Schizogony and gametogony of the vaccine, oocyst-deficient, strain T-263 of Toxoplasma gondii

Authors: Dubey, Jitender

Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/24/2017
Publication Date: 10/15/2017
Citation: Dubey, J.P. 2017. Schizogony and gametogony of the vaccine, oocyst-deficient, strain T-263 of Toxoplasma gondii. Veterinary Parasitology. 245:160-162.

Interpretive Summary: Toxoplasma gondii is a single-celled parasite of all warm-blooded hosts worldwide. It causes mental retardation and loss of vision in children, and abortion in livestock. Cats are the main reservoir of T. gondii because they are the only hosts that can excrete the resistant stage (oocyst) of the parasite in the feces. Humans become infected by eating under cooked meat from infected animals and food and water contaminated with oocyst. It would be desirable to have a non-infectious vaccine for the prevention of T. gondii infection in cats and to understand mechanism of immunity to excretion of oocysts. An initial step will be to indentify stage/ stages of the parasite for induction of immunity. A chemically-induced mutant of T. gondii, T-263, is immunogenic but lacks the capacity to form oocysts in cats. Cats fed live bradyzoites of T-263 do not excrete oocysts after challenge with oocyst producing strains. However, it is not known at what stage of the parasite development the oocyst formation is halted. In the present study, the author found that the T-263 forms schizonts (asexual stages), and both male and female gamonts but no oocysts. The results demonstrate that the T-263 strain is defecting in oocyst formation and the observations should help future studies in identification of genes/factors responsible for oocyst formation in the intestine of cats. . The results will be useful for parasitologists, biologists, and epidemiologists.

Technical Abstract: Oocysts are important stage for the spread of Toxoplasma gondii because they are environmentally resistant. Among all hosts of T. gondii, only felids can excrete oocysts. Cats that have excreted T. gondii oocysts after primary infection become immune to re-excretion of oocysts, and this immunity appears to be long lasting. It would be desirable to have a non-infectious vaccine for the prevention of T. gondii infection in cats and to understand mechanism of immunity to excretion of oocysts. An initial step will be to indentify stage/ stages of the parasite for induction of immunity. A chemically-induced mutant of T. gondii, T-263, is immunogenic but lacks the capacity to form oocysts in cats. Cats fed live bradyzoites of T-263 do not excrete oocysts after challenge with oocyst producing strains. However, it is not known at what stage of the parasite development the oocyst formation is halted. Here, four cats were fed live tissue cysts of the T-263 strain and examined for enteroepithelial stages and oocyst production. Schizonts, male, and female gamonts but no oocysts were detected in two cats euthanized 5 and 7 days post inoculation; these cats were administered methyl prednisolone aceatate (20 mg/kg) once intramuscularly. The remaining two cats did not excrete oocysts examined 3-14 days post inoculation, but both seroconverted and developed antibody titers of 1:400 tested by the modification agglutination test, indicating exposure to the parasite. The results demonstrate that the T-263 strain is defecting in oocyst formation and the observations should help future studies in identification of genes/factors responsible for oocyst formation in the intestine of cats.