La toxoplasmose acquise est une infection parasitaire qui touche l’ensemble des cellules cérébrales lors de la phase aiguë. Il paraît donc surprenant que cette infection soit sans conséquence sur le fonctionnement du cerveau de l’individu infecté. Nous nous proposons ici de faire une revue de la littérature des modifications neurologiques induites par le parasite chez l’animal, ainsi que de l’ensemble des modifications psychiatriques chez l’homme significativement associées à une infection à Toxoplasma gondii. D’après les données de la littérature, les plus probantes concernent l’association entre la toxoplasmose et le déclenchement d’une schizophrénie : les sujets souffrant d’un premier épisode psychotique lors du déclenchement d’une schizophrénie ont 2,7 fois plus de chances d’avoir une sérologie positive que les sujets sains. Certains traitements antipsychotiques font, de plus, diminuer les taux d’immunoglobulines G antitoxoplasmiques in vivo, et ont démontré une action antiparasitaire in vitro. Mais les conséquences de l’infection toxoplasmique acquise ne semblent pas s’arrêter à la schizophrénie, puisque d’autres résultats significatifs ont été récemment rapportés dans des populations de patients atteints de troubles obsessionnels compulsifs. Des modifications de traits de personnalité ont également été rapportées. Les études sur les conséquences psychiatriques de l’infection acquise à T. gondii doivent être poursuivies, pour mieux comprendre les mécanismes des modifications cérébrales induites par le parasite, explorer l’ensemble des pathologies psychiatriques, dont le premier épisode pourrait statistiquement être associé à une sérologie toxoplasmique positive, et pour savoir si cette sérologie positive doit orienter le clinicien vers la prescription d’un traitement psychotrope à activité antiparasitaire, comme l’halopéridol et l’acide valproïque.

Toxoplasma gondii is the most common protozoan parasite in developed nations. Up to 43% of the French population may be infected, depending on eating habits and exposure to cats, and almost one third of the world human’s population may be infected. Two types of infection have been described: a congenital form and an acquired form. Although the medical profession treats these latent cases as asymptomatic and clinically unimportant, results of animal studies and recent studies of personality profiles, behavior, and psychomotor performance have led to reconsider this assumption.

Among rats: parasite cysts are more abundant in amygdalar structures than those found in other regions of the brain. Infection does not influence locomotion, anxiety, hippocampal-dependent learning, fear conditioning (or its extinction) and neophobia in rats. Rats’ natural predator is the cat, which is also T. gondii’s reservoir. Naturally, rats have an aversion to cat urine, but the parasite suppresses this aversion in rats, thus influencing the infection cycle. Tachyzoites may invade different types of nervous cells, such as neurons, astrocytes and microglial cells in the brain, and Purkinje cells in cerebellum. Intracellular tachyzoites manipulate several signs for transduction mechanisms involved in apoptosis, antimicrobial effectors functions, and immune cell maturation. Dopamine levels are 14% higher in mice with chronic infections. These neurochemical changes may be factors contributing to mental and motor abnormalities that accompany or follow toxoplasmosis in rodents and possibly in humans. Moreover, the antipsychotic haloperidol and the mood stabilizer valproic acid most effectively inhibit Toxoplasma growth in vitro with synergistic activity.

The effects of the parasite are not due to the manipulation in an evolutionary sense but merely due to neuropathological or neuroimmunological effects of the parasite’s presence. Toxoplasmosis and schizophrenia: epidemiological studies point to a role for toxoplasmosis in schizophrenia’s etiology, probably during pregnancy and early life, this association being congruent with studies in animal models indicating that animal exposures of the developing brain to infectious agents or immune modulating agents can be associated with behavioral changes that do not appear until the animal reaches full maturity. Psychiatric patients have increased rates of toxoplasmic antibodies, the differences between cases and controls being greatest in individuals who are assayed near the time of the onset of their symptoms. The increase of dopamine in the brain of infected subjects can represent the missing link between toxoplasmosis and schizophrenia. Toxoplasmosis and Obsessive Compulsive Disorder (OCD): the seropositivity rate for anti-T. gondii IgG antibodies among OCD patients is found to be significantly higher than the rate in healthy volunteers. Infection of basal ganglia may be implicated in the pathogenesis of OCD among Toxoplasma seropositive subjects. Toxoplasmosis and personality: infected men appear to be more dogmatic, less confident, more jealous, more cautious, less impulsive and more orderly than others. Conversely, infected women seem warmest, more conscientious, more insecure, more sanctimonious and more persistent than others. It is possible that differences in the level of testosterone may be responsible for the observed behavioral differences between Toxoplasma-infected and Toxoplasma-free subjects.

In the future two major avenues for research seem essential. On one hand, prospective studies and research efforts must still be carried out to understand the mechanisms by which the parasite induces these psychiatric disorders. On the other hand, it has not yet been demonstrated that patients with positive toxoplasmic serology may better respond to haloperidol’s or valproic acid’s antiparasitic activity. These results may appear as a major issue in the drug’s prescribing choices and explain variability in response to the treatment of patients with schizophrenia that is not explained by the genetic polymorphism.