Amoebiasis

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Amoebiasis is caused by the protozoan Entamoeba histolytica.[1] Amoebiasis is often asymptomatic but may cause dysentery and invasive extra-intestinal disease.[2] Entamoeba dispar, another species, has been thought in the past to be non-pathological but in vitro and in vivo experiments suggest it is capable of causing liver damage.[3] 

  • Humans are the only reservoir, and infection occurs by ingestion of mature cysts in food or water, or on hands contaminated by faeces.[4]
  • The cysts of E. 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 - eg, the liver, lungs and brain, via the venous system.
  • Asymptomatic carriers pass cysts in the faeces and the asymptomatic carriage state can persist indefinitely. E. dispar is the parasite most commonly found in such carriers, Cysts remain viable for up to two months.
  • Invasive amoebiasis most often causes an amoebic liver abscess but may affect the lung, heart, brain, urinary tract and skin.[5] 
  • E. histolytica infects approximately 50 million people worldwide, of which approximately 100,000 die annually.[6] 
  • It is the third most common cause of death (after schistosomiasis and malaria) from parasitic infections.[7] 
  • It is very common in South and Central America, West Africa and Southeast Asia. It is rare in temperate climates.[8] 
  • Increasing prevalence is seen in men who have sex with men who engage in oral-anal sex.[9] 
  • Travellers and immigrants and residents of institutions are also at risk.[10] 
  • About 90% of infections are asymptomatic and the remaining 10% produce a spectrum of disease varying from dysentery to amoebic liver abscess.[2] 

The incubation period may be as short as seven days and tissue invasion mostly occurs during first four months of infection.

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Intestinal amoebiasis

  • The most common type of amoebic infection is the asymptomatic passage of cysts, found to be mainly associated with E. dispar infection.[2] 
  • 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. The patient is usually generally well with mild or moderate abdominal pain. Symptoms often fluctuate over weeks or even months with the patient becoming debilitated.
  • Abdominal tenderness in one or both iliac fossae but may be generalised. There is palpably thickened gut, and low fever. There is abdominal distension in more severely ill patients passing relatively small amounts of stool sometimes.
  • Amoebic colitis without dysentery: a change in bowel habit, bloodstained stools, flatulence and colicky pain, tenderness in the right iliac fossa or other places over the colon. This may disappear or progress to dysentery.
  • Rectal bleeding: this may occasionally be the only sign, with or without tenesmus (common in children).
  • Amoeboma:
    • Abdominal mass, which is usually in the 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: this is more likely in children and in patients taking steroids; high-grade fever, severe abdominal pain, increasing distension of the 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 infection. May also resemble simple appendicitis, often with signs of dysentery.

Hepatic amoebiasis

  • There is usually no current, and often no history of, dysentery.
  • It usually occurs within eight weeks to one year of infection.
  • It presents with sweating and pyrexia, a painful liver or diaphragm, together with weight loss often appearing insidiously, but pain may appear abruptly.
  • Fever is typically remitting with a prominent evening rise with brief rigors and profuse sweating.
  • Often there is anaemia and dry painful cough.
  • There is liver enlargement with localised tenderness in the right hypochondrium, epigastrium and intercostal spaces overlying the liver.
  • An epigastric mass from a left-lobe lesion may be found.
  • Upward enlargement may cause bulging of the right chest wall with raised upper level of liver dullness on percussion. Reduced breath sounds or crepitations at the right lung base may be heard.
  • Abscess may extend into adjacent structures, usually the right chest, peritoneum and pericardium. If it extends into the lung, it produces hepatobronchial fistula with expectoration of brownish, necrotic liver tissue. May also cause peritonitis, pericarditis, brain abscess or genitourinary disease.
  • FBC (leukocytosis), raised ESR, abnormal LFTs (raised alkaline phosphatase and transaminases).[2] 
  • Stool examination:
    • Microscopic stool examination for trophozoites should be performed in patients with diarrhoea..Examination of 3 to 6 stool samples and concentration techniques may be required due to low specificity. [5]  
    • E. histolytica should be differentiated from other Entamoeba spp.[4] The World Health Organization now recommends that intestinal amoebiasis should be diagnosed with specific stool E. histolytica testing (eg, cultures, antigen testing or PCR) rather than examining stool for ova and parasites.
  • Serology: antibody testing is positive in nearly 100% of cases of liver abscess, 89-100% of invasive bowel disease and nearly 100% of patients with amoeboma.[11][12]  
  • PCR tests (faeces, abscess aspirate or other tissues).
  • Barium studies are contra-indicated 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.
  • Ultrasound- or CT-guided liver abscess aspiration.
  • Proctoscopy, sigmoidoscopy or colonoscopy: mucosal scrapings for biopsy and E. histolytica testing.
  • Abscesses resolve slowly and may increase in size during treatment and so clinical response, rather than repeated scans, is more important in monitoring progress.
  • Fluid and electrolyte replacement, gastric suction and blood transfusion may be required.
  • Diloxanide furoate is the drug of choice for asymptomatic patients with E. histolytica cysts in the faeces (metronidazole and tinidazole are relatively ineffective).
  • Metronidazole is the first choice for treatment of acute invasive amoebic dysentery. Tinidazole is also effective.
  • Treatment with metronidazole or tinidazole is followed by a 10-day course of diloxanide furoate to destroy any amoebae in the gut.
  • Diloxanide furoate is also given as a 10-day course for chronic infections.
  • Amoebic abscesses of the liver:
    • Metronidazole and tinidazole are effective for amoebic abscesses of the liver.
    • Diloxanide furoate is ineffective against hepatic amoebiasis but a 10-day course should be given at the completion of metronidazole or tinidazole treatment to destroy any amoebae in the gut.
    • Surgical drainage of an uncomplicated amoebic liver abscess is unnecessary and should be avoided.
    • However, the abscess should be drained if there is a risk that it may rupture or if metronidazole leads to no improvement after 72 hours of treatment. 
    • Aspiration is largely being replaced by percutaneous catheter drainage.[14]  
    • In patients unsuitable for percutaneous drainage (elderly, frail, septic shock, multilocular cysts) laparoscopy is the preferred option.[15] 
    • Laparotomy is usually required for rupture of a liver abscess but can occasionally be managed by ultrasound-guided percutaneous catheter drainage.[16] 
  • Amoebic colitis may lead to fulminant or necrotising colitis, toxic megacolon, amoeboma or a rectovaginal fistula. 
  • Amoebic liver abscess: may extend and/or rupture into the abdomen or chest, or disseminate and cause a brain abscess.

