Assessing the impact of host predation with Holling II response on the transmission of Chagas disease

Abstract

Chagas disease is a zoonosis caused by the protozoan parasite Trypanosoma cruzi and transmitted by a broad range of blood-sucking triatomine species. Recently, it is recognized that the parasite can also be transmitted by host ingestion. In this paper, we propose a Chagas disease model incorporating two transmission routes of biting-defecation and host predation between vectors and hosts with Holling II functional response. The basic reproduction number R_v of triatomine population and basic reproduction numbers R_0 of disease population are derived analytically, and it is shown that they are insufficient to serve as threshold quantities to determine dynamics of the model. Our results have revealed the phenomenon of bistability, with backward and forward bifurcations. Specifically, if R_v>1, the dynamic is rather simple, namely, the disease-free equilibrium is globally asymptotically stable as R_0<1 and a unique endemic equilibrium is globally asymptotically stable as R_0>1. However, if R_v<1, there exists a backward bifurcation with one unstable and one stable positive vector equilibria, and bistability phenomenon occurs, revealing that different initial conditions may lead to disease extinction or persistence even if the corresponding R_0>1. In conclusion, predation transmission in general reduces the risk of Chagas disease, whilst it makes the complexity of Chagas disease transmission, requiring an integrated strategy for the prevention and control of Chagas disease.