Toxoplasma gondii infection and behaviour – location, location, location?

Abstract

SummaryParasite location has been proposed as an important factor in the behavioural changes observed in rodents infected with the protozoan Toxoplasma gondii. During the chronic stages of infection, encysted parasites are found in the brain but it remains unclear whether the parasite has tropism for specific brain regions. Parasite tissue cysts are found in all brain areas with some, but not all, prior studies reporting higher numbers located in the amygdala and frontal cortex. A stochastic process of parasite location does not, however, seem to explain the distinct and often subtle changes observed in rodent behaviour. One factor that could contribute to the specific changes is increased dopamine production by T. gondii. Recently, it was found that cells encysted with parasites in the brains of experimentally infected rodents have high levels of dopamine and that the parasite encodes a tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of this neurotransmitter. A mechanism is proposed that could explain the behaviour changes due to parasite regulation of dopamine. This could have important implications for T. gondii infections in humans.

Infection of male rats with Toxoplasma gondii results in enhanced delay aversion and neural changes in the nucleus accumbens core

“…B 282: 20150042 tyrosine hydroxylase-like genes from T. gondii can result in subregion-specific changes in dopamine concentrations [43]. This is pertinent because T. gondii does not exhibit an exclusive tropism to nucleus accumbens or its sub-regions [44]. Toxoplasma gondii has earlier been reported to cause structural changes in neurons of host brain [45].…”

Toxoplasma gondii and Schizophrenia: A Relationship That Is Not Ruled Out

“…Experiments in cell cultures have demonstrated that dopamine increases the replication of T. gondii tachyzoites [118]. This biochemical mechanism may play a role in the behavioral changes observed, which would result from the involvement of catecholaminergic neurons and consequent dopaminergic hyperactivity [19].…”

“…Therefore, this parasite has genes that allow it to "manipulate" the behavior of the host and facilitate its capture by the cat, its definitive host, thereby favoring parasite survival. The presence of these genes is consequently an evolutionary advantage of T. gondii [19].…”

“…This reactivation is often associated with nervous system symptoms, such as Guillain-Barré syndrome, diffuse encephalopathy, meningoencephalitis, or brain abscesses [17,18]. Human parasitizations, although generally considered asymptomatic, may cause behavioral disorders and the development of a psychiatric disease such as schizophrenia due to damage resulting from the initial infection, from the host immune response to the parasite, or from the persistence of cysts in the CNS [19]. Accordingly, the concept of asymptomatic chronic parasitization is currently under debate [20].…”

Humans as Superorganisms: How Microbes, Viruses, Imprinted Genes, and Other Selfish Entities Shape Our Behavior

“…On top of that, Toxoplasma directly synthesizes an enzyme that can increase the host's dopamine production even further (Gaskell, Smith, Pinney, Westhead, & McConkey, 2009). Indeed, in vitro, dopamine release has been found to be seven times larger in Toxoplasma--infected mouse cells than in uninfected ones; in vivo, the effect is estimated to be larger still (Prandovszky et al, 2011; for discussion of related evidence, see McConkey et al, 2013). Up--regulation of the dopamine system has been associated with both reckless sensation seeking (e.g., Norbury, Manohar, Rogers, & Husain, 2013) and positive schizophrenia symptoms (for a review, see Kantrowitz & Javitt, 2010).…”