Benznidazole Treatment of Chagasic Encephalitis in Pregnant Woman with AIDS

Margarita Bisio

, Jaime Altcheh, Jorge Lattner, Guillermo Moscatelli, Valeria Fink, Juan M. Burgos, Facundo García Bournissen, Alejandro G. Schijman, and Héctor Freilij

Author affiliations: Hospital de Niños Ricardo Gutiérrez, Buenos Aires, Argentina (M. Bisio, J. Altcheh, G. Moscatelli, F. García Bournissen, H. Freilij); Instituto de Investigaciones en Ingeniería Genética y Biología Molecular Dr Héctor N. Torres, Buenos Aires (M. Bisio, A.G. Schijman); Hospital Juan A. Fernández, Buenos Aires (J. Lattner, V. Fink); Facultad de Medicina de la Universidad de Buenos Aires, Buenos Aires (J.M. Burgos)

Abstract

We report a case of chagasic meningoencephalitis reactivation in a pregnant woman co-infected with Trypanosoma cruzi and HIV that was successfully managed with benznidazole and highly active antiretroviral therapy. Early diagnosis enabled rapid specific treatment that improved the health of the patient and her baby.

Chagas disease, caused by the protozoan Trypanosoma cruzi, is transmitted to humans mainly by triatomine bugs (vector-borne route), through blood transfusions, or from mother to child through the placenta (transplacental route) (1). In patients co-infected with HIV, Chagas disease reactivation generally occurs in persons with CD4 T-cell counts < 200 cells/mm³ and results in severe meningoencephalitis or myocarditis (2). Confirmation of central nervous system (CNS) reactivation requires T. cruzi detection in 1) cerebrospinal fluid, 2 brain tissue, or 3) blood, with neurologic manifestations and clinical response to parasiticidal treatment (2). CNS reactivation is associated with a high mortality rate, and management consists of combining anti–T. cruzi drugs (benznidazole or nifurtimox) with highly active antiretroviral therapy (HAART) to favor immune reconstitution (2,3).
Migration by persons from Chagas disease–endemic areas to vector-free urban centers, and changes in the epidemiologic profile of HIV, have led to a large overlap in the geographic distribution of the 2 infections (4). In fact, the prevalence of T. cruzi infection among HIV-seropositive patients from disease-endemic regions was found to be 1.3% in Brazil and 1.9% in Spain (4,5).
Because safety of benznidazole in pregnancy has not been established (6), its use in treating pregnant women is contraindicated (7,8). Prevalence of vertical transmission of T. cruzi infection from immunocompetent women to their fetus varies from 0.1% to 18% among regions (7), and such transmission is strongly associated with the maternal blood-parasite load (7,9). However, patients co-infected with HIV exhibit higher levels of parasitemia and a higher congenital transmission rate (10) than those who are not co-infected. Indeed, in our experience, 6 of 7 co-infected pregnant women transmitted T. cruzi infection (11). We describe a noteworthy case-patient from that series, a woman who experienced reactivation of T. cruzi infection during the third trimester of pregnancy but did not transmit the parasite infection, probably because she received, without delay, treatment with benznidazole and HAART.