Understanding how ecological interactions affect vector-borne disease dynamics is crucial in the context of rapid biodiversity loss and increased emerging vector-borne diseases. Although there have been many studies on the impact of interspecific competition and host competence on disease dynamics, few of them have addressed the case of a vector-borne disease. Using a simple compartment model with two competing host species and one vector, we investigated the combined effects of vector preference, host competence, and interspecific competition on disease risk in a vector-borne system. Our research demonstrated that disease transmission dynamics in multi-host communities are more complex than anticipated. Vector preference and differences in host competence shifted the direction of the effect of competition on community disease risk, yet interspecific competition quantitatively but not qualitatively changed the effect of vector preference on disease risk. Our work also identified the conditions of the dilution effect and amplification effect in frequency-dependent transmission mode, and we discovered that adding vector preference and interspecific competition into a simple two-host-one-vector model altered the outcomes of how increasing species richness affects disease risk. Our work explains some of the variation in outcomes in previous empirical and theoretical studies on the dilution effect.
4 October 2022 in Frontiers in Ecology and Evolution
Rapid global biodiversity loss and increasing emerging infectious diseases underscore the significance of identifying the diversity-disease relationship. Although experimental evidence supports the existence of dilution effects in several natural ecosystems, we still know very little about the conditions under which a dilution effect will occur. Using a multi-host Susceptible-Infected-Recovered model, we found when disease transmission was density-dependent, the diversity-disease relationship could exhibit an increasing, decreasing, or non-monotonic trend, which mainly depended on the patterns of community assembly. However, the combined effects of the host competence-abundance relationship and species extinction order may reverse or weaken this trend. In contrast, when disease transmission was frequency-dependent, the diversity-disease relationship only showed a decreasing trend, the host competence-abundance relationship and species extinction order did not alter this decreasing trend, but it could reduce the detectability of the dilution effect and affect disease prevalence. Overall, a combination of disease transmission mode, community assembly pattern, and host community composition determines the direction or strength of the diversity-disease relationship. Our work helps explain why previous studies came to different conclusions about the diversity-disease relationship and provides a deeper understanding of the pathogen transmission dynamics in actual communities.
A stochastic nutrient–phytoplankton–zooplankton model with instantaneous nutrient recycling is proposed and analyzed in this paper. When the nutrient uptake function and the grazing function are linear and the ingested phytoplankton is completely absorbed by the zooplankton, we establish two stochastic thresholds and , which completely determine the persistence and extinction of the plankton. That is, if , both the phytoplankton and the zooplankton eventually are eliminated; if and , the phytoplankton is persistent in mean but the zooplankton is extinct; while for , the entire system is persistent in mean. Furthermore, sufficient criteria for the existence of ergodic stationary distribution of the model are obtained and the persistent levels of the plankton are estimated. Numeric simulations are carried out to illustrate the theoretical results and to conclude our study. Our results suggest that environmental noise may cause the local bloom of phytoplankton, which surprisingly can be used to explain the formation of algal blooms to some extent. Moreover, we find that the nonlinear nutrient uptake function and grazing function may take credit for the periodic succession of blooms regardless of whether they are in the absence or presence of the environmental noises.
A central goal of disease ecology is to identify the factors that drive the spread of infectious diseases. Changes in vector richness can have complex effects on disease risk, but little is known about the role of vector competence in the relationship between vector richness and disease risk. In this study, we firstly investigated the combined effects of vector competence, interspecific competition, and feeding interference on disease risk through a two‐vector, one‐host SIR‐SI model, and obtained threshold conditions for the occurrence of dilution and amplification effects. Secondly, we extended the above model to the case of N vectors and assumed that all vectors were homogeneous to obtain analytic expressions for disease risk. It was found that in the two‐vector model, disease risk declined more rapidly as interspecific competition of the high‐competence vector increased. When vector richness increases, the positive effects of adding a high‐competence vector species on disease transmission may outweigh the negative effects of feeding interference due to increased vector richness, making an amplification effect more likely to occur. While the addition of a highly competitive vector species may exacerbate the negative effects of feeding interference, making a dilution effect more likely to occur. In the N‐vector model, the effect of increased vector richness on disease risk was fully driven by the strength of feeding interference and interspecific competition, and changes in vector competence only quantitatively but not qualitatively altered the vector richness–disease risk relationship. This work clarifies the role of vector competence in the relationship between vector richness and disease risk and provides a new perspective for studying the diversity–disease relationship. It also provides theoretical guidance for vector management and disease prevention strategies.