Criptosporidiosis: una zoonosis de reciente interés

Abstract

Cryptosporidium, a coccidium described in 1907. causes subclinical infections and diarrhea in many vertebrates including man. It departs from other Cryptosporidiiae in its localization on the brush border of epithelial cells, without intracytoplasmic multiplication. The life cycle is direct, with merogonia, endogenous sporogonia and formation of gametes. Thin-walled oocysts maintain the endogenous cycle; thick-walled oocysts excreted into the environment infect other vertebrates. Cryptosporidium infects the intestinal epithelium of immunocompetent individuals. The pathogenesis is unknown; morphologic alterations and the existence of a toxin or moiety may induce fluid and electrolyte loss. Cryptosporidium invades epithelia of the respiratory tract and gall bladder inducing chronic and emaciating diarrhea and eneumonia in persons with an altered immune system. Most Cryptosporidium diarrheas olve within a few days; dehydration is rapidly corrected by oral or intravenous therapy with glucose-salt solution. There is no specific therapy against the parasite. The most severe manifestations are in non-breast-fed and prematurely weaned infants. Cryptosporidium investigated through two years of systematic study of acute diarrheas in Costa Rica showed a frequency of 3% , but in the warm and humid months of the year the frequency was as high as 2564 . The transmission of Cryptosporidium may involve domestic animals. Oocysts are resistant to laboratory desinfectants but are susceptible to freezing. Diagnosis consists in finding oocysts in feces by direct examination, or after fixation and staining with Ziehl-Neelsen or Giemsa. Tissue forms are detected in histologic preparations, and the parasite can be implanted in suckling mice, embryonated eggs, or tissue culture.