Amebiasis A06.9

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 18.07.2022

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Acanthamöbiasis; Amebiasis; Amoeba dysentery; Amoebiasis

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Löch, 1875; Osler, 1890; Councilman and Lafleur, 1891; Walker and Sellards, 1913; Brumpt, 1925; Diamond and Clark, 1993

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Infection with pathogenic amoebae. Within the genus Entamoebia, Entamoeba histolytica is the most important pathogenic form. Infection by swallowing the cyst forms of the pathogen with drinking water or from food. The genus Acanthamoeba causes mainly opportunistic infections.

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Acanthamoebae as well as 3 other amoebae genera (Naegleria, Balamuthia, Sappinia) are among the free-living amoebae responsible for opportunistic and non-opportunistic infections. Entry points are skin and upper respiratory tract.

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Apathogenic amoebiasis: no health problems.

Pathogenic amoebiasis (acanthamoebiasis):

  • Cysts or minute forms: No significant health problems.
  • Magnaforms: adherence to colonic mucosa. By proteolytic and cytolytic properties penetration into the intestinal mucosa. Caused diseases:
    • Amoebecolitis (invasive intestinal amoebiasis, amoebic dysentery)
    • amoebic liver abscess
    • Amoeboma.

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Worldwide prevalence: approx. 50 million people worldwide contract invasive amebiasis annually, up to 100,000 deaths annually (WHO, 1997).

Occurrence: predominantly in warm countries with low hygienic standards, autochthonous infections in temperate zones are rather rare (e.g. sewer workers). In Central Europe, about 1% of the population has an asymptomatic intestinal infection.

Frequent occurrence in male homosexuals (oral-anal contact, rectal lavage). In this population, the incidence is about 20%!

The species of the aquatic and soil-dwelling genus Acanthomoeba play a role in immunocompromised individuals as triggers of granulomatous amoebic encephalitis and chronic granulomatous dermatitis.

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Faecal-oral uptake of cysts with contaminated food; release of smaller, vegetative forms, so-called minuta forms (trophozoites) from cysts in the intestine. Trophozoites multiply by bifurcation and form cysts which are excreted with the stool in a mature, quadrenuclear state. When trophozoites penetrate the intestinal wall and phagocytise erythrocytes, they become so-called magnaforms.

Clinical features
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Cutaneous amoebiasis: Cutaneous abscesses, ulcerations, fistulas or gangrenous inflammation of the skin and subcutis are present, mostly secondary to active amoebic colitis or amoebic liver abscess. Affected are mainly the perianal and genital region, buttocks, chest region and abdominal wall. Occasionally, there is a presence of sooted papules or extensive aggregated sooted papules/plaques which resemble condylomata acuminata, but in which the entamoeba (or acanthamoeba species) can be detected histologically without doubt. The occurrence of Purpura Schönlein-Henoch in patients with amoebiasis is described on the basis of individual case reports. Localised or also disseminated granulomatous cutaneous infections caused by Acanthamoeba spp. are mainly observed as opportunistic infections (especially in HIV-infected persons). Predilection sites are the face, trunk and extremities.

Amoebecolitis (invasive intestinal amoebiasis, amoebic dysentery): abdominal pain, fever, "raspberry jelly-like", slimy-bloody diarrhoea, milder forms: mushy-watery diarrhoea (more frequent), ulcerations reaching into the submucosa (so-called bottleneck or canteen ulcers), gradual development over several weeks to years. Chronic courses are possible.

Amoebic liver abscess: acute upper abdominal pain (mainly on the right side) radiating to the back, thorax, shoulder, fever, lesions: necrotic material, exudate and remains of granulocytes lysed by amoebae; slow development (on average 3-5 months after infection). Chronic forms with low feeling of illness are rare.

Amoeboma: localized granulomatous inflammation of the colon wall which can proliferate into large tumors.

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In the chair:

  • Stool culture (to exclude simultaneous bacterial infections)
  • Stool microscopy (sensitivity of 70%): MIFC method in stool (preferably in native stool, fresh stool/mucus flake [in 3 stool samples]): Microscopic detection of cysts, minota forms and magnaforms in stool. Pathogenic and apathogenic forms of intestinal lumen cannot be differentiated, characteristics of cysts: E. histolytica larger than 10 µm, E. histolytica maximum 4 nuclei. Detection of magnaforms is proven by amoebic colitis.
  • Antigen detection (ELISA, sensitivity comparable with microscopy)
  • PCR (highest sensitivity).

In serum (indication of invasion):

  • serum antibodies (ELISA)
  • Transaminases, cholestasis parameters
  • Inflammation parameters
  • Blood count
  • Electrolytes.

Imaging (abscess, perforation, toxic megacolon):

  • Abdominal sonography
  • Computer tomography
  • Colonoscopy.

Differential diagnosis
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  • Diseases that may be associated with similar clinic:
    • Diarrhoea induced by bacterial toxins
    • Shigellose
    • Salmonellosis
    • Campylobacter infection
    • Yersiniosis
    • Chronic inflammatory intestinal diseases
    • Bacterial abscess
    • Pyomyositis
    • Melioidosis
    • Biliary ascariasis
    • Fascioliasis
    • Malignant tumor.

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  • Acute abdomen:
  • Pleural Empyema
  • Lung abscess
  • hepatobronchial fistula
  • Pericardial abscess.

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Standard: Metronidazole 3 times/day 10 mg/kg bw (max. 3 times/day 800 mg) i.v. or orally over 10 days (dosage for adults and children).

In mild cases: Tinidazole 2 g/day orally for 5 days (children: 30 mg/kg bw/day, maximum 2 g/day). Tinidazole is no longer approved in Germany, but is available from pharmacies abroad ( off-label use).

Subsequently cyst treatment: Paromomycin 3 times/day 500 mg/day p.o. for 9-10 days (children: 10 mg/kg bw/day).

Alternatively: Diloxanidfuroat, Nimorazol, Chloroquin.

In pregnant women: treatment indicated (however, 5-nitroimidazole should not be given in the 1st trimester).

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Food hygiene (ice cubes, salads, ice cream, open juices)

Avoid oral-anal sexual contacts and rectal lavage.

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Control of the success of therapy: in severe cases: blood count, liver values, cholestasis and inflammation parameters during and after treatment, time intervals according to the severity of the disease.

Stool examination: 6 weeks after the end of treatment.

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  1. Annesley J (1828) Researches into the causes, nature and treatment of the more prevalent diseases of warm climates generally. Longman, Rees, Orme, Brown and Green, London, Vol. 2 p. 247
  2. Budd, G 1857 On diseases of the liver. Churchill, London, United Kingdom
  3. Burchard GD et al (2003) Therapy of tropical diseases after returning from travel. Internist 44: 633-642
  4. Carrero JC et al (2019) Intestinal amoebiasis: 160 years of its first detection and still remains as ahealth
    problem in developing countries. Int J Med Microbiol:151358.
  5. Kucik CJ et al. (2004) Common intestinal parasites. Am Fam Physician 69: 1161-1168
  6. Losch FA (1975) Massive development of amebas in the large intestine. Translation from the original in Russian. Am J Trop Med Hyg 24: 383-392
  7. Trabelsi H et al (2012) Pathogenic free-living amoebae: epidemiology and clinical review. Pathol Biol (Paris) 60:399-405.


Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 18.07.2022