Elsevier

The Lancet

Volume 361, Issue 9362, 22 March 2003, Pages 1025-1034
The Lancet

Seminar
Amoebiasis

https://doi.org/10.1016/S0140-6736(03)12830-9Get rights and content

Summary

Amoebiasis is the second leading cause of death from parasitic disease worldwide. The causative protozoan parasite, Entamoeba histolytica, is a potent pathogen. Secreting proteinases that dissolve host tissues, killing host cells on contact, and engulfing red blood cells, E histolytica trophozoites invade the intestinal mucosa, causing amoebic colitis. In some cases amoebas breach the mucosal barrier and travel through the portal circulation to the liver, where they cause abscesses consisting of a few E histolytica trophozoites surrounding dead and dying hepatocytes and liquefied cellular debris. Amoebic liver abscesses grow inexorably and, at one time, were almost always fatal, but now even large abscesses can be cured by one dose of antibiotic. Evidence that what we thought was a single species based on morphology is, in fact, two genetically distinct species—now termed Entamoeba histolytica (the pathogen) and Entamoeba dispar (a commensal)—has turned conventional wisdom about the epidemiology and diagnosis of amoebiasis upside down. New models of disease have linked E histolytica induction of intestinal inflammation and hepatocyte programmed cell death to the pathogenesis of amoebic colitis and amoebic liver abscess.

Section snippets

The organism

Unlike many protozoan parasites, E histolytica has a simple lifecycle, existing as either the infectious cyst form or the amoeboid trophozoite stage. Human beings, and perhaps some non-human primates, are the only natural hosts. Infection usually begins with the ingestion of the cysts in food or water that has been contaminated by human faeces. E histolytica cysts are round, usually 10–15 μm in diameter, and are surrounded by a refractile wall that may include chitin. They contain four nuclei,

Epidemiology—E histolytica, the doppelganger

E histolytica is distributed throughout the world, and is a substantial health risk in almost all countries where the barriers between human faeces and food and water are inadequate. Remarkably, our understanding of the worldwide and regional prevalence of E histolytica infection is now changing, thanks to the discovery that the organism called E histolytica on the basis of its morphology is, in fact, two genetically distinct species. Brumpt8 suggested in 1925 that the genus Entamoeba included

Pathophysiology

The pathological range of amoebic colitis encompasses mucosal thickening, multiple discrete ulcers separated by regions of colonic mucosa of normal appearance, diffusely inflamed and oedematous mucosa, and necrosis and perforation of the intestinal wall (figure 2). The gross findings can strongly resemble those seen in inflammatory bowel disease.48 Disease begins when E histolytica trophozoites adhere to colonic epithelial cells, probably through the galactose/N-acetylgalactosamine specific

Gastrointestinal

Many individuals with E histolytica infection have no symptoms, and can clear their infection without any signs of disease. However, 4–10% of asymptomatic individuals infected with E histolytica develop disease over a year.19, 90 Patients with amoebic colitis present with bloody diarrhoea and abdominal pain and tenderness.91, 92 The onset is often gradual, with patients reporting several weeks of symptoms. Multiple small volume mucoid stools are common, but profuse, watery diarrhoea might be

Diagnosis

The diagnosis of amoebic colitis rests on the demonstration of E histolytica in the stool or colonic mucosa of patients with diarrhoea. For years this diagnosis was done by microscopic examination of stool, a technique that probably identified most cases of amoebic colitis when used by skilled individuals (differentiation of E histolytica trophozoites from leucocytes and other intestinal protozoa can be difficult), and with the examination of at least three properly prepared stool samples.119,

Amoebiasis

In an age where drug resistance has become the rule, rather than the exception, for many microbial pathogens, I find it refreshing to report that the cornerstone of treatment for amoebiasis remains the nitroimidazole derivatives (metronidazole, tinidazole, ornidazole). Because metronidazole is the only nitroimidazole available in the USA, my recommendations (table 3) focus on this agent, but the other tinidazole agents are equally or slightly more effective. Amoebic colitis is treated by

The future

Walker and Sellards141 discovered that two different individuals infected with the same stool sample from a patient with amoebic dysentery could show completely different clinical manifestations (asymptomatic cyst passer or amoebic colitis). Since then, investigators have questioned why some hosts seem to be more susceptible to disease, and whether E histolytica isolates might differ in their virulence. We now have the techniques to try and answer both of those queries. Studies in the mouse

Search strategy

I obtained sources for this review by searching PubMed until Aug 31, 2002, with the keywords: Entamoeba histolytica, amebiasis, amoebiasis, amebic liver abscess, amoebic liver abscess, amebic colitis, amoebic colitis, amebic dysentery, and amoebic dysentery. The search was restricted to papers in the English language.

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