Cyclosporiasis pathophysiology: Difference between revisions

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*Absence of [[parasitic]] vacuoles in biopsied samples
*Absence of [[parasitic]] vacuoles in biopsied samples


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[[Immunocompromised]] patients are more prone to develop chronic inflammation of the epithelium of gastrointestinal tract.
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 completed 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.
 
In 1999, Connor et al. (42) described additional lesions in three patients with cyclosporiasis. They reported an accumu- lation of myelin-like material (MLM) between the base and sides of the enterocytes. In one of the cases, these dense MLM appeared later in the infection, suggesting an ongoing inflam- matory or immunologic process.  
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==References ==
==References ==

Revision as of 19:00, 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]

Life cycle of Cyclosporiasis- Center for Disease Control and Prevention(CDC)[3]

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. Infected patients showed evidence of intestinal injury on endoscopy, such as erythema of the mucosa.

Histologic samples of small bowel of these patients showed affection of the lamina propria, with moderate inflammation of this region, and neutrophils in some cases. All studied patients had evidence of chronic inflammation, with identification of plasma cells in the mucosa.[5]

The infected epithelial cells of the gastrointestinal tissue include the following alterations:[5]

  • Shortened villi
  • Increased length of crypts and increased mitosis
  • Absence of parasitic vacuoles in biopsied samples

Immunocompromised patients are more prone to develop chronic inflammation of the epithelium of gastrointestinal tract.

References

  1. 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.
  2. 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. 3.0 3.1 "Cyclosporiasis".
  4. 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.
  5. 5.0 5.1 Connor BA, Shlim DR, Scholes JV, Rayburn JL, Reidy J, Rajah R (1993). "Pathologic changes in the small bowel in nine patients with diarrhea associated with a coccidia-like body". Ann Intern Med. 119 (5): 377–82. PMID 8338291.

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