top of page

Transmission route

  1. Vector-borne: contact with the feces of an infected triatomine bug (or "kissing bug")

  2. Non vector-borne: mother-to-child transmission (congenital), contaminated blood
    transfusions, transplantation



  1. Endemic: Mexico, Central America, South America (8 million infected people)

  2. Non-endemic: North America (Canada & US), Western Pacific Region (Australia & Japan),
    Europe (due to migration)


Clinical presentation

  1. Acute phase (parasites circulate in the blood): 2 months after infection, asymptomatic or
    mild symptoms: skin lesion or swelling of an eye-lid (purple), fever, headache,
    swollen lymph glands, muscle pain, abdominal & chest pain, pallor

  2. Chronic phase (parasites hide in the heart and digestive muscles): cardiac disorders (arrhythmias),
    digestive problems (colon/oesophagus enlargement), neurological alterations



  • Yes, if treatment is started in an early (acute) stage

  • 10.000 deaths yearly


Pregnant women

  1. Serological testing of pregnant women recommended for: (a) women living in endemic areas, (b) receivers of blood transfusion in endemic areas, (c) women born (or that have lived) in endemic areas, (d) women whose mothers were born in endemic areas.

  2. Seropositive pregnant women: anti-parasitic treatment (benznidazole and nifurtimox) is not recommended during pregnancy (teratogenic risks insufficiently known).

  3. In case Anti-T.cruzi antibodies are present in maternal serum, the fetus might be infected. Microscopical examination of cord/peripheral blood of the neonate on the presence of mobile T. cruzi trypomastigotes (microhematocrit test) is necessary.

  4. Early diagnosis of acute congenital infection in newborns and treatment with anti-parasitic therapy is key to reduce side-effects, to obtain high cure rates and to avoid lifelong chronic infections.


Maternal-foetal transmission

  • An average of 5% vertical transmission in case of chronically infected mothers in endemic areas (huge variation in numbers between different endemic regions).

  • Probably no transmission via breast milk and amniotic fluid or transuterine.

  • Probable route of transmission: transplacental (during second-third trimester and perinatal)

  • Congenital infection gives an increased risk of premature delivery, low birth weight, premature ruptures of membranes.

  • 20 to 183 cases of congenital Chagas disease in Europe annually.


Factors that can play a role in transmission

1) Parasite: parasitic load, virulency, genotype (strain), capacity to invade placental cells.

2) Mother:

  • Parasitaemia increases during pregnancy (especially in the second and third trimester) and is associated with congenital transmission.

  • Immune status of the pregnant women (reactivated infection has a higher transmission risk than an acute infection, a chronic infection often has a low parasitaemia).

  • Co-infection with HIV/malaria/plasmodium vivax increases the risk of transmission.

3) Placenta  

  • T. Cruzi can infect and multiply within villous trophoblastic cells.

  • Via the placental marginal zone and placental breaches/tears, parasites can enter and multiply in the chorionic plate and reach the umbilical cord and the fetus.

4) Foetus

  • Most neonates of infected mothers are asymptomatic, 2 - 10% present with respiratory distress, meningoencephalitis, myocarditis, hepatosplenomegaly, etc.


Ultrasound markers to look out for

There are various possible signs of intrauterine infections, among which:



  • Growth restriction

Amniotic Fluid Index

  • Polyhydramnion


  • (Unilateral) ventriculomegaly

  • Microcephaly

  • Colpocephaly

  • Mega-Cisterna Magna


  • Ventricular hypertrophy


  • Hepatosplenomegaly (hyperechogenic)

Fetal hydrops

  • Cord edema

  • Ascites

  • Pleural effusion

  • Pericardial effusion

Differential Diagnosis

- TORCH infections (Toxoplasmosis, Rubella, CMV, Herpes)

- Congenital Hepatitis

- Syphilis

- Leptospirosis


A proper anamnesis can put you on track of Chagas Disease.

*  *  *


American Trypanosomiasis

WHO Fact Sheet

Centres for Disease Control and Prevention

Congenital Transmission of Chagas Disease — Virginia, 2010 Weekly, July 6, 2012 / 61(26);477-479. See:

Carlier, Y. et al. (2011). Congenital Chagas Disease: Recommendations for Diagnosis, Treatment and Control of Newborns, Siblings and Pregnant Women. PloS Negl Trop Dis., 5(10): e1250. Doi: 10.1371/journal.pntd.0001250

Carlier, Y. et al. (2015). Congenital Chagas disease: an update. Mem. Inst. Oswaldo Cruz., 110(3): 363–368. Doi: 10.1590/0074-02760140405 See:

Cevallos, A. & Hernandez, R. (2014). Chagas’ Disease: Pregnancy and Congenital Transmission. BioMed Research International. Doi: 10.1155/2014/401864
Flores-Chavez, M. et al. (2008) Fatal congenital Chagas' disease in a non-endemic area: a case report. Cases J., 1: 302. Doi: 10.1186/1757-1626-1-302

Chagas   Disease  

Named after

Brazilian physician Carlos Chagas (1909) 

Also known as

American trypanosomiasis


protozoan parasite Trypanosoma cruzi (T. cruzi)

bottom of page