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Amebiasis Treatment & Management

  • Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 24, 2016
 

Approach Considerations

Treatment of amebiasis includes pharmacologic therapy, surgical intervention, and preventive measures, as appropriate. Most individuals with amebiasis may be treated on an outpatient basis. Several clinical scenarios may favor inpatient care, as follows:

  • Severe colitis and hypovolemia requiring intravenous (IV) volume replacement
  • Liver abscess that is of uncertain etiology or is not responding to empiric therapy
  • Fulminant colitis requiring surgical evaluation
  • Peritonitis and suspected amebic liver abscess rupture

Intestinal amebiasis may be mistakenly treated as if it were inflammatory bowel disease (IBD). Accordingly, in all patients with suspected IBD, lower gastrointestinal (GI) endoscopy should be performed before treatment with steroids is initiated.

The following consultations may be helpful:

  • Infectious disease specialist
  • General surgeon
  • GI specialist

Follow-up stool examination after therapy completion is recommended to ensure intestinal eradication. No special diet is recommended.

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Pharmacologic Therapy

In endemic areas, asymptomatic infections are not treated. In nonendemic areas, however, asymptomatic infection should be treated[61] ; luminal agents that are minimally absorbed by the GI tract (eg, paromomycin, iodoquinol, and diloxanide furoate) are best suited for such therapy.[62, 63] This recommendation is based on 2 arguments: first, that invasive disease may develop, and second, that shedding of E histolytica cysts in the environment is a public health concern.[4]

Asymptomatic E dispar infections should not be treated, but because this organism is a marker of fecal-oral contamination, educational efforts should be initiated.[4]

Metronidazole is the mainstay of therapy for invasive amebiasis.[61, 64, 65] Tinidazole has been approved by the US Food and Drug Administration (FDA) for intestinal or extraintestinal amebiasis. Other nitroimidazoles with longer half-lives (ie, secnidazole and ornidazole) are currently unavailable in the United States.

Nitroimidazole therapy leads to clinical response in approximately 90% of patients with mild-to-moderate amebic colitis. Because intraluminal parasites are not affected by nitroimidazoles, nitroimidazole therapy for amebic colitis should be followed by treatment with a luminal agent (eg, paromomycin or diloxanide furoate) to prevent a relapse.[4]

Amebic liver abscess of up to 10 cm can be cured with metronidazole without drainage.[66] Clinical defervescence should occur during the first 3-4 days of treatment. Failure of metronidazole therapy may be an indication for surgical intervention. Treatment with a luminal agent should also follow.[4]

Chloroquine has also been used for patients with hepatic amebiasis. Dehydroemetine (available from the Centers for Disease Control and Prevention [CDC] Drug Service [404-639-3670]) has been successfully used but, because of its potential myocardial toxicity, is not preferred.

Broad-spectrum antibiotics may be added to treat bacterial superinfection in cases of fulminant amebic colitis and suspected perforation. Bacterial coinfection of amebic liver abscess has occasionally been observed (both before and as a complication of drainage), and adding antibiotics to the treatment regimen is reasonable in the absence of a prompt response to nitroimidazole therapy.

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Surgical and Percutaneous Intervention

Surgical intervention is required for acute abdomen that is due to any of the following[67] :

  • Perforated amebic colitis
  • Massive GI bleeding
  • Toxic megacolon (rare and typically associated with the use of corticosteroids)

Surgical intervention is usually indicated in the following clinical scenarios[4] :

  • Uncertain diagnosis (possibility of pyogenic liver abscess)
  • Concern about bacterial suprainfection in amebic liver abscess
  • Failure to respond to metronidazole after 4 days of treatment
  • Empyema after amebic liver abscess rupture
  • Large left-side amebic liver abscess representing risk of rupture in the pericardium
  • Severely ill patient with imminent amebic liver abscess rupture

Unlike pyogenic liver abscess, uncomplicated amebic liver abscess generally responds to medical therapy alone; drainage is seldom necessary and is usually best avoided. When drainage is necessary, image-guided percutaneous intervention (ie, needle aspiration or catheter drainage[68] ) has replaced surgical intervention as the procedure of choice. The indications for drainage of amebic liver abscess include the following:

  • Presence of a left-lobe abscess more than 10 cm in diameter
  • Impending rupture and abscess that does not respond to medical therapy within 3-5 days

Percutaneous catheter drainage improves treatment outcomes in amebic empyema and is life-saving in amebic pericarditis. It should be used judiciously in the setting of localized intra-abdominal fluid collections.

