RCH logo

Immigrant Health Service

Chagas disease

  • Background

    Chagas disease (American Trypanosomiasis) is a chronic systemic parasitic infection caused by the protozoan parasite Trypanosoma cruzi. The condition was first described by the Brazilian physician Carlos Chagas in 1909, and was recognised as a neglected tropical disease by the World Health Organization (WHO) in 2005.1 

    Transmission - T. cruzi is primarily transmitted by infected triatomine insect vectors ('kissing bugs') - see life cycle.2 Triatomine bugs are found in housing with earthen walls/floors, and most species feed nocturnally. Triatomine bugs transmit the infection through taking a blood meal and releasing trypomastigotes in faeces, contaminating the bite wound. Trypomastigotes can also enter the host through intact mucosal membranes (e.g. oral mucosa, conjunctivae). Other modes of transmission include vertical (during pregnancy/birth causing congenital disease),3 and through blood transfusion, solid organ or bone marrow transplant, laboratory accidents, and ingestion of food or liquid contaminated with faeces of infected triatomine bugs.1,4

    Epidemiology - Chagas disease is endemic in rural areas of Mexico, Central and South America, and associated with overcrowding and poverty. Countries endemic for Chagas include Argentina, Belize, Bolivia, Brazil, Chile, Columbia, Costa Rica, Ecuador, El Salvador, French Guiana, Guatemala, Guyana, Honduras, Mexico, Nicaragua, Panama, Paraguay, Peru, Suriname, Uruguay and Venezuela.1 T cruzi is endemic in vectors and wildlife reservoirs across the Americas, from the southern parts of the US to Argentina.2 WHO estimates more than 100 million people are at risk of infection,1 and there were an estimated 10.5 million cases of Chagas disease in 2023.5 Prevalence has decreased in endemic countries since 1990 with vector control strategies, however non-endemic regions have experienced an increase due to global movement and migration.5,6 A 2016 systematic review of Chagas screening in migrants found equal or higher prevalence compared to source country estimates,7 and American Heart Association guidelines on Chagas cardiomyopathy note the vast majority of cases occur in immigrants.6

    Clinical presentation

    The incubation period after vector borne exposure is 1-2 weeks (up to 4 months in transplant/transfusion related cases). Chagas disease subsequently has two phases:

    1. Initial acute phase - lasts 8-12 weeks and is characterised by circulating trypomastigotes (parasitaemia).
      • Usually asymptomatic, may cause mild flu like symptoms (malaise, fever, anorexia, lymphadenopathy).
      • Characteristic lesions may be present at inoculation sites, such as skin swelling (Chagoma) or unilateral eyelid swelling (Romana's sign).8
      • Severe acute disease is uncommon (<1%),9 but may present with acute myocarditis,6 pericardial effusion or meningoencephalitis (the latter is more common in infants <2 years and in reactivation cases).10
      • Congenital infection (classified as acute disease3,9 and diagnosed by detection of the parasite or PCR testing) is mostly sub-clinical, but can cause prematurity, low birthweight, fever, hepatosplenomegaly or anaemia. Rare presentations include meningoencephalitis, pneumonitis and neonatal death. Congenital disease is uncommon (pooled transmission rate 4.7% [95% CI 3.9, 5.6] in infants of infected mothers).11

    2. Chronic phases - in the absence of successful treatment, T. cruzi infection is lifelong 
      • Latent (indeterminate) stage - patients are asymptomatic, with positive serology, but no end-organ manifestations and a normal ECG.6,8 This stage can last decades, or be lifelong.
      • Symptomatic (determinate) stage - after 10-30 years, 20-40% of infected individuals develop symptoms of chronic infection. 
        • Cardiac involvement is the most common complication (20-30%). Parasite infection causes fibrosing myocarditis, which can progress to an arrhythmogenic dilated cardiomyopathy with atypical angina, heart failure, conduction disturbances, ventricular arrhythmias, sudden cardiac death and thromboembolic events.6,8 ECG changes (e.g. right bundle branch block, left anterior fasicular block, ST changes) are the earliest sign of progression.6,10
        • Gastrointestinal (GI) smooth muscle involvement (10-15%) can lead to progressive dysmotility, causing megaesophagus and megacolon.  Patients may present with reflux symptoms, dysphagia, or constipation.8
        • Neurological involvement11 (~10%) neuritis, sensory impairment, abnormal reflexes, and rarely, CNS presentations (including those related to thromboembolic events).10
        • Reactivation - associated with parasitaemia and may cause acute clinical manifestations, including severe acute disease, can occur with immune suppression from any cause.

