eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Trypanosomiasis: Differential Diagnoses & Workup

Author: 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
Coauthor(s): Antonio Muñiz, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Texas Medical School at Houston; Medical Director of the Pediatric Emergency Department, Children's Memorial Hermann Hospital
Contributor Information and Disclosures

Updated: Jan 27, 2009

Differential Diagnoses

African Trypanosomiasis (Sleeping Sickness)
Malaria
Amebic Meningoencephalitis
Meningitis, Aseptic
Aspiration Syndromes
Meningitis, Bacterial
Atrioventricular Block, Second Degree
Mononucleosis and Epstein-Barr Virus Infection
Atrioventricular Block, Third Degree, Acquired
Mumps
Atrioventricular Block, Third Degree, Congenital
Myocardial Infarction in Childhood
Bronchiectasis
Myocarditis, Nonviral
Bundle Branch Block, Left
Myocarditis, Viral
Bundle Branch Block, Right
Nephrotic Syndrome
Cardiomyopathy, Dilated
Parvovirus B19 Infection
Constipation
Pericardial Effusion, Malignant
Cytomegalovirus Infection
Pericarditis, Bacterial
Encopresis
Pericarditis, Constrictive
Gastroesophageal Reflux
Pericarditis, Viral
Herpes Simplex Virus Infection
Rheumatic Heart Disease
Hirschsprung Disease
Sinus Node Dysfunction
Intestinal Malrotation
Sinusitis
Intestinal Volvulus
Syphilis
Intussusception
Toxoplasmosis
Leishmaniasis
Tuberculosis
Leprosy
Lymphadenopathy

Other Problems to Be Considered

Achalasia
Arteriosclerotic heart disease
Collagen vascular diseases
Congenital megacolon
Congestive heart failure
Conjunctivitis
Cellulitis
Parotitis

Workup

Laboratory Studies

  • During the acute phase of trypanosomiasis, the CBC count may reveal leukocytosis with relative lymphocytosis, and transaminase levels are often elevated.
  • During acute illness (ie, the first 6-12 wk), parasites are frequently seen in blood smears, using either Giemsa staining or direct wet-mount preparations (in which motile parasites may be seen). Sensitivity is 80-90%. Thickly-stained and thinly-smeared blood can allow morphologic characterization of the parasite and differentiation from other trypanosomes, but these preparations are less sensitive (60%). Concentration using centrifugation after red-cell lysis or clotting and examination of the buffy coat increases detection to 90-100%.
  • In late infections, low levels of parasitemia are present; therefore, blood smear results are often negative. To confirm the diagnosis, parasites in the blood must be cultured on a special medium or identified by means of xenodiagnosis.
  • Serologic tests for anti– T cruzi immunoglobulin M (IgM) play a limited role in the diagnosis because these tests are not widely available or standardized. In recent human infections, antibodies of the IgM class appear in the blood stream 15 days after infection, peak 17-45 days after infection, and persist for years. Antibodies of the IgM isotype predominate during the acute phase. Later, in the latent and chronic stages, antibodies are primarily from the IgG and IgA classes. Serologic tests include complement fixation (CF), indirect hemagglutination (IHA), and indirect immunofluorescence. False-positive results can occur with leishmaniasis, malaria, collagen vascular disease, and syphilis.
    • The CF test, or Machado-Guerreiro test, is considered the most reliable immunodiagnostic method for diagnosis. The indirect fluorescent antibody test (IFAT) is rapid and easy to perform, has a high sensitivity, and can be used to differentiate IgM antibodies from IgG antibodies. Enzyme-linked immunosorbent assay (ELISA) is as sensitive as the IFAT and can also be used to differentiate IgM antibodies from IgG antibodies.
    • Several agglutination tests have been developed that detect the presence of antibodies against T cruzi, such as the indirect IHA, direct agglutination (DA), latex agglutination (LA), and flocculation tests. IFAT reveals the earliest positive results for IgM antibodies after initial infection, followed by the DA method. All of these tests have been reported to provide positive results in more than 95% of the sera from infected humans.
    • A persistent problem with these tests is false-positive reactions. These have been observed with leishmaniasis, malaria, syphilis, infectious mononucleosis, tuberculosis, leprosy, and collagen vascular disease. The use of a minimum of 2 different, independently performed serologic tests is recommended to confirm infection.
    • In the United States, CF and IFAT are available from the Centers for Disease Control and Prevention (CDC). In addition, the Food and Drug Administration has approved assays based on the ELISA format for use in clinical testing; these are performed at Abbott Laboratories in Illinois and Gull Laboratories in Utah.
    • T cruzi kinetoplast DNA has been observed using polymerase chain reaction (PCR) amplification,3,4 which can be used to identify as few as 1 parasite in 20 mL of blood with a sensitivity of 96-100%.
  • Xenodiagnosis is the best method for parasitologic diagnosis in the latent or chronic phases. It consists of allowing laboratory-reared reduviid nymphs to feed on blood from an infected patient. The feces and intestines of the nymphs are examined 20-60 days later for the presence of the parasites. Test results are positive in approximately 50% of individuals.
  • PCR has been used to detect T cruzi in congenital cases of trypanosomiasis and to follow the efficacy of patients treated for Chagas disease.
  • Blood cultures have positive results in 100% of patients with acute-phase illness but only 40-50% in those with chronic illness.
  • Blood banks in areas of endemic disease use either the IHA or LA tests for disease detection. Recent studies involving the use of ELISA for the detection of antibodies to T cruzi and a radioimmunoprecipitation assay had a sensitivity and specificity of 100%.
  • In people who are immunosuppressed and thought to have Chagas disease, examine other specimens, such as lymph node aspirates, bone marrow, cerebrospinal fluid, and pericardial fluid, if the presence of T cruzi cannot be confirmed in the blood.
  • In congenital Chagas disease, an indirect immunofluorescence test with anti-IgM has been introduced recently and it is effective in confirming acute congenital disease. Test infants of seropositive mothers as soon as possible for the presence of circulating parasites and specific IgM antibody.
  • Atrial natriuretic factor is a sensitive marker capable of detecting gradual impairments in cardiac function and suggests poor survival in patients with Chagasic cardiomyopathy.  Brain natriuretic peptide has also been shown to be a marker for severity of disease in Chagas disease.
  • N -terminal proBNP has been shown to be a marker of impaired left ventricular dysfunction.5

