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.

Isospora-type oocysts were excreted by cats following the ingestion of Toxoplasma fromn infected mice. Oocysts appeared 3 to 5 days after cyst. were ingested and 8 to 10 days after trophozoites were ingested, and also 21 to 24 days after the administration of infective fecal suspensions from cats. A close quanititative and biologic correlation between oocysts and Toxoplasma infectivity of the feces was observed which could not be separated by density gradient centrifugation and filtration methods. Toxoplasma is an intestinal coccidian of cats which is fecally spread. It has evolved to multiply in brain and muscle and in other species, making it possible for carnivorism to become another means of transmission.

Toxoplasma infection is c o m m o n in m a n and animals, yet for 60 years the life cycle of Toxoplasma gondii remained unknown. R e c e n t l y a new form of Toxoplasma was found in the feces of cats that had eaten Toxoplasma-infected mice (for review of earlier work see [1]). This fecal form is biologically different from the known stages of Toxoplasma. While searching the feces of cats for a morphological equivalent of Toxoplasma, several candidate forms such as fungi, cysts of flagellates, and coccidian oocysts resembling those of Isospora fells, I. rivolta, and I. bigemina were found. Of these only oocysts resembling [. bigemina were constantly and q u a n t i t a t i v e l y associated with fecal Toxoplasma infectivity. W e will describe and characterize these oocysts and show b y a series of m u t u a l l y independent determinations that they should be regarded as oocysts of Toxoplasma got~dii. Some of these findings were briefly reported (2). DEFINITION O F TER3£STrophozoites refer to intracellular and free forms of Toxoplasma which are actively proliferating in the tissues of acutely infected animals (Fig. 1). Free trophozoites are quickly digested in solutions of pepsin at pH 1.3.Cyst refers to an accumulation of Toxoplasma (merozoites) characteristically occurring in the brain and muscle of chronically infected animals (Fig. 2). Cysts are surrounded by an elastic argyrophilic and periodic acid Schiff positive wall and contain much stored glycogen. The cyst wall is destroyed immediately on exposure to pepsin but the released merozoites survive in it for some time.

Toxoplasma oocysts in cat feces were marked with a tracer amount of strontium-85 (85-SR), and were superficially buried simulating the natural disposal of feces by cats. Oocyst infectivity in Costa Rica was followed qualitatively and persisted for 1 year in three shaded sites, two moist, and one relatively dry site. Oocyst infectivity was quantitated in the Kansas deposit over a period of 18 months, including two winters. After initial mixing in soil, the level of infectivity remained fairly stable. Infectivity was recovered, probably from the surface on one Musca, several isopods, and earthworms. These data on persistence of Toxoplasma oocysts in soil support the concept that Toxoplasma infectivity in nature may be increased logarithmically by cats.

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We critically review and summarize information on the prevalence of Toxoplasma gondii infections in rats, mainly Rattus norÕegicus, and their possible role as a source of infection for larger carnivores and omnivores. We also review information on immunology and natural resistance, contributing to the model value of rats in the analysis of human infection. Rats can be Ž . Ž . successfully infected with oocysts sporozoites , tissue cysts bradyzoites , and tachyzoites. Even adult rats, that are resistant to clinical toxoplasmosis, can be infected orally with a few oocysts or tissue cysts. Infections with tachyzoites of the RH strain are highly variable. Congenital transmission of T. gondii occurs at a high rate when rats are infected during pregnancy. Congenitally infected rats can harbor viable T. gondii in the absence of detectable antibodies to T. gondii and rats with low antibody titers may harbor few or no organisms. The isolation of viable T. gondii by bioassay is the only reliable means to determine persistence of chronic T. gondii infection in feral rats. No evidence was found for maintenance of T. gondii in rats by vertical transmission in the absence of cats. q 1998 Elsevier Science B.V. Ž . PII S 0 3 0 4 -4 0 1 7 9 7 0 0 2 2 7 -6 ( ) J.P. Dubey, J.K. Frenkelr Veterinary Parasitology 77 1998 1-32 2

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 samll 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 x 13 mum. The prepatent period i 5s 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 mum in length and 40 and 95 mu-m 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.