Amoebiasis pathophysiology

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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

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.

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.^[1]

E. histolytica trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.^[1]
E. histolytica is also thought to contain glycosidases that cleave glycsolyated mucin molecules, resulting in mucin degradation.^[2]^[3]
Once the mucin layer is degraded, E. histolytica then adheres to plasma membrane of enterocytes and uses lectins, amebapores, and proteases to cause damage by a characteristic "hit and run" phenomenon.^[1]

Lectin: responsible for adhesion of the parasite on Gal-GalNAc residues on enterocytes
Amebapore: Protein that forms channels that induce cytolysis in a process similar to perforin-mediated cytolysis of cytotoxic T-cells
Protrease: Enzymes that metabolize cellular proteins

As the trophozites creates interglandular lesions and degrades the extracellular matrix, it is propelled forward by locomotion.^[1]^[4]^[5]

As the trophozoites invade, IL-8 and TNF-alpha secretion is upregulated, and the host immune cells are activated.^[6]^[7]
Neutrophils migrate to the site of invasion and contribute to the inflammatory damage induced by E. histolytica, but are generally incapable of destroying the organism. The mechanism may which E. histolytica evades neutrophils is unknown.^[6]^[7]^[1]
Once neutrophils are recruited, macrophages and eosinophils are also activated.^[1]

On gross pathology, the following findings may be present in patients with amebiasis:^[1]

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)

On microscopic pathology, amebiasis is characterized by a flask ulcer (deep, microhemorrhagic ulceration involving the submucosa), which is a characteristic of advanced disease.^[1]
Additional findings may be present in patients with amebiasis:^[1]