Amebiasis may be asymptomatic or produce intermittent diarrhea with abdominal pain. Invasion of the mucosa is typical and may spread to the liver, where an ab- scess is produced.
E. histolytica infection rates are higher in warm climates, particularly in areas where thelevel of sanitation is low. Worldwide, this organism is thought to produce more deaths than any other parasite, except those that cause malaria and schistosomiasis. Reports of amebic liver abscess, for instance, emanate primarily from Mexico, western South America, South Asia, and West and South Africa. For reasons apparently unrelated to exposure, symptomatic illness is much less common in women and children than in men.
Although stool surveys in the United States indicate that 1 to 5% of the population harbors Entamoeba, the vast majority of these are now known to be colonized with the nonpathogenic E. dispar. The incidence of invasive amebiasis in the United States de-creased sharply over several decades, reaching a nadir in 1974. Since then, the numbers have increased steadily. It is now seen particularly in institutionalized individuals, Indian reservations, migrant labor camps, victims of acquired immunodeficiency syndrome (AIDS), and travelers to endemic areas.
Symptomatic amebiasis is usually sporadic, the result of direct person-to-person fecal–oral spread under conditions of poor personal hygiene. Venereal transmission is seen in male homosexuals, presumably the result of oral–anal sexual contact. Food- and water-borne spread occur, occasionally in epidemic form. Such outbreaks, however, are seldom as explosive as those produced by pathogenic intestinal bacteria. One outbreak of intestinal amebiasis was due to colonic irrigation at a chiropractic clinic.
A number of virulence factors have been identified in E. histolytica. In an experimental setting, invasiveness correlates well with endocytic capacity, the production of extracellular proteinases capable of activating complement and degrading collagen, the presence of a galactose-specific lectin apparently capable of mediating attachment of the organism to colonic mucosa, and perhaps most importantly, the capacity to lyse host cells on contact. The latter phenomenon is initiated by the galactose-specific lectin-mediated adherence of the trophozoite to a target cell. Following adherence, the ameba releases a pore-forming protein that polymerizes in the target cell membrane, forming large tubular lesions. Cytolysis rapidly follows.
In most cases of infections, however, tissue damage is minimal, and the host remains symptom free, suggesting that host factors may modulate the invasiveness of virulent strains. These factors are still poorly understood, but changes in host resistance, the colonic milieu, or the parasite itself may amplify tissue damage and clinical manifesta-tions. Protein malnutrition, high-carbohydrate diets, corticosteroid administration, child-hood, and pregnancy all appear to render the host more susceptible to invasion. Certain colonic bacteria appear to enhance invasiveness, possibly by providing a more favorable redox potential for survival and multiplication or by facilitating the adherence of the para-site to colonic mucosa. Finally, it is known that the pathogenic strains in the tropics are more invasive than those isolated in temperate areas, possibly because poor sanitation re-sults in more frequent passage through humans.
Amebas contact and lyse colonic epithelial cells, producing small mucosal ulcerations. There is little inflammatory response other than edema and hyperemia, and the mucosa be-tween ulcers appears normal. Trophozoites are present in large numbers at the junction be-tween necrotic and viable tissue. Once the lesion penetrates below the superficial epithe-lium, it meets the resistance of the colonic musculature and spreads laterally in the submucosa, producing a flask-like lesion with a narrow mucosal neck and a large submu-cosal body. It eventually compromises the blood supply of the overlying mucosa, resulting in sloughing and a large necrotic ulcer. Extensive ulceration leads to secondary bacterial infection, formation of granulation tissue, and fibrotic thickening of the colon. In approxi-mately 1% of patients, the granulation tissue is organized into large, tumor-like masses known as amebomas. The major sites of involvement, in order of frequency, are the cecum, ascending colon, rectum, sigmoid, appendix, and terminal ileum. Amebas may also enter the portal circulation and be carried to the liver or, more rarely, to the lung, brain, or spleen. In these organs, liquefaction necrosis leads to the formation of abscess cavities.
Although E. histolytica elicits both humoral and cellular immune responses in humans, it is still not clear which, and to what degree, these responses are capable of modulating ini-tial infection or thwarting reinfection. In endemic areas, the prevalence of gastrointestinal colonization increases with age, suggesting that the host is incapable of clearing E. his-tolytica from the gut. However, the relative infrequency with which populations livingin these areas suffer repeated bouts of severe amebic colitis or liver abscess indicates that those who experience such infections have protection against recurrent disease.
Patients with invasive disease are known to produce high levels of circulating antibod-ies. Nevertheless, there is no correlation between the presence or concentration of such antibodies and protective immunity, possibly because pathogenic E. histolytica tropho-zoites have the capacity to aggregate and shed attached antibodies and are resistant to the lytic action of complement. The susceptibility to invasive amebiasis of malnourished populations, pregnant women, steroid-treated individuals, and AIDS patients indicates that cell-mediated immune mechanisms may be directly involved in the control of tissue invasion.
Pathogenic E. histolytica strains produce a lectin-like substance that is mitogenic for lymphocytes. It has been suggested that this substance could stimulate viral replication of human immunodeficiency virus–infected lymphocytes as does another mitogen, phyto-hemagglutinin.
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