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Amebiasis Workup

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

Laboratory Studies

Laboratory diagnosis of amebiasis is made by demonstrating the organism or by employing immunologic techniques.[48, 49, 50, 51, 52]

Findings from basic blood tests may include the following:

  • Leukocytosis without eosinophilia (80% of patients)
  • Elevated alkaline phosphatase level (80%)
  • Elevated transaminase levels
  • Mildly elevated bilirubin level
  • Reduced albumin level
  • Mild anemia
  • Elevated erythrocyte sedimentation rate (ESR)

Other laboratory studies employed for diagnosis include microscopy, culture, serologic testing, and polymerase chain reaction (PCR) assay.

Microscopy

Microscopic examination of fresh stool smears for trophozoites that contain ingested red blood cells (RBCs) is commonly done (see the image below).[16] The presence of intracytoplasmic RBCs in trophozoites is diagnostic of E histolytica infection, though some studies have demonstrated the same phenomenon with E dispar.

Trichrome stain of Entamoeba histolytica trophozoi 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.

Examination of a single stool sample has a sensitivity of only 33-50%; however, examination of 3 stool samples over no more than 10 days can improve the detection rate to 85-95%. It should be kept in mind that routine microscopy cannot be relied on to distinguish the pathogenic E histolytica from the nonpathogenic E dispar and E moshkovskii.

Stool leukocytes may be found, but in fewer numbers than in shigellosis.

Stool examination findings in patients with amebic liver abscess are usually negative. Repeated stool sampling in patients with proven amebic liver abscess is positive in 8-40% of cases. Identification of the parasite in a liver abscess aspirate is only 20% sensitive.

The World Health Organization (WHO) recommends that intestinal amebiasis be diagnosed with an E histolytica -specific test, thus rendering the classic ova-and-parasite stool examination obsolete.

Culture

Cultures can be performed either with fecal or rectal biopsy specimens or with liver abscess aspirates.[16] Culture has a success rate of 50-70%, but it is technically difficult. Overall, culture is less sensitive than microscopy.

Xenic cultivation, first introduced in 1925, is defined as the growth of the parasite in the presence of an undefined flora. This technique is still in use today, using modified Locke-egg media. Axenic cultivation, first achieved in 1961, involves growing the parasite in the absence of any other metabolizing cells. Only a few strains of E dispar have been reported to be viable in axenic cultures.

Antigen detection

Enzyme-linked immunosorbent assay (ELISA) is used to detect antigens from E histolytica in stool samples. Several kits are commercially available.[16]

Antigen-based ELISA kits using monoclonal antibodies against the galactose/N -acetylgalactosamine (GAL/GalNAc)–specific lectin of E histolytica (E histolytica II, TechLab, Blacksburg, VA) yield an overall sensitivity of 71-100% and a specificity of 93-100%. One study showed a much lower sensitivity (14.2%). In patients with amebic liver abscess, serum and liver aspirate antigen detection using the same kit was shown to yield a sensitivity of 96% in serum and 100% in liver aspirate.

Other stool detection kits use monoclonal antibodies against the serine-rich antigen of E histolytica (Optimum S; Merlin Diagnostika, Bornheim-Hersel, Germany) or against other specific antigens (Entamoeba CELISA-PATH, Cellabs, Brookvale, Australia; ProSpecT EIA, Remle Inc, Lenexa, KY).

No specific antigen tests are available for the detection of E dispar and E moshkovskii from clinical samples.

Antibody detection

Serum antibodies against amebae are present in 70-90% of individuals with symptomatic intestinal E histolytica infection.[16] Antiamebic antibodies are present in as many as 99% of individuals with liver abscess who have been symptomatic for longer than 1 week. Serologic examination should be repeated 1 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.

ELISA, the assay most commonly used worldwide, measures the presence of serum antilectin antibodies (immunoglobulin G [IgG]). 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 antiamebic antibody response occurs. The sensitivity of ELISA for detection of antibodies to E histolytica in patients with amebic liver abscess is 97.9%, and its specificity is 94.8%. False-negative results can occur within the first 7-10 days after infection.

Immunofluorescent assay (IFA) is also rapid, reliable, and reproducible. In the setting of amebic liver abscess, the sensitivity and specificity of IFA were shown to be 93.6% and 96.7%, respectively.

Indirect hemagglutination assay (IHA) 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 very specific (99.1%), but it is less sensitive than ELISA. It is not useful in differentiating acute infection from previous infection, because high titers may persist for years after successful treatment. False-positive reactions at titers higher than 1:256 are rare. ELISA has replaced IHA in most laboratories.[53]

Immunoelectrophoresis, counterimmunoelectrophoresis (CIE), and immunodiffusion (ID) use the precipitation property of antigen-antibody complexes in agar. CIE is time-consuming but has a sensitivity of 100% in invasive amebiasis. ID is simple to perform and thus ideal for laboratories that only rarely perform amebic serology; however, it requires a minimum of 24 hours, compared with 2 hours for IHA or ELISA. ID is slightly less sensitive than IHA and ELISA but is equally specific. Complement fixation (CF) is less sensitive than other techniques.

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%.

