Amoebic infections

Two very different groups of amoebic species infect humans. (1) Obligate anaerobic gut parasites—including the major pathogen Entamoeba histolytica, Dientamoeba fragilis (which causes relatively mild colonic involvement with diarrhoea), and eight non-pathogenic species including Entamoeba dispar. (2) Aerobic free-living, water and soil amoebae—these can become facultative tissue parasites in humans after cysts or trophozoites are inhaled, ingested, or enter damaged skin or mucosae.

Entamoeba histolytica infection

The term amoebiasis (when unqualified) generally refers to E. histolytica infection, which is common in Mexico, South America, Natal, the west coast of Africa, and South-East Asia; nearly all amoebic disease seen in temperate countries is acquired elsewhere. Transmission is by the faecal–oral route; following ingestion of infective cysts, a population of trophozoites becomes established in the caecum and proximal colon.

Clinical features—clinical features range from minimal changes in bowel habit to severe dysentery. Onset is usually gradual or intermittent, with initially mild constitutional upset, colicky abdominal pain, and foul-smelling stools that always contain visible or occult blood. Less typical presentations of amoebic colitis include (1) fulminant; (2) amoebic colitis without dysentery; (3) amoeboma—presenting as an abdominal mass, most frequently in the right iliac fossa; (4) localized perforation and amoebic appendicitis; (5) rectal bleeding. The most significant complication is hepatic amoebiasis.

Diagnosis, treatment, and prognosis—examination of dysenteric stool, bowel-wall scrapings, liver abscess aspirate, or other samples in temporary wet mounts is critical, with identification of live erythrocytophagous trophozoites confirming the diagnosis of invasive amoebic disease. Other diagnostic methods include (1) demonstration of amoebal DNA in faeces/tissues by PCR; (2) serology—but seropositivity does not distinguish current and past tissue invasion. Aside from supportive care, metronidazole for 5 days is usually the first-choice treatment, with the addition of diloxanide to eliminate infection from the bowel and so prevent recurrence of tissue invasion or transmission to others. Uncomplicated invasive intestinal disease (and uncomplicated hepatic amoebiasis) should have mortality less than 1%, but this may reach 40% for amoebic peritonitis with multiple gut perforation.

Hepatic amoebiasis—less than 50% of patients give any convincing history of dysentery and few have concurrent dysentery. Presentation is typically with fever, sweating, liver or diaphragmatic pain, weight loss, and tender hepatomegaly. Diagnosis is usually achieved by demonstration of a (most often solitary) liver abscess on ultrasonography or CT and positive serological testing, with a therapeutic amoebicide trial generally being preferable to diagnostic needling of the liver.

Prevention—simple hygienic measures and health education provide considerable protection: boiling water for 5 min kills cysts. Travellers to endemic areas may need a medical check on their return; but chemoprophylaxis is not appropriate.

Free-living amoebae

Three genera of free-living amoebae, Naegleria, Acanthamoeba, and Balamuthia, cause human disease. Naegleria causes a primary meningoencephalitis after bathing or diving in fresh water; amphotericin B is an effective drug, but most cases are fatal, partly because of diagnostic delays. Acanthamoeba causes a painful keratitis, mainly in contact lens users, which usually responds to intensive local amoebicides, although corneal grafting may be needed; it also causes a highly fatal granulomatous encephalitis in immunocompromised patients. Balamuthia causes an encephalitis similar to that of Acanthamoeba in both immunocompromised and immunocompetent individuals; primary skin or facial lesions are common.