Cyst‐Induced Toxoplasmosis in Cats*

Abstract

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.

Seroprevalence of Toxoplasma gondii in cats (Felis catus, Linnaeus 1758) living in Lima, Peru

“…Over one million non-sporulated oocysts can be dispersed to the environment in cat feces FRENKEL, 1972). When environmental conditions are favorable (water, wetland, average temperature of 25°C, and enough oxygen), the sporulated oocysts become infective within three days, thus explaining the high incidence of infection in tropical or subtropical areas (LEGUÍA, 2002).…”

Isolation and Genotyping ofToxoplasma GondiiCausing Fatal Systemic Toxoplasmosis in an Immunocompetent 10-Year-Old Cat

“…The main pathologic features of systemic toxoplasmosis in cats after both experimental and natural infection have been well characterized 10,11,20 and include interstitial pneumonia, hepatitis, splenitis, lymphadenomegally, and ophthalmitis. In addition, myocarditis and central nervous system disease may occur.…”

Mechanics of the Toxoplasma gondii oocyst wall

“…The oocyst is the result of sexual multiplication of T. gondii in the intestinal epithelium of cats (19)(20)(21). A few days postinfection, unsporulated (uninfective) spheroid oocysts (10 × 12 μm) are excreted in cat feces and become rapidly infective following aerobic sporulation (22).…”