CRYPTOSPORIDIOSIS : CLINICAL ASPECTS
Immunocompetent patients usually note the onset of explosive, profuse, watery diarrhea 1 to 2 weeks after exposure. Typically, the illness persists for 5 to 11 days and then rapidly abates. Occasionally, purging, accompanied by a mild malabsorption and weight loss, continues for up to 1 month. A few patients complain of nausea, anorexia, vomiting, and low-grade fever. Except for its shorter duration, more prominent abdominal pain, and rel-ative lack of flatulence, the clinical manifestations of cryptosporidiosis closely resemble those produced by G. lamblia. Radiographic and endoscopic examinations of the gut are either normal or demonstrate mild, nonspecific abnormalities. Recovery is complete, and neither relapse nor reinfection has been reported.
Cryptosporidiosis has been described in patients with a broad range of immunodefi-ciencies, including childhood malnutrition in third world countries, AIDS, and congenital hypogammaglobulinemia, and in those resulting from cancer chemotherapy and immuno-suppressive management of organ transplants. In such patients, cryptosporidiosis is usu-ally indolent in onset and manifestations are similar to those seen in normal hosts, but the diarrhea is more severe. Fluid losses of up to 25 L/day have been described. Patients with biliary cryptosporidiosis present with typical manifestations of cholecystitis and cholan-gitis. Unless the immunologic defect is reversed, the disease usually persists for the dura-tion of the patient’s life. Weight loss is often prominent. The prognosis depends on the nature of the underlying immunologic abnormality; half of patients with AIDS die within 6 months. Although other intercurrent infections are usually the direct cause of death, malnutrition and complications of parenteral nutrition contribute.
The diagnosis of cryptosporidiosis is established by the recovery and identification of Cryptosporidium oocysts in a recently passed or preserved diarrheal stool. Oocyst excre-tion is most intense during the first week of illness, tapers during the second week, and generally stops with the cessation of diarrhea. Because cryptosporidia oocysts are one of the few acid-fast particles found in feces, a definitive identification can be established with any one of the acid-fast staining procedures developed for mycobacteria. A direct immunofluorescence antibody stain using a monoclonal antibody to oocyst wall has been recently introduced that appears to be superior to acid-fast stains. When direct examina-tions are negative, concentration procedures are used and the concentrate restained. Im-munofluorescence and EIAs for the detection of anticryptosporidial antibodies are now available.
In the immunocompetent patient, the disease is self-limited and attempts at specific an-tiparasitic therapy are not warranted; rehydration may be required in small children. In the immunocompromised host, the severity and chronicity of the diarrhea warrants thera-peutic intervention. Unfortunately, there is no uniformly effective anticryptosporidial agent available at this time. Paromomycin, a luminal antimicrobic, has been shown to re-duce the intensity of diarrhea in some patients, and parenteral octreotide acetate, a so-matostatin analog, has been useful in decreasing stool volumes. The only uniformly suc-cessful approach has been the reversal of underlying immunologic abnormalities. When appropriate, withdrawal of cancer chemotherapy agents or immunosuppressive drugs may result in a cure.
The stools of patients with cryptosporidiosis are infectious. Stool precautions should be instituted at the time the diagnosis is first suspected; for the immunosuppressed pa-tient, this should be whenever diarrhea, regardless of presumed etiology, is first noted. This is particularly important in cancer chemotherapy and transplantation units, where spread of the disease from a symptomatic patient to other immunosuppressed patients can have life-threatening consequences.
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