Are tiny parasites messing with our brains?

Think before you swallow

Reverie, 1872, Edward Radford (Wikicommons)

Toxoplasma gondii is a tiny protozoan. It’s also a parasite. Like a surprising number of parasites, it can infiltrate brain tissue and make its host behave in ways that help it spread to new hosts.

For example, an infected rat is attracted to the smell of cat urine and ends up getting eaten by a cat, the only host in which T. gondii can sexually reproduce. Once inside a host, the parasite targets the amygdala—an area of the brain that stores emotional memories. Autopsies of infected rodents show twice the density of T. gondii cysts in the amygdala as in other brain regions (Vyas et al., 2007). Primates can also get infected, and the behavioral changes are similar. Infected chimpanzees like the smell of leopard urine (Poirotte, 2016).

Humans too can get infected—between 13 and 43% of adults 25 to 50 years of age in Europe, with lower rates in North America and higher ones in Brazil and Africa (Friesema et al., 2025). Some strains seem to have adapted specifically to human hosts. Of the three main lineages, Type II strains are the most common ones in our species (Hosseini et al., 2019; Xiao & Yolken, 2015).

Infection causes humans, like other animals, to change mentally and behaviorally. Men become more jealous, women more easy-going, and both sexes slower to respond to threats, as shown by a higher risk of traffic accidents and longer reaction time. The last finding proves the direction of causality: the longer you have been infected, the slower you react. Slower reaction time does not increase your risk of infection (Flegr et al., 2005; Havlíček et al., 2001; Latifi et al., 2025).

At the extremes of sexual behavior, infected individuals, particularly men, feel more drawn to masochism, rape fantasies, bondage, same-sex experiences, and anal sex. Women with latent toxoplasmosis also report feeling more drawn to violent sexual practices and same-sex experiences. But such fantasies are, if anything, less often acted out by infected individuals. Real changes to sexual behavior seem confined to a greater propensity for sexual promiscuity, oral sex and, among male homosexuals, anal sex (Flegr, 2017; Flegr & Kuba, 2016; Latifi et al., 2025).

T. gondii manipulates not only behavior but also physical appearance. Infected men are taller, and women rate them as being more dominant and masculine. Infected men also have lower second-to-fourth digit ratios, a sign of greater exposure to the male hormones (Flegr et al., 2005; Hodková et al., 2007; Latifi et al., 2025). This physical manipulation is in line with a strategy of making infected males more attractive to prospective hosts (Mackey & Immerman, 2003).

Can this behavioral and physical manipulation be demonstrated under controlled conditions? Such research would be difficult because we cannot experiment with humans as we do with lab animals. Humans also live long. Decades may pass between the initial infection and the ultimate pay-off for the parasite (Cochran et al., 2000; Frost, 2020).

Nonetheless, a group of Czech researchers is convinced that some strains of T. gondii have evolved the ability to manipulate human behavior, specifically sex. Infected men not only seek more sexual partners but also engage in sexual practices that transmit the parasite more efficiently, i.e., into the partner’s oral cavity or anal canal. The existing host gets no reproductive benefit; in fact, his fertility is reduced through lower sperm counts and lower sperm motility (Hlaváčová et al., 2021; Kaňková et al., 2020).

T. gondii cyst in a mouse brain (Wikicommons, J.P. Dubey)

We know that T. gondii is present in male ejaculate as cysts containing thousands of spores. We also know that the cysts are spread from one body to another through fellatio, anal sex, or vaginal sex. The transmission is male to female or male to male, but not female to male.

Sexual transmission, particularly from a male host, is indicated by several lines of evidence:

• In heterosexual couples, an infected male partner increases the female partner’s risk of infection, but an infected female partner does not increase the male partner’s risk of infection.

• In women, the risk of infection correlates with sex work, unprotected sex before pregnancy, and history of genital injuries. In men it correlates with sexual promiscuity, and in male homosexuals with unprotected anal sex.

• Seroprevalence of T. gondii is higher in fellating individuals of either sex than in non-fellating controls.

• Seroprevalence is higher in homosexuals and promiscuous individuals.

• Seroprevalence is positively correlated with the prevalence of STDs across countries, including HIV.

• Seroprevalence is higher in women than in men. The gender difference emerges in the 10-to-14 age group and peaks among 20-to-39-year-olds (Flegr et al., 2005; Latifi et al., 2025).

