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Cryptosporidiosis - Causes and Pathogenesis
Last reviewed: 04.07.2025
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Causes of cryptosporidiosis
The cause of cryptosporidiosis is coccidia of the genus Cryptosporidium, family Cryptosporidiae, class Sporozoasida, subclass Coccidiasina. The genus Cryptosporidium includes 6 species, of which C. parvum is pathogenic for humans. Cryptosporidia are obligate parasites that infect the microvilli of the mucous membranes of the gastrointestinal tract and respiratory tract of animals and humans.
The life cycle of cryptosporidia occurs in the body of one host, includes the stages of schizogony, merogony, gametogony and sporogony. Cryptosporidia are localized in a parasitiform vacuole formed by intestinal microvilli, therefore the parasite is located intracellularly, but extraplasmically. First-generation merozoites are capable of proliferating in two directions: into first-generation schizonts or second-generation schizonts, therefore the number of parasites increases. Two types of oocysts are formed in the host's body: thick-walled - leaving the host's body with feces. and thin-walled - releasing sporozoites in the intestine, as a result of which autoinfection is possible.
Cryptosporidium oocysts, when preserved in the environment, are capable of invasion for 18 months at a temperature of 4 °C and 1 week at -10 °C. When heated to 72 °C, they die within 1 minute.
Oocysts are resistant to disinfectants, especially those containing chlorine. Due to this, as well as their small size (4-7 µm), which allows them to pass through many filters, it is impossible to purify water from cryptosporidia using modern technologies, therefore the infection spreads by water.
Currently, there is no sufficiently effective drug to which cryptosporidia would be sensitive.
[ Pathogenesis of cryptosporidiosis
The pathogenesis of cryptosporidiosis has not been sufficiently studied. The prevalence of cholera-like profuse watery diarrhea in the clinical picture of the disease suggests the production of enterotoxin, but despite numerous searches, the toxin has not been found in cryptosporidia. Some studies have shown the presence in cryptosporidia of a gene responsible for the production of a protein with hemolytic activity similar to that of E. coli 0157 H7. The most typical localization of the process is the distal parts of the small intestine. After oocysts enter the intestine, increased reproduction of the parasite begins; the resulting merozoites spread and affect a large number of enterocytes, causing degenerative changes in them (villous atrophy). This is accompanied by crypt hypertrophy, mono- and polymorphonuclear infiltration of the basement membrane and leads to the appearance of crater-like depressions on the surface of the epithelium. In severe forms of the disease, total damage to the microvilli occurs.
As a result of massive damage to the microvilli, the absorption of water and electrolytes is disrupted, their secretion through the intestinal wall increases, which is manifested by watery diarrhea. The enzymatic activity of the intestine is disrupted, secondary malabsorption and steatorrhea occur. In patients with severe immunodeficiency, damage to not only the gastrointestinal tract, but also the hepatobiliary system and respiratory tract is possible.
The most important factor determining susceptibility to invasion and severity of cryptosporidiosis is the state of immunity. The role of humoral immunity has been proven, but the most important is the impairment of T-cell function.