Cryptosporidiosis is an infectious disease caused by a protozoan called Cryptosporidium parvum, and its specific causes and mechanisms of action are described as follows.
1Causes of Disease
Cryptosporidium is a parasitic protozoan that grows intracellularly, belonging to the sporozoan class, coccidia subclass, Eimeriida order, Eimeriina subclass, Cryptosporidiidae family, Cryptosporidium genus. The body is spherical, with a diameter of2～4μm, with a life cycle similar to that of other protozoa in the sporozoan class, including asexual merogony, sexual reproduction, and sporogony, all of which occur within the same host. The oocysts are oval-shaped, with a diameter of2～6μm, the oocyst wall is smooth, and the mature oocyst contains4新月形子孢子。When eaten by humans or animals, the sporozoites are excreted from the oocyst wall through the gaps, attach to the microvillus brush along the small intestinal epithelial cells, and are enclosed in the parasitophorous vacuole for development into trophozoites for asexual reproduction. Initially, they develop into trophozoites containing8small nuclei, which then further develop into trophozoites with8of the first type of meronts. After the meronts mature and rupture, the sporozoites re-enter other small intestinal epithelial cells, continuing the first type of meront reproduction or developing into trophozoites containing only4of the second type of meronts. The sporozoites released from mature second type meronts then differentiate and develop into male and female gametocytes, which produce male and female gametes, and finally, the male and female gametes combine to form zygotes and develop into oocysts.
The oocysts have thin-walled and thick-walled types, with the former accounting for20％，has 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 body, with a double-layered wall that is resistant to the external environment. After being excreted in feces, they become infectious.10％ formaldehyde solution or5％ ammonia water can inactivate it, after65℃30min can also cause the infectivity of oocysts to be lost.
It is currently believed that at least6Cryptosporidium infections in humans and mammals are almost always caused by Cryptosporidium parvum.
2Pathogenesis
The exact pathogenesis of the 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.
The pathogenic changes caused by Cryptosporidium in human and animal bodies are basically similar, mainly affecting the small intestine and colon, with the stomach and esophagus also potentially involved. The villi in the lesion site of the small intestine atrophy and become shorter or even disappear, while the crypt epithelial cells proliferate simultaneously and the crypts become significantly deeper. The surface epithelial cells of the mucosa appear as short cylindrical, with irregularly arranged nuclei. Mononuclear cells and multinucleated inflammatory cells can be seen in the epithelial layer and the lamina propria. The pathological changes of the colon mucosa are similar to those of the small intestine. After recovery, the above lesions can return to normal. When the infection extends to the gallbladder, it can cause acute and necrotic 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 can be seen with infiltration of multinucleated cells. In the lung biopsy samples of patients with Cryptosporidium infection in the lungs, lesions such as active bronchitis and focal interstitial pneumonia can be observed.
