproducts of the cell’s breakdown) build up in the host’s brain cells. This build up of enzymes and chemicals may lead to the neurotransmitter imbalances that cause all the behavioral changes that make Toxoplasma unique [4]. Ultimately, Toxoplasmosis is usually considered subclinical in all its stages and in any animal it infects. It has some scary-sounding correlations, but it’s primarily benign. In fact, most people who have latent Toxoplasmosis don’t ever know that they have it. If you’re still worried, though, you have a pretty big support group: about one third of the global population carries Toxoplasma parasites. Guess the cat’s out of the bag on this one – we could all be controlled by a single celled protist, and we wouldn’t even notice.
[1] Dubey, J. P. (1998). Advances in the life cycle of Toxoplasma gondii. International Journal for Parasitology, 28(7), 1019–1024. https://doi.org/10.1016/S0020-7519(98)00023-X
[2] Ihara, F., Nishimura, M., Muroi, Y., Mahmoud, M. E., Yokoyama, N., Nagamune, K., & Nishikawa, Y. (2016). Toxoplasma gondii Infection in Mice Impairs Long-Term Fear Memory Consolidation through Dysfunction of the Cortex and Amygdala. Infection and Immunity, 84(10), 2861–2870. https://doi.org/10.1128/IAI.00217-16
[3] Dalimi, A., & Abdoli, A. (2012). Latent Toxoplasmosis and Human. Iranian Journal of Parasitology, 7(1), 1–17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488815/
[4] Hinze-Selch, D., Däubener, W., Eggert, L., Erdag, S., Stoltenberg, R., & Wilms, S. (2007). A Controlled Prospective Study of Toxoplasma gondii Infection in Individuals With Schizophrenia: Beyond Seroprevalence. Schizophrenia Bulletin, 33(3), 782–788. https://doi.org/10.1093/schbul/sbm010