Effects of Toxoplasma gondii Infection on the Brain

Abstract

Toxoplasma gondii, an intracellular protozoan parasite, can infect humans in 3 different ways: ingestion of tissue cysts, ingestion of oocysts, or congenital infection with tachyzoites. After proliferation of tachyzoites in various organs during the acute stage, the parasite forms cysts preferentially in the brain and establishes a chronic infection, which is a balance between host immunity and the parasite's evasion of the immune response. A variety of brain cells, including astrocytes and neurons, can be infected. In vitro studies using non-brain cells have demonstrated profound effects of the infection on gene expression of host cells, including molecules that promote the immune response and those involved in signal transduction pathways, suggesting that similar effects could occur in infected brain cells. Interferon-gamma is the essential mediator of the immune response to control T. gondii in the brain and to maintain the latency of chronic infection. Infection also induces the production of a variety of cytokines by microglia, astrocytes, and neurons, which promote or suppress inflammatory responses. The strain (genotype) of T. gondii, genetic factors of the host, and probably the route of infection and the stage (tachyzoite, cyst, or oocyst) of the parasite initiating infection all contribute to the establishment of a balance between the host and the parasite and affect the outcome of the infection.

A rare presentation of toxoplasma encephalitis in systemic lupus erythematous patient: case report and review of literature

“…[1][2][3] Toxoplasma gondii can infect humans in 3 different ways: ingestion of tissue cysts, ingestion of oocysts, or congenital infection with tachyzoites. 4 Within a short period of time the tachyzoite form of the parasite actively crosses the gastrointestinal barrier by penetrating enterocytic cells in the small intestine and entering submucosal tissue. 5,6 Intracellular tachyzoites form a parasitophorous vacuole that ruptures following multiple cycles of replication.…”

“…[7][8][9] Latent infection with T. gondii involves an elaborate interplay between the parasite and the host in which the parasite ensures its survival and proliferation but avoids fatal damage to the host at the same time. 10 By definition, latent infections involve a complex interplay between parasite and host, producing some degree of harmony. In humans, T. gondii performs a delicate balancing act that involves, on the one hand, modification of its proximal (and perhaps distal) environment in ways to promote its survival and transmission and, on the other hand, avoidance of overt tissue damage (directly from the parasite or indirectly from the immune response) that would lead to the demise of its host.…”

Toxoplasmosis and psychosis: environment makes a difference

“…gondii, which can lead to abnormalities in these regions [4]. Another hypothesis that could explain the biological plausibility is the interference of T. gondii with neurotransmitter function.…”

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

“…Studies of animal brain biopsies have shown T. gondii to have high neurotropism, with the capacity to infect glial cells (especially microglia and astrocytes) and neurons, forming persistent cysts in brain tissue [69]. Although no tropism for specific brain regions has been observed, with cysts being detected in many areas, the most frequently parasitized regions are the hippocampus, thalamus, cerebral cortex, cerebellum, olfactory bulb, and, especially, the amygdala [70][71][72][73].…”