18.7
Amebiasis is a gastrointestinal infection caused by the protozoan Entamoeba histolytica.
It is typically transmitted through the fecal-oral route by ingestion of cysts present in contaminated food or water.
After ingestion, the cysts release trophozoites in the intestine, where they adhere to colonic epithelial cells using a galactose-N-acetylgalactosamine lectin.
This adherence induces epithelial cell death through cytolysis and apoptosis. It also triggers the release of interleukin-1α and the precursor interleukin-1β.
Interleukin-1β then activates NF-κB in nearby cells, promoting the production of other cytokines that attract neutrophils and macrophages.
Trophozoites can directly damage neutrophils, causing additional epithelial injury and mediator release.
In response, macrophages release tumor necrosis factor alpha, which amplifies inflammation and tissue damage.
The resulting pathology includes mucosal inflammation, ulceration, and tissue necrosis.
These pathological changes can lead to symptoms such as abdominal pain, diarrhea, and, in severe cases, dysentery.
Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.
Etiology and Transmission
The infective cyst stage of E. histolytica is transmitted via the fecal–oral route, primarily through ingestion of contaminated water or food. Once ingested, cysts excyst and release trophozoites, which adhere to colonic epithelial cells through a specific galactose‑N‑acetylgalactosamine (Gal/GalNAc) lectin. This adherence triggers epithelial cytolysis and apoptosis, followed by the release of IL‑1α and pro‑IL‑1β. Activated IL‑1β incites NF‑κB signaling in surrounding intestinal cells, promoting expression of inflammatory mediators, including COX‑2 and IL‑8. Concurrently, cysteine proteinases from the trophozoites convert pro‑IL‑1β to its active form, amplifying the inflammatory cascade.
Pathophysiological Responses
The ensuing inflammatory milieu recruits neutrophils and macrophages. Neutrophils subjected to trophozoite assault exacerbate epithelial injury, while macrophages contribute additional cytokines like TNF‑α. Histopathologically, this process manifests as mucosal inflammation, thickening, ulceration, and necrosis, with potential progression to perforation. Cysteine proteinases also facilitate immune evasion by cleaving and inactivating complement components (C3a, C5a) and immunoglobulins (IgA, IgG). Trophozoites may disseminate hematogenously, with a predilection for hepatic colonization, culminating in abscess formation and tissue necrosis. Some trophozoites can also differentiate back into cysts, which are shed in feces and can infect new hosts, completing the life cycle.
Epidemiological and Demographic Aspects
Globally, E. histolytica remains the third leading cause of death among parasitic infections. Risk factors for complicated disease include pregnancy, corticosteroid therapy, malignancy, malnutrition, and alcoholism. Notably, amebic liver abscesses occur predominantly in middle‑aged males, while certain behavioral factors—such as oral‑anal sexual practices among men who have sex with men—are associated with increased transmission risk.
Amebiasis is a gastrointestinal infection caused by the protozoan Entamoeba histolytica.
It is typically transmitted through the fecal-oral route by ingestion of cysts present in contaminated food or water.
After ingestion, the cysts release trophozoites in the intestine, where they adhere to colonic epithelial cells using a galactose-N-acetylgalactosamine lectin.
This adherence induces epithelial cell death through cytolysis and apoptosis. It also triggers the release of interleukin-1α and the precursor interleukin-1β.
Interleukin-1β then activates NF-κB in nearby cells, promoting the production of other cytokines that attract neutrophils and macrophages.
Trophozoites can directly damage neutrophils, causing additional epithelial injury and mediator release.
In response, macrophages release tumor necrosis factor alpha, which amplifies inflammation and tissue damage.
The resulting pathology includes mucosal inflammation, ulceration, and tissue necrosis.
These pathological changes can lead to symptoms such as abdominal pain, diarrhea, and, in severe cases, dysentery.
From Chapter 18:
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