Entamoeba Histolytica and Other Aamoebae
Amoebiasis affects around 480 million people worldwide, with an annual mortality of 40,000110,000 persons. It is now established that in addition to the amoeba E. histolytica, which is pathogenic to humans, there is another amoeba that looks just like it; E. dispar is a harmless commensal organism that is much more common than E. histolytica. Infection with E. dispar can coexist with E. histolytica infection, and in up to 20% of E. dispar infections, antibodies develop that can crossreact with the reagents used for the standard immunodiagnosis of E. histolytica infection. E. dispar can now be reliably identified by assays based on the polymerase chain reaction.
The clinical spectrum of intestinal E. histolytica infection ranges from an asymptomatic carrier state to severe invasive disease. Asymptomatic cyst carriage occurs with E. histolytica as well as E. dispar. Most E. histolytica-infected individuals clear the infection spontaneously, with only about 10% going on to develop colitis. Acute amoebic colitis ranges from mild to severe, and can be fulminant, leading to colon perforation. Amoebic liver abscess is the most common extraintestinal form of invasive amoebiasis. About 20% of patients with liver abscess have previously had clinical dysentery. Infection can spread from the liver by direct extension into the pleuropulmonary cavity and the pericardial cavity. Occasionally, usually in immunosuppressed individuals, infection might be widely disseminated and affect other organs, including bone and the brain.
Luminal amoebicides (such as paromomycin, diloxanide furoate and iodoquinol) act on organisms in the intestinal lumen, but are ineffective against organisms in tissue. Metronidazole (and other nitroimidazole derivatives) is effective in the treatment of invasive disease, but less effective in the treatment of luminal forms of the parasite.
Asymptomatic Patients. In nonendemic areas, asymptomatic patients should preferably be treated with paromomycin (2535 mg/kg per day, divided into three doses, for 7 days). Alternative treatments include diloxanide furoate (500 mg three times daily for 10 days) or iodoquinol (650 mg three times daily for 20 days). Iodoquinol and its analog iodochlorhydroxyquin have been reported to cause myelo-optic neuropathy after long-term use, and their use is therefore no longer encouraged; however, myelo-optic neuropathy has never been reported with the doses used to treat protozoan infections. The value of treatment of asymptomatic carriers in endemic areas is questionable, because of the high rate of reinfection.
Intestinal Infection. Nitroimidazole derivatives are the drugs of choice for treatment of amoebic colitis, as they are very effective against the trophozoite form of the parasite (metronidazole 750800 mg three times daily for 510 days, or tinidazole 2 g daily for 3 days). These drugs have little effect on amoebic cysts, however, and standard advice is that treatment should be followed by an agent (such as paromomycin or diloxanide furoate) that acts on the organism in the lumen. There have not, however, been any studies published in the past decade that have critically evaluated whether this advice is still robust.
Liver Abscess. Metronidazole 750800 mg three times daily for 10 days, or tinidazole followed by a luminal amoebicide, is the treatment of choice. The potential cardiovascular and gastrointestinal adverse effects of dehydroemetine and emetine hydrochloride limit their use and are now rarely used. Aspiration of the abscess might be necessary in some cases. The need for open surgical drainage has decreased, however, since the success of percutaneous drainage. Surgery should be reserved for patients with a ruptured abscess, with bacterial superinfection, or when an abscess cannot be accessed by the percutaneous route.
Nat Clin Pract Gastroenterol Hepatol. 2006;3(8) © 2006 Nature Publishing Group
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