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Trypanosoma cruzi Infection Does Not Decrease Survival or Reproduction of the Common Bed Bug, Cimex lectularius

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  • 1 Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania;
  • 2 Facultad de Salud Pública y Administración, Universidad Peruana Cayetano Heredia, Lima, Peru

Although not presently implicated as a vector of human pathogens, the common bed bug, Cimex lectularius, has been suspected of carrying human pathogens because of its close association with humans and its obligate hematophagy. Recently, we characterized the vectorial competence of C. lectularius for the parasite Trypanosoma cruzi, the causative agent of Chagas disease. We observed that C. lectularius can acquire T. cruzi infection when fed on T. cruzi–carrying mice, and subsequently transmit T. cruzi to uninfected mice. This led us to ask why has C. lectularius not been implicated in the transmission of T. cruzi outside of the laboratory? We hypothesized that T. cruzi reduces C. lectularius fitness (i.e., survival and/or reproduction) as an explanation for why C. lectularius does not to transmit T. cruzi in natural settings. We tested this hypothesis by comparing the survival and reproduction of uninfected and T. cruzi–infected C. lectularius. We observed that T. cruzi had a variable effect on C. lectularius survival and reproduction. There were negligible differences between treatments in juveniles. Infected adult females tended to live longer and produce more eggs. However, no effect was consistent, and infected bugs showed more variation in survival and reproduction metrics than control bugs. We did not observe any negative effects of T. cruzi infection on C. lectularius survival or reproduction, suggesting that decreased fitness in T. cruzi–infected C. lectularius is not why bed bugs have not been observed to transmit T. cruzi in natural settings.

    • Supplementary Materials

Author Notes

Address correspondence to Jennifer K. Peterson or Michael Z. Levy, Department of Biostatistics and Epidemiology, University of Pennsylvania, 714 Blockley Hall, 423 Guardian Drive, Philadelphia, PA 19104. Email: jenni.peterson@gmail.com and mzlevy@pennmedicine.upenn.edu

Financial support: This work was supported by the National Institutes of Health 5R01 AI101229.

Authors’ addresses: Jennifer K. Peterson, Ricardo Castillo-Neyra, Casey Bartow-McKenney, Dylan Tracy, and Michael Z. Levy, Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, E-mails: jenni.peterson@gmail.com, cricardo@upenn.edu, casb@pennmedicine.upenn.edu, tradylan@sas.upenn.edu, and mzlevy@pennmedicine.upenn.edu. Renzo Salazar, Katty Borrini, Carlos Condori, and César Náquira, Universidad Peruana Cayetano Heredia/University of Pennsylvania Zoonotic Disease Research Lab, Urbanización Las Begonias D-11, Distrito José Luis Bustamante y Rivero, Arequipa, Perú, E-mails: rendaths@gmail.com, yttakbm@gmail.com, carlosedcopino@gmail.com, and cesar.naquira@gmail.com.

These authors contributed equally to this work.

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