eMedicine Specialties > Gastroenterology > Liver

Amebic Hepatic Abscesses

Author: Daniel Matei Brailita, MD, Chief of Infectious Diseases, Mary Lanning Memorial Hospital
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; KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant Professor of Public Health, University of Texas School of Public Health; Ambrish Ojha, MD, Staff Physician, Department of Internal Medicine, Texas Tech University Health Sciences Center; Harvey Kantor, MD, Chief, Professor, Department of Internal Medicine, Division of Infectious Diseases, Texas Tech University Health Science Center
Contributor Information and Disclosures

Updated: Sep 19, 2008

Introduction

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.

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 apoptosis2 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.

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 areas3  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.

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.5 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.

Clinical

History

The signs and symptoms of amebic liver abscess often are nonspecific, resembling those of pyogenic liver abscess or other febrile diseases.6,7,8,9

  • Time of onset
    • Patients with amebic liver abscess usually present acutely (duration of symptoms <14 d), with the most frequent complaints being fever and abdominal pain. This presentation is characteristic of younger patients.
    • The subacute presentation is characterized by weight loss, and, in less than half the cases, abdominal pain and fever are present.
  • Abdominal pain
    • Abdominal pain is the most common element in the history and is present in 90-93% of patients.
    • The pain most frequently is located in the right upper quadrant (54-67%) and may radiate to the right shoulder or scapular area.
    • Pain increases with coughing, walking, and deep breathing, and it increases when patients rest on their right side.
    • The pain usually is constant, dull, and aching.
  • Constitutional symptoms
    • Fever is present in 87-100% of cases.
    • Rigors are present in 36-69% of cases.
    • Nausea and vomiting are present in 32-85% of cases.
    • Weight loss is present in 33-64% of cases.
  • Diarrhea
    • Diarrhea is present in less than one third of patients at the time of diagnosis.
    • Some patients describe a history of having had dysentery within the previous few months.
    • Bloody diarrhea is present in 7% of cases.
  • Pulmonary symptoms
    • Pulmonary symptoms are present in 18-26% of cases.
    • The most frequent symptoms are cough and chest pain, which may represent a sign of secondary pulmonary involvement by abscess rupture in the pleural cavity.
    • When coughing produces an odorless brown substance similar to anchovy paste, a bronchopleural fistula has developed.10
  • Recent travel to endemic areas
    • Onset of symptoms usually occurs within 8-12 weeks from the date of travel.
    • In 95% of cases, onset occurs within 5 months of returning from travel to an endemic area.
    • A remote travel history of as many as 12 years has been reported.

Physical

  • Fever is the most common sign and is found in as many as 99% of cases.
  • Hepatomegaly is present in some cases.
    • The frequency varies widely in different series published, reporting as high as 63% in one series and as low as 18% in another.
    • Hepatomegaly with pain upon palpation is one of the most important signs of amebic liver abscess.
    • Point tenderness over the liver, below the ribs, or in the intercostal spaces is a typical finding.
  • Abdominal tenderness
    • In 55-75% of cases, abdominal tenderness is located in the right upper abdominal quadrant.
    • When the abscess is located in the left lobe (28% of cases), epigastric tenderness is noted.
  • Pulmonary abnormalities
    • Pulmonary abnormalities are present in 20-45% of cases and consist of dullness and rales at the right lung base and nonproductive cough.
    • Breath sounds over the right lung base may be diminished.
    • Pleural rub may be audible.
  • Jaundice (<10% of cases) mostly occurs in complicated cases with multiple abscesses or a large abscess compressing the biliary tract.
  • Signs of complications
    • Signs of peritoneal irritation, such as rebound tenderness, guarding, and absence of bowel sounds, are present when the abscess ruptures in the peritoneal cavity. Peritonitis occurs in 2-7% of cases.
    • Pericardial friction rub can be audible when the abscess extends into the pericardium. This sign is associated with very high mortality.
    • Signs of pleural effusion are present when the abscess ruptures in the pleural cavity.

Causes

The following are the risk factors associated with amebic liver abscess:

  • Immigrants from endemic areas
  • Institutionalized persons, especially people with mental retardation
  • Crowding and poor hygiene
  • Men who have sex with men (secondary to sexually acquired amebic colitis)
  • Presence of immunosuppression (eg, HIV infection, malnutrition with hypoalbuminemia, alcohol abuse, chronic infections, posttraumatic splenectomy, steroid use)

More on Amebic Hepatic Abscesses

Overview: Amebic Hepatic Abscesses
Differential Diagnoses & Workup: Amebic Hepatic Abscesses
Treatment & Medication: Amebic Hepatic Abscesses
Follow-up: Amebic Hepatic Abscesses
Multimedia: Amebic Hepatic Abscesses
References
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References

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Further Reading

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Keywords

amebic hepatic abscesses, amebic hepatic abscess, amebic liver abscesses, amebic liver abscess, hepatic amebiasis, amebic colitis, Entamoeba histolytica, E histolytica

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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; Adjunct Assistant 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.

Medical Editor

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

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

Alex J Mechaber, MD, FACP, 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; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
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 and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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