    History and examination

    Assess for:

    • Exposure risk factors - living conditions, transfusion history, family history
    • Cardiac symptoms - symptoms of heart failure (e.g. exertional dyspnoea), atypical angina, palpitations, stroke/thromboembolic history
    • GI symptoms - dysphagia, gastro-oesophageal reflux (GOR), constipation
    • Neurological symptoms - sensory impairment
    • Complete full physical examination, including cardiac and GI exam, and peripheral nervous system exam.

    Testing

    Testing (serology) should be offered to all humanitarian entrants originating from or transiting through Central and South America, and all children of mothers with confirmed infection. Testing is a priority for women of reproductive age (including pregnant women) and people who are immunosuppressed (or at risk of immunosuppression) who have lived in endemic areas. Testing is also a priority for all children of mothers with confirmed infection, including Australian born children (testing varies in infants - see below).

    • In the acute stage - diagnosis is via direct microscopy of parasites in blood (thick and thin films) or CSF, or PCR testing.2,9 Note - direct transmission can occur with needlestick injuries in acute infection/parasitaemia.2
      • Molecular testing (PCR assay)2 is available internationally, and has higher sensitivity (65-70% on a single specimen, 85% on multiple specimen testing). PCR testing is usually reserved for acute infection (including transfusion or transplant related cases), reactivation with immune suppression, congenital disease and laboratory exposures. 

    • In the chronic stages - circulating trypomastigotes are usually not identified, and serology is recommended for screening. If initial serology is positive, a second confirmatory test using a different assay is required, sensitivity and specificity of commercially available assays varies.2
      • In Australia, T. cruzi serology (ELISA) is available through the Institute Of Clinical Pathology And Medical Research (ICPMR) at Westmead. If confirmatory testing is required, this will be arranged by ICPMR.
      • False positive serology can occur with Leishmaniasis and syphilis infection (see RCPA manual).
      • In general, PCR is not a useful diagnostic test for chronic T.cruzi infection.13
      • In end-organ disease, amastigotes may be found in muscle biopsy specimens with hematoxylin and eosin or Giemsa staining.
    • In infants of mothers from endemic areas - see CDC algorithms. If maternal serology confirmed positive, complete cord/whole blood microscopy and PCR in infants twice in the 1st 3 months, as parasitaemia increases in the first month.9 Infant serology <9 months of age will reflect maternal antibodies, but is useful where maternal serology has not been tested and as a baseline. Infant serology should be tested at 9-12 months of age.3,9 

    Management

    Staging 

    Following confirmation of positive T. cruzi serology, assess staging (indeterminate vs determinate) and monitor for end organ damage with:13  

    • Repeat history and examination - baseline and annually.
    • ECG with 30s lead II rhythm strip6 - baseline and annually. 
    • CXR - baseline and each 3-5 years, or if clinically indicated.
    • Echocardiogram - baseline and each 3-5 years, or if clinically indicated.
    • Consider barium swallow +/- AXR and contrast studies if GI symptoms.

    Note diagnostic criteria for indeterminate vs determinate stages are controversial, and variably include echocardiogram and GI imaging.

    Referrals

    Consult with infectious diseases unit for all confirmed cases. Refer to cardiac or gastroenterology units if end-organ involvement. 

    Treatment

    Treatment at the acute stage is curative, however given the acute stage is largely asymptomatic, anti-parasitic therapy is not often offered, resulting in chronic infection.14 US guidelines9,13,15 recommend treatment for:

    • All cases of acute or reactivated Chagas disease and for chronic T. cruzi infection in children up to age 18 years. 
    • Adults <50 years with chronic infection, who do not yet have advanced cardiomyopathy. Treatment for adults 50 years and older is on a case by case basis.

    Treatment is with either benznidazole (nitroimidazole derivative, launched 1971) or nifurtimox (nitrofuran compound, launched 1965).16 Both drugs have significant side effects (up to 40%), potential for genotoxicity and carcinogenicity, and they are contraindicated in renal disease, liver disease and during pregnancy. Benznidazole is generally better tolerated and more often used as first line therapy,9,13 nifurtimox is often better tolerated in children. More recent trials are examining different treatments, including the use of combination regimens and miltefosine.17

