- Clinical science
Chagas disease (American trypanosomiasis) is an infectious disease caused by the protozoan parasite Trypanosoma cruzi (T. cruzi), which is typically transmitted by triatomine bugs of the reduviid family. Chagas disease is endemic to Central and South America and most cases that occur in the US are reported in immigrants from endemic regions. Patients present initially with fever, swelling at the site of inoculation of triatomine feces, and generalized lymphadenopathy. These symptoms resolve within a few weeks, and the patient enters an asymptomatic latent phase, which may last for 10–20 years. Eventually, 10–30% of all infected patients enter a chronic phase and develop symptoms of Chagas cardiomyopathy and/or gastrointestinal disease characterized by achalasia and progressive dilation of the colon. The disease is diagnosed by thin and thick peripheral smears in the acute phase and by serological tests in the chronic phase. Chagas disease patients are treated with the antitrypanosomal drugs benznidazole and nifurtimox. Supportive therapy is required for Chagas cardiomyopathy and gastrointestinal disease. Treatment of Chagas disease is most effective when initiated early (in the acute phase).
- Global statistics
- Prevalence in the US: > 300,000 infected individuals
Epidemiological data refers to the US, unless otherwise specified.
Life cycle of T. cruzi in the triatomine insect
- Ingestion of the trypomastigote form of T. cruzi by the triatomine insect occurs during a blood meal.
- Transformation of the trypomastigotes into epimastigotes in the midgut and transformation of into metacyclic trypomastigotes in the hindgut occurs after 8–10 days.
- Metacyclic trypomastigotes are shed in feces.
Life cycle of T. cruzi in the human host
- Metacyclic trypomastigotes enter cells that are located in the vicinity of the wound site and/or mucosal membranes (e.g. conjunctiva).
- Within the cells, the metacyclic trypomastigote is converted into an amastigote, which then multiplies within the infected cell by binary fission.
- Intracellular amastigotes transform into trypomastigotes
- Both trypomastigotes and amastigotes are released into the blood stream by lysis of the infected cell.
Trypomastigotes can reinfect host cells and perpetuate the cycle within the host.
- The parasite causes immune-mediated tissue damage as a result of cross-reaction with T. cruzi antigens.
- Incubation period: 1–2 weeks
Acute phase (lasts ∼ 8–12 weeks)
- Fever, malaise, loss of appetite
- Cutaneous manifestations
- Generalized lymphadenopathy and hepatosplenomegaly
- Rarely (∼ 1% of cases): myocarditis, meningoencephalitis
- Indeterminate phase: Patient enters an asymptomatic latent phase.
Chronic phase (develops after ∼ 10–20 years)
- Chagas cardiomyopathy
- Gastrointestinal tract
- Rarely: infection of CNS tissue (esp. in immunocompromised patients)
- Confirmatory tests
- Additional tests
Chagas disease should be suspected in immigrants from endemic regions!
Treatment against Chagas disease is most effective when initiated early (in the acute phase). Drug toxicity is usually low in infants and younger children. Antitrypanosomal drugs are not FDA approved and can only be obtained from the CDC as an expanded access drug.
- First-line: benznidazole
- Second-line: nifurtimox
|Indication for antitrypanosomal therapy in Chagas' disease|
|Patient group||Antitrypanosomal therapy|
|Intermediate and chronic phase||< 18 years||✓|
|18–50 years||Patients in the indeterminate phase||✓|
|Patients in the chronic phase with early Chagas cardiomyopathy||?|
|Patients with advanced Chagas cardiomyopathy||×|
|> 50 years||?|
- Chagas cardiomyopathy
|Chagas cardioembolism score||Annual stroke risk||Stroke prophylaxis|
|3||2.1%||Warfarin or aspirin|
- Megaesophagus: see “Therapy” in
Instructions for people traveling to or working in endemic regions
- Use insect repellents and insecticide-treated bed nets.
- Avoid sleeping in poorly constructed houses with thatched roofs and cracked walls.
- Public health measures