Toxoplasma gondii

Life Cycle
  • Humans and other mammals can be infected with T. gondii either by ingestion of infective oocysts shed in cat feces, or by ingestion of bradyzoites encapsulated in tissue cysts within the flesh of infected mammals. Once ingested, the oocysts or bradyzoites transform into rapidly dividing tachyzoites which invade through the GI mucosa and disseminate widely throughout the body. A healthy immune system is rapidly capable of eliminating most of the organisms; however, some enter dormancy within encapsulated cysts primarily in the CNS.
  • These bradyzoites can remain dormant and viable for years and may reactivate once host immunity wanes. It is important to note that T. gondii only undergoes sexual reproduction within felines and thus cats are the protozoa's definitive host.
Transmission
  • As described above, most individuals acquire T. gondii through oral ingestion of either oocysts from feline feces or through ingestion of encapsulated tissue cysts from undercooked meat of infected mammals. Active infection during pregnancy can result in trans-placental mother-to-child transmission, thus allowing categorization of T. gondii as a TORCHES Organism.
Clinical Consequences
  • Overview
    • T. gondii infection can cause a variety of syndromes depending on the immune status of the patient and age of infection.
  • Primary Infection in Healthy Adult
    • Primary infection in a healthy, immunocompetent adult is subclinical in the vast majority of individuals. When the disease does manifest, the only signs may be cervical lymphadenopathy along with some constitutional symptoms such as headache, mild fever, and malaise. Whatever the case, symptomology is self-limited and healthy adults rapidly recover; however, dormant encysted bradyzoites may remain for years in the individuals CNS.
  • Infection in Immunocompromised Adult
    • Immunocompromised patients, such as AIDS patients, are highly prone to a more severe infection with T. gondii. Infection may be due to primary infection or due to recrudescence of previously-acquired dormant disease due to reactivation of dormant encysted bradyzoites. Whatever the case, the syndrome centers around the CNS and usually manifests as encephalitis. Radiography will display multifocal growing mass lesions within the brain and brainstem. Clinically, focal neurological impairments, altered mental status, headaches, and seizures are common.
  • Fetal Infection
    • Congenital toxoplasmosis can result if there is a primary T. gondii infection in a pregnant mother. Trans-placental infection of T. gondii does not occur in healthy pregnant women who have been previously exposed. For this reason, it is recommended that household felines be removed during pregnancy. Infection early during pregnancy is much more severe than that occurring later during gestation
    • Early infection may result in stillbirth, microcephaly, or other major abnormalities. Later infection may result in chorioretinitis (see below) and other neurological abnormalities that may manifest years later.
  • Chorioretinitis
    • T. gondii infection of the retina can result in blindness and can be observed as a fluffy white, cotton-like lesions on the retina. T. gondii chorioretinitis most commonly occurs following congenital infection but can also occur in immunocompromised patients.
Treatment
  • Pyrimethamine and sulfadiazine can be used for active infections.