Amoebiasis

Amoebiasis is an intestinal and, in a proportion of cases, invasive extraintestinal infection caused by Entamoeba histolytica. This protozoan parasite is transmitted through the faecal oral route via ingestion of infective cysts from contaminated food or water. It is distinguished from the morphologically identical but non pathogenic Entamoeba dispar and Entamoeba moshkovskii.

The great majority of infections remain asymptomatic (colonisation without invasive disease). A minority progress to invasive intestinal disease (amoebic colitis) or, through haematogenous spread, extraintestinal disease, most notably amoebic liver abscess.

It is an important global cause of morbidity and mortality, particularly in regions with inadequate sanitation infrastructure.

Pathophysiology

• Following ingestion, cysts excyst within the small intestine to release trophozoites, which colonise the large intestine.
• Invasive disease occurs when trophozoites penetrate the colonic mucosa. This is facilitated by specific parasite virulence factors including a galactose specific lectin mediating adherence and subsequent cytolysis of host cells.
• The result is characteristic flask shaped ulcers with a narrow neck and broader base extending into the submucosa.
• Extraintestinal disease results from haematogenous spread of trophozoites via the portal venous system, predominantly to the liver.
• Amoebic liver abscess overlaps diagnostically with, and must be distinguished from, pyogenic liver abscess.
• Less commonly, a hepatic abscess spreads further to the lung, pleura, pericardium or, rarely, brain.

• The large majority of infected individuals remain asymptomatic, with Entamoeba histolytica colonisation identified incidentally on stool examination. Some subsequently clear infection spontaneously without ever developing invasive disease.
• Amoebic colitis presents with gradual onset (over one to several weeks, distinguishing it from the more acute onset typical of bacterial dysentery) abdominal pain, cramping and bloody, mucoid diarrhoea (dysentery), with tenesmus.
• It typically occurs without significant fever, a further point of distinction from many bacterial causes of dysentery. This distinction is imperfect and cannot be relied upon in isolation.
• Fulminant amoebic colitis, an uncommon but severe complication, presents with severe abdominal pain, high fever and systemic toxicity.
• It carries substantial risk of colonic perforation and peritonitis, and toxic megacolon. Together these represent a surgical emergency requiring urgent recognition.
• Amoeboma, a rare complication comprising a mass forming inflammatory lesion within the colonic wall, can mimic colonic carcinoma both clinically and radiologically. Careful diagnostic distinction is required.
• Amoebic liver abscess presents with fever, right upper quadrant pain and hepatomegaly, typically as a solitary lesion within the right hepatic lobe.
• Concurrent active intestinal symptoms are frequently absent at the time of liver abscess presentation. The absence of diarrhoea does not exclude this diagnosis in a patient with a compatible hepatic presentation and relevant travel history.

• Stool microscopy can identify characteristic trophozoites or cysts. Trophozoites containing ingested red blood cells in invasive disease are a relatively specific though inconsistently observed finding.
• Microscopy cannot reliably distinguish pathogenic Entamoeba histolytica from the morphologically identical non pathogenic species. This limits the clinical utility of microscopy alone for confirming invasive disease.
• Stool antigen testing or polymerase chain reaction testing, where available, offers specific identification of Entamoeba histolytica, distinguishing it from the non pathogenic morphologically identical species. It is the preferred diagnostic approach where accessible.
• Serological testing is particularly useful for suspected invasive disease (amoebic colitis or liver abscess), given a strong antibody response in the context of tissue invasion.
• A positive result in the appropriate clinical context (particularly imaging showing a compatible hepatic lesion) is generally sufficient to support the diagnosis without further invasive sampling.
• Colonoscopy, where performed for suspected amoebic colitis, may show characteristic flask shaped ulcers. Biopsy from the ulcer edge supports diagnosis, rather than from the base, which is frequently necrotic and less likely to yield diagnostic organisms.
• Caution regarding perforation risk is warranted in the acutely unwell patient with suspected fulminant disease.
• Imaging (ultrasound or computed tomography) confirms a hepatic abscess where suspected. The diagnostic approach and distinction from pyogenic liver abscess are detailed further under that specific condition.

• Invasive disease (amoebic colitis or liver abscess) is treated with metronidazole 750 mg orally or intravenously three times daily for seven to ten days, or tinidazole 2 g orally once daily for three to five days. Both are highly effective against the invasive trophozoite form.
• Following completion of tissue active treatment (metronidazole or tinidazole), give a luminal acting agent, typically paromomycin 25 to 35 mg per kg per day in three divided doses for seven days. This eradicates any residual intraluminal cyst colonisation.
• This second agent is essential, because metronidazole and tinidazole have relatively poor activity against the luminal cyst form. Omitting it risks ongoing asymptomatic cyst passage, with continued transmission risk and potential relapse.
• Asymptomatic cyst passage is treated with a luminal agent alone (paromomycin). It must be confirmed as pathogenic Entamoeba histolytica through specific antigen or molecular testing, because non pathogenic species do not require treatment.
• The rationale is the recognised potential, albeit at low absolute frequency, for asymptomatic colonisation to progress to invasive disease, together with the public health relevance of reducing ongoing transmission.
• Amoebic liver abscess generally does not require drainage, given the typically excellent response to metronidazole alone in the majority of cases. This contrasts with pyogenic liver abscess.
• Percutaneous or surgical drainage is reserved for very large abscesses (particularly with risk of imminent rupture), and abscesses not responding adequately to medical therapy alone within several days.
• Drainage is also used for left lobe abscesses, given proximity to the pericardium and risk of pericardial rupture, a rare but life threatening complication.
• Drainage is also used where diagnostic uncertainty persists and drainage is required to exclude an alternative diagnosis such as pyogenic abscess.
• Fulminant amoebic colitis with suspected or confirmed perforation requires urgent surgical assessment and intervention alongside antiparasitic treatment, following general principles applicable to any perforated viscus with associated peritonitis.
• Prevention through safe water and food hygiene practices and improved sanitation infrastructure is the primary preventive strategy, given the absence of any available vaccine for this infection.
• Hygiene practices include boiling or appropriate filtration of water in endemic settings, thorough washing of fresh produce, and avoidance of potentially contaminated ice.