Amebic Hepatic Abscesses Workup

  • Author: Daniel Matei Brailita, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Nov 22, 2011
 

Laboratory Studies

  • Hematology
    • Approximately three fourths of patients with an amebic liver abscess have leukocytosis. This most likely will appear if symptoms are acute or complications have developed.
    • Eosinophilia is rare.
    • Anemia may be present, but the cause usually is multifactorial.
  • Chemistry
    • Hyperbilirubinemia is present in only a small proportion of cases.
    • In acute liver abscess, the aspartate aminotransferase (AST) levels are high.
    • In chronic liver abscess, the alkaline phosphatase level tends to be elevated and the AST level tends to be within normal limits. Overall, the alkaline phosphatase level is elevated in about 70% of cases of amebic liver abscess.
    • Similar CBC count and liver test abnormalities are found in patients with pyogenic liver abscesses and are not specific.
  • Stool examination
    • The role of microscopic stool examination is limited. Less than 30-40% of patients with amebic liver abscess have concomitant intestinal amebiasis, and 10% of the population is infected with the nonpathogenic strain of E dispar. Hence, the microscopic examination of the stool for the identification of cysts is of little value. If positive, it may suggest the diagnosis.
    • Fecal findings suggestive of amebic colitis include a positive test for heme, a paucity of neutrophils, and the presence of Charcot-Leyden crystal protein. The stool examination is still of value if the serologic and antigen identification tests are not available.
    • Examination of the stool for hematophagous trophozoites of E histolytica must be made on at least 3 fresh specimens because the trophozoites are very sensitive and may be excreted intermittently. A combination of wet mount, iodine-stained concentrates, and trichrome-stained preparations is used.
    • Upon examination of the stool, trophozoites may be confused with neutrophils. Cysts must be differentiated morphologically from nonpathogenic Entamoeba hartmanni, Entamoeba coli, and Endolimax nana. Nonpathogenic E dispar cannot be differentiated morphologically and require fecal antigen detection.
  • Stool antigen detection
    • Stool antigen detection facilitates early diagnosis before an antibody response occurs (< 7 d) and differentiates pathogenic from nonpathogenic Entamoeba infection. The primary drawbacks are the requirement for fresh, unpreserved stool specimens[12] and the lack of intestinal amebiasis in as many as 60% of patients with amebic liver abscess.
    • Stool antigen detection kits based on enzyme immunoassay (EIA) are most common and still quite sensitive compared to polymerase chain reaction (PCR)-based methods.[13]
    • The PCR stool test shows high sensitivity for detecting E histolytica and for distinguishing nonpathogenic amoebas.[14, 15, 16] However, this test is expensive. Real-time (rapid) PCR is sensitive but not well standardized[17] and is not widely available.
  • Stool culture for amoeba is sensitive but has limited availability.
  • Serologic testing
    • Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
    • EIA has now largely replaced indirect hemagglutination (IHA) testing and counter immunoelectrophoresis (CIE) testing. EIA is relatively simple and easy to perform, rapid, inexpensive, and more sensitive.[18, 19]
      • The EIA test detects antibodies specific for E histolytica in approximately 95% of patients with extraintestinal amebiasis, in 70% of patients with active intestinal infection, and in 10% of persons who are asymptomatic cyst passers.
      • The EIA serology findings revert to negative in 6-12 months following eradication of infection. Even in highly endemic areas, fewer than 10% of patients who are asymptomatic have positive amebic serology findings.
      • Initial negative test results may appear in as many as 10% of patients with amebic liver abscess. Under these circumstances, order repeat serology testing in 1 week. This test result will usually be positive.
  • Serum antigen detection
    • E histolytica galactose lectin antigen is detectable by enzyme-linked immunosorbent assay (ELISA) in at least 75% of serum samples obtained from patients with amebic liver abscess. Studies reported an antigen seropositivity of 96% with a reversal rate of 82% after 1 week of treatment with metronidazole. This test may be useful for patients who present acutely, before an antibody response occurs. The sample needs to be obtained before starting the treatment, as the treatment leads to rapid antigen loss. This test can be used for rapid diagnosis in highly endemic areas, where serology can be misleading, but it is not widely available.[12]
    • Rapid antigen and antibody tests are currently being evaluated and seem very promising.[20]
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Imaging Studies

