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Amebic Hepatic Abscesses

  • Author: Daniel Matei Brailita, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Apr 15, 2015
 

Background

Amebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection. This infection is caused by the protozoa E histolytica, which enter the portal venous system from the colon. 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.

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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.

Race-, sex-, and age-related demographics

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

Amebic liver abscess is marked by a 7-12–fold higher incidence in males than in females despite an equal sex distribution of noninvasive colonic amebic disease among adults.[3] However, no sexual preponderance exists among children.

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

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[4] and sometimes as high as 55%.[5] 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.[6]

Complications

Pleuropulmonary infection is the most common complication. Mechanisms of infection include development of a sympathetic serous effusion; rupture of a liver abscess into the chest cavity, leading to empyema; or hematogenous spread, resulting in parenchymal infection.

Bronchopleural fistula may occur in rare instances when patients expectorate a substance that resembles anchovy paste. Trophozoites may be demonstrated in the fluid. Occasionally, this complication may be followed by a spontaneous cure of the amebic liver abscess.

Cardiac involvement results following the rupture of an abscess involving the left lobe of the liver. It usually is associated with very high mortality.

Intraperitoneal rupture occurs in 2-7% of patients. Left lobe abscesses are more likely to progress to rupture because of their later clinical presentation.

Bacterial superinfection can occur.

Rupture into peritoneal organs (eg, stomach) and mediastinum can occur.

Cases of hepatic artery pseudoaneurysm have been reported.

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Contributor Information and Disclosures
Author

Daniel Matei Brailita, MD Infectious Disease Specialist, Mary Lanning Healthcare and Central Nebraska Infectious Diseases

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

Disclosure: Nothing to disclose.

Coauthor(s)

KoKo Aung, MD, MPH, FACP Chief, Division of General Internal Medicine, O Roger Hollan Professor of Internal Medicine, Director, Office of Educational Programs, Department of Medicine, University of Texas Health Science Center at San Antonio

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Received consulting fee from GI Dynamics for consulting; Received honoraria from NovoNordisk, Inc for board membership.

Ambrish Ojha, MBBS 

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

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, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

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.

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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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