Cryptosporidia (“hidden-spore”) are small parasites that can infect the intestinal tract of a wide range of mammals, including humans. Like other sporozoan parasites, they are ob-ligate intracellular organisms that exhibit alternating cycles of sexual and asexual repro-duction. As with Toxoplasma, both cycles are completed within the gastrointestinal tract of a single host. Long recognized as an important cause of diarrhea in animals, cryp-tosporidia were not identified as causes of human enteritis until 1976.
Regardless of animal host, all strains of this tiny (2 to 6μm) parasite appear morphologi-cally identical. Although all strains can reasonably be regarded as a single species, the one that infects humans and cattle is often referred to as C. parvum. The organisms ap-pear as small spherical structures arranged in rows along the microvilli of the epithelial cells. They are readily stained with Giemsa and hematoxylin–eosin. Although they remain external to the cytoplasm of the intestinal epithelial cell, they are covered by a double membrane derived from the reflection, fusion, and attenuation of the microvilli, and are thus, by definition, intracellular organisms. Oocysts shed into the intestinal lumen mature to contain four sporozoites; their cell wall provides the unusual property of acid fastness, allowing them to be visualized with stains generally employed for mycobacteria.
Infective oocysts are excreted in the stool of the parasitized animal. Unlike those of Toxo-plasma, cryptosporidia oocysts are fully mature and immediately infective on passage inthe feces. Following ingestion by another animal, sporozoites are released from the oocyst and attach to the microvilli of the small bowel epithelial cells, where they are transformed into trophozoites. These divide asexually by multiple fission (schizogony) to form schizonts containing eight daughter cells known as type 1 merozoites. On release from the schizont, each daughter cell attaches itself to another epithelial cell, where it re-peats the schizogony cycle, producing another generation of type 1 merozoites.
Eventually, schizonts containing four type 2 merozoites are seen. Incapable of continued asexual reproduction, these develop into male (microgamete) and female (macrogamete) sexual forms. Following fertilization, the resulting zygote develops into an oocyst that is shed into the lumen of the bowel. The majority possess a thick protective cell wall that ensures their intact passage in the feces and survival in the external environment.
Approximately 20% fail to develop the thick protective wall. The cell membrane rup-tures, releasing infective sporozoites directly into the intestinal lumen and initiating a new “autoinfective” cycle within the original host. In the normal host, the presence of innate or acquired immunity dampens both the cyclic production of type 1 merozoites and the for-mation of thin-walled oocysts, halting further parasite multiplication and terminating the acute infection. In the immunocompromised, both presumably continue, explaining why such individuals develop severe, persistent infections in the absence of external reinfection.
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