Leishmania spp. and Trypanosoma cruzi are protozoan parasites that cause leishmaniasis and Chagas disease, respectively. In the United States, autochthonous transmission cycles of both Leishmania and T. cruzi have been documented, particularly in the southern and southwestern regions. Previous studies in El Paso, Texas, have identified dogs, cats, and several sylvatic mammals as infected hosts for these pathogens; however, the role of bats has remained largely unexplored. Here, we conducted a cross-sectional, observational study of 29 wild bats, opportunistically collected from domestic and peridomestic urban environments in El Paso, Texas, as part of local rabies surveillance. DNA extracted from available heart, spleen, skin, and lung tissues was analyzed by quantitative PCR targeting T. cruzi satellite DNA and Leishmania 18S rDNA, followed by DNA sequencing for confirmation. PCR-based molecular detection identified Leishmania spp. in six bats (24.1%) and Trypanosoma cruzi in thirteen bats (44.8%). DNA sequencing analysis confirmed the presence of parasite-specific DNA in four Leishmania -positive samples and twelve Trypanosoma cruzi -positive samples. Restriction fragment length polymorphism (RFLP) analysis showed that the digestion patterns of the T. cruzi samples differed from those observed in the TcBat reference control. However, given the limited characterization and known genetic variability of the TcBat lineage, as well as the constraints of PCR-RFLP–based typing, these findings do not conclusively exclude the possibility that the detected strains belong to the TcBat genotype. Co-detection of both parasites was detected in 3 out of 18 Tadarida brasiliensis specimens. Mapping of capture sites showed infected bats occurring in both urban and suburban areas of El Paso County. This study provides evidence of the molecular detection of Leishmania spp. and T. cruzi in bats from El Paso, Texas. These findings highlight bats as sylvatic hosts for medically important trypanosomatids in the U.S.–Mexico border region and emphasize the need for expanded surveillance to assess zoonotic risk and its environmental drivers.
Silva-Espinoza et al. (2026) studied this question.