Amebiasis (Entamoeba histolytica)

Amebiasis is caused by Entamoeba histolytica, a pathogenic protozoan that must be distinguished from morphologically identical but non-pathogenic Entamoeba dispar and Entamoeba moshkovskii. The life cycle alternates between infective cyst (4-nucleated, resistant to environmental conditions and chlorinated water) and invasive trophozoite (motile, contains ingested erythrocytes pathognomonically). Transmission is fecal-oral via contaminated food/water, person-to-person (especially in MSM), or vertical, with global distribution but highest endemicity in tropical/subtropical regions (Mexico, India, Africa, Central/South America).

Pathogenesis involves cyst ingestion, excystation in small intestine, colonization of large intestine by trophozoites, and in 10% invasive disease through colonic epithelial penetration via Gal/GalNAc lectin adhesion, amebapore-mediated cytolysis, and cysteine proteinases. Clinical syndromes include asymptomatic intestinal infection (90%), amebic colitis (gradual bloody diarrhea over 1-3 weeks, abdominal pain, weight loss, can mimic IBD), fulminant amebic colitis with toxic megacolon (rare, high mortality), and extraintestinal disease — most commonly amebic liver abscess (90% of extraintestinal cases, right lobe predominance, single 'anchovy paste' abscess), pleuropulmonary, brain, peritoneal.

Diagnosis includes stool ova and parasites (low sensitivity, cannot distinguish E. histolytica from E. dispar), stool antigen detection (TechLab E. histolytica II), PCR (gold standard for species discrimination), serology (positive in 90% of invasive disease, ELISA IgG, useful for amebic liver abscess), and imaging (US for liver abscess - hypoechoic right lobe lesion). Colonoscopy with biopsy shows flask-shaped ulcers with trophozoites containing ingested RBCs.