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What Causes Intestinal Cryptosporidiosis?

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Cryptosporidiosis is a type of gastroenteritis caused by a zoonotic enteric parasite of the genus Cryptosporidium. The disease is typically characterized by acute diarrhea that is self-limited in immunocompetent individuals. In immunocompromised persons such as those with HIV/AIDS it can become chronic. In such individuals, it may be linked to life-threatening complications caused by massive fluid loss and subsequent dehydration.

Species of the genus Cryptosporidium have been found to infect mammals, reptiles, amphibians, birds and fish. Two species that most commonly affect humans are Cryptosporidium hominis (essentially limited to humans) and Cryptosporidium parvum (wide range of hosts, including domestic livestock species of animals).

Taxonomic and Genetic Characteristics of Cryptosporidium

The first Cryptosporidium was described by an American parasitologist and physician Ernest Edward Tyzzer in 1907, when he discovered Cryptosporidium muris in the gastric glands of laboratory mice. Two years later he described Cryptosporidium parvum, but it was only in the 1970s that Cryptosporidium was determined to be a prominent cause of intestinal disease in humans.

The genus Cryptosporidium is one of over 300 genera in the phylum Apicomplexa, which includes other significant parasitic protists and human pathogens such as Plasmodium, Isospora, Cyclospora, Toxoplasma and Babesia. All members of the genus Cryptosporidium are intracellular parasites with specific biological and morphological features.

There are more than twenty species and sixty genotypes of Cryptosporidium described to date. These have been classified according to their genetic diversity. Sequence variations in the non-repeat regions are employed to separate different subtype families. More pronounced genetic diversity is usually observed in developing countries, most notably in rural settings.

Life Cycle of the Parasite

The primary site of infection with Cryptosporidium hominis and Cryptosporidium parvum is the small intestine. Like other members of the phylum Apicomplexa, Cryptosporidium undergoes a complex life cycle that has asexual and sexual stages, but also invasive stages with the characteristic apical complex (from which the name of the whole phylum is derived).

The sporulated oocyst (which is the only documented exogenous stage) is excreted from the body of an infected host in the feces. This oocyst is composed of a robust trilaminar wall that surrounds and preserves the viability of four internal sporozoites under unfavorable environmental conditions. These sporozoites ultimately represent the source of new infection.

After ingestion, the sporozoites are liberated from the oocysts, so they can attach to the lining of the intestine in order to invade intestinal epithelial cells. The cells then engulf the parasites into a parasitophorous vacuole where they enlarge to form the trophozoites.

Asexual multiplication known as merogony (or schizogony) occurs when the trophozoite nucleus divides. As a result, type I meronts are formed, within which six or eight merozoites bud off from the residual body that is located next to the parasite-host cell junction. These merozoites are motile and they reattach to epithelial cells of the intestine. Here they may continue the asexual cycle or may undergo sexual multiplication that results in type II meronts.

The type II meronts can further differentiate into microgamonts and macrogamonts. Flagellum-free microgametes found in the microgamont can exit from this structure and fertilize an adjoining macrogamont, forming the only diploid stage in the cryptosporidial life cycle – the zygote.

The zygote further develops into two different types of oocysts: the thick-walled oocyst (commonly excreted from the host) and the thin-walled oocyst (primarily involved in autoinfection). Oocysts are infective upon excretion, therefore permitting direct and immediate fecal-oral transmission, when this life cycle can be reiterated.

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