Toxoplasma gondii () is a parasitic protozoan (specifically an apicomplexan) that causes toxoplasmosis. Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals, but felids are the only known definitive hosts in which the parasite may undergo sexual reproduction.
In rodents, T. gondii alters behavior in ways that increase the rodents' chances of being preyed upon by felids. Support for this "manipulation hypothesis" stems from studies showing that T. gondii-infected rats have a decreased aversion to cat urine while infection in mice lowers general anxiety, increases explorative behaviors and increases a loss of aversion to predators in general. Because cats are one of the only hosts within which T. gondii can sexually reproduce, such behavioral manipulations are thought to be evolutionary adaptations that increase the parasite's reproductive success since rodents that do not avoid cat habitations will more likely become cat prey. The primary mechanisms of T. gondii–induced behavioral changes in rodents occur through epigenetic remodeling in neurons that govern the relevant behaviors (e.g. hypomethylation of arginine vasopressin-related genes in the medial amygdala, which greatly decrease predator aversion).
In humans, particularly infants and those with weakened immunity, T. gondii infection is generally asymptomatic but may lead to a serious case of toxoplasmosis. T. gondii can initially cause mild, flu-like symptoms in the first few weeks following exposure, but otherwise, healthy human adults are asymptomatic. This asymptomatic state of infection is referred to as a latent infection, and it has been associated with numerous subtle behavioral, psychiatric, and personality alterations in humans. Behavioral changes observed between infected and non-infected humans include a decreased aversion to cat urine (but with divergent trajectories by gender) and an increased risk of several psychiatric disorders – particularly schizophrenia and bipolar disorder. Preliminary evidence has suggested that T. gondii infection may induce some of the same alterations in the human brain as those observed in rodents. Many of these associations have been strongly debated and newer studies have found them to be weak, concluding:
T. gondii is one of the most common parasites in developed countries; serological studies estimate that up to 50% of the global population has been exposed to, and may be chronically infected with, T. gondii; although infection rates differ significantly from country to country. Estimates have shown the highest IgG seroprevalence to be in Ethiopia, at 64.2%, as of 2018.
Structure
T. gondii contains organelles called rhoptries and micronemes, as well as other organelles.
Lifecycle
The lifecycle of T. gondii may be broadly summarized into two components: a sexual component that occurs only within cats (felids, wild or domestic), and an asexual component that can occur within virtually all warm-blooded animals, including humans, cats, and birds. Because T. gondii can sexually reproduce only within cats, cats are therefore the definitive host of T. gondii. All other hosts – in which only asexual reproduction can occur – are intermediate hosts.
Sexual reproduction in the feline definitive host
When a feline is infected with T. gondii (e.g. by consuming an infected mouse carrying the parasite's tissue cysts), the parasite survives passage through the stomach, eventually infecting epithelial cells of the cat's small intestine. Inside these intestinal cells, the parasites undergo sexual development and reproduction, producing millions of thick-walled, zygote-containing cysts known as oocysts. Felines are the only definitive host because they lack expression of the enzyme delta-6-desaturase (D6D) in their intestine. This enzyme converts linoleic acid; the absence of expression allows systemic linoleic acid accumulation. Recent findings showed that this excess of linoleic acid is essential for T. gondii sexual reproduction.
Feline shedding of oocysts
Infected epithelial cells eventually rupture and release oocysts into the intestinal lumen, whereupon they are shed in the cat's feces. Oocysts can then spread to soil, water, food, or anything potentially contaminated with the feces. Highly resilient, oocysts can survive and remain infective for many months in cold and dry climates.