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INTRODUCTION

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. Host range is largely a function of species, as a given species of parasite most efficiently maintains infection within a few species of hosts.

PATHOGENESIS AND EPIDEMIOLOGY

Cryptosporidium completes its life cycle within a single host (Fig. 340-1). Infection occurs after ingesting the sporulated, thick-walled oocysts. Excystation occurs in the small intestine after exposure to bile salts and pancreatic enzymes, releasing 4 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 account for persistent and occasionally severe disease, even when a low inoculum of cysts is ingested.

Figure 340-1

Cryptosporidium life cycle. (Reproduced with permission from Smith HV, Nichols RA, Grimason AM: Cryptosporidium excystation and invasion: getting to the guts of the matter, Trends Parasitol. 2005 Mar;21(3):133-142.)

The principal mode of transmission is fecal-oral, through either a waterborne or person-to-person route. The median infectious dose has been estimated at 132 oocysts, although disease can occur with ingestion of as few as 10 oocysts. Infectious dose tends to be lower with Cryptosporidium hominis. Infected individuals may shed oocysts for up to 5 weeks after an acute diarrheal episode.

In the immunocompetent host, Cryptosporidium primarily infects the proximal small bowel. The exact mechanism whereby Cryptosporidium causes diarrhea is unknown. The organism disrupts epithelial tight junctions in several in vitro epithelial cell models, resulting in a loss of barrier function. Pathologic findings include loss of intestinal epithelium, villous atrophy with loss of epithelial architecture and surface area, and infiltration of the lamina propria with mononuclear and polymorphonuclear cells. Various stages of the parasite can be seen immediately below the brush border of epithelial cells in biopsy samples.

The mechanisms of recovery and immunity to cryptosporidiosis has not been fully elucidated. An intact cell-mediated immune system with CD4 lymphocytes and interferon is crucial for recovery from disease. Animal models support a pivotal ...

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