 Prognosis[2] 

  • In uncomplicated disease, the mortality rate is less than 1% but is much higher in complicated severe disease - eg, fulminant amoebic colitis, chest involvement or cerebral amoebiasis.
  • More severe illness occurs in children (especially neonates), the immunosuppressed, malnourished, pregnancy and postpartum.
  • Recurrence is common if amoebae are not completely eradicated.
  • The bowel heals rapidly and completely; hepatic abscesses usually disappear within 8 months to 2 years.
  • 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 but progress has been made in the identification of possible candidates, the route of application and the understanding of the immune response. It is hoped that this will lead to a vaccine being developed within the next few years.[18] 

Further reading & references

  • Wilson IW, Weedall GD, Hall N; Host-Parasite interactions in Entamoeba histolytica and Entamoeba dispar: what have we learned from their genomes? Parasite Immunol. 2012 Feb-Mar;34(2-3):90-9. doi: 10.1111/j.1365-3024.2011.01325.x.
  1. Stanley SL Jr; Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34.
  2. Ximenez C, Moran P, Rojas L, et al; Novelties on amoebiasis: a neglected tropical disease. J Glob Infect Dis. 2011 Apr;3(2):166-74. doi: 10.4103/0974-777X.81695.
  3. Dolabella SS, Serrano-Luna J, Navarro-Garcia F, et al; Amoebic liver abscess production by Entamoeba dispar. Ann Hepatol. 2012 Jan-Feb;11(1):107-17.
  4. Amebiasis, DPDx, Centers for Disease Control & Prevention
  5. Pearson R, Amebiasis, Merck Manual, 2009 (Updated 2012)
  6. Choudhuri G, Rangan M; Amebic infection in humans. Indian J Gastroenterol. 2012 Jul;31(4):153-62. Epub 2012 Aug 19.
  7. Haque R; Human intestinal parasites. J Health Popul Nutr. 2007 Dec;25(4):387-91.
  8. Amoebiasis and giardiasis, World Health Organization, 2013
  9. Hung CC, Chang SY, Ji DD; Entamoeba histolytica infection in men who have sex with men. Lancet Infect Dis. 2012 Sep;12(9):729-36. doi: 10.1016/S1473-3099(12)70147-0.
  10. Zibaei M, Firoozeh F, Azargoon A; Infantile amoebiasis: a case report. Case Rep Infect Dis. 2012;2012:614398. doi: 10.1155/2012/614398. Epub 2012 Jun 21.
  11. Fotedar R, Stark D, Beebe N, et al; Laboratory diagnostic techniques for Entamoeba species. Clin Microbiol Rev. 2007 Jul;20(3):511-32, table of contents.
  12. Leo M, Haque R, Kabir M, et al; Evaluation of Entamoeba histolytica antigen and antibody point-of-care tests for the rapid diagnosis of amebiasis. J Clin Microbiol. 2006 Dec;44(12):4569-71. Epub 2006 Oct 11.
  13. British National Formulary
  14. Alkofer B, Dufay C, Parienti JJ, et al; Are pyogenic liver abscesses still a surgical concern? A Western experience. HPB Surg. 2012;2012:316013. doi: 10.1155/2012/316013. Epub 2012 Feb 19.
  15. Aydin C, Piskin T, Sumer F, et al; Laparoscopic drainage of pyogenic liver abscess. JSLS. 2010 Jul-Sep;14(3):418-20. doi: 10.4293/108680810X12924466006567.
  16. Bukhari AJ; Ruptured amebic liver abscess. J Coll Physicians Surg Pak. 2003 Mar;13(3):159-60.
  17. Alavi KA; Amebiasis. Clin Colon Rectal Surg. 2007 Feb;20(1):33-7. doi: 10.1055/s-2007-970198.
  18. Parija SC; Progress in the research on diagnosis and vaccines in amebiasis. Trop Parasitol. 2011 Jan;1(1):4-8. doi: 10.4103/2229-5070.72108.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Last Checked:
07/06/2013
Document ID:
1798 (v23)
© EMIS

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