Infection with cryptosporidium occurred in 12 immunocompetent persons who had direct contact with the feces of infected calves during three unrelated outbreaks of calf cryptosporidiosis. Nine of the twelve subjects had diarrhea and abdominal cramps that lasted 1 to 10 days. Infections were diagnosed and monitored by detection of oocysts in feces, with a modified Sheather's flotation technique and phase-contrast microscopy. Oocysts of cryptosporidium were isolated from calves but not from other animals with which these subjects had been in contact. Oocysts of cryptosporidium were also detected during repeated examinations of feces from two immunodeficient patients with persistent cryptosporidiosis. An apparently identical infection was transmitted to calves and mice, using oocysts from infected calves and human beings. Oocysts from an immunodeficient person also produced infections in kittens, puppies, and goats. This study shows that cryptosporidium may produce a moderate self-limited illness in immunocompetent persons, which contrasts sharply with the prolonged severe diarrhea in immunocompromised patients who contract cryptosporidiosis. Calves with diarrhea should be considered a potential source of human infection, and immunocompromised persons should avoid contact with such animals.

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The endogenous development of Isospora suis Biester 1934 is described in piglets inoculated with 150,000 or 200,000 sporulated oocysts. Endogenous stages developed within villous epithelial cells throughout the small intestine. Two distinct types of meronts were seen in tissue sections. Type I meronts, which were seen at 3 days postinoculation, were binucleate, elongate, and 10.5 by 4.7 micron. They produced two to 14 Type I merozoites per parasitophorous vacuole. Type I merozoites were 10.0 by 3.6 micron. They produced two to 14 Type I merozoites per parasitophorous vacuole. Type I merozoites were 10.0 by 3.6 micron. Type II meronts, which were seen at 4 days postinoculation, were elongate and contained three to 12 nuclei. Type II meronts were 11.4 by 5.3 micron, and one to four were found per parasitophorous vacuole. Type II merozoites were 6.3 by 2.1 micron, and three to 16 were found per parasitophorous vacuole. The peak of asexual development occurred 4 days postinoculation. Fully developed microgamonts, macrogamonts, and oocysts were seen 5 days postinoculation. The prepatent period was 5 days, and the patent period was 5 to 8 days. No extraintestinal stages were seen.

Abstract. A species of porcine coccidia, Zsospora suis, when inoculated into piglets, produced diarrhea, dehydration, weight loss and death. Gross lesions were characterized by a fibrinonecrotic membrane within the jejunum and ileum. Villous atrophy and variable erosion, often with an adhered necrotic membrane, were seen microscopically. Asexual and sexual stages of I. suis were seen within the intestinal epithelium and oocysts were recovered from the feces. The seventy of clinical disease and lesions were dose-related.In 1934, researchers recognized pig diarrhea and enteritis associated with coccidia and identified a new species of porcine coccidia as Isospora suis [2]. The oocysts of eight species of Eimeria and one species of Isospora in swine have been described [ 131. Although coccidia are widespread in the swine population [15], most authors have considered swine coccidia not to be of clinical importance [ I l , 141. With confinement swine facilities now a common husbandry practice, clinical coccidiosis has been seen more frequently [3, 5 , 101. Investigators at the Veterinary Diagnostic and Investigational Laboratory at Tifton, Ga., have described in piglets a clinical and pathologic entity associated with coccidiosis [lo]. In 1978, sporulated oocysts of I. suis were recovered from 23 (49%) of 47 clinical cases studied. Oocysts of I. suis were given to five litters of piglets in an attempt to reproduce the disease seen by practitioners and the laboratory diagnosticians. Materials and MethodsThe original I. suis inoculum was obtained from a 10-day-old piglet with clinical coccidiosis from which only oocysts of 1. suis were recovered. Feces from this piglet were placed in 2.5% potassium dichromate in petri dishes or aerated flasks for 3 to 5 days for sporulation of oocysts. The fecal suspension was passed through wire mesh sieves, centrifuged at 1,500 rpm for 5 minutes, and the supernatant discarded. The oocyst pellet was resuspended in Sheathers sugar solution (1 2 9 specific gravity) and the oocysts harvested, washed in water to remove potassium dichromate and sugar and counted with a hemacytometer. Ten of 12 counts (discarding high and low counts) were averaged and the dose calculated. These sporulated oocysts were passed through young pigs shown to be negative for coccidial oocysts in the feces. The pigs were maintained in individual wire bottom cages and used to obtain oocysts to dose litters 1 and 2. Subsequent litters (3,4 and 5) were dosed with I. suis oocysts from these pigs and from piglets of litters I and 2.

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