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Prevention

Amebiasis is prevented by eradicating fecal contamination of food and water through improved sanitation, hygiene, and water treatment. In nonendemic areas, disease transmission can be reduced by early treatment of carriers.

Amebic cysts are not killed by soap or low concentrations of chlorine or iodine; therefore, water in endemic areas should be boiled for more than 1 minute and vegetables should be washed with a detergent soap and soaked in acetic acid or vinegar for 10-15 minutes before consumption.

Avoiding sexual practices that involve fecal-oral contact may reduce the risk of sexual transmission of infective cysts. Because reinfection is possible, family members or close contacts of an index case should be screened.

In humans, natural E histolytica infection does not seem to result in long-term immunity: individuals with a previous amebic liver abscess are as susceptible to a new infection as other members of the population are.[4]

Vaccinations using native and recombinant forms of Gal-lectin have been successful in protecting animals against intestinal amebiasis and amebic liver abscess. Protection against amebic liver abscesses has also been reported by targeting other E histolytica components, including the serine-rich protein and the 29-kDa-reductase antigen. To date, vaccines against the Gal-lectin hold the most promise, but clinical trials are required to validate its efficacy in humans.

Development of a vaccine for invasive amebiasis is still in its infancy.[69, 70, 71] Many components of the ameba are immunogenic and may serve as targets for a future vaccine, including the galactose/N -acetylgalactosamine lectin, the serine-rich E histolytica protein, cysteine proteinases, lipophosphoglycans, amebapores, and the 29-kd protein. Quach et al recently reviewed current strategies involved in the development of a vaccine against E histolytica.[72]

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Contributor Information and Disclosures
Author

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Pfizer Inc for speaking and teaching.

Coauthor(s)

Kerry O Cleveland, MD Professor of Medicine, University of Tennessee College of Medicine; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Methodist Healthcare of Memphis

Kerry O Cleveland, MD is a member of the following medical societies: American College of Physicians, Society for Healthcare Epidemiology of America, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

J Robert Cantey, MD Professor, Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina

J Robert Cantey, MD is a member of the following medical societies: Alpha Omega Alpha, American Society for Microbiology, International Society of Travel Medicine, Southern Society for Clinical Investigation, Musculoskeletal Infection Society, American Society for Clinical Investigation, Infectious Diseases Society of America, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Michael Stuart Bronze, MD Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Maria A Horga, MD Assistant Professor, Department of Pediatric Infectious Diseases, Bristol-Myers Squibb

Disclosure: Nothing to disclose.

Alexandre Lacasse, MD, MSc Internal Medicine Faculty, Assistant Director, Medicine Clinic, Infectious Disease Consultant, St Mary's Health Center

Alexandre Lacasse, MD, MSc is a member of the following medical societies: American College of Physicians, American Medical Association, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, and Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Thomas R Naparst, MD Clinical Instructor in Emergency Medicine, New York University School of Medicine; Consulting Staff, Department of Emergency Medicine, New York Downtown Hospital

Thomas R Naparst, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michael D Nissen, MBBS, FRACP, FRCPA Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Robert Swords, MD Fellow, Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina

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

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Trichrome stain of Entamoeba histolytica trophozoites in amebiasis. Two diagnostic characteristics are observed. Two trophozoites have ingested erythrocytes, and all 3 have nuclei with small, centrally located karyosomes.
Trichrome stain of Entamoeba histolytica cyst in amebiasis. Each cyst has 4 nuclei with characteristically centrally located karyosomes. Cysts measure 12-15 mm.
Entamoeba histolytica trophozoite. Image courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica cyst. Image courtesy of Centers for Disease Control and Prevention.
Life cycle of Entamoeba histolytica.
Gross pathology of intestinal ulcers due to amebiasis. Image courtesy of Centers for Disease Control and Prevention.
Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Image courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica in liver aspirate, trichrome stain. Image courtesy of Centers for Disease Control and Prevention.
Histopathology of amebiasis. Image courtesy of Centers for Disease Control and Prevention.
 
 
 
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