Diagnosis Clinical Manifestations and Pathology

Diagnosis depends on microscopic examination of stools, serologic tests, and clinical symptoms. The classic method, discovery of trophozoites or cysts in stools, is tedious and requires considerable skill, even with modern equipment and staining techniques. Trophozoites remain active only in fresh specimens and must be distinguished from commensal species and white blood cells. Preserved fecal specimens may be concentrated and stained, but detecting the adults and cysts and identifying them accurately are still difficult procedures. Furthermore, since trophozoites and cysts are not continually passed, more than one sample must be examined. Three or more specimens collected on separate days will find 80 to 90 percent of infections; fewer will be needed in symptomatic cases, as trophozoites are most readily detected in bloody patches in stools. Serologic tests also have limitations. Antibodies do not form unless amebas reach the bloodstream. It has been estimated that antibodies circulate in 85 to 90 percent of patients with liver abscess but in only 50 to 80 percent of those with severe dysentery. Serologic tests detect antibodies from recovered as well as active cases, which further limits the use of such methods in prevalence surveys.

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 conflu ent, 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 form 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. Diagnosis is by biopsy or serology. Chronic amebiasis, both intestinal and hepatic, is sometimes very difficult 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 to 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.

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