Amebiasis (Amebic dysentery, hepatic amebiasis)
Primary Distribution: World-wide.
Agent and Vector: Entamoeba histolytica (an ameba) is ingested via water or food contaminated with human feces (Centers for Disease Control [CDC], 1999).
Incubation: The incubation period for amebic dysentery is usually 1- 4 weeks, but may be shorter or substantially longer (CDC, 1999).
Clinical Findings and Treatment
Signs and Symptoms: About 90% of infected persons are asymptomatic. There are two basic types of amebiasis: intestinal and extraintestinal disease, which may exist simultaneously. In symptomatic intestinal amebiasis common signs and symptoms are fever, gradual onset of colicky abdominal pain, increased number of stools (often intermittent, > 6 stools/day, usually containing mucous and blood), jaundice, anorexia, weight loss, and tenesmus. Severe infections may have an acute onset and be characterized by severe abdominal pain, frequent and profuse bloody diarrhea (sometimes containing necrotic tissue), more rapid weight loss, and the potential for dehydration. Rarely, a form of chronic amebic colonitis develops which mimics irritable bowel disease. The most common extraintestinal amebiasis is hepatic amebiasis (abscess). Symptoms of hepatic amebiasis include a gradual or acute onset of fever, right upper quadrant pain (sometimes radiating to the right shoulder), hepatomegaly and tenderness, nausea and vomiting, anorexia, weight loss, and malaise. Intercostal tenderness is common. Prompt treatment is necessary to prevent the hepatic abscess from rupturing. Other extraintestinal infections include perianal skin infections and rare metastatic infections to the brain, lungs, and genitalia. (CDC, 1999; Goldsmith, 1999; Weissman & Salata, 2000).
Complications: Untreated patients (in undeveloped areas of the world) may develop megacolon, vomiting, high fever, dehydration and circulatory collapse. Perforation may occur, leading to peritonitis, pericarditis, and pleurisy (Goldsmith, 1999).
Common Laboratory Findings: Multiple fresh stool examinations in optimal conditions will only detect organisms in about 80% of the infections as the trophozoites (immature amebas) rapidly autolyze. If a patient has taken antibiotics, antimalarials, antidarrheals, or mineral oil specimen collection should be delayed for 10-14 days (Goldwater, 1999). Guaic is positive and eosinophilia is often present. In patients with dysentery, WBCs are increased, but not in patients with mild colitis.
Diagnosis: Detection of trophozoites containing digested red blood cells is diagnostic. Endoscopy is used when stools are negative, but suspicion is high. Serology testing is available but is positive only in severe intestinal infections and not mild cases. A positive serum antibody can be a result of both the avirulent Entamoeba. dispar as well as Entamoeba histolytica. The indirect hemagglutination test is sensitive but will not distinguish past from present infections. The agar gel method is less sensitive but will indicate whether infection is present or past.
Differential Diagnosis: Diarrhea: ulcerative colitis, bacillary dysentery, diverticulitis, appendicitis, carcinoma, tuberculosis, irritable bowel syndrome. Hepatic amebiasis: cancer, pyogenic abscess, echinococcal cyst.
Treatment: Tissue amebicides (dehydroemetine, emetine, and metronidazole) act on amebas in the bowel wall but not the lumen. Luminal amebicides (diloxanide furoate, idoquinol, and paromomycin act on amebas in the bowel lumen. Tetracycline inhibits bacterial growth in both the bowel wall and lumen. Metronidazole effects both the bowel wall and lumen but if given alone has a 50% fail rate as it needs a luminal amebicide to augment its action. Asymptomatic patients are treated with iodoquinol 30-40 mg/kg/24 (maximum 650 mg/dose) po tid for 20 days or paromomycin 25-35mg/kg/24 hr po tid for 7 days. Diloxanide furoate is available only from the CDC for treatment of asymptomatic amebiasis. Patients with invasive amebiasis and symptoms are treated with metronidazole 30-50 mg/kg/24 hours (maximum 500-700 mg/dose) po tid for 10 days. This amount of metronidazole often causes severe nausea that can be prevented by taking promethazine one hour prior to dosing. Some experts recommend adding a luminal amebicide such as paromomycin. Patients with hepatic amebiasis are treated with metronidazole 750 mg po tid for 10 days or 500 mg IV every 6 hours for 10 days. Some references recommend diloxanide furoate or iodoquinol, followed by chloroquine (Goldsmith, 1999; Rosenblatt, 1999). Follow up care includes examination of stools at 2-3 day intervals starting at 4 weeks and up to 3 months after the end of treatment.
Notes From the Field: Prevention is essential, and includes hand washing, proper food handling, and boiling questionable water to 55 degrees C. Research on the antiamebic effect of various plants in Africa has shown that swallowing fresh whole papaya seeds can prevent amebiasis. Two tablespoons of fresh papaya seeds twice a week may reduce the incidence of amebiasis. (Sohni, Kaimal, & Bhatt 1995; Tona, Kambu, Ngimbi, Cimanga, & Vlietinck, 1998).
Authors: Amy Roberts, FNP & Charles Kemp, FNP
Centers for Disease Control and Prevention. (1999). Amebiasis infection. Retrieved January 9, 2000, from the World Wide Web: http://www.cdc.gov/ncidod/dpd/amebias.htm.
Goldsmith, R.S. (1999). Infectious diseases: Protozoal and helminthic. In L.M. Tierney, S.J. McPhee, & M.A. Papadakis (Eds.), Current medical diagnosis & treatment (38th ed.) (pp.1356-1361). Stamford Connecticut: Appleton & Lange.
Rosenblatt, J.E. (1999). Antiparasitic agents. Mayo Clinic Proceedings. 74(11), 1161-1175.
Sohni, Y., Kaimal,P., & Bhatt, R. (1995). The antiamoebic effect of a crude drug formulation of herbal extracts against Entamoeba histolytica in vitro and in vivo. Journal of Ethnopharmacology, 19(1), 29-32.
Tona, L., Kambu, K., Ngimbi, N., Cimanga, K., & Vlietinck, A. (1998). Antiamoebic and phytochemical screening of some Congolese medicinal plants. Journal of Ethnopharmacology, 61(1), 57-65.
Weissman, S., & Salata, R. (2000). Amebiasis. In R. Behrman, R. Kliegman, & H. Jenson (Eds.). Nelson textbook of pediatrics (16th ed.) (pp. 1035-1036). Philadelphia: W.B. Saunders Company.