THE MERCK VETERINARY MANUAL
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Overview of Amebiasis

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Amebiasis is an acute or chronic colitis, characterized by persistent diarrhea or dysentery, that is prevalent in tropical and subtropical areas worldwide. Its prevalence has declined in the USA over the past several decades, but the disease is still important in many tropical areas, particularly in times of disasters. It is common in people and nonhuman primates, sometimes seen in dogs and cats, and rare in other mammals. Several species of amebae are found in mammals, but the only known pathogen is Entamoeba histolytica. People are the natural host for this species and the usual source of infection for domestic animals. Mammals become infected by ingesting food or water contaminated with feces containing infective cysts. E dispar is a noninvasive, nonpathogenic ameba that is molecularly distinct but morphologically indistinguishable from the pathogenic species E histolytica. E invadens of reptiles is also morphologically identical to E histolytica, but it is not transmissible to mammals.

E histolytica is a pathogen with variable virulence. It lives in the lumen of the large intestine and cecum and may produce no obvious clinical signs, or it may invade the intestinal mucosa and produce mild to severe, ulcerative, hemorrhagic colitis. In acute disease, fulminating dysentery may develop, which may be fatal, progress to chronicity, or resolve spontaneously. Chronic cases may show weight loss, anorexia, tenesmus, and chronic diarrhea or dysentery, which may be continual or intermittent. In addition to the colon and cecum, amebae may invade perianal skin, genitalia, liver, brain, lungs, kidneys, and other organs. Signs may resemble those of other colonic diseases (eg, trichuriasis, balantidiasis). Invasive amebiasis is exacerbated by immunosuppression.

Definitive diagnosis depends on finding E histolytica trophozoites or cysts in feces. Trophozoites are best seen in direct saline smears or in stained sections of affected colonic tissue. These parasites are difficult to find, because many animals with extraintestinal amebiasis have no concurrent intestinal infection. Colonoscopy with scraping or biopsy of ulcerations is more effective than fecal examination in diagnosing amebic colitis. In intestinal infections, repeated examinations may be necessary, because parasites may be passed periodically in the feces.

Trophozoites range in size from 10 to 60 μm but usually are >20 μm in diameter, have a single vesicular nucleus (usually with a central karyosome), are motile, and may contain ingested RBCs. Feces should be examined promptly, because the trophozoites die quickly once outside the body. Fecal leukocytes may be mistaken for amebae, so fixed and stained fecal smears (iodine, trichrome, iron hematoxylin, or periodic acid-Schiff reaction) may be necessary for identification.

Cysts range from 10 to 20 μm in diameter; the usual size is 12–15 μm. Mature cysts have four nuclei, whereas immature cysts may have one or two. In primates, the cysts may be recovered and identified on zinc sulfate flotations or in fixed and stained preparations (iodine, trichrome, or iron hematoxylin); however, E histolytica cysts are seldom, if ever, excreted by dogs or cats. An ELISA-based antigen test, available for diagnosis in people, may also aid diagnosis in other mammals. Immunostaining may also be useful.

Scant information on treatment in animals is available. Metronidazole (10–25 mg/kg, PO, bid for 1 wk) or furazolidone (2–4 mg/kg, PO, tid for 1 wk) has been suggested. Dogs may continue to shed trophozoites after therapy. Treatment recommendations for people are available from the Centers for Disease Control and Prevention website (http://www.dpd.cdc.gov/dpdx/HTML/Amebiasis.htm). For asymptomatic infections in people, the CDC lists iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the USA) as drugs of choice, and for symptomatic intestinal disease or extraintestinal infections in people (eg, hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate.

Last full review/revision July 2013 by Sharon Patton, MS, PhD

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