Unhealthy herds and the predator spreader: understanding when predation increases disease incidence and prevalence

Abstract

Disease ecologists now recognize the limitation behind examining host-parasite interactions in isolation: community members – especially predators – dramatically affect host-parasite dynamics. Although the initial paradigm was that predation should reduce disease in prey populations (“healthy herds hypothesis”), researchers have realized that predators sometimes increase disease in their prey. These “predator-spreaders” are now recognized as critical to disease dynamics, but empirical research on the topic remains fragmented. In a narrow sense, a “predator-spreader” would be defined as a predator that mechanically spreads parasites via feeding. However, predators affect their prey and, subsequently, disease transmission in many other ways such as altering prey population structure, behavior, and physiology. We review the existing evidence for these mechanisms and provide heuristics that incorporate features of the host, predator, parasite, and environment to understand whether or not a predator is likely to be a predator-spreader. We also provide guidance for targeted study of each mechanism and quantifying the effects of predators on parasitism in a way that yields more general insights into the factors that promote predator-spreading. We aim to offer a better understanding of this important and underappreciated interaction and a path towards being able to predict how changes in predation will influence parasite dynamics.

Contrasting effects of sheep and cattle grazing on foliar fungal diseases by changing plant community characteristics

“…We found only few direct effects of herbivores on the pathogens. Sheep directly increased biotrophic pathogen load, in line with findings for other mammalian grazers (Zhang et al., 2020) and studies in other systems (Richards et al., 2023) showing, for instance, that coral predators can increase disease through wounding and vectoring pathogens (Renzi et al., 2022). However, sheep grazing only directly facilitated the biotrophs, which might benefit especially from wounding (as shown for snail‐fungal interactions, Silliman & Newell, 2003), as they often consumed the upper parts of grass leaves (Liu, Duan, et al., 2021).…”

“…We focused on vertebrate herbivores and found that sheep grazing increased biotrophic pathogens, while cattle grazing decreased biotrophic and necrotrophic pathogen load. Theory and some empirical work suggest that herbivores could regulate disease in host populations (Hudson et al., 1992; Liu, Mipam, et al., 2021; Packer et al., 2003), however the impacts of herbivores will depend on how they alter various aspects of community structure and the opposite pattern is also possible (Richards et al., 2023). Our approach to disentangle direct and indirect effects, combining structural equation modelling and a manipulative experiment to test particular pathways, was able to identify the mechanisms by which large grazers affected foliar pathogens and revealed that sheep and cattle affected pathogen groups via different mechanisms.…”

“…Most obviously they can consume the pathogens present in host tissue and reduce infection levels overall if they target diseased hosts (Packer et al., 2003). Alternatively: herbivory can cause wounds, which allows pathogens to enter the host and cause infection (Daleo et al., 2009; Renzi et al., 2022); herbivores can vector pathogens directly (Richards et al., 2023), or alter induced plant defences or lower host quality (Hatcher & Paul, 2000; Thaler et al., 2010). In this study, we consider all effects mediated by changes in individual hosts, rather than community composition, as “direct” effects.…”