Submitted to: Journal of Eukaryotic Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 20, 1997
Publication Date: N/A
Interpretive Summary: Infections by the single-celled parasite Toxoplasma gondii are widely prevalent in humans and animals. The ingestion of food or water contaminated with resistant Toxoplasma (oocysts) from cat feces or the ingestion of tissue cysts in undercooked meat are the 2 major ways of postnatal transmission of T. gondii. After infection with any infective stage of T. gondii, tachyzoites (rapidly dividing stage) multiply in a variety of cells and eventually encyst in several tissues, particularly in the brain. Tissue cysts persist for a long time, perhaps for the life of the host. It has been hypothesized that tissue cysts rupture occasionally and the released bradyzoites (slow developing stage) are killed in immunocompetent hosts. However, in immunosuppressed hosts, such as AIDS patients, encysted T. gondii (bradyzoites) released from tissue cysts may multiply locally and spread to other organs. Encephalitis is the predominant clinical manifestation of toxoplasmosis in AIDS patients and is believed to be due to reactivation of latent infections. The mechanism of reactivation of toxoplasmosis is unknown. A scientist at the Beltsville Agricultural Research Center studied the migration pathway of T. gondii in mice after feeding encysted Toxoplasma. This paper documents conversion time from bradyzoites to tachyzoites then to bradyzites. The sequence of events described will be of interest to biologists, public health workers and parasitologists in general.
Technical Abstract: The development of Toxoplasma gondii was studied in mice fed bradyzoites. At 2 h after oral inoculation (HAI), bradyzoites were found in cells of the surface epithelium and the lamina propria of the small intestine, primarily the ileum. Division into 2 tachyzoites was first observed at 18 HAI in the intestine. At 24 HAI, organisms were also seen in mesenteric lymph nodes. Organisms were first detected in the brain at 6 days after oral inoculatio with bradyzoites (DAI) but not consistently until 10 DAI. Immunohistochemical staining with bradyzoite specific (BAG-5 antigen) anti- serum showed that bradyzoites retained their BAG-5 reactivity even after the first division into 2 tachyzoites in the intestine at 24 HAI. BAG-5 positive organisms were not seen 2 - 5 DAI. BAG-5 antigens reappeared in T. gondii at 6 DAI. Whole mice and individual tissues of mice fed bradyzoites were bioassayed in cats and mice for the presence of bradyzoites. Feces of cats fed murine tissues were examined for oocyst shedding for short prepatent periods. Bradyzoites were present in the intestines of mice up to 12 HAI but not at 18 HAI, and tachyzoites and not bradyzoites disseminated to other tissues from the intestine. Bradyzoites were again detected 6 DAI. Using the mouse bioassay, T. gondii was first detected in peripheral blood at 24 HAI and more consistently at 48 HAI. Using a pepsin-digestion procedure and mouse bioassay, organisms were demonstrated in many tissues of mice 15 and 49 DAI.