Cryptosporidium

Causative agent of cryptosporidiosis

■ Cryptosporidiosis in humans is predominantly caused by Cryptosporidium hominis (= human genotype of C. parvum) and the bovine genotype of C. par-vum. Humans are infected by peroral ingestion of infective oocysts. In immunocompetent persons, the infection remains inapparent or manifests as a self-limiting diarrhea. Persistent, choleralike, life-threatening diarrheas are observed in AIDS patients. ■

Parasite species and occurrence. At least 10 species of the genus Cryptospor-idium and several genotypes are currently known that occur mainly as parasites of the intestine (and rarely of other organs) in humans and numerous species of mammalian animals, birds, and reptiles. Cryptosporidium hominis is a parasite of humans and monkeys, the bovine genotype of C. parvum infects many species of mammalian animals (ruminants, dogs, cats, rabbits, rodents, etc.) and humans. Other species originating from animals have been found occasionally in AIDS patients, including Cryptosporidium canis (host: dog) Cryptosporidium felis (host: cat), Cryptosporidium meleagridis and Cryp-tosporidium baileyi (hosts: birds).

Cryptosporidiosis occurs worldwide. The mean prevalences in humans differ in developed and developing countries and are about 2% and 6% respectively for immunocompetent persons with diarrhea and 14% and 24% respectively in HIV-positive patients. Prevalences exceeding 50% are also known in the latter group. Among domesticated animals, particularly high prevalences are observed among young calves (often 20-100%).

Morphology and life cycle. C. hominis and C. parvum inhabit mainly the small intestine and produce oocysts 4-5 im in diameter. Following peroral ingestion of infectious oocysts, each of which contains four sporozoites, the released sporozoites invade enterocytes where each stage resides within a parasitophorous vacuole just beneath the cell membrane in the microvillus region of the host cell. This localization is typical of cryptosporidia (Fig. 9.15). Following formation of type I meronts with eight merozoites, the latter can infect new cells. In the further course, type II meronts with four merozoites are produced that give rise to sexual forms (gamogony). The fertilized zygote encysts to produce about 80% thick-walled and 20% thin-walled oocysts. The oocysts sporulate while still intracellular in the intestine. Each sporulated oocyst contains four free sporozoites (i.e., not enclosed in a sporocyst). Thin-walled oocysts can burst within the host, releasing sporozoites that cause endogenous autoinfections. After a brief prepatent period (two to four, sometimes up to 12 days), thick-walled oocysts are shed with feces and can immediately infect new hosts. It is assumed that persistent infections in immunodeficient persons are due to endogenous autoinfections by sporozoites from thin-walled oocysts or by merozoites from type I meronts.

Epidemiology. C. hominis is transmitted within the human population. Humans may also acquire zoonotic infections with the bovine type of C. parvum (main source of infection: calves) or rarely with other species or genotypes of animal origin.

Transmission of the oocysts is by the direct fecal-oral route or in contaminated foods or drinking water. The oocysts of C. parvum remain viable in cool water for months. This explains the etiology of major epidemics due to fecal contamination and improper processing of drinking water such as occurred in Milwaukee in 1993 with 403 000 persons involved. Sewage contained up to 13 000 oocysts per liter, surface bodies of water up to 112 oocysts per liter. As few as 30-100 oocysts are sufficient to induce an infection in humans.

Clinical manifestations. Cryptosporidia inhabit mainly the small intestine, where they may cause destruction of microvilli, shortening, swelling, and fusion of the villi and cellular infiltration of the mucosa. The severity and course of an infection depends on the immune status of the infected person.

■ Immunocompetent persons. Infections either take an inapparent course or result, after incubation periods of five to 28 days, in acute, self-limiting, in most cases mild illnesses lasting one to 26 days with diarrhea and various generalized symptoms.

■ Immunodeficient persons. Chronic infections with severe diarrhea and long periods of oocyst excretion, e.g., in AIDS patients. The diarrhea is watery, voluminous, choleralike and often associated with other symptoms (abdominal pain, nausea, vomiting, mild fever, etc.). In HIV patients, cryptosporidia

— Cryptosporidium: Life Cycle -

— Cryptosporidium: Life Cycle -

Life Cycle Cryptosporidium Cat

Fig. 9.15 1 Infective oocyst; 2 sporozoite before penetration into an enterocyte; 3 type I schizont with eight merozoites; 3a free merozoite; 4 type II schizont with 4 merozoites; 4a, b free merozoites; 5 microgamont; 5a microgamete; 6 macro-gamont; 7 macrogamete being fertilized by a microgamete; 8 thick-walled oocyst (shed with feces); 9,10 thin-walled oocyst from which sporozoites are released in the host intestine (autoinfection).

Fig. 9.15 1 Infective oocyst; 2 sporozoite before penetration into an enterocyte; 3 type I schizont with eight merozoites; 3a free merozoite; 4 type II schizont with 4 merozoites; 4a, b free merozoites; 5 microgamont; 5a microgamete; 6 macro-gamont; 7 macrogamete being fertilized by a microgamete; 8 thick-walled oocyst (shed with feces); 9,10 thin-walled oocyst from which sporozoites are released in the host intestine (autoinfection).

are also found in other localizations (gallbladder, bile, and pancreatic ducts, esophagus, stomach, large intestine, respiratory tract).

Diagnosis, therapy, and prevention. Cryptosporidium oocysts can be diagnosed in stool smears after staining (e.g., modified Ziehl-Neelsen stain) (Fig. 9.11i, p. 504, Fig. 9.14c, p. 516), or visualization by immunofluorescence using monoclonal antibodies. In addition, coproantigens are detectable by ELISA. The only drug with efficacy against Cryptosporidium is nitazoxanide (see also Giardia).

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