T. gondii seems to have become sexually transmissible through three stages of coevolution with our species:

• Entry into a human population, apparently via contact with cats. This animal began to coexist with humans some 10,000 years ago in the Middle East (Galal et al., 2022).

• Passive sexual transmission. The parasite was spread initially to new hosts via sex and other forms of intimate contact without any behavioral modification. Meanwhile, natural selection favored those strains that could adapt to a life cycle within human bodies.

• Active sexual transmission. Natural selection increasingly favored those strains that could increase sexual transmission by modifying the host’s sexual behavior.

We are only now realizing that T. gondii is sexually transmitted. At present, medical research is biased toward obvious STDs whose symptoms occur soon after infection, are easily observable, and develop over a short time. But these characteristics are not optimal for a long-lived host, like our own. In such species, harming the host reduces the prospects for infection of new hosts over a potentially long lifetime. The prospects are better if the parasite remains discreet and does as little harm as possible, at least as long as its host remains sufficiently young and useful.

Indeed, many diseases of old age may be due not to old age itself but to long-present parasites that no longer have anything to lose. From the latter’s standpoint, the host has served its purpose and can be harmed without incurring any penalty.

Are other parasites messing with our sex lives?

T. gondii may be one of many microorganisms that have evolved to manipulate human behavior. We are too good to pass up. Our complex neural circuitry, our social nature, and our dense populations make us ideal vectors. Even if a parasite initially has no ability to manipulate human behavior, such an ability could evolve soon enough. All of the right conditions are in place.

The following are several disorders that may be caused by behavior-manipulating parasites. Again, the disorder itself could represent the final destructive stage of a long-term infection.

HIV-Associated Neurocognitive Disorders (HAND)

Although HIV-associated neurocognitive disorders (HAND) are widely attributed to HIV, the relationship between the two remains circumstantial. In fact, HAND occurs even in individuals who have lost all detectable traces of HIV through antiretroviral therapy. One study found that 21% of such individuals nonetheless go on to develop dementia (McArthur & Brew, 2010).

The causal agent seems to exist as an AIDS cofactor—not by making an HIV infection worse but by increasing the host’s appetite for behaviors that increase the risk of HIV infection. This cofactor may be hiding in plain sight among the opportunistic infections currently blamed on the host’s compromised immune system. While such infections primarily target the lungs, the brain is the second most-common target (Masliah et al., 2000; Jellinger et al., 2000).

The existence of a brain-manipulating cofactor is consistent with the profile of AIDS victims in a study from Bologna, Italy. In that country, AIDS is transmitted mainly via intravenous drug use, yet transmission via homosexuality/bisexuality is ten times more often associated with cognitive impairment (De Ronchi et al., 2002; Wikipedia, 2025). Certainly, AIDS does impair cognition, as shown by an association between low white cell counts and HAND in the Bologna study. But some cofactor must also be impairing cognition via the homosexuality/bisexuality route.

The cofactor might be the hepatitis C virus (HCV). In a large cohort of people with HIV, the risk of HAND was higher among those with antibodies to HCV (Mastrorosa et al., 2023).

Sexually transmissible strains of Candida albicans (vaginal yeast)

Candida has been implicated in several neurodegenerative diseases, notably Alzheimer's, multiple sclerosis, and autism spectrum disorders. It has thus evolved the ability to cross the blood-brain barrier and adhere to tissues in the central nervous system, particularly white matter. Because of antibody cross-reactivity, the actual Candida species is difficult to identify, though C. albicans is the main suspect (Denaro et al., 1995; Jong et al., 2001).

Keep in mind that C. albicans encompasses many strains that differ substantially from each other in various ways: single nucleotide polymorphisms, inversions, copy number changes, loss of heterozygosity, and whole or partial chromosomal aneuploidies. At least one of these changes is responsible for altering the balance between commensalism and pathogenesis (Hirakawa et al., 2015; see also Tian et al., 2021).

C. albicans can colonize many body sites, but some strains have adapted specifically to the vagina. A few are responsible for vulvovaginal candidiasis (VVC, commonly known as vaginal yeast infection), which affects 70 to 75% of sexually active women at least once and 5 to 8% recurrently (Li et al., 2008). In China, two strains account for almost 60% of all VVC cases, with neither being present at extragenital sites (Li et al. 2008).

Sexual transmission is indicated by several lines of evidence:

• Once a vaginal infection develops, it can spread to the male partner’s glans penis via vaginal sex or to his oral cavity via cunnilingus (Li et al., 2008; Schmid et al., 1995).

