Cryptosporidiosis is an infectious disease caused by a Cryptosporidium called Cryptosporidium parvum, and its specific etiology and mechanism of action are described as follows.
1. Etiology
Cryptosporidium is a parasitic protozoan that grows intracellularly, belonging to the class Sporozoa, subclass Eucoccidia, order Eimeriida, suborder Eimeriina, family Cryptosporidiidae, genus Cryptosporidium. The body is spherical, with a diameter of 2-4 μm. Its life cycle is similar to that of other protozoa in the class Sporozoa, including asexual schizogamy, sexual reproduction, and sporogony, all of which occur within the same host. The oocysts are oval, with a diameter of 2-6 μm, with smooth walls. The mature oocysts contain 4 crescent-shaped sporozoites. When ingested by humans or animals, the oocysts are released in the small intestine, and the sporozoites escape from the cracks in the oocyst wall and attach to the microvillus brush along the intestinal epithelial cells, being enclosed in parasitophorous vacuoles for development into trophozoites for asexual reproduction. Initially, they develop into trophozoites containing 8 small nuclei, and then further develop into the 1st type schizonts containing 8 schizonts. After the schizonts mature and rupture, the schizonts re-infect other intestinal epithelial cells, continuing the 1st type schizogamy or developing into the 2nd type schizonts containing only 4 schizonts. The schizonts of the mature 2nd type release schizonts that differentiate and develop into female (large) and male (small) gametocytes, which then produce female and male gametes, respectively. Finally, the male and female gametes combine to form zygotes, which develop into oocysts.
Oocysts have thin-walled and thick-walled types, with the former accounting for about 20%, which have weak resistance to the external environment. After the sporozoites escape, they directly侵入 new host cells to continue asexual reproduction, causing repeated infections in the host body. The thick-walled oocysts sporulate within the host, with a double-layered wall that is highly resistant to the external environment. After being excreted out of the body with feces, they become infectious. They can be inactivated with 10% formalin solution or 5% ammonia water, and their infectivity can also be lost after being treated at 65°C for 30 minutes.
It is currently believed that there are at least 6 species of Cryptosporidium, and infections in humans and mammals are almost always caused by Cryptosporidium parvum.
2. Pathogenesis
The exact pathogenesis of this disease is not yet fully understood. Most people believe that it may be due to widespread damage to the intestinal mucosal epithelial cells and villous atrophy, leading to malabsorption.
Cryptosporidium causes pathogenic changes in humans and animals that are basically similar, with lesions mainly occurring in the small intestine and colon, while the stomach and esophagus may also be involved. The villi in the lesion sites of the small intestine atrophy and become shorter, even disappearing, while the crypt epithelial cells proliferate and the crypts become significantly deeper. The epithelial cells on the mucosal surface are short columnar, with irregularly arranged nuclei. Mononuclear cells and multinucleated inflammatory cells can be seen in the villous epithelium and lamina propria. The pathological changes in the colon mucosa are similar to those in the small intestine. After recovery, the above lesions can return to normal. When the infection extends to the gallbladder, it can cause acute and necrotizing cholecystitis, with thickening and hardening of the gallbladder wall, flattening of the mucosal surface, and the possibility of ulcers. Under the microscope, necrosis of the gallbladder wall and infiltration by multinucleated cells can be observed. In the lung biopsy samples of patients with Cryptosporidium infection in the lungs, lesions such as active bronchitis and focal interstitial pneumonia can be seen.