In most infected persons, the organism lives as a commensal, and the carrier is without symptoms. With symptomatic disease, diarrhea may begin within a week of infection, although an incubation period of 2–4 weeks is more common, with gradual onset of abdominal pain and diarrhea. Fever is uncommon. Periods of remission and recurrence may last days to weeks or longer. Abdominal examination may show distention, tenderness, hyperperistalsis, and hepatomegaly. Microscopic hematochezia is common. More severe presentations include colitis and dysentery, with worse diarrhea (10–20 stools per day) and bloody stools. With dysentery, physical findings include high fevers, prostration, vomiting, abdominal pain and tenderness, hepatic enlargement, and hypotension. Severe presentations are more common in young children, pregnant women, those who are malnourished, and those receiving corticosteroids. Thus, in endemic regions, corticosteroids should not be started for presumed inflammatory bowel disease without first ruling out amebiasis. Fulminant amebic colitis can progress to necrotizing colitis, intestinal perforation, mucosal sloughing, and severe hemorrhage, with mortality rates over 40%. More long-term complications of intestinal amebiasis include chronic diarrhea with weight loss, which may last for months to years; bowel ulcerations; and amebic appendicitis. Localized granulomatous lesions (amebomas) can present after either dysentery or chronic intestinal infection. Clinical findings include pain, obstructive symptoms, and hemorrhage and may suggest intestinal carcinoma.
2. Extraintestinal amebiasis
The most common extraintestinal manifestation is amebic liver abscess. This can occur with colitis, but more frequently presents without history of prior intestinal symptoms. Patients present with the acute or gradual onset of abdominal pain, fever, an enlarged and tender liver, anorexia, and weight loss. Diarrhea is present in a small number of patients. Physical examination may show intercostal tenderness. Abscesses are most commonly single and in the right lobe of the liver, and they are much more common in men. Without prompt treatment, amebic abscesses may rupture into the pleural, peritoneal, or pericardial space, which is often fatal. Amebic infections may rarely occur throughout the body, including the lungs, brain, and genitourinary system.
Laboratory studies with intestinal amebiasis show leukocytosis and hematochezia, with fecal leukocytes not present in all cases. With extraintestinal amebiasis, leukocytosis and elevated liver function studies are seen.
Diagnosis is typically made by finding E histolytica or its antigen or by serologic tests. However, each method has limitations. Molecular diagnosis is possible from multi-pathogen panels, which are sensitive and specific but expensive.
Diagnosis is most commonly made by identifying organisms in the stool. E histolytica and E dispar cannot be distinguished, but the identification of amebic trophozoites or cysts in a symptomatic patient is highly suggestive of amebiasis (eFigure 35–12). Stool evaluation for organisms is not highly sensitive (~30–50% for amebic colitis), and at least three stool specimens should be evaluated after concentration and staining. Multiple serologic assays are available; these tests are fairly sensitive, although sensitivity is lower (~70% in colitis) early in illness, and they cannot distinguish recent and old disease, as they remain positive for years after infection. Commercially available stool antigen tests (TechLab II, CELISA, QUIK CHEK) can distinguish E histolytica from nonpathogenic species and offer improved sensitivity (greater than 90% for colitis). The QUIK CHEK assay is FDA-approved, offers rapid point-of-care diagnosis, and is available in a combined assay for amebiasis, giardiasis, and cryptosporidiosis. Highly sensitive molecular tests are not used routinely but available in some high resource settings within commercial panels for identifying gut pathogens. Colonoscopy of uncleansed bowel typically shows no specific findings in mild intestinal disease; in severe disease, ulcers may be found with intact intervening friable mucosa, resembling inflammatory bowel disease (Figure 35–7). Examination of fresh ulcer exudate for motile trophozoites and for E histolytica antigen may yield a diagnosis.
Trophozoites of Entamoeba histolytica with ingested erythrocytes stained with trichrome. The ingested erythrocytes appear as dark inclusions. Erythrophagocytosis (ingestion of red blood cells by the parasite) is the only morphologic characteristic that can be used to differentiate E histolytica from the nonpathogenic Entamoeba dispar. However, erythrophagocytosis is not typically observed on stained smears of E histolytica. The parasites above show nuclei that have the typical small, centrally located karyosome, and thin, uniform peripheral chromatin. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.)
Gross pathology showing intestinal ulcers due to amebiasis. (From Dr. Mae Melvin, Public Health Image Library, CDC.)
Serologic tests for anti-amebic antibodies are almost always positive, except very early in the infection. Thus, a negative test in a suspicious case should be repeated in about a week. The TechLab II antigen test can be used to test serum with good sensitivity if used before the initiation of therapy. Examination of stools for organisms or antigen is frequently negative; the antigen test is positive in ~40% of cases. As imaging studies cannot distinguish amebic and pyogenic abscesses, when a diagnosis is not available from serologic studies, percutaneous aspiration may be indicated, ideally with an image-guided needle. Aspiration typically yields brown or yellow fluid. Detection of organisms in the aspirate is uncommon, but detection of E histolytica antigen is very sensitive and diagnostic. The key risk of aspiration is peritoneal spillage leading to peritonitis from amoebas or other (pyogenic or echinococcal) organisms.
Liver abscesses can be identified by ultrasonography, CT, or MRI, typically with round or oval low-density nonhomogeneous lesions, with abrupt transition from normal liver to the lesion, and hypoechoic centers. Abscesses are most commonly single, but more than one may be present. The right lobe is usually involved.