Kaplinski and colleagues evaluated T. cruzi vertical transmission rates and risks of cardiomyopathy in urban and rural women in Bolivia. Of 1696 study participants, 1213 were from an urban area of Bolivia where housing changes and vector control have essentially removed residential exposure to the triatomine bug that serves as the vector of Chagas disease. The other 483 participants were in a rural part of Bolivia where mud- or dirt-walled homes are commonly infested with T. cruzi-infected vectors.

Pregnant women presenting for delivery were eligible for study entry. Infection with T. cruzi was confirmed when two or more conventional tests were positive. T. cruzi-infected study subjects underwent electrocardiography (ECG) and had cord blood tested at delivery. Infants of infected mothers were further evaluated for T. cruzi antigenemia and/or serology at 1, 6, and 9 months of age.

Overall, 456 (26.9%) of the women were infected with T. cruzi. Women from rural areas were much more likely to be infected with T. cruzi at the time of delivery than women from urban areas (47.4% vs 18.7%, respectively; P < 0.0001). Also, there was an inverse relationship between vertical transmission to the infant and duration of living in rural areas. The women who reported never having lived in a vector-infested house had a higher rate of vertical transmission than the women who had resided in a house known to contain triatomines (9.7% vs 4.6%, respectively; P = 0.04).

Of 302 infected women who underwent electrocardiography, 28 (9.3%) had ECG changes that were consistent with Chagas cardiomyopathy. The most common types of ECG change were bradycardia and bundle branch block. Women with abnormal ECGs had been residents of infected houses longer than women with normal ECGs (17.5 vs 1.0 years; P = 0.001). Women with abnormal ECGs were similarly likely to transmit T. cruzi to their infants as were women with normal ECGs (3.6% vs 8.0%, respectively; P = 0.40).

Thus, Kaplinski and colleagues showed that women who have longer exposure to T. cruzi are more at risk for Chagas cardiomyopathy as they get older. But they are less likely to transmit T. cruzi to their infants than are women who have less vector exposure.


In the Americas, T. cruzi causes more disease than any other parasite; it is estimated that 6 million people are infected. Approximately one-fourth of the infected individuals will develop life-altering cardiomyopathy.1 There could be as many as 1 million infected individuals in the United States,2 where transmission occurs congenitally, via blood transfusion, and even via insect vectors.3

Infection triggers immunity that alters parasite loads, but this immunity neither eradicates the infection nor protects from future infection. And, the immune response is implicated in the pathogenesis of the inflammatory cardiomyopathy.

When treatment is not given and household insect vectors repeatedly induce recurrent infection, the body struggles to keep a tenuous balance between suppressed infection (with, as shown by this study, lower parasite loads and less congenital transmission) and immunity-triggered pathology (such as cardiomyopathy). With urbanization and improved housing, previously infected women develop less cardiomyopathy but are at greater risk of congenital transmission of infection.

So, what can be done? Clearly, we need a multifaceted approach.

Improvements in housing with resultant decreases in housing-related triatomine bugs will reduce the overall incidence of infection. Development efforts must continue to promote improved housing in areas of Latin America where Chagas disease is endemic. Similarly, improved access to medical care would allow for more timely diagnosis and effective treatment of infected individuals in rural areas.

Medication can also help, especially when given early after infection (whether the infection was acquired congenitally or from insects). Benznidazole and nifurtimox can eradicate some infection, and benznidazole is associated with relatively fewer side effects. In adult infection, benznidazole can eradicate detectable parasites in 94% of patients.4 However, benznidazole, even while decreasing parasite load, does not seem to reverse or even prevent progression of established Chagas cardiomyopathy.5 Priority should be placed on the treatment of congenitally infected children (since children experience both better cure rates and fewer side effects than adults) and young adults, especially women who risk transmitting the infection to their offspring.6


  1. World Health Organization. Chagas Disease. http://www.who.int/mediacentre/factsheets/fs340/en/. Accessed Sept. 10, 2015.
  2. Hotez PJ, Dumonteil E, Betancourt Cravioto M, et al. An unfolding tragedy of Chagas disease in North America. PLoS Negl Trop Dis 2013;7:e2300.
  3. Garcia MN, Aguilar D, Gorchakov R, et al. Evidence of autochthonous Chagas disease in southeastern Texas. Am J Trop Med Hyg 2015;92:325-330.
  4. Molina I, Gomez i Prat J, Salvador F, et al. Randomized trial of posaconazole and benznidazole for chronic Chagas’ disease. N Engl J Med 2014;370:1899-1908.
  5. Morillo CA, Marin-Neto JA, Avezum A, et al. Randomized trial of benznidazole for chronic Chagas’ cardiomyopathy. N Engl J Med [In press.] 2015. doi 10.1056/NEJMoa1507574.
  6. Maguire JH. Treatment of Chagas’ disease — time is running out. N Engl J Med [In press.] 2015. doi: 10.1056/NEJMe1510170.