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Notes: Tissue cyst induced Toxoplasma gondii infections were examined in 2 beagle dogs orally inoculated with tissue cysts. Neither dog developed clinical signs of toxoplasmosis. Both dogs developed low antibody titers to T. gondii. The MAT and IFAT were superior to the LAT and IHT tests for detecting antibodies to T. gondii.

Notes: . The development of Toxoplasma gondii was studied in mice fed bradyzoites. At one hour 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 two tachyzoites was first observed at 18 HA1 in the intestine. At 24 HAI, organisms were also seen in mesenteric lymph nodes. Organisms were first detected in the brain at six days after oral inoculation 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 two tachyzoites in the intestine at 18 HAL 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 HA1 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 HA1 and more consistently at 48 HAL Using a pepsin-digestion procedure and mouse bioassay, organisms were demonstrated in many tissues of mice 15 and 49 DAI.

Notes: SYNOPSIS. The life cycle of Toxoplasma gondii is described from cats orally inoculated with Toxoplasma cysts. Five new structural stages of Toxoplasma designated as “types” A-E were found in the epithelial cells of the small and large intestine. Type A is the smallest of all 5 intestinal Toxoplasma types. It occurs as collections of 2-3 organisms in the jejunum 12–18 hr after infection. Type B organisms are characterized by a centrally located nucleus, a prominent nucleolus and dark blue cytoplasm giving rise to the appearance of bipolar staining with Giemsa. Type B occurs 12–54 hr after infection and appears to divide by simple endodyogeny and by multiple endodyogeny (endopolygeny). Type C organisms are elongate with subterminal nuclei and strongly PAS-positive cytoplasm. They occur at 24–54 hr and divide by schizogony. Type D organisms are smaller than type C and contain only a few PAS-positive granules. They occur from 32 hr to 15 days after inoculation and account for over 90% of all parasites in the small intestine during this time. Three subtypes divide by endodyogeny, schizogony and by splitting of their merozoites from the main nucleated mass without leaving a residual body. Type E organisms resemble one of the subtype D which divide by schizogony, but they leave a residual body. They occur from 3–15 days after inoculation.Gametocytes occur thruout the small intestine but more commonly in the ileum 3-15 days after infection. Male gametocytes contain on an average of 12 microgametes and comprise 2–4% of the gametocyte population. The prepatent period after cystinduced infection is 3–5 days with the peak oocyst production between 5–8 days and a patent period varying from 7–20 days.Variable numbers of trophozoites are present in the lamina propria of the small intestine and in the extra-intestinal tissues within a few hr after inoculation. After 9–10 days cysts were seen in the heart and later in the brain.The lesions of toxoplasmosis are compared in newborn and weanling kittens and in adult cats after oral and subcutaneous inoculation with cysts. After the ingestion of cysts, newborn kittens developed enteritis, hepatitis, myocarditis, myositis, pneumonitis and encephalitis and were moribund by the 9th day. Kittens aged 2 weeks and older developed enteritis, myocarditis, encephalitis and myositis but often survived; adult cats usually remained asymptomatic. After subcutaneous inoculation of cysts, newborn and weanling kittens died of acute toxoplasmosis with severe pneumonia, myocarditis, encephalitis and hepatitis.

Notes: An isolate of Sarcocystis neurona. (SN6) was obtained from the spinal cord of a horse from Oregon with neurologic signs. The parasite was isolated in cultures of bovine monocytes and equine spleen cells. The parasite divided by endopolygeny and completed at least one asexual cycle in cell cultures in three days. Two gamma interferon knockout mice inoculated with cell culture-derived merozoites became ill 35 d later and S. neurona schizonts and merozoites were found in encephalitic lesions. The parasite in tissue sections of mice reacted with S. neurona-specific antibodies and S. neurona was reisolated from the brain of knockout mice.

Notes: SYNOPSIS. Evidence is presented that Isospora felis and I. rivolta invade the extra-intestinal tissues of cats. Kittens were fed sporocysts of I. felis and I. rivolta. At specific intervals the kittens were killed and suspensions of extra-intestinal tissues were fed to indicator kittens less than a day old. Oocyst production by the indicator kittens within the regular prepatent period was taken as evidence that coccidian stages were present in the inoculum consisting of extra-intestinal tissues of cats.Tissues of kittens infected with I. felis for 5–104 days were infectious to newborn kittens as follows: liver and spleen mixture 3 out of 5 times, mesenteric lymph nodes 4 out of 4 times, brain and muscle mixture 1 out of 5 times, lungs 1 out of 5 times. The prepatent period in kittens consuming oocysts of I. felis was 7-11 days; after consuming extra-intestinal tissues of kittens it was 4–8 days. Distinct coccidian stages unlike those present in the gut were found singly and in groups of 2–15 in lymphoreticular cells of mesenteric lymph nodes of 2 kittens infected for 2–4 days.Tissues of kittens infected with I. rivolta for 5–21 days were infectious to newborn kittens as follows: liver and spleen mixture 3 out of 5 times, mesenteric lymph nodes 1 out of 5 times, brain, muscle and lung mixture none of 5 times. The prepatent period in kittens consuming oocysts of I. rivolta or extra-intestinal tissues of cats was 5–7 days. Coccidian stages occurred singly or in pairs, intracellularly or free in the mesenteric lymph nodes of 3 out of 10 kittens infected for 1–8 days.

Notes: Abstract A method for isolation of enteroepithelial stages of Toxoplasma gondii from the intestinal mucosa of experimentally infected cats was developed using Percoll density-gradient centrifugation. Gamonts and merozoites were obtained essentially free of host-cell debris. A recovery rate of nearly 30% of the parasites in the original preparations was obtained by this method. Merozoites were separated from gamonts by filtration through a 3-μm polycarbonate filter.

Notes: Abstract A direct agglutination test was evaluated for the detection and quantitation of IgG antibodies to Neospora caninum in both experimental and natural infections in various animal species. As compared with results obtained by the indirect fluorescent antibody test, the direct agglutination test appeared reliable for the serologic diagnosis of neosporosis in a variety of animal species. The direct agglutination test should provide easily available and inexpensive tools for serologic testing for antibodies to N. caninum in many host species.