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Cryptosporidium parvum

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Disease. cryptosporidiosis

Geographic distribution. Worldwide in temperate and tropical zone

Infection rate. Cryptosporidium parvum is ubiquitous, infecting most mammals, and is highly infectious. Thus everyone is at some risk of acquiring cryptosporidiosis. Prevalence rates of cryptosporidiosis in diarrheal illness range from a few per cent in cooler, more developed countries (0.1-2% overall), to 0.5-10% in warmer, less developed countries. Recent data suggest that 3-4% of AIDS patients in the USA and Europe will become infected with cryptosporidiosis during their symptomatic period. In the developing contries the equivalent numbers are much higher up to 50% in hospital patients with AIDS.

Life cycle. Genus cryptosporidium has a wide range of hosts such as humans, mammals, birds, reptiles, and fishes. Oocyst-contaminated water, soil, and vegetables cause infections. Sporozoites released from oocyst are attached intestinal epithelial cells after excystation and develop into trophozoite. Trophozoite undergo asexual life cycle (merogony) and then sexual multiplication. Oocysts are produced and excreted through the feces after fertilization of macrogamete and microgamete. Thin walled oocysts could induce autoinfection by being excysted in intestinal lumen.

Morphology. Round to oval oocyst has 4-6 ㎛ in diameter. Oocyst seems often refractile at wet smear. Black dot or small vacuoles in oocyst could be seen after modified acid fast staining. Sporozoite and merozoites have apical complex (microneme, rhoptry, conoid, preconoidal ring) at the anterior most part.

Pathology and clinical symptoms. Watery diarrhea is the most frequent symptom, and can be accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. In immunocompetent persons, symptoms are limited within 1 to 2 weeks; they can be chronic and more severe in immunocompromised patients, especially those with CD4 counts < 200/ul. Microvilli of the small intestine disappear and loss of the ability to produce digestive enzymes and decrease of digestion area can cause indigestion and malabsorption.

Diagnosis. Detection of oocysts in the stool using modified acid fast staining, indirect fluorescent antibody test or PCR.

Prevention. Improved personal hygiene, adequate washing of vegetables, and filtration or boiling of drinking water are necessary.

Comments. The oocysts are not always detectable and repeated examinations of stool may be needed in clinically suspicious patients.

Jae-Ran Yu


Oocyst of Cryptosporidium parvum. Fecal smear stained with modified acid fast method. 5 ㎛.

Jae-Ran Yu


Oocysts of Cryptosporidium parvum labeled by indirect fluorescent antibody test using oocyst wall specific monoclonal antibody (CMYL30).

Jae-Ran Yu


Oocysts of Cryptosporidium parvum stained with monoclonal antibody (CMYL30) and DAPI. Blue dots in the oocysts are sporozoites stained with DAPI.

Jae-Ran Yu


Oocyst of Cryptosporidium parvum (A) (Ziehl-Neelsen stain, 1000x).

DY Min/MH Ahn/JS Ryu


Oocyst of Cryptosporidium parvum (B) (Fluorescent antibody test, 1000x).

DY Min/MH Ahn/JS Ryu


Mouse small intestine infected with Cryptosporidium parvum. Small basophillic bodies seem to be on the surface of epithelial cells are various developmental stages of C. parvum enveloped by host cell membrane. H & E stain.

Jae-Ran Yu


Merozoites of Cryptosporidium parvum.

Jae-Ran Yu


Trophozoite of Cryptosporidium parvum located on the surface of intestinal epithelial cell.

Jae-Ran Yu


Meront stage of Cryptosporidium parvum under asexual division (endopolygeny).

Jae-Ran Yu


Mature type I meront including eight merozoites.

Jae-Ran Yu


Macrogametocyte of Cryptosporidium parvum including many wall forming bodies, and amylopectin granules.

Jae-Ran Yu


Microgametocyte of Cryptosporidium parvum. About sixteen microgamets could be seen when microgametocyte is fully matured.

Jae-Ran Yu


Immature oocyst of Cryptosporidium parvum.

Jae-Ran Yu