Amebic Liver/Hepatic Abscesses

Updated: Mar 07, 2017
  • Author: Daniel Matei Brailita, MD; Chief Editor: BS Anand, MD  more...
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Overview

Background

Amebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection. This infection is caused by the protozoa E histolytica, which enters 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 by E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver where they typically form one or more abscesses. The E histolytica galactose/N-acetyl-D-galactosamine (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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Etiology

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, human immunodeficiency virus [HIV] infection, malnutrition with hypoalbuminemia, alcohol abuse, chronic infections, posttraumatic splenectomy, steroid use)
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Epidemiology

United States data

Amebic liver abscess is rare and is currently seen almost exclusively in immigrants or travelers to the United States. In 1994, 2,983 cases of amebiasis were reported to the Centers for Disease Control and Prevention (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 data

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.

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Prognosis

In most cases, rapid clinical improvement is observed in less than 1 week with antiamebic drug therapy alone. Radiological resolution lags behind the resolution of clinical symptoms. The average time to radiological resolution is approximately 12 months, with a range of 3 months to more than 10 years.

Death occurs in approximately 5% of persons having extraintestinal infection, including liver abscess. Rupture into the peritoneal cavity and the pericardium are responsible for most deaths.

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 a 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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Patient Education

Direct patient and public education at sanitary measures; personal hygiene, including hand washing; and food hygiene.

Educate travelers to endemic areas about the precautions needed. These details are discussed below.

Control of amebiasis can be achieved by exercising proper sanitary measures and avoiding fecally contaminated food and water, including the following:

  • Regular examination of food handlers and thorough investigation of diarrheal episodes may identify the source of infection in some communities.
  • Vegetables must be cleaned with a strong detergent soap and soaked in acetic acid or vinegar for approximately 15 minutes to eradicate the cyst forms.
  • Boiling is the only effective means of eradicating the cysts in water.

Change in sexual practices to avoid fecal-oral contamination is of importance in the male homosexual population.

Travelers to areas with suboptimal sanitation and hygiene should eat only cooked foods or fruits peeled by themselves and should avoid drinking local water, including ice cubes frequently used for cocktails. Notably, many types of bottled water in developing countries are not properly disinfected.

No prophylactic vaccine currently is available for amebiasis, but efforts to better define antigenic candidates and wider use of animal models are encouraging. [7, 8] Note the following:

  • A serine-rich E histolytica protein (SREHP) has been expressed in avirulent vaccine strains of Salmonella species.
  • E histolytica galactose/ N -acetyl-D-galactosamine (Gal/GalNAc) [9] and synthetic enhanced intranasal lectin-based amebiasis subunits [10] have been extensively studied as attractive candidates for vaccine development.

Gal-inhibitable lectin shows promise in animal studies. [11]

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