Amebiasis results from infection with the intestinal protozoan Entamoeba histolytica. A recent clarification within the genus Entamoeba has resulted from the use of zymodemes (electrophoretic mobility patterns of parasitic isoenzymes) to distinguish between two morphologically identical species: E. histolytica - usually asymptomatic, but may be pathogenic; and E. dispar - the more prevalent species by 10-fold, but always asymptomatic. Although most patients ( 90%) infected with E. histolytica are asymptomatic, amebiasis in the remaining symptomatic patients ( 10%) accounts for the third most common cause of death from parasitic disease worldwide (following Schistosomiasis and Malaria). About 10% of the world's population is infected by either E. histolytica or E. dispar, resulting in 50 million cases of invasive amebiasis and 100,000 deaths (all due to E. histolytica). The prevalence of E. histolytica and E. dispar in the U.S. is 4%, but it is more common in lower socioeconomic groups, the institutionalized mentally retarded, homosexuals, and some immigrants.
Ingestion of cysts of either E. histolytica or E. dispar is followed by excystation in the small bowel and invasion of the colon by trophozoites. In 90% of patients, trophozoites re-encyst and produce asymptomatic infection. Most asymptomatic carriers terminate infection within 12 months. Invasive disease begins with adherence of E. histolytica to colonic mucins, epithelial cells, and leukocytes; a process mediated by the parasite's galactose-inhibitable adherence lectin. After adherence, trophozoites of E. histolytica invade the colonic epithelium by means of proteolytic enzymes, and produce either nonspecific thickening of the mucosa or the classic flask-shaped amebic ulcers. Trophozoites may ascend the portal veins to produce acellular liver abscesses filled with proteinaceous debris. E. histolytica trophozoites lyse target cells by using its lectin to bind to the target cell's membrane and using the parasite's ionophore-like protein to induce a Na+ , K+ , Ca2+ leak from target cell cytoplasm.
Amebic Colitis often presents with a 1-2 week history of abdominal pain, diarrhea containing blood and mucous, and tenesmus, but fever is often absent. Although endoscopy reveals hemorrhagic ulcers dispersed over a normal-appearing mucosa, fecal leukocytes are absent because of the lytic activity of ameba. Fulminate Colitis presents with severe bloody diarrhea, fever, and diffuse abdominal pain, and has a mortality rate of > 50%. Chronic Amebic Colitis presents with recurrent episodes of dysentery, and can mimic inflammatory bowel disease, or when Ameboma is present, carcinoma. Extraintestinal Amebiasis most often results in liver abscess, but any organ may be involved. Diagnosis of invasive amebiasis depends on the presenting symptoms, detection of antiamebic antibodies, and blood in the stool, a finding that should lead to examination of the stool for trophozoites. E. histolytica ingests red blood cells and stimulates production of antiamebic antibodies. Infection with E. dispar does not result in production of antibodies, and E. dispar does not ingest RBCs.
Prophylaxis: When traveling outside of the U.S., avoid drinking contaminated water, eat only cooked food or self-peeled fruit. Therapy: Invasive colitis or liver abscess: Metronidazole 750 mg PO tid or 500 mg IV q6 hr. X 10 days, followed by Dilozanide furoate 500 mg po tid X 10 days.
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John W. King, M.D / Professor & Program Director / Section of Infectious Diseases
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