Pediatric Amebiasis Workup

  • Author: Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA; Chief Editor: Russell W Steele, MD   more...
 
Updated: May 10, 2012
 

Laboratory Studies

  • Laboratory diagnosis of amebiasis is made through the demonstration of the organism or immunologic techniques.[29, 30, 31, 32, 33]
  • Stool
    • Light microscopy: Examination of a fresh stool smear for trophozoites that contain ingested RBCs is rather insensitive. Routine microscopy cannot distinguish the E dispar and E moshkovskii (nonpathogenic amebae) from E histolytica.
    • An enzyme immunoassay kit to specifically detect E histolytica in fresh stool specimens is commercially available.
    • PCR-based diagnostic tests have been developed but are not widely available.[34, 35, 36] Field studies that directly compared PCR with stool culture or antigen-detection tests for the diagnosis of E histolytica infection suggest that these methods are equally comparable. PCR assay can also be used for detection of E histolytica in the liver aspirate for the diagnosis of amoebic liver abscess.[37]
      • The stool samples are always heme positive.
      • Fecal leukocytes may be absent.
  • Serum tests
    • Antibody tests: Serum antibodies against amebae are present in 70-90% of individuals with symptomatic intestinal E histolytica infection. Antiamebic antibodies are present in as many as 99% of individuals with liver abscess who have been symptomatic for longer than a week. Serologic examination should be repeated a week later in those with negative test on presentation. However, serologic tests do not distinguish new from past infection because the seropositivity persists for years after an acute infection. Several methods are commercially available for antibody detection.
      • Indirect hemagglutination antibody (IHA) test detects antibody specific for E histolytica. The antigen used in IHA consists of a crude extract of axenically cultured organisms. Antibody titers of more than 1:256 to the 170-kd subunit of the galactose-inhibitable adherence lectin are noted in approximately 95% of patients with extraintestinal amebiasis, 70% of patients with active intestinal infection, and 10% of asymptomatic individuals. IHA is not useful in differentiating acute from previous infection because high titers may persist for years after successful treatment. False-positive reactions at titers higher than 1:256 are rare.
      • EIA is as sensitive and specific as the IHA test and has replaced IHA in most laboratories.[38]
      • Immunodiffusion (ID) is simple to perform, making it ideal for the laboratory that has only an occasional request for amebic serology. However, it requires a minimum of 24 hours to complete, compared with 2 hours for the IHA or EIA test. ID is slightly less sensitive than IHA and EIA, but is equally specific.
      • Although detection of immunoglobulin M (IgM) antibodies specific for E histolytica has been reported, sensitivity in patients with current invasive disease is only about 64%.
    • The galactose lectin antigen is present in the serum of 75% of subjects with amebic liver abscess and may be particularly useful in patients presenting acutely, before an IgG serum anti-amebic antibody response occurs.
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Imaging Studies

  • Chest radiography may reveal an elevated right hemidiaphragm and a right-sided pleural effusion in patients with amebic liver abscess.
  • Ultrasonography is preferred for the evaluation of amebic liver abscess because of its low cost, rapidity, and lack of adverse effects. A single lesion is usually seen in the posterosuperior aspect of the right lobe of the liver. Multiple abscesses may occur in some patients. In an ultrasonographic evaluation of 212 patients, 34 (16%) had multiple abscesses, 75 (35%) had an abscess in the left lobe, and the remaining 103 (49%) had a solitary abscess in the right lobe.
  • CT may be slightly more sensitive than ultrasonography. In cerebral amebiasis, CT shows irregular lesions without a surrounding capsule or enhancement.
  • MRI reveals high signal intensity on T2-weighted images. Perilesional edema and enhancement of rim are noted after injection of gadolinium (86%).
  • Complete resolution of liver abscess may take as long as 2 years. Repeat imaging is not indicated if the patient is otherwise doing well.
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Other Tests

  • Leukocytosis without eosinophilia is observed in 80% of cases.
  • Mild anemia may be noted.
  • Liver function tests reveal elevated alkaline phosphatase levels (in 80% of patients), elevated transaminase levels, mild elevation of serum bilirubin level, and reduced albumin levels.
  • The erythrocyte sedimentation rate is elevated.
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Procedures

  • Rectosigmoidoscopy and colonoscopy with biopsy or scraping at margin of colonic mucosal ulcer provides valuable materials for diagnostic information in intestinal amebiasis. Small mucosal ulcers covered with yellowish exudates are observed. The mucosal lining between ulcers appears normal (see image below). Rectosigmoidoscopy and colonoscopy should be considered before using steroids in patients in whom inflammatory bowel disease is suspected. In a multivariate analysis, the best combination of findings to predict amebic colitis was the presence of cecal lesions, multiple lesions, and exudates.[39]
  • Biopsy results and a scraping of ulcer edge may reveal trophozoites. Indications for endoscopy in suspected intestinal amebiasis include the following:
    • Stool examination findings are negative, but the serum antibody test findings are positive.
    • Stool examination findings are negative, but immediate diagnosis is required.
    • Stool examination and antibody test results are negative, but amebiasis is strongly suspected.
    • Evaluation of chronic intestinal syndromes or mass lesions is desired.
  • Aspiration of the liver abscess is occasionally required to rule out a pyogenic abscess. Aspiration amebic liver abscess yields an anchovy-pastelike material that lacks WBCs due to lysis by the parasite. Amebae are visualized in the abscess fluid in a minority of patients with amebic liver abscess. Aspiration of liver is indicated only for large abscesses (>12 cm), imminent abscess rupture, failure of medical therapy, or presence of left lobe abscesses. Gross pathology of intestinal ulcers due to amebiaGross pathology of intestinal ulcers due to amebiasis. Courtesy of Centers for Disease Control and Prevention.
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Histologic Findings

  • Histopathologic findings include nonspecific mucosal thickening and focal ulcerations with or without amebae in a diffusely inflamed mucosal layer.
  • Classic flask-shaped ulcers may be seen with ulceration extending through the mucosa and muscularis mucosa into the submucosa (see following images). Histopathology of typical flask-shaped ulcer of inHistopathology of typical flask-shaped ulcer of intestinal amebiasis. Courtesy of Centers for Disease Control and Prevention. Histopathology of amebiasis. Courtesy of Centers fHistopathology of amebiasis. Courtesy of Centers for Disease Control and Prevention.
  • Staining with periodic acid–Schiff or immunoperoxidase and antilectin antibodies aid in the visualization of amebae.
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Contributor Information and Disclosures
Author

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

Coauthor(s)

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.

Specialty Editor Board

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.

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.

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.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

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.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Maria A Horga, MD, to the development and writing of this article.

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Entamoeba histolytica trophozoite. Courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica cyst. Courtesy of Centers for Disease Control and Prevention.
Life cycle of Entameba histolytica.
Gross pathology of intestinal ulcers due to amebiasis. Courtesy of Centers for Disease Control and Prevention.
Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica in liver aspirate, trichrome stain. Courtesy of Centers for Disease Control and Prevention.
Histopathology of amebiasis. Courtesy of Centers for Disease Control and Prevention.
 
 
 
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