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.