Modeling the impact of non-human host predation on the transmission of Chagas disease.

In addition to the traditional transmission route via the biting-and-defecating process, non-human host predation of triatomines is recognized as another significant avenue for Chagas disease transmission. In this paper, we develop an eco-epidemiological model to investigate the impact of predation on the disease's spread. Two critical thresholds, R v p (the basic reproduction number of triatomines) and R 0 p (the basic reproduction number of the Chagas parasite), are derived to delineate the model's dynamics. Through the construction of appropriate Lyapunov functions and the application of the Bendixson–Dulac theorem, the global asymptotic stabilities of the equilibria are fully established. The vector-free equilibrium E 0 is globally stable when R v p < 1. E 1 , the disease-free equilibrium, is globally stable when R v p > 1 and R 0 p < 1 , while the endemic equilibrium E ∗ is globally stable when both R v p > 1 and R 0 p > 1. Numerical simulations highlight that the degree of host predation on triatomines, influenced by non-human hosts activities, can variably increase or decrease the Chagas disease transmission risk. Specifically, low or high levels of host predation can reduce R 0 p to below unity, while intermediate levels may increase the infected host populations, albeit with a reduction in R 0 p. These findings highlight the role played by non-human hosts and offer crucial insights for the prevention and control of Chagas disease. • A novel model integrating systemic and non-human predation transmission is developed. • Two thresholds of R v p and R 0 p are derived to delineate the model dynamics. • The global stabilities of the equilibria for the high-dimensional model are shown. • The work offers the crucial insight for the prevention and control of Chagas disease. [ABSTRACT FROM AUTHOR]