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This is a PatientPlus article. PatientPlus articles are written for doctors and so the language can be technical, however some people find that they add depth to the patient information leaflets. You may find the abbreviations record helpful.

Amoebiasis is caused by a protozoa, of the 9 species of amoebae harboured by humans, only Entamoeba histolytica is a pathogen.1

  • Humans are the only reservoir, and it is commonly spread by water or food contaminated by faeces.
  • The cysts of Entamoeba histolytica enter the small intestine and release active amoebic parasites (trophozoites), which invade the epithelial cells of the large intestines, causing flask-shaped ulcers. Infection can then spread from the intestines to other organs, e.g. liver, lungs and brain, via the venous system.
  • Asymptomatic carriers pass cysts in the faeces and the asymptomatic carriage state can persist indefinitely. Cysts remain viable for up to 2 months.
Epidemiology
  • About 10 percent of the world's population is infected with E.histolytica.
  • It is the third most common cause of death (after schistosomiasis and malaria) from parasitic infections, and second protozoal cause (after malaria).
  • Very common in South and Central America, West Africa and Southeast Asia. Rare in temperate climates.
  • About 90% of infections are asymptomatic and the remaining 10% produce a spectrum of disease varying from dysentery to amoebic liver abscess.
Presentation

Incubation period may be as short as 7 days and tissue invasion mostly occurs during first 4 months of infection.

Intestinal amoebiasis

  • The most common type of amoebic infection is asymptomatic cyst passage. Symptomatic patients initially have lower abdominal pain and diarrhoea and later develop dysentery (with blood and mucus in stool).
  • Amoebic colitis with dysentery: loose stools with fresh blood. Patient is usually generally well with mild or moderate abdominal pain. Symptoms often fluctuate over weeks or even months with patient becoming debilitated.
  • Abdominal tenderness in one or both iliac fossae but may be generalised. Palpably thickened gut. Low fever. Abdominal distension in more severely ill patients passing relatively small amounts of stool sometimes.
  • Amoebic colitis without dysentery: change in bowel habit, blood stained stools, flatulence and colicky pain, tenderness in right iliac fossa or other places over colon. May disappear or progress to dysentery.
  • Rectal bleeding: may occasionally be only sign, with or without tenesmus (common in children).
  • Amoeboma:
    • Abdominal mass usually in right iliac fossa
    • May be painful and tender
    • Fever, altered bowel habit and there may be intermittent dysentery
    • May be symptoms of partial or intermittent bowel obstruction
  • Fulminant colitis: more likely in children and patients taking steroids; high grade fever, severe abdominal pain, increasing distension of abdomen with vomiting plus watery diarrhoea. Absent bowel sounds. X-ray may show free peritoneal gas with acute gaseous dilatation of the colon.
  • Localised perforation and appendicitis: deep ulcer may cause sudden perforation with peritonitis or may leak causing pericolic abscess or retroperitoneal cellulites. May also resemble simple appendicitis, often with signs of dysentery.

Hepatic amoebiasis

  • Usually no current and often no history of dysentery
  • Usually occurs within 8 weeks to 1 year of infection
  • Presents with sweating and pyrexia, painful liver or diaphragm together with weight loss often appearing insidiously, but pain may appear abruptly.
  • Fever is typically remitting with prominent evening rise with brief rigors and profuse sweating
  • Often anaemia and dry painful cough
  • Liver enlargement with localised tenderness in right hypochondrium, epigastrium and intercostal spaces overlying liver
  • May find epigastric mass from left-lobe lesion
  • Upward enlargement may cause bulging of right chest wall with raised upper level of liver dullness on percussion. May hear reduced breath sounds or crepitations at right lung base.
  • Abscess may extend into adjacent structures, usually the right chest, peritoneum and pericardium. If extends into lung produces hepatobronchial fistula with expectoration of brownish, necrotic liver tissue. May also cause peritonitis, pericarditis, brain abscess, or genitourinary disease.
Differential diagnosis
Investigations
  • Stool examination: neutrophils and Charcot-Leyden crystals may be seen; trophozoites are diagnostic. Since trophozoites are killed rapidly by water or drying, at least three fresh stool specimens have to be examined for a positive diagnosis. Fresh stool or concentrated stool examination is positive in 75% to 95% of patients.
  • Serology: antibody testing is positive in 95% of cases of liver abscess, 60% of invasive bowel disease and nearly 100% of patients with amoeboma.2
  • Barium studies are contraindicated in acute amoebic colitis because of the risk of perforation.
  • Ultrasound, CT and MRI scans of the abdomen can be useful in diagnosing hepatic amoebiasis.
  • Proctoscopy or sigmoidoscopy: mucosal scrapings; should also see ulcers.
  • Abscesses resolve slowly and may increase in size during treatment and so clinical response is more important in monitoring progress rather than repeated scans.
Management
  • Fluid and electrolyte replacement, gastric suction and blood transfusion
  • Asymptomatic patients (i.e. E. histolytica cysts in the faeces) can be treated with luminal amoebicides, e.g. diloxanide furoate or paromomycin. Metronidazole and tinidazole are ineffective.
  • Metronidazole is the first choice for treatment of acute invasive amoebic dysentery. Tinidazole is also effective.
  • Metronidazole and tinidazole are also effective for hepatic amoebiasis. Treatment with metronidazole or tinidazole is then followed by a 10-day course of diloxanide furoate to destroy any amoebae in the gut.
  • Metronidazole and tinidazole are effective for amoebic abscesses of the liver. The abscess should be aspirated if there is a risk that it may rupture or if metronidazole leads to no improvement after 72 hours of treatment. Aspiration may need to be repeated.
  • Laparotomy is required for rupture of liver abscesses.
Prognosis
  • In uncomplicated disease, mortality rate is less than 1% but is higher in complicated severe disease:
    • Over 50% in fulminant amoebic colitis
    • 40% for pericarditis
    • 15-20% for pleuropulmonary amoebiasis
    • 90% for cerebral amoebiasis
  • More severe illness occurs in children (especially neonates), the immunosuppressed, malnourished, pregnancy and post-partum.
  • Recurrence is common if not completely freed of amoebae.
  • Bowel heals rapidly and completely; hepatic abscesses disappear within approximately 8 months to 2 years.
Prevention
  • Successful control of amoebiasis depends on prevention of infection through adequate sanitation, safe food and water and good personal hygiene of the population.
  • No vaccine is yet available.

Document References
  1. Stanley SL Jr; Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34. [abstract]
  2. Heckendorn F, N'Goran EK, Felger I, et al; Species-specific field testing of Entamoeba spp. in an area of high endemicity. Trans R Soc Trop Med Hyg. 2002 Sep-Oct;96(5):521-8. [abstract]
Acknowledgements EMIS is grateful to Dr Colin Tidy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2007.
DocID: 1798
Document Version: 20
DocRef: bgp457
Last Updated: 2 Oct 2007
Review Date: 1 Oct 2009

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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