Amoebiasis

What is amoebiasis?

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

How common is amoebiasis? (Epidemiology)⁶

• E. histolytica infects approximately 50 million people worldwide, of which approximately 100,000 die annually.⁷

• It is the third most common cause of death (after schistosomiasis and malaria) from parasitic infections.⁸

• The majority of amoebiasis cases occur in developing countries. In industrialised countries, risk groups include immunocompromised persons, and institutionalised populations.⁴

• Amoebic dysentery is transmitted in areas where poor sanitation allows contamination of drinking water and food with faeces. In these areas, up to 40% of people with diarrhoea may have amoebic dysentery.

• Estimates on the prevalence of Entamoeba spp. infection range from 1% to 40% of the population in Central and South America, Africa, and Asia, and from 0.2% to 10.8% in endemic areas of developed countries such as the US. However, these estimates are difficult to interpret, mainly because infection can remain asymptomatic or go unreported, and because many older reports do not distinguish E. histolytica from the non-pathogenic, morphologically identical species E. dispar.

• 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

Amoebiasis symptoms⁶

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

About 90% of infections are asymptomatic and the remaining 10% produce a spectrum of disease.²

Symptoms include severe dysentery and associated complications. Severe chronic infections may lead to further complications such as peritonitis, perforations, and the formation of amoebic granulomas (amoeboma). Amoebic liver abscesses are the most common manifestation of extraintestinal amoebiasis. Pleuropulmonary abscess, brain abscess, and necrotic lesions on the perianal skin and genitalia may also occur.⁴

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 a 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.

Differential diagnosis

• Other causes of infective colitis, ulcerative colitis, colorectal cancer.

• In chronic infection, other possible diagnoses include Crohn's disease, ileocaecal tuberculosis, diverticulitis, anorectal lymphogranuloma venereum.

• Amoebic liver abscess has to be differentiated from pyogenic abscess which may occur particularly in older patients with underlying bowel disease or after surgery.

Investigations¹¹

• 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.

  • 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.^{12 13}

• 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.

Amoebiasis treatment²

• 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

Complications^{6 17}

Fulminant amoebic dysentery is often fatal. Other complications include perforation of the colon, colonic ulcers, amoeboma, or chronic carriage.

• 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.

Prognosis²

• 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.

Amoebiasis 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 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