Partial Predation
In the simplest case of predator-spreading via partial predation, the predator causes a wound that provides a direct route of entry for parasites. Moreover, devoting energy to repairing the wound renders prey less able to invest in immune function and other defenses against parasitism. In addition to this simple scenario, it can also be the case that the predator acts as a mechanical vector for disease. In these cases, the predator contaminates itself with the parasite (smeared on/in its mouth or other body parts) when it preys on an infected prey individual, and then exposes another individual by preying on but not killing it (practicing partial predation). In some ways, this latter scenario is similar to sloppy predation, but, in this case, the predator is directly bringing the parasite into contact with the prey. An iconic example of partial predation, and of partial predation predator-spreading, is corals and their corallivorous predators. Corallivores are generally associated with increased disease in corals across a wide array of systems and have been experimentally demonstrated to “vector” infection from an infected coral to an uninfected one through partial predation (Renzi et al. 2022). Although these predators are typically considered alternate hosts or reservoirs of the infection (Aeby 1998; Gignoux-Wolfsohn et al. 2012), the actual mechanism for the parasite transfer is often uncharacterized (Clemens & Brandt 2015) and the line between mechanically and biologically vectoring infection through partial-predation is far from crisp. (Because our focus in this review is on scenarios where the predator does not become infected we do not consider common “biological” vectors such as mosquitoes, though these processes are reviewed extensively elsewhere.) The importance of partial predation predator-spreading in these systems stems from the sessile life-style of the prey. Partial predators can spread infection over much longer distances than direct contact between prey and with much more specificity than passive dispersal through the water (Renzi et al. 2022). Partial-predation predator spreading is not, however, restricted to sessile prey. For example, sub-lethal parasitoids are known to frequently vector viral pathogens between prey individuals when ovipositing. However, even in this case, there is still a large difference in dispersal distance, given that parasitoids travel much more than larval prey (Cossentine 2009). Plants are also sessile organisms which are frequently victims of partial predation; while they are generally beyond the scope of this review we discuss them briefly in Box 2.
The study of partial predation predator-spreading is rich and continuing to develop rapidly. We suggest an additional, new focus on the importance of incidental partial predation or failed predation in predator spreading. Systems in which prey typically survive potentially lethal predation attempts may be prone to the transfer of parasites via contaminated mouthparts, talons, and claws. Regular wounding through partial predation may also produce a subset of the prey population whose immune defense systems are substantially compromised. As in the case of coral partial predation predator-spreading, these processes should prove most important in systems with low contact or opportunities for direct transmission between prey.
Recent work has explored how the transport of parasites between contaminated locations by vectors (e.g., a pollinator in a plant-pollinator interaction) or by passive abiotic processes can influence levels of parasitism in the population, finding that the outcome depends on the dose-infectivity relationships (Ng et al.2022) whether they be accelerating, linear, or decelerating (Fig. 2a); the same should be true of partial predation predator-spreading. In cases where the minimum infective dose is high, vector-based spread does not result in as much parasitism as would be expected from a simpler compartment model (dashed line in Fig. 2b) or as in cases with a low minimum infectious dose (solid line in Fig. 2b). In contrast, passive abiotic processes, such as wind or water current dispersal, which contaminate additional sites can lead to faster than expected spread of disease when there is an accelerating dose-infectivity curve (that is, when the relationship between dose and infection is concave up, as shown in Fig. 1a; (Ng et al. 2022)); while accelerating dose-infectivity curves are not common, they do occur (Clay et al. 2021). These results suggest that it would be interesting to expand the work of Ng et al. to cases where predators are responsible for parasite spread and, as we discuss more in the next section (‘Parasite passes through predator’), to consider the impact of dose-response relationships.
Study of partial predation predator spreading should focus on those systems with diffuse or patchy prey who frequently survive predation attempts. Direct testing of predator attack surfaces for parasites combined with tests of parasite persistence on similar surfaces should provide evidence for whether the predator is a viable spreader. Finally, experimental inoculation through wounding of prey could provide insights into this putative mechanism and nicely complement ecological studies of rates of infection after sublethal predation wounding.