Imaging Studies

  • In patients with cardiac involvement, chest radiography may reveal cardiac enlargement with clear lung fields.
  • In patients with advanced esophageal involvement, chest radiography may reveal a tubular mass along the aorta and air-fluid level, which reflects the retention of swallowed material in the esophagus.
  • Fluoroscopic esophagrams obtained with barium often show the absence of mucosal irregularities and a variably dilated esophagus with a narrow, conical segment at its lower end that represents the nonrelaxing sphincter (bird-beak appearance). In advanced disease, the diameter is grossly enlarged, causing it to fold over the diaphragm.
  • Cine-esophagrams may show tertiary contractions and accumulation of the contrast material.
  • Manometry in patients with Chagas disease typically reveals loss of peristalsis upon deglutition and an abnormally elevated pressure in the lower esophageal sphincter, which fails to relax.
  • Scintigraphy is as sensitive as manometry in depicting esophageal dysmotility and it reveals patterns of transit similar to those described in idiopathic achalasia.
  • In colonic involvement, barium enema examination is the cornerstone for diagnosis. The sigmoid colon is frequently dilated and elongated in nearly all cases, and the rectum is dilated in 80% of cases.
  • Echocardiography is used to assess for evidence of acute chagasic myocarditis or chronic Chagas cardiomyopathy.6  In the acute setting, echocardiography may reveal pleural effusions, apical or anterior dyskinesis, and left ventricular dilatation. In patients with chronic disease, echocardiography may reveal left ventricular aneurysm, segmental wall abnormalities, left ventricular dilatation, decreased left ventricular ejection fraction, diastolic dysfunction, tricuspid, and mitral regurgitation.
  • Thallium stress-redistribution myocardial perfusion scintigraphy may reveal reversible and irreversible perfusion defects in chronic Chagas cardiomyopathy. The perfusion defects occur in the presence of normal epicardial coronary arteries and probably represent myocardial fibrosis, coronary microvasculature abnormalities, or extensive impairment of cardiac sympathetic function.
  • Cardiac MRI has been shown to be the most accurate method to detect myocardial fibrosis in patients with Chagas disease. CMR offers a wide variety of imaging tools to evaluate morphology, function, and other tissue characterization abilities, such as edema and fat.

Other Tests

  • Electrocardiography may be useful.
    • The most common electrocardiographic abnormalities in acute infection include sinus tachycardia, prolongation of the PR interval, S-T segment depression and T-wave inversion, low voltage of the QRS complex, and prolongation of the QT interval.7
    • The most common electrocardiographic manifestations in chronic disease are intraventricular blocks (right bundle branch block and left anterior hemiblock), sinus bradycardia, atrioventricular (AV) block (first degree, second degree, complete), sinoatrial block, atrial fibrillation, and premature ventricular beats.
  • Lumbar puncture may demonstrate pleocytosis with a predominance of lymphocytes and elevated protein level; often, it reveals the presence of T cruzi.
  • Complex ventricular dysrhythmias during stress testing are a clinical marker for progressive cardiomyopathy in Chagas disease. 

Procedures

  • Endoscopy is not essential to the diagnosis of chagasic achalasia. Its main value is in the identification of other disorders, such as gastric and esophageal cancer, which are more common in patients with chagasic megaesophagus.

Histologic Findings

  • The lesion at the parasite's portal of entry has a predominance of lymphocytic, monocytic, and eosinophilic infiltration, with the presence of giant cells. When the heart is invaded, myocardial fibers are often edematous and undergo various stages of focal necrosis, which primarily involves the contractile and conduction systems.
  • Interspersed among the degenerating fibers is a markedly mixed inflammatory cell exudate consisting of granulocytes, lymphocytes, monocytes, mast cells, and plasma cells.
  • Diffuse inflammation of the myocardium is present, as well as dense foci of fibrosis in the interstitial spaces and invasion of lymphocytes, plasma cells, and macrophages. In two thirds of the cases, the detection of parasites in the myocardium is difficult.

More on Trypanosomiasis

Overview: Trypanosomiasis
Differential Diagnoses & Workup: Trypanosomiasis
Treatment & Medication: Trypanosomiasis
Follow-up: Trypanosomiasis
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

trypanosomiasis, American trypanosomiasis, Chagas disease, Chagas' disease, chagasic heart disease, chagasic megaesophagus, chagoma, chronic Chagas disease, chronic chagasic cardiopathy, contraction band necrosis, dyspepsia, focal myonecrosis, interstitial fibrosis, Kinetoplastida, lymphocytic infiltration, megacolon, megaduodenum, megaesophagus, parasitemia, parasitic disease, Romaña sign, Romaña's sign, Schizotrypanum, triatomid, Trypanosoma cruzi, T cruzi, Trypanosomatina

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Contributor Information and Disclosures

Author

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: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

Antonio Muñiz, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Texas Medical School at Houston; Medical Director of the Pediatric Emergency Department, Children's Memorial Hermann Hospital
Antonio Muñiz, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Medical Association, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital
Ashir Kumar, MBBS, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association of Physicians of Indian Origin, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine
Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

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: None None None

 
 
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