18 December 2011

What the Cat Dragged In

This time, it’s Toxoplasma gondii, one of the strangest parasites I have ever heard of, and one that is estimated to infect up to a staggering 1/3 of the world’s human population. (Infection is much higher in developing countries; recent testing in the US determined that infection rates are around 10% of the population).3

Tox. gondii begins its life cycle in warm-blooded mammal intermediate hosts, preferably rodents that will be eaten by cats, thus allowing the parasite to complete its life cycle and sexually reproduce. While most rats avoid cats and cat odors, rats infected with toxoplasmosis suddenly display unique behavioral changes. These rats develop what has been called a “fatal attraction” to cats, increasing their chances of being eaten and thereby increasing the parasite’s chances of sexual reproduction. The rats become more active, less fearful, slower to react, slower to learn, less averse to cat odors, and less averse to cat-populated areas. It is interesting that this effect is so selective; in other matters such as competition for mates and social status, the rats behave normally.1 6

Humans can become infected with Tox. gondii if they are exposed to oocytes found in animal meat and cat feces. Transmission can also occur through the placenta, but only in immunosuppressed mothers who are initially infected while pregnant. Once oocytes are injested by the intermediate host (rat/human/other mammal), the parasite undergoes asexual reproduction, with rapidly dividing tachyzoites and more slowly dividing bradyzoites. These go on to form cysts in the host’s brain, heart, and other tissues. An innate and adaptive response in the host is activated, and antibody is made. Acute toxoplasmosis is a relatively mild and short-lived disease in most immunocompetent people, and it transitions quickly into the latent phase: the cysts remain, potentially for the rest of the host’s life.5

The most interesting thing about these cysts is that they may actually cause a change in a human host’s personality. Multiple studies have concluded that infected humans have slower reaction times, have been in more traffic accidents, and are less novelty-seeking. Infected woman may be more warm and prone to guilty feelings, and infected men may be more suspicious and have higher testosterone levels.2 (However, it should be noted that many of these human studies are correlational. In fact, one reported study has shown that infection with CMV is also correlated with less novelty-seeking.4 So, there is some evidence that the mechanism may be general brain infection and not a specific parasitic action.) Tox. gondii is associated with incidences of schizophrenia and mood disorders, and may affect the host’s levels of dopamine. One recent study actually found that infected men were less averse to the smell of cat urine, while infected women were more averse (aversions to other animals’ urine were normal).2

Tox. gondii is only one example out of many parasites that have learned to control their host’s behavior in order to increase their reproductive potential. It is fascinating to me that this is even possible, and especially that infection with Tox. gondii is so rampant throughout the world.

Take-home message? Keep your cat away from raw meat!



1 Berdoy, M., Webster, J.P., & Macdonald, D.W. (2000). Fatal attraction in rats infected with Toxoplasma gondii. Proceedings. Biological Sciences/The Royal Society, 267(1452), 1591-4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1690701/pdf/11007336.pdf

2 Flegr, J., et al. (2011). Fatal attraction phenomenon in humans - cat odour attractiveness increased for toxoplasma-infected men while decreased for infected women. PLoS Neglected Tropical Diseases, 5(11), e1389. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210761/?tool=pubmed

3 Jones, J. L., et al. (2007). Toxoplasma gondii infection in the United States, 1999–2004, decline from the prior decade. American Journal of Tropical Medicine and Hygiene, 77(3), 405-10. http://www.ajtmh.org/content/77/3/405.long

4 Novotná , et al. (2005). Probable neuroimmunological link between Toxoplasma and cytomegalovirus infections and personality changes in the human host. BMC Infectious Diseases, 5, 54. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187888/?tool=pubmed

5 Tenter, A.M., Heckeroth, A.R., & Weiss, L.M. (2000). Toxoplasma gondii: from animals to humans. International Journal for Parisitology, 30(12-13), 1217-1258. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109627/?tool=pubmed

6 Webster, J.P. (2007). The effect of Toxoplasma gondii on animal behavior: playing cat and mouse. Schizophrenica Bulletin, 33(3), 752-756. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526137/?tool=pubmed

4 comments:

  1. Very interesting- A couple first questions wile reading your post. Was it mentioned in your research about how the parasites get into the brain? Are they small enough to penetrate the blood-brain barrier or can they physically poke a hole through? Also, when cysts form on the brain, do they selectively target a specific area- thus an explanation for possible behavioral changes in the host?

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  2. Hi Hanan, whoa really interesting post. I never knew about this.

    What is the incidence of Toxoplasma gondii in the US? It doesn't seem like we hear much about these diseases as a noxious effect of ingesting raw meat. I like my steaks medium rare, could I get the disease?

    What kind of immunological mechanisms could be at play so that the Toxoplasma gondii can persist within a host to cause psychological and or neurological changes? Morgado et al. 2011, showed that Toxoplasma gondii upregulated B7-2 expression on the surface of mouse bone-marrow derived macrophages and human peripheral blood monocytes. Their studies imply a parallel in mechanism of B7-2 regulation by T. gondii and mammals.

    Morgado P, Ong YC, Boothroyd JC, Lodoen MB. Toxoplasma gondii induces B7-2 expression through activation of JNK signal transduction. Infect Immun. 2011, 79(11):4401-12.

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  3. Very interesting questions, Randy! For now, here is an article that explains how T. gondii might get through the blood-brain barrier:

    http://www.ncbi.nlm.nih.gov/pubmed/21106256

    It seems that the disease may modulate gene expression to increase chemokines and adhesion molecules in brain endothelial cells, increasing its chances of being actively transported across the BBB like a “Trojan horse.” Infected antigen-presenting cells may carry tachyzoites across the barrier.

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  4. @Julie: The incidence in the US is estimated at around 10% of the population, which I feel is pretty high. However, this is nothing to the incidence in the rest of the world, which varies from 9-100% depending on environmental factors (around a third of the world's pop has been exposed). The oocytes may be transported through unpasteurized milk and infectious tissue cysts are found in infected meat. Wild animals (60% of birds, rats and mice) are more likely to be infected.In Europe and in the USA, pork is considered to be a major source of T. gondii infection in humans. The incidence of cysts in meat is dependent on the living conditions and exposure rates of the animal, and rates have been falling in the US.

    Tissue cysts are resistant to freezing, but can be killed by tempertures of 67 degrees C and higher. So, it is important to properly cook your meat!

    Extreme amounts of detail about the spread of Tox. gondii from animals to humans (routes, prevention, rates, mechanisms) can be found here:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109627/?tool=pubmed

    Enjoy your steak! :) The good news is that rates in beef are lower than in pork!

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