• The same strains seem to infect both the vagina and the glans penis (Ge et al., 2012; see also Tian et al., 2021).

• In both men and women, genital yeast infections are associated with a higher number of sexual partners (Warszawski et al., 1996).

• There seems to have been selection for sexual transmissibility, particularly via oral sex. Vaginal strains adhere better than other strains to saliva-coated surfaces (Schmid et al. 1995).

Transmission is woman to man and not man to woman. Infected people do not have higher rates of vaginal sex, but they do have higher rates of oral sex, notably cunnilingus (Hellberg et al., 1995; Reed et al., 2003). C. albicans in the male partner’s oral cavity does not predict recurrence of VVC in the female partner (Reed et al., 2003), and treatment of the male partner with antifungals does not prevent recurrence of VVC in the female partner (Bisschop et al., 1986; Buch et al. 1982). It looks as if a parasite is acting on the female partner, specifically on her sexual behavior, by weakening her inhibitions and by motivating her to engage in vaginal contact with the male’s partner's body, particularly his mouth.

Infection seems to proceed in three stages: 1) colonization of the vagina as a commensal with low virulence and no VVC, potentially for a long period of relative latency; 2) colonization of brain sites that influence sexual behavior; and 3) activation of the most virulent stage (i.e., VVC), when the pathogen can now spread to a male partner.

Multiple sclerosis

This disease can cause lesions throughout the nervous system, but a recurring symptom is impairment of social cognition through damage to the limbic system, particularly the amygdala (Batista et al., 2016; Hillyer et al., 2023; Meyer-Arndt et al., 2022). As we have seen with T. gondii, this brain region is a primary target for manipulation of behavior.

Multiple sclerosis (MS) seems to be associated with a fungal parasite that infiltrates the brain and nervous system, perhaps a form of Candida. In people with MS, this association is indicated by:

• Antibodies against various Candida species

• High levels of immune defense proteins that bind to mannoproteins, which are ubiquitous in fungal cell walls but rare in bacterial and mammalian cell walls

• High levels of chitotriosidase, which the immune system produces to destroy chitin—a component of fungal cell walls but not of bacterial and mammalian cell walls.

• Successful treatment of MS with a fungicide, dimethyl fumarate (Benito-Leon & Laurence, 2017).

MS seems to be sexually transmitted. It is rare before puberty, two to three times more common in women, more common in women taking oral contraceptives, and associated with smoking—a sociological marker of sexual activity among women. It is also associated with herpes simplex virus type 2 (Benito-Leon & Laurence, 2017; Golden & Voskuhl, 2017; Hawkes, 2002).

Unlike the unknown parasite that may cause HAND, this one begins doing harm early in adulthood, at around 30 years of age, perhaps because this is when female hosts tend to abandon their multi-partner lifestyle. Consequently, the parasite no longer has anything to gain from keeping its host healthy. The mean age of onset for MS has nonetheless risen in recent decades (Golden & Voskuhl, 2017; Romero-Pinel et al., 2022).

A role in alternative sexualities?

We will now go beyond medical disorders and consider alternative sexual lifestyles. Could they also be due, in some cases, to behavioral manipulation by unknown parasites?

The words “in some cases” should be highlighted, since such parasites would first evolve sexual transmissibility before acquiring the capacity to manipulate behavior. They would thus tend to manipulate an existing sexual behavior, usually by increasing the number of sexual partners. Nonetheless, as we shall see, the creation of novel sexual behaviors is not excluded.

Exclusive male homosexuality

More than two decades ago, Greg Cochran argued for the existence of a “gay germ,” i.e., a pathogen that reorients male sexual preferences to increase the number of hosts it can infect via sexual relations (Cochran et al., 2000). He ruled out a genetic cause because of the high fitness cost of exclusive male homosexuality and its heritability of only 20%. Instead, the cause may be a pathogen that targets the limbic system. “Indeed, anecdotal reports indicate that changes in human sexual orientation have occurred following changes in the limbic area due to trauma or infection.” The pathogen may be exploiting a niche that provides more opportunities for sexual transmission. “[H]omosexual behavior could facilitate spread because of the larger numbers of partners homosexual males may have on average, relative to heterosexual males” (Cochran et al., 2000).

This theory has received new support with the recent discovery that the gut microbiome is different in men who have sex with men; specifically, there are fewer of the commensal bacteria that help repair and preserve the intestinal lining. Perhaps an invasive pathogen destroys them in order to facilitate its entry into the body. Although this change to the gut microbiome seems to pave the way for HIV infection, having been in fact discovered through AIDS research, HIV itself does not seem to be responsible (Armstrong et al., 2018; Lin et al., 2024; Tuddenham et al., 2020).

