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Cryptosporidium species are tiny (2–6 μm), obligate intracellular parasites related to other coccidian protozoan, including Toxoplasma, Cyclospora, Isospora, Plasmodium, Eimeria, and Sarcocystis.Cryptosporidium species primarily infect the gastrointestinal tract of a variety of vertebrate hosts, including humans.1 Host range is largely a function of species, as a given species of parasite most efficiently maintains infection within a few species of hosts.

Over 20 species of Cryptosporidium have been described, but there is some debate as to the exact number of species.2 Two species, C hominis and C parvum, account for nearly all of the disease caused by Cryptosporidium species in humans and are the species of public health significance. C parvum was formerly divided into two genotypes (genotypes I and II), but current classification separates genotype I into a separate species known as C hominis.3 This distinction is important, as humans are essentially the only known reservoir of C hominis, and the species is more efficient at causing disease in humans. Furthermore, studies that distinguish between the two species in cohorts of infected patients generally find a higher prevalence of C hominis; however, the exact prevalence of either species depends on the principal mode of spread (human-to-human vs. zoonotic), sanitation, and living conditions.6-10

Cryptosporidium completes its life cycle within a single host1,11(Fig. 345-1). Infection occurs after ingesting the sporulated, thick-walled oocysts. Excystation occurs in the small intestine after exposure to bile salts and pancreatic enzymes, releasing four sporozoites. These sporozoites penetrate a surface epithelial cell in the intestinal mucosa and form an intracellular parasitophorous vacuole. They then differentiate into uninuclear trophozoites, which undergo asexual replication (merogony) to form type I meronts. The type I meront can then autoinfect other surface epithelial cells or differentiate into a type II meront. The type II meront then undergoes gametogomy, producing both microgametocytes and macrogametocytes. These gametocytes fertilize to produce oocysts. The life cycle is complete when the oocysts undergo sporogomy, resulting in infectious sporozoites within the oocysts. Approximately 80% of the oocysts produced in this fashion are environmentally resistant, thick-walled cysts that are excreted in the feces. The remaining 20% are thin-walled cysts that undergo another autoinfective stage. The autoinfectious stages are important features in the parasite’s life cycle and accounts for persistent and occasionally severe disease, even when a low inoculum of cysts are ingested.

Figure 345-1.

Cryptosporidium life cycle. The infectious sporulated oocyst is ingested by a susceptible host. Exposure to digestive enzymes and bile salts releases four motile sporozoites that immediately attach and invade adjacent epithelial cells. The sporozoites develop in a parasitophorous vacuole that is intracellular but extracytoplasmic; there, they form trophozoites that differentiate through nuclear division into schizonts. Type I schizonts contain 6 to 8 nuclei that mature into 6 to 8 merozoites, which then infect neighboring cells and continue the asexual multiplication cycle or ...

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