Overview of Toxoplasma Gondii
Following ingestion, gastric enzymes and bile degrade the cyst walls of the infective sporozoites or bradyzoites, releasing the parasites into the small intestine where they rapidly invade host cells. Once in the intracellular milieu, the invading parasite resides in a parasitophorous vacuole (PV) witH no to little replication before quickly undergoing a developmental switch to the tachyzoite form (red).
Tachyzoites rapidly replicate within the PV, exit from infected cells, and disseminate to other organs and tissues during the acute phase of infection. In response to unknown stimuli, possibly including the host’s immune response, tachyzoites convert back to the encysted bradyzoite form, establishing a chronic infection. In summary, T. gondii will interconvert between three developmental forms during infection in a single intermediate host: the non-replicating sporozoites, the rapidly growing tachyzoites (red), and the slowly dividing bradyzoites (green).
The life cycle is completed when an infected animal is eaten by a definitive feline host (e.g., a domestic cat preying on an infected mouse), which will shed the oocysts into the environment. Although infection with T. gondii is usually self-limiting in healthy adult humans, severe disease does sometimes occur in immunocompromised individuals, such as the fetus, patients with HIV and transplant patients.
There exists no effective therapy to treat a chronic infection. This presents serious challenges should a chronically infected individual become immunocompromised, as reactivation of tissue cysts can lead to severe complications, especially in HIV-AIDS and transplant patients.