    • Benznidazole (US FDA approved age 2-12 years in 2017) - via special access scheme. See product information and patient information.
      • Dosing (see table in product information):
        • 2-12 years: 5-8 mg/kg per day orally in 2 divided doses for 60 days (i.e. 2.5-4 mg/kg twice daily for 60 days).
        • >12 years: 5 mg/kg per day in 2 divided doses for 60 days (i.e. 2.5 mg/kg twice daily for 60 days)
      • Tablet size 12.5mg and 100mg, scored, dispersible. Half life ~13 hours.
      • Side effects include abdominal pain, rash (including severe hypersensitivity reactions), decreased appetite/weight, headache, nausea, vomiting, neutropenia, urticaria, pruritus, eosinophilia and peripheral neuropathy.
      • Contraindicated if allergy to metronidazole, renal impairment, liver impairment, avoid all alcohol.
      • Contraindicated during pregnancy and breastfeeding - pregnancy test before treatment in reproductive age females and contraception during treatment and for 5 days after stopping treatment. 

    • Nifurtimox (US FDA approved age 0-17 years in 2020) - via special access scheme. See product information and patient information. 
      • Dosing (see table in product information):
        • 0-17 years:
          • Weight 2.5 - 40 kg: 10-20 mg/kg per day orally in 3 divided doses for 60 days (i.e. 3.3-6.6 mg/kg three times daily for 60 days)
          • Weight 41 kg or greater: 8-10 mg/kg per day orally in 3 divided doses for 60 days (i.e. 2.7-3.3 mg/kg three times daily for 60 days)
        • 18 years and older: 8-10 mg/kg per day orally in 3 divided doses for 60-90 days (i.e. 2.7-3.3 mg/kg three times daily for 60-90 days)
      • Tablet size 30mg and 120mg, scored tablets, dispersible, given with food. Half life ~3 hours.
      • Side effects include abdominal pain, headache, decreased appetite, nausea, pyrexia, rash and peripheral neuropathy.
      • Contraindicated if renal impairment, liver impairment, extreme caution in porphyria, avoid all alcohol.
      • Contraindicated during pregnancy - pregnancy test prior to treatment in females of reproductive age and avoid pregnancy for 6 months after treatment. Males should also use contraception during and 3m after treatment.   

    Monitoring during treatment - baseline FBE, LFT, UEC, repeat day 7,21 and 60.18

    Serological cure is achieved in 90-100% of infants with congenital disease if they are treated in the 1st year, and 60-85% of patients with acute disease.9,10 Treatment efficacy decreases with age and chronic disease (60-93% in children aged up to 13 years and 2-40% in adults with late chronic disease),16 however treatment with benznidazole is associated with positive effects on disease progression and survival (reviewed in 10).  Treatment of women of reproductive age is prioritised and associated with a 95% reduction in congenital transmission.19

    Follow up

    • Provide education about Chagas disease, long-term follow-up requirements and use recall systems.
      • Repeat history and examination - annually.
      • ECG with 30s lead II rhythm strip - annually. 
      • CXR - each 3-5 years, or if clinically indicated.
      • Echocardiogram - each 3-5 years, or if clinically indicated.
      • Consider barium swallow +/- AXR and contrast studies if GI symptoms.
    • Discuss blood donation - Australian blood banks will only accept donations of plasma for people who have lived in Chagas endemic areas.
    • Discuss pregnancy and risks of immunosuppression where relevant.  
    • CDC patient information, UpToDate patient information.

