The closely related species Entamoeba coli and Entamoeba hartmanni are commensals, and infection with E. histolytica is also often asymptomatic. Pathogenic amebas cause light to severe intestinal damage ( amebic dysentery ) and sometimes spread to the liver, lungs, brain, and other organs.
Characteristics
The parasite exists in two forms during its life cycle. Active adults, trophozoites, multiply in the lumen of the colon.They frequently live there harmlessly, feeding on the contents of the intestine. Some strains are generally commensal; others are highly pathogenic. Under conditions of stress, lowered host resistance, or when a particularly pathogenic strain is involved, amebas invade the intestinal wall and cause abscesses. As they pass lower into the large intestine, the drier environment stimulates them to form a cyst wall. The original cell nucleus divides twice, producing four daughter nuclei.Cysts are passed with the feces and are infective when swallowed. Excystation takes place in the small intestine, and the young trophozoites, four from each cyst, are carried in the fecal stream to the large intestine. When dysentery occurs, trophozoites are swept out too rapidly to encyst. Even though huge numbers of amebas may be passed, they die quickly and are not infective. Persons with mild or no symptoms produce infective cysts, and it is they, not the patients with dysentery, who spread the disease. Infection is by the fecal-oral route.
Direct infection can take place in circumstances of extreme crowding, among inmates of institutions, and among male homosexuals. Indirect spread, however, by fecal contamination of food and water, is more common. Waterborne epidemics of amebic dysentery are not so frequent as those of bacillary dysentery , but the former do occur when sewage contaminates wells or water pipes. Fruits and vegetables can become covered with cysts when human feces are used as fertilizer, or when fruits are washed in contaminated water or are handled by a carrier.
Flies and cockroaches can transmit cysts from feces to food. The disease thus flourishes in poor sanitary conditions but is rare where good personal hygiene is practiced and where water and sewer systems function properly. Dogs, cats, and monkeys can be infected in the laboratory, but there is no evidence that animal reservoirs have an epidemiological significance. Infection with E. histolytica occurs around the world, although both commensal and pathological amebiasis is more common in poor, tropical countries.
Prevalence rates vary greatly, as does the proportion of infections that result in clinical disease. Amebiasis, especially clinical disease, is rare today in developed countries. In the United States, 3,000–4,000 cases were reported annually through the late 1970s. However, a spurt to roughly twice that level occurred in 1979–84. The disease was concentrated in Texas and California and probably resulted from increased immigration from Mexico and Southeast Asia. But annual case rates may be significantly underreported. Asymptomatic and clinical amebiasis is much more common in Third World countries.
Surveys have shown prevalence rates of up to 60 percent, reflecting real differences as well as technical difficulties. It is clearly a major public-health problem in much of South and Southeast Asia, China, Africa, and parts of Latin America. Mexico appears to have an unusually high prevalence. Estimates in the latter part of the twentieth century indicated that about 480 million people were infected throughout the world: 290 million in Asia, 80 million in Africa, 90 million in the Americas, and – remarkably – 20 million in Europe. Serious disease, however, strikes only a small percentage of those infected, and those who die of it constitute a very tiny fraction indeed.
Amebas cause disease when they invade the mucosal and submucosal layers of the large intestine, producing characteristic flask-shaped lesions. In severe cases, the lesions become large and confluent, resulting in substantial tissue destruction, bleeding, loss of fluids, and sloughing of patches of mucosa. Damage to the intestinal wall reduces water absorption, and loose stools with blood and mucous are passed. In addition to severe and perhaps fatal damage to the gut, amebas sometimes penetrate through the muscular coat of the bowel, where they enter the bloodstream and are carried to other organs, especially the liver. Intestinal perforation may result in fatal peritonitis. Large abscesses may f orm in the liver, with grave and sometimes fatal consequences.
Amebas may also migrate from the liver through the diaphragm to the lungs and cause new abscesses there. Brain abscesses are rare, but lethal. Very destructive skin ulcerations can also occur, especially around the anus. Clinical symptoms of intestinal amebiasis range from mild diarrhea and abdominal discomfort to frequent loose stools with blood mucus, severe pain, emaciation, and prostration. Onset is generally insidious. Liver involvement may develop without evidence of intestinal disease. Symptoms include severe, continuous pain, enlarged and tender liver, fever, and weakness. Chronic amebiasis, both intestinal and hepatic, is sometimes very dif ficult to identify. Differential diagnosis must rule out bacillary dysentery.
Amebic dysentery tends to be a chronic disease with a gradual onset and little or no fever. The stools tend to be more abundant but less frequent and not to be bright red with blood, as is common in bacillary dysentery. Amebic dysentery has a longer incubation period, 20–90 days or more, compared to 7 days or less for the bacillary form. Finally, with its shorter incubation period and greater probability of water transmission, bacillary dysentery is more likely to occur in dramatic epidemics.
History
Amebiasis probably did not become a serious problem until people began to adopt a sedentary, agricultural way of life. Dysentery has been described in early medical writings of Europe and Asia, and outbreaks were frequent in military units, on slave ships, and in prisons. It is generally impossible, however, to determine whether amebic or bacillary dysentery was involved in any particular outbreak of the “flux.” British doctors in India provided good clinical accounts of amebiasis in the early nineteenth century. In 1828, James Annesley clearly linked the intestinal and hepatic aspects of the disease.The pathogen was described in 1875 by Russian physician Fedor L ̈ osch, who noted the clinical course of the disease, identified the ameba, and induced similar lesions in dogs by feeding them ameba-rich stools from his patient. L ̈ osch, however, believed that something else initially caused the disease and that the ameba merely “sustained” it. Technical problems, especially in identifying amebas and determining which were pathogenic and which were harmless, greatly impeded further research. Stephanos Kartulis kept interest in the subject alive in the 1880s, establishing that an ameba was the probable cause of “tropical” dysentery.
Then in 1890, Canadian Henri Lafleur and American William Councilman published a definitive study of the pathology of the disease. German researchers H. Quincke and E. Roos distinguished between pathogenic and commensal human amebas. Still, the situation remained confused, as ameba identification and taxonomy was controversial, and many research results could not be replicated. Doubts about the significance of pathogenic amebas were widespread in the early 1900s.
Even Patrick Manson, perhaps the most important figure in tropical medicine, expressed skepticism about the role of amebas in dysentery as late as 1909. In 1913, American scientist Ernest Walker established the basic outline of the life cycle of E. histolytica and cleared some of the confusion about nonpathogenic forms. The discovery in 1925 of methods to raise amebas in culture has contributed to further clarification. Many mysteries remain, however, as to distinctions between pathogenic and nonpathogenic strains, and factors such as diet, stress, and concomitant infections that trigger invasiveness in longstanding, asymptomatic infections.
K. David Patterson
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