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Amebiasis denotes the disease caused solely by Entamoeba histolytica, although there are 2 other morphologically identical Entamoeba species that can also infect humans—Entamoeba dispar and Entamoeba moshkovskii. E dispar is about 10 times more prevalent than E histolytica in most endemic areas for amebiasis. Recent reports suggest that infection of E moshkovskii, which was once considered a free-living amoeba, is also common in some parts of the world such as Bangladesh, India, and Australia. Most cases of E moshkovskii infection occur concomitantly with E dispar or E histolytica infections. Free-living amoebic infections are discussed in Chapter 343.
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PATHOGENESIS AND EPIDEMIOLOGY
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E histolytica is a protozoan with an invasive, motile trophozoite and infectious cyst stages that is responsible for person-to-person transmission of infection. The trophozoite varies in diameter from approximately 10 to 60 μm, has a clear ectoplasm, and a single nucleus. The cyst averages 12 mm in diameter and has 1 to 4 nuclei (Figs. 336-1 and 336-2). Humans are the only reservoir for E histolytica. Cysts that are passed in the feces of infected individuals survive in a moist environment for months. Following their ingestion in contaminated food or water, the cysts travel to the small intestine, the multinucleated metacystic amoeba is activated and emerges through a hole in the cyst wall, and immediately after excysting, it undergoes division into 8 uninucleate trophozoites. These organisms do not colonize the small intestine but are usually carried to the cecum where they become established. In 90% of patients, the trophozoites re-encyst and produce asymptomatic infection, which usually spontaneously resolves within 12 months. In 10% of patients, the parasite causes symptoms. Invasion of trophozoites then occurs, causing intestinal and hepatic abscesses.
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Human and parasite genetic differences are likely to play important roles in determining the pathogenicity of infection. Certain human leukocyte antigen (HLA) class II alleles appear to provide independent leptin receptor polymorphisms and appear to provide protection against E histolytica infection. On the other hand, E histolytica genotypes have been shown to differ among those infected and presenting with no symptoms, diarrhea/dysentery, or liver abscess. A cell-mediated immune response is likely to be important in clearing established infection by generating interferon-γ and tumor necrosis factor-α to activate macrophages and neutrophils to kill the trophozoite. Hepatic lesions illustrate lytic destruction of the hepatic parenchyma with abscess formation. The smallest lesions can measure a few millimeters in diameter, whereas others can extend ...