Amebic Hepatic Abscesses 

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

Background

Amebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection. This infection is caused by the protozoa E histolytica, which ascends the portal venous system. Amebic liver abscess is an important cause of space-occupying lesions of the liver, mainly in developing countries. Prompt recognition and appropriate treatment of amebic liver abscess lead to improved morbidity and mortality rates.

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Pathophysiology

E histolytica exists in 2 forms. The cyst stage is the infective form, and the trophozoite stage causes invasive disease. People who chronically carry E histolytica shed cysts in their feces; these cysts are transmitted primarily by food and water contamination. Rare cases of transmission via oral and anal sex or direct colonic inoculation through colonic irrigation devices have occurred. Cysts are resistant to gastric acid, but the wall is broken down by trypsin in the small intestine. Trophozoites are released and colonize the cecum. To initiate symptomatic infection, E histolytica trophozoites present in the lumen must adhere to the underlying mucosa and penetrate the mucosal layer.

Liver involvement occurs following invasion of E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver where they typically form large abscesses. The Gal/GalNAc lectin is an adhesion protein complex that sustains tissue invasion.[1] The abscess contains acellular proteinaceous debris, which is thought to be a consequence of induced apoptosis[2] and is surrounded by a rim of amebic trophozoites invading the tissue.

The right lobe of the liver is more commonly affected than the left lobe. This has been attributed to the fact that the right lobe portal laminar blood flow is supplied predominantly by the superior mesenteric vein, whereas the left lobe portal blood flow is supplied by the splenic vein.

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Epidemiology

Frequency

United States

Amebic liver abscess is rare and is currently seen almost exclusively in immigrants or travelers. In 1994, 2,983 cases of amebiasis were reported to the Centers for Disease Control (CDC). The disease was removed from the National Notifiable Diseases Surveillance System in 1995. An estimated 4% of patients with amebic colitis develop an amebic liver abscess.

An estimated 10% of the population is infected with Entamoeba dispar. Previously thought to be a nonpathogenic strain of E histolytica, this type of amoeba does not produce clinical symptoms even in the immunocompromised host.

International

Worldwide, approximately 40-50 million people are infected annually, with the majority of infections occurring in developing countries. The prevalence of infection is higher than 5-10% in endemic areas[3] and sometimes as high as 55%.[4] The highest prevalence is found in developing countries in the tropics, particularly in Mexico, India, Central and South America, and tropical areas of Asia and Africa.

Mortality/Morbidity

Infection with E histolytica ranks second worldwide among parasitic causes of death, following malaria.

  • Annually, 40,000-100,000 deaths are caused by infection with E histolytica.
  • Per year, a 10% risk of developing symptomatic invasive amebiasis exists after the acquisition of a pathogenic strain.[5]

Race

All races can be affected by amebic liver abscess. Risk factors for infection include travel or residence in endemic areas.

Sex

Amebic liver abscess is marked by a 7-12 times higher incidence in males than in females despite an equal sex distribution of noninvasive colonic amebic disease among adults.[6] However, no sexual preponderance exists among children.

Age

Peak incidence of amebic liver abscess occurs in people in their third, fourth, and fifth decades, although it can occur in any age group.

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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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