Polymerase chain reaction assay

A wide variety of PCR-based methods targeting different genes, including a small-subunit rRNA gene (18S rDNA), a 30-kd antigen gene, a serine-rich protein gene, a chitinase gene, a hemolysin gene, and extrachromosomal circular DNA, have been described for the detection and differentiation of E histolytica, E dispar, and E moshkovskii.[16]

Sensitivities can vary according to sampling and the specific target gene used. Field studies that directly compared PCR with stool culture or antigen-detection tests for the diagnosis of E histolytica infection found these methods to be comparably effective. PCR assay can also be used for detection of E histolytica in liver aspirates for the diagnosis of amoebic liver abscess.[54]

PCR-based tests have been strongly endorsed by the WHO. However, application of PCR-based methods in routine diagnosis is still very limited[55, 56, 57] ; the generation of nonspecific DNA fragments from environmental and clinical samples often leads to false-positive results.

Loop-mediated isothermal amplification assay

The loop-mediated isothermal amplification (LAMP) assay has been applied to the detection of E histolytica in cases of hepatic amebiasis. A study that compared this test with PCR testing in 50 patients with clinical suspicion of amebic liver abscess found that LAMP assay detected 5 additional abscesses that were missed by PCR assay.[58] The rapidity, operational simplicity, high specificity and sensitivity, and high yield of LAMP assay suggest that it may prove to be a better diagnostic tool than PCR assay for diagnosis of hepatic amebiasis.

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Radiography, Ultrasonography, CT, and MRI

Chest radiography may reveal an elevated right hemidiaphragm and a right-side pleural effusion in patients with amebic liver abscess.

Both ultrasonography and CT scanning are sensitive but nonspecific for amebic liver abscess. Ultrasonography is preferred for the evaluation of amebic liver abscess because of its low cost, rapidity, and lack of adverse effects. CT may be slightly more sensitive than ultrasonography. In cerebral amebiasis, CT shows irregular lesions without a surrounding capsule or enhancement.

On ultrasonograms, amebic liver abscesses usually appear as a solitary homogenous hypoechoic round lesion in the posterosuperior aspect of the right lobe of the liver (70-80% of cases), though 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.

On CT scans with intravenous (IV) contrast, amebic liver abscess can appear as a rounded, low-attenuation lesion with an enhancing rim. Furthermore, the abscess may be homogenous or septated, with or without observable fluid levels.

Magnetic resonance imaging (MRI) reveals high signal intensity on T2-weighted images. Perilesional edema and enhancement of rim are noted after injection of gadolinium (86% of cases).

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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Liver Aspiration

Ultrasound- or CT-guided needle aspiration of the liver should be performed when a diagnosis must be established very rapidly; pyogenic liver abscess can present and appear in similarly to amebic liver abscess.

Liver abscess aspirate is usually an odorless thick yellow-brown liquid classically referred to as “anchovy paste.” This liquid lacks white blood cells (WBCs) as a result of lysis by the parasite. Amebae are visualized in the abscess fluid in a minority of patients with amebic liver abscess (see the image below). Liver aspiration is indicated only if abscesses are large (> 12 cm), abscess rupture is imminent, medical therapy has failed, or abscesses are present in the left lobe.


Entamoeba histolytica in liver aspirate, trichrom Entamoeba histolytica in liver aspirate, trichrome stain. Image courtesy of Centers for Disease Control and Prevention.

The aspirate can be sent for microscopy, culture, antigen detection, and PCR, where available. A Gram stain should also be performed if a pyogenic etiology is suspected clinically.

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Lower GI Endoscopy

Rectosigmoidoscopy and colonoscopy with biopsy or scraping at the margin of a colonic mucosal ulcer provide valuable materials for diagnostic information in intestinal amebiasis. Tissue can be sent for microscopic evaluation, culture, and PCR assay, where available.

Indications for endoscopy in suspected intestinal amebiasis include the following:

  • Stool examination findings are negative, but 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

Fulminant colitis is a relative contraindication to colonoscopy, because it increases the risk of intestinal perforation.

On endoscopic examination, small mucosal ulcers covered with yellowish exudates are observed. The mucosal lining between the ulcers appears normal. The mucosa resembles that seen in inflammatory bowel disease (IBD). Biopsy results and a scraping of ulcer edge may reveal trophozoites. Ameboma (a carcinomalike annular lesion) can also be seen, usually in the cecum and ascending colon.[4, 59]

Rectosigmoidoscopy and colonoscopy should be considered before steroids are used in patients with suspected IBD. In a multivariate analysis, the best combination of findings for predicting amebic colitis was the combination of cecal lesions, multiple lesions, and exudates.[60]

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Histologic Findings

The intestinal biopsy specimen should be taken from the edge of ulcers and evaluated for motile trophozoites.

Histopathologic findings may include nonspecific mucosal thickening, multiple discrete ulcers separated by regions of normal-appearing colonic mucosa, diffusely inflamed and edematous mucosa, necrosis, or wall perforation (see the image below).

Gross pathology of intestinal ulcers due to amebia Gross pathology of intestinal ulcers due to amebiasis. Image courtesy of Centers for Disease Control and Prevention.

Amebic invasion through the mucosa and into submucosal tissues is the hallmark of amebic colitis; lateral extension through the submucosal tissues gives rise to the classic flask-shaped ulcer of amebic colitis (see the images below).

Histopathology of amebiasis. Image courtesy of Cen Histopathology of amebiasis. Image courtesy of Centers for Disease Control and Prevention.
Histopathology of typical flask-shaped ulcer of in Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Image courtesy of Centers for Disease Control and Prevention.

Different chemical stains can be used (see the image below), including periodic acid−Schiff stain, which makes E histolytica appear magenta in color.

Trichrome stain of Entamoeba histolytica cyst in a Trichrome stain of Entamoeba histolytica cyst in amebiasis. Each cyst has 4 nuclei with characteristically centrally located karyosomes. Cysts measure 12-15 mm.
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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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