Amoebiasis pathophysiology: Difference between revisions

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==Pathogenesis==
==Pathogenesis==
*Following transmission, ''E. histolytica'' trophozoites inhabit in the large intestine of the human host.
*Following transmission, ''E. histolytica'' trophozoites inhabit in the large intestine of the human host.
*In the large intestine, the trophozoites invades the intestinal mucosa into the bloodstream. Simultaneously, they form resistant cysts that are then excreted in human stools.
*In the large intestine, the trophozoites invades the intestinal mucosa into the bloodstream. Simultaneously, they form resistant cysts in the large intestines that are then excreted in human stools.
*Once in the bloodstream, the trophozoite migrates into the portal circulation and develops amebic liver abscess.
*Once in the bloodstream, the trophozoite migrates into the portal circulation and develops amebic liver abscess.



Revision as of 17:57, 10 March 2016

Amoebiasis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Overview

Transmission

  • E. histolytica cyst is usually transmitted by the fecal-oral route through contaminated drinking water or food)
  • E. histolytica cyst may also be transmitted indirectly through direct contact with infected individuals.

Pathogenesis

  • Following transmission, E. histolytica trophozoites inhabit in the large intestine of the human host.
  • In the large intestine, the trophozoites invades the intestinal mucosa into the bloodstream. Simultaneously, they form resistant cysts in the large intestines that are then excreted in human stools.
  • Once in the bloodstream, the trophozoite migrates into the portal circulation and develops amebic liver abscess.

Invasion of Intestinal Mucosa

  • E. histolytica trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.
  • E. histolytica is

Pathology

Gross Pathology

On gross pathology, the following findings may be present in patients with amebiasis:

  • Wavy surface epithelium (results from focal release of mucin and spasm of the muscular layer)
  • Nodular and/or irregular ulcers in the cecum (most common), sigmoid colon, and rectum. Early ulcers are usually in the interglandular epithelium.
  • Nodular: small (sub-centrimetric), rounded, elevated lesions with necrotic center and edematous rim
  • Irregular: large (1-5 cm), shallow with broad elevated margins

Note: the mucosal folds may occasionally hide small colonic ulcers (false-negative results)

Microscopic Pathology

  • On microscopic pathology, amebiasis is characterized by a flask ulcer (deep, microhemorrhagic ulceration involving the submucosa), which is a characteristic of advanced disease.
  • Additional findings may be present in patients with amebiasis:
  • Interglandular ulceration
  • Hyperemia
  • Thickened mucosa
  • Reactive glandular hyperplasia
  • Stromal edema
  • Infiltration of neutrophils, eosinophils, and macrophages
  • Lymphoid aggregates
  • Detection of amebas on surface exudate
  • Tissue necrosis, usually fibrinoid (advanced lesion)
  • Formation of granulation tissue (advanced lesion)

Gallery

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 "Public Health Image Library (PHIL)".


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