Trypanosoma cruzi - Chagas Disease

Chagas disease or American trypanosomiasis is caused by Trypanosoma cruzi, a protozoan transmitted by infected Triatominae insects. Diagnosis is generally made by testing with at least two different serologic tests; IgG confirms chronic disease.


Indications for Testing

  • Residency in endemic area
  • Recent travel to endemic area
  • Cardiomyopathy or prototypical gastrointestinal disease without obvious etiology

Laboratory Testing

  • Trypanosomiasis diagnosis (CDC, 2014)
  • Acute phase (first 60-90 days)
    • Direct detection of parasites on blood smear (Giemsa stain)
    • IgM may be useful in acute infection
    • Polymerase chain reaction (PCR) is very sensitive when available
  • Nonacute (chronic) phase (>90 days)
    • IgG confirms chronic disease – by indirect fluorescent antibody (IFA), enzyme-linked immunosorbent assay (ELISA), or indirect hemagglutination antibody (IHA)
      • World Health Organization (WHO) recommends at least two tests to confirm disease
    • Cross-reactivity with Leishmania spp may occur
    • PCR requires further validation

Differential Diagnosis



  • Prevalence
    • U.S. – almost exclusively found in immigrants from Central and South America
    • Worldwide – 16-18 million individuals infected
  • Transmission
    • Triatominae vector species (kissing bug)
    • Maternal transplacental transfer (congenital)
    • Blood transfusion from infected donor
    • Organ transplantation
    • Ingestion of contaminated food/water (rare)


  • The genus Trypanosoma contains many species of protozoans
    • Only three cause human disease – T. cruziT. brucei gambiense, and T. brucei rhodesiense
    • Vectorborne from the reduviid Triatoma gerstaeckeri and others
      • Exposure to feces deposited on skin by infected bugs

Clinical Presentation

  • Acute phase
    • Mild symptoms occur for 2 weeks to 3 months
      • Romaña sign – unilateral painless edema of palpebral and periocular tissues
    • Initial signs include malaise, fever, anorexia, rash, and edema
    • Acute myocarditis in small percentage of cases
    • Indurated area of erythema and swelling (chagoma) may indicate parasite entry site
    • Frequently undetected at this stage
  • Chronic phase
    • May manifest decades later
    • Cardiomyopathy with arrhythmia
      • ~20-30% of patients (Bern, 2015)
      • Earliest sign is conduction defects – patient usually asymptomatic
      • Symptoms of biventricular failure – peripheral edema, hepatomegaly
      • ~60% experience sudden cardiac death
    • Digestive system complications
      • Megacolon
      • Ranges from mild achalasia to megaesophagus
  • Congenital disease
    • Highest risk for infection when maternal parasitemia is high during acute phase
    • Prematurity, hepatosplenomegaly, meningitis/encephalitis
  • Immunocompromised hosts
    • Organ transplant recipients – more severe clinical spectrum that can include acute myocarditis and congestive heart failure
    • Immunocompromised patient with reactivation – most common presentations are meningoencephalitis, brain abscess, and acute myocarditis

ARUP Laboratory Tests

Screen for and detect spirochetes and blood parasites, including microfilaria, Babesia, Trypanosoma, and Plasmodium species

Patient's travel history is necessary to aid in test interpretation

Aid in the diagnosis of Chagas disease (T. cruzi); may be useful in acute phase of disease

Order in conjunction with blood parasite screen

Aid in the diagnosis of nonacute (chronic phase) Chagas disease (T. cruzi)

If test results are equivocal, repeat testing in 10-14 days

Medical Experts



Marc Roger Couturier, PhD, D(ABMM)
Associate Professor of Pathology (Clinical), University of Utah
Medical Director, Parasitology/Fecal Testing, Infectious Disease Antigen Testing, Bacteriology, and Molecular Amplified Detection, ARUP Laboratories


Patricia R. Slev, PhD, D(ABCC)
Associate Professor of Pathology (Clinical), Codirector, Clinical Chemistry Fellowship program, University of Utah
Section Chief, Immunology; Medical Director, Immunology Core Laboratory; Medical Director, Serologic Hepatitis and Retrovirus and Immunology Core Laboratory; Medical Director, Microbial Immunology, ARUP Laboratories


Additional Resources