Cyclosporiasis pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
''''C. cayetanensis'' infects epithelial cells of the small intestine, especially those of the jejunum. | |||
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Nine patients with gastrointestinal illness caused by CLBs (now called Cyclospora) in Nepal were examined endo- scopically. They had histological evidence of small bowel in- jury. Five had moderate to marked erythema of the distal duodenum. Oocysts were observed in the duodenal aspirates. All patients had mild to moderate acute inflammation of the lamina propria, and neutrophils were observed in 5 of 9 cases. Additionally, diffuse chronic inflammation of mild to moderate degree was present in all samples. An increase of plasma cells in the lamina propria was also observed (44). Histopathologi- cal alterations of the epithelial tissue included focal vacuoliza- tion at the tips of the villi of the surface epithelium, loss of the brush border, and alteration of cells from a columnar to cuboid shape. The architecture of the tissues showed mild to moder- ately severe partial villous atrophy and crypt hyperplasia, char- acterized by shortened blunted villi and increased crypt length and mitosis. Interestingly, no parasitic vacuoles were observed in any of the biopsy sections examined (44). In 1996, Deluol et al. (52) described supranuclear intracytoplasmic vacuoles with 6 to 8 comma-shaped structures (merozoites) in a patient with Cyclospora infection (Fig. 1). The same year, Sun et al. (178) described the presence of multiple parasitic vacuoles containing asexual-stage Cyclospora organisms in intestinal bi- opsies of an HIV-positive patient who had just returned from the Dominican Republic. This patient had a low CD4 cell count (224 cells/l) and presented with chronic inflammation of the duodenum and stomach. Organisms were present in the supranuclear location of the mucosal villi and absent in the crypts. Histological examination of biopsies of the stomach, rectum, and transverse and sigmoid colon did not reveal any organisms. In 1997, Ortega et al. (140) demonstrated the pres- ence of sexual-stage coccidian organisms in 17 patients with Cyclospora infection. The presence of sexual and asexual stages in the same host is suggestive that the life cycle can be com- pleted within one host. Two types of meronts, the asexual stages, were observed. Type I had 8 to 12 merozoites, each measuring about 0.5 by 3 to 4 m. Type II meronts had 4 merozoites, measuring 0.7 to 0.8 by 12 to 15 m. Biopsies of these patients showed diffuse edema and infiltration of the | |||
villous mucosa by mixed inflammatory cells. Plasma cells and lymphocytes were notoriously present, and eosinophils were also numerous in 4 of 17 cases. | villous mucosa by mixed inflammatory cells. Plasma cells and lymphocytes were notoriously present, and eosinophils were also numerous in 4 of 17 cases. | ||
Revision as of 18:35, 18 September 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Fresh produce and water can serve as vehicles for transmission and the sporulated oocysts are ingested (in contaminated food or water). The oocysts excyst in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine.
Pathogenesis
Life Cycle
Unsporulated oocysts of Cyclospora cayetanensis are excreted from infected persons. When freshly passed in stool, the oocyst is not infective (thus, direct fecal-oral transmission cannot occur, which differentiates Cyclospora from another important coccidian parasite, Cryptosporidium). Under adequate temperatures (23-32ºC), these take about 7-15 days to sporulate, in order to become infectious. After being ingested, from contaminated water and food, oocysts excyst to release elongated sporozoites. Sporozoites will then infect epithelial cells of the gastrointestinal tract, particularly those of the duodenum and jejunum. The sporozoites undergo asexual reproduction, originating meronts type I and II, which will then differentiate into gametocytes. These last will be fertilized to produce a zygote.[1][2] Inside the cells, zygotes undergo asexual multiplication and sexual development to mature into oocysts, which will be shed in stool.[3]
C. cayetanensis oocysts have also been isolated from non gastrointestinal sites, namely from sputum of immunocompromised patients with HIV and concomitant TB. This leads to hypothesis that C. cayetanensis may be an opportunistic pathogen.[4]
Transmission
The protozoan lives out its lifecycle intracellularly within the host’s epithelial cells and gastrointestinal tract. Infection is transmitted through the oral-fecal route, and begins when a person ingests oocysts in fecally contaminated food or water.
- Fresh produce and water can serve as vehicles for transmission and the sporulated oocysts are ingested (in contaminated food or water).
Microscopic Pathology
''C. cayetanensis infects epithelial cells of the small intestine, especially those of the jejunum.
References
- ↑ Eberhard ML, Ortega YR, Hanes DE, Nace EK, Do RQ, Robl MG; et al. (2000). "Attempts to establish experimental Cyclospora cayetanensis infection in laboratory animals". J Parasitol. 86 (3): 577–82. doi:10.1645/0022-3395(2000)086[0577:ATEECC]2.0.CO;2. PMID 10864257.
- ↑ Ortega YR, Sanchez R (2010). "Update on Cyclospora cayetanensis, a food-borne and waterborne parasite". Clin Microbiol Rev. 23 (1): 218–34. doi:10.1128/CMR.00026-09. PMC 2806662. PMID 20065331.
- ↑ 3.0 3.1 "Cyclosporiasis".
- ↑ Di Gliullo AB, Cribari MS, Bava AJ, Cicconetti JS, Collazos R (2000). "Cyclospora cayetanensis in sputum and stool samples". Rev Inst Med Trop Sao Paulo. 42 (2): 115–7. PMID 10810327.