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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: . Opossums (Didelphis marsupialis), act as intermediate hosts for Besnoitia darlingi and could be infected orally with sporozoites (oocysts) and bradyzoites (tissue cysts), or intraperitoneally (i.p.) with tachyzoites. Infections could presumably be transmitted through cannibalism. Cats (Felis catus), the definitive host, could be infected only with bradyzoites but not sporozoites. Oocysts shed by cats measure about 12 × 12 μm, resemble similarly sized oocysts of Toxoplasma gondii and Hammondia hammondi, and must be differentiated by the appearance of tissue cysts after experimental infection of intermediate hosts. Cats did not form tissue cysts of B. darlingi. Tachyzoites from the related B. jellisoni could be used in the Sabin-Feldman dye test to determine the development of antibody to B. darlingi in opossums after infection.

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: SYNOPSIS. The development of Toxoplasma cysts was studied in mice inoculated with tachyzoites by several routes. After 1–30 days of infection, murine tissues were examined microscopically, and portions or whole carcasses were fed to mice and cats. The feces of the cats were examined for oocyst shedding.Cyst-like structures containing distinct PAS-positive granules were first seen after 3 days of infection with tachyzoites, and became numerous by 6 days. Argyrophilic walls were first seen after 6 days, and became numerous by 16 days of infection with tachyzoites.Prepatent periods to oocyst shedding (PPO) were either “short” (3–10 days) or “long” (19–48 days). The “short” PPO was found only in cats that had ingested mice infected for 3 days or longer, and was related to the development of PAS-positive granules in T. gondii, and to high, 60–100%, oral infectivity rates for cats. The “long” PPO followed the ingestion of mice infected for only 1–2 days, and was related to tachyzoites without distinct PAS-positive granules and low, 32% or less, infectivity for cats. The “long” PPO followed also the ingestion of oocysts and the parenteral inoculation of tachyzoites, bradyzoites, or sporozoites.Using the “short” PPO as a criterion for detecting cysts in tissues, it was shown that (a) numerous cysts developed in mice 5 days after inoculation with tachyzoites, 7–9 days after inoculation with cysts, and 9–10 days after inoculation with oocysts, and (b) cysts developed faster and more frequently in the brain and muscle than in lungs, liver, spleen, and kidneys of mice inoculated with tachyzoites.

Notes: SYNOPSIS. Toxoplasma gondii, passed from mouse to mouse in the tachyzoite stage for 30–35 generations, developed cysts, which, when fed to cats, failed to produce oocysts. Besnoitia jellisoni, passed similarly for 20 generations, lost the capacity to form cysts. These phenomena are explained by a loss of genomes or gene products during the rapid passage selecting for tachyzoites.

Notes: Summary A 40 year old woman with Hodgkin's disease twice developed signs of encephalitis while being treated with prednisone and cyclophosphamide for 10 months. Since on both occasions herToxoplasma dye test titer was 1 : 8000 or higher, she was treated on suspicion of toxoplasmosis with sulfadiazine and pyrimethamine. Her tumor therapy was changed to bleomycin with lower doses of prednisone for 12 months. After death from central pontine myelinolysis,Toxoplasma and cytomegalovirus could be isolated, but no lesions attributable to these infectious agents were present. Maintenance of the patient's immune competence suggested an inquiry into the effects of the chemotherapeutic agents and of tumor infiltration for their respective interference with immunity. Using hamsters with chronic latent toxoplasmosis, it was found that both cortisone and cyclophosphamide caused recrudescence of chronic inapparent infection, that vinblastine and bleomycin interfered only slightly with the development of immunity, whereas an infiltrating lymphoma permitted immunity to develop normally. It is concluded that greater attention should be directed to the immunosuppressive effects of tumor treatment. By choice of an effective tumor therapy which is least immunosuppressive, and if necessary under cover of antimicrobial therapy, a patient with Hodgkin's disease can be aided in developing immunities which he may subsequently be able to maintain.

Notes: Summary Hammondia hammondi gen.nov.,sp.nov. (Eimeriorina:Sarcocystidae) is described as an obligate heteroxenous protozoon of domestic cats (final host) and laboratory mice (experimental intermediate host). Oocysts from the final host are infectious only for the intermediate host; and cysts from the intermediate host are infectious only for the final host. Intracellular cysts develop principally in striated muscle of mice that ingest oocysts, with a few cysts in the brain and perhaps elsewhere. Cysts are without septa or radial spines; bradyzoites are slender, there is no evidence of metrocytes. Cysts are not infectious for mice. After the ingestion of cysts by cats, a multiplicative cycle precedes the development of gametocytes in the epithelium of the small intestine. Oocysts are shed unsporulated, sporogony is outside of the host, resulting in two sporocysts with four sporozoites each. Oocysts of the species average 11×13 μm. The prepatent period is 5 to 8 days, and oocyst shedding persists for 10 to 28 days followed by immunity. Cysts in skeletal muscle measured between 100 and 340 μm in length and 40 and 95 μm in width. Experimental intermediate hosts are laboratory mice, rats, hamsters, guinea pigs, Peromyscus and Mastomys. Some of the intermediate hosts develop low levels of antibody and some cross-immunity against Toxoplasma; however, this has not been observed in cats.