    References

    1. World Health Organization. Chagas disease (also known as American Trypanosomiasis). World Health Organization, 2025; [cited 2025 Dec 22]. Available from: https://www.who.int/news-room/fact-sheets/detail/chagas-disease-(american-trypanosomiasis)
    2. Centers for Disease Control and Prevention. DPDx - Laboratory Identification of Parasites of Public Health Concern. Centers for Disease Control and Prevention, 2025; [cited 2026 Jan 05]. Available from: https://www.cdc.gov/dpdx/trypanosomiasisamerican/index.html 
    3. Centers for Disease Control and Prevention. Clinical Considerations for Congenital Chagas Disease. Centers for Disease Control and Prevention, 2025; [cited 2026 Jan 05]. Available from: https://www.cdc.gov/chagas/hcp/considerations/index.html  
    4. Rassi A Jr, Rassi A, Marin-Neto JA. Chagas disease. The Lancet. 2010 Apr; 375(9723):1388–402. Available from: https://doi.org/10.1016/S0140-6736(10)60061-X
    5. Cousin E, Nascimento BR, Whisnant JL, Zimsen SRM, Harris AA, Machado IE, et al. Global, regional, and national burden of Chagas disease, 1990–2023: a systematic analysis for the Global Burden of Disease Study 2023. Lancet Infect Dis. 2025 Nov [cited 2025 Dec 22];S1473309925005626. Available from: https://linkinghub.elsevier.com/retrieve/pii/S1473309925005626
    6. Nunes MCP, Beaton A, Acquatella H, Bern C, Bolger AF, Echeverría LE, Dutra WO, Gascon J, Morillo CA, Oliveira-Filho J, Ribeiro ALP, Marin-Neto JA; American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; and Stroke Council. Chagas Cardiomyopathy: An Update of Current Clinical Knowledge and Management: A Scientific Statement From the American Heart Association. Circulation. 2018 Sep 18;138(12):e169-e209. doi: 10.1161/CIR.0000000000000599.
    7. Conners EE, Vinetz JM, Weeks JR, Brouwer KC. A global systematic review of Chagas disease prevalence among migrants. Acta Trop [Internet]. 2016 Apr [cited 2025 Nov 7];156:68–78. Available from: https://linkinghub.elsevier.com/retrieve/pii/S0001706X16300018
    8. Suárez C, Nolder D, García-Mingo A, Moore DA, Chiodini PL. Diagnosis and Clinical Management of Chagas Disease: An Increasing Challenge in Non-Endemic Areas. Res Rep Trop Med. 2022 Jul;13:25–40. Available from: https://www.dovepress.com/diagnosis-and-clinical-management-of-chagas-disease-an-increasing-chal-peer-reviewed-fulltext-article-RRTM
    9. Bern C. Chagas disease: Acute and congenital Trypanosoma cruzi infection. In: UpToDate, Weller PF, Bogorodskaya M (Eds), Wolters Kluwer. (cited 2026 Jan 5)
    10. Nunes MCP, Bern C, Clark EH, Teixeira AL, Molina I. Clinical features of Chagas disease progression and severity. Lancet Reg Health Am. 2024 Sep 13;37:100832. doi: 10.1016/j.lana.2024.100832. 
    11. Howard EJ, Xiong X, Carlier Y, Sosa-Estani S, Buekens P. Frequency of the congenital transmission of Trypanosoma cruzi: a systematic review and meta-analysis. BJOG. 2014 Jan;121(1):22-33. doi: 10.1111/1471-0528.12396.
    12. Córdova E, Maiolo E, Corti M, Orduña T. Neurological manifestations of Chagas' disease. Neurol Res. 2010 Apr;32(3):238-44. doi: 10.1179/016164110X12644252260637. 
    13. Bern C, Marin-Neto A. Chagas disease: Chronic Trypanosoma cruzi infection. In: UpToDate, Weller PF, Bogorodskaya M (Eds), Wolters Kluwer. (cited 2026 Jan 5)
    14. Haberland A, Munoz Saravia SG, Wallukat G, Ziebig R, Schimke I. Chronic Chagas disease: from basics to laboratory medicine. Clin Chem Lab Med. 2013 Feb;51(2):271–94. Available from: https://www.degruyter.com/document/doi/10.1515/cclm-2012-0316/html
    15. Centers for Disease Control and Prevention. Clinical Care of Chagas Disease. Centers for Disease Control and Prevention, 2025; [cited 2026 Jan 05]. Available from: https://www.cdc.gov/chagas/hcp/clinical-care/index.html
    16. Pérez-Molina JA, Crespillo-Andújar C, Bosch-Nicolau P, Molina I. Trypanocidal treatment of Chagas disease. Enfermedades Infecciosas y Microbiología Clínica. 2021;39(9):458-470. https://doi.org/10.1016/j.eimc.2020.04.011.
    17. Porta EOJ, Kalesh K and Steele PG. Navigating drug repurposing for Chagas disease: advances, challenges, and opportunities. Front. Pharmacol. 2023; Volume 14. Available from: https://doi.org/10.3389/fphar.2023.1233253
    18. Pinto A, Pett S, Jackson Y. Identifying Chagas disease in Australia: an emerging challenge for general practitioners. Aust Fam Physician. 2014 Jul;43(7):440-2.
    19. Bern C. Chagas disease: Epidemiology, screening, and prevention. In: UpToDate, Weller PF, Bogorodskaya M (Eds), Wolters Kluwer. (cited 2026 Jan 5)

    Immigrant health clinic resources, Authors: Toni Maldari, Rachel Claydon, Georgie Paxton. Updated 5 Jan 2026, Contact: georgia.paxton@rch.org.au