Cuckold fetish

Other pathogens may be responsible for certain paraphilias, such as the cuckold fetish—where a male host abandons mate guarding and even feels pleasure at the prospect of being cuckolded. This fetish is absent from Greco-Roman literature, which nonetheless attests to a wide range of alternative sexualities. The earliest references come from 17th century England, particularly among English merchants.

The date and milieu point to an external source—most likely, slaves imported through trade from West Africa. Because of that region’s high polygyny rate, conditions were ideal for the evolution of STDs that can spread from one polygynous household to another by inhibiting, or even inversing, male sexual jealousy. Keep in mind that the barriers to transmission were already low. On the one hand, the head of household was generally an older man who could not satisfy all his wives; on the other, the latter were often solicited by young single men, as inevitably happens in a polygynous society (Frost, 2023).

This point is made by anthropologist Pierre van den Berghe:

The temporary celibacy of young men in polygynous societies is rarely absolute, however. While it often postpones the establishment of a stable pair-bond and the procreation of children, it often does not preclude dalliance with unmarried girls, adultery with younger wives of older men, or the rape or seduction of women conquered in warfare. Thus, what sometimes looks like temporary celibacy is, in fact, temporary promiscuity. (van den Berghe, 1979, pp. 50-51)

Polygynous households were thus vulnerable to any STD that could overcome the already low barriers to entry. Once this behavioral niche was colonized, selection favored those strains that could lower the barriers even more.

Conclusion

In theory, all sexually transmitted parasites should be under selection to manipulate host behavior. Their very existence depends on how the host behaves, and even a slight behavioral change could significantly improve their ability to infect other individuals. Sexual transmission is an ideal target for manipulation because it provides the parasite with potentially numerous opportunities for spreading to new hosts.

Such manipulation can take different forms. Some parasites may simply make their male or female host less discriminating, as appears to be the case with T. gondii. Others may reorient their host’s sexual orientation. Still others may cause sexual fetishes and other paraphilias.

It is difficult to determine the full extent of this phenomenon, given our current state of knowledge. One avenue for research would be to study the human brain to see how far it has gone in evolving strategies to counter behavioral manipulation, as two evolutionary biologists have already wondered:

How much of our neural complexity is a necessary defense against manipulative invaders? How much of the enormous redundancy is to provide system level functionality if part of the system is attacked? How much of the complex process of wiring a brain during development is to prevent pathogen re-wiring? (Read & Braithwaite, 2012, p. 195)

These defensive strategies achieve their aim in three ways: 1) restrict access to the brain, primarily through the blood-brain barrier; 2) increase the costs of manipulation, either by increasing the amount of neuroactive substance needed for a behavioral response or by making this substance toxic at the microscopic level; and 3) increase robustness, by creating redundant or modular neural systems as “backups” to maintain the integrity of behavioral responses (Del Giudice, 2019).

Specifically, we can look for decoy surface molecules. Such decoys mimic the surface molecules used by pathogens to enter a cell while not allowing them to enter. An example in humans is CEACAM3, which mimics the normal surface molecule CEACAM1. It is fast-evolving, apparently because it has been coevolving with certain pathogens: the latter evolve to avoid this surface molecule, which in turn evolves to bind the pathogen even more (Del Giudice, 2019). Are such decoys specifically produced by our neural tissues?

Evolutionary psychologist Marco Del Giudice is skeptical about the possibility that behavior-manipulating parasites have adapted to human bodies, notably because we have large complex brains with much redundancy and because we are much larger than microbes and can thus invest much more, metabolically, in counter-measures to fight them.

On the other hand, we have much longer generation times than any behavior-manipulating parasite currently known. The latter thus has a coevolutionary advantage: it can outmaneuver our counter-measures faster than we can evolve new ones. Our large, complex brains also create more opportunities for manipulation. Then again, the very largeness of our brains works in our favor: we can create so much neural redundancy that the parasite has to pull too many switches in too many places to produce a substantial effect.

Finally, we have another advantage: we can fight invasive parasites through cultural rules and prohibitions. Rules against sexual promiscuity and non-vaginal sex may reflect a vague awareness that the sex act can transmit not only semen but also unwanted free riders (Mackey & Immerman, 2001; Mackey & Immerman, 2003).

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