  • Ultrasonography is the preferable initial diagnostic test. It is rapid, inexpensive, and is only slightly less sensitive than CT scan (75-80% sensitivity vs 88-95% for CT scan).
    • Ultrasonography simultaneously evaluates the gallbladder and avoids radiation exposure.
    • As opposed to scanning with technetium-99m, sonography often can distinguish an abscess from a tumor or other solid focal lesion.
    • The lesions tend to be round or oval, with well-defined margins, and hypoechoic.
  • CT scan is sensitive but the findings are not specific.
    • The abscess typically appears low density with smooth margins and a contrast-enhancing peripheral rim.
    • The use of injected contrast may differentiate hepatic abscesses from vascular tumors. See the images below.CT scan of the abdomen with IV and oral contrast iCT scan of the abdomen with IV and oral contrast is shown. Note the thick-walled cavity with low attenuation center and contrast-enhanced periphery. CT scan of the abdomen with contrast showing largeCT scan of the abdomen with contrast showing large amebic abscess with multiloculated appearance and atypical left liver lobe location. CT scan cannot differentiate amebic liver abscess from pyogenic liver abscess.
  • MRI is sensitive, but the findings are not specific. This test provides information comparable with less expensive imaging procedures.
  • Technetium-99m liver scanning is useful for differentiating an amebic liver abscess from a pyogenic abscess; however, it is not used as a first-line test.
    • Because amebic liver abscesses do not contain leukocytes, they appear as cold lesions on hepatic nuclear scanning, with a typical hot halo or a rim of radioactivity surrounding the abscess.
    • In contrast, pyogenic liver abscesses contain leukocytes and, therefore, typically appear as hot lesions on nuclear scanning.
  • Gallium scanning is helpful in differentiating pyogenic abscess (similar to technetium-99m nuclear hepatic scanning) but requires delayed images, which makes the test less helpful.
  • Hepatic angiography is only useful to differentiate liver abscesses from vascular lesions.
  • Plain chest or abdominal films may show elevation and limitation of motion of the right diaphragm, basilar atelectasis, and right pleural effusion or gas within the abscess cavity.
  • None of the imaging tests can definitely differentiate a pyogenic liver abscess, an amebic abscess, or malignant disease. Clinical, epidemiological, and serological correlation is needed for diagnosis.
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Procedures

  • Aspiration of the abscess content is indicated only if rupture of the abscess is thought to be imminent, differentiation between amebic abscess and pyogenic abscess is critical, or no response to antiprotozoal therapy occurs in 5-7 days (see Surgical Care).
    • Aspiration may be performed under CT scan or sonographic guidance.
    • Send the collected specimen for Gram stain and cultures.
    • Amebas rarely are recovered from the aspirate (15%), and often they are present only in the peripheral parts of the abscess, invading and destroying adjacent tissue.
    • Amebic liver abscesses only rarely yield positive bacterial cultures following secondary bacterial infection of the abscess cavity.
    • Detecting E histolytica antigen in the aspirate is possible and is accomplished as previously described for stool specimens. It is highly specific. The sensitivity was only 20% using ELISA, but newer PCR-based assays have a sensitivity of 83% and a specificity of 100%.[21, 22] However, currently, PCR-based detection is not widely available.
  • Many possible complications are associated with aspiration of the abscess.
    • The most common complications are infection and bleeding.
    • Other complications include amebic peritonitis or inadvertent puncture of an echinococcal cyst.
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Histologic Findings

The liver involvement in amebiasis consists of necrotic abscesses and periportal inflammation. The abscess contains acellular proteinaceous debris and is surrounded by a rim of amebic trophozoites invading tissue. The abscess contains a chocolate-colored fluid that resembles anchovy paste and consists predominantly of necrotic hepatocytes. Triangular areas of hepatic necrosis, possibly due to ischemia from amebic obstruction of portal vessels, have been observed. E histolytica can also induce hepatocyte and neutrophilic apoptosis. Some authors postulate that amebic liver abscess probably results from the coalescence of small microabscesses. Periportal fibrosis may be present, but whether this represents prior trophozoite invasion or a host reaction to amebic antigens or toxins is not known.

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Contributor Information and Disclosures
Author

Daniel Matei Brailita, MD  Chief of Infectious Diseases, Mary Lanning Memorial Hospital

Daniel Matei Brailita, MD is a member of the following medical societies: HIV Medicine Association of America and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Ildiko Lingvay, MD, MPH  Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas

Ildiko Lingvay, MD, MPH is a member of the following medical societies: Endocrine Society and Texas Medical Association

Disclosure: Nothing to disclose.

KoKo Aung, MD, MPH, FACP  Associate Professor, Department of Medicine, University of Texas Health Science Center at San Antonio; Adjunct Associate Professor of Public Health, University of Texas School of Public Health

KoKo Aung, MD, MPH, FACP is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Ambrish Ojha, MD  Staff Physician, Department of Internal Medicine, Texas Tech University Health Sciences Center

Ambrish Ojha, MD is a member of the following medical societies: American College of Physicians and American Medical Association

Disclosure: Nothing to disclose.

Harvey Kantor, MD  Chief, Professor, Department of Internal Medicine, Division of Infectious Diseases, Texas Tech University Health Science Center

Harvey Kantor, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Illinois State Medical Society, Infectious Diseases Society of America, New York Academy of Sciences, Royal Society of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert J Fingerote, MD, MSc, FRCPC  Consultant, Clinical Evaluation Division, Biologic and Gene Therapies, Directorate Health Canada; Consulting Staff, Department of Medicine, Division of Gastroenterology, York Central Hospital, Ontario

Robert J Fingerote, MD, MSc, FRCPC is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Oscar S Brann, MD, FACP  Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group

Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

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CT scan of the abdomen with IV and oral contrast is shown. Note the thick-walled cavity with low attenuation center and contrast-enhanced periphery.
CT scan of the abdomen with contrast showing large amebic abscess with multiloculated appearance and atypical left liver lobe location. CT scan cannot differentiate amebic liver abscess from pyogenic liver abscess.
 
 
 
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