The intestinal protozoan cryptosporidium is known to cause diarrhea in immunocompromised patients, but few cases have been reported in detail in immunocompetent persons. During a 12-month period, we identified cryptosporidium in the stools of 43 immunocompetent patients. The numbers of cases were increased in those under 4 years old and in those from 30 to 39 years old. Of 30 index cases, 23 (77 per cent) were diagnosed in the late summer or the fall. Fifteen of the 43 patients (35 per cent) had other gastrointestinal pathogens, of which only Giardia lamblia was statistically associated with cryptosporidium. In the 28 patients in whom other gastrointestinal pathogens were not identified, the clinical manifestations were predominantly watery, nonbloody diarrhea and, less commonly, abdominal discomfort, anorexia, fever, nausea, and weight loss. The infection was self-limited in all 43 patients. Clustering of cases occurred in a day-care center and in two families. These clinical observations confirm worldwide findings and suggest that cryptosporidium is a relatively common nonviral cause of self-limited diarrhea in immunocompetent persons in the northeastern United States.

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The (NZB x NZW)F1 mouse strain develops a syndrome of accelerated autoimmunity including severe renal disease and early death. Evidence suggests that class II molecules play a central role in this process. Previous studies have suggested that the NZW strain contributes at least one gene to the development of accelerated autoimmunity that is linked to the H-2 complex, and antibodies to murine class II molecules have been used to ameliorate disease in (NZB x NZW)F1 mice. We therefore wished to sequence the class II molecules from NZW mice to identify any unique sequences that may contribute to disease development. We constructed oligonucleotide primers corresponding to the 5' and 3' regions of the second exon of class II genes from a variety of haplotypes, and used these primers in a polymerase chain reaction to sequence the second exon of the NZW I-A alpha, I-A beta, and I-E beta genes. We report that the second exons of NZW I-A alpha, I-A beta, and I-E alpha are identical to their counterparts of the previously sequenced u haplotype, and that the second exon of NZW I-E beta is identical to its counterpart from u except for a single base change that results in a substitution of arginine for threonine at amino acid 72. This base and amino acid are identical to those found at the same positions in the s haplotype.

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