Optimal killing for obligate killers: the evolution of life histories and virulence of semelparous parasites

Abstract

SUMMARYMany viral, bacterial and protozoan parasites of invertebrates first propagate inside their host without releasing any transmission stages and then kill their host to release all transmission stages at once. Life history and the evolution of virulence of these obligately killing parasites are modelled, assuming that within-host growth is density dependent. We find that the parasite should kill the host when its per capita growth rate falls to the level of the host mortality rate. The parasite should kill its host later when the carrying capacity, K, is higher, but should kill it earlier when the parasite-independent host mortality increases or when the parasite has a higher birth rate. When K(t), for parasite growth, is not constant over the duration of an infection, but increases with time, the parasite should kill the host around the stage when the growth rate of the carrying capacity decelerates strongly. In case that K(t) relates to host body size, this deceleration in growth is around host maturation.

Free-living pathogens: Life-history constraints and strain competition

“…The predicted positive association between FLP persistence and virulence appears in other models (Gandon, 1998;Kamo and Boots, 2004), as a consequence of different assumptions. The intuitive prediction that pathogens reproducing more through a particle burst at host death, and less through shedding during infection, should induce virulent disease has appeared previously (Ebert and Weisser, 1997;Day, 2002;Kamo and Boots, 2004). Half of our predictions follow from hypothesized interaction between FLP decay rate and traits other than virulence; these results apparently are novel.…”

“…γ = 0; β > 0. Suppose that no FLP are shed from living hosts, so that pathogen reproduction occurs only as a burst following the death of each infected host (Ebert and Weisser, 1997). Then, S* simplifies to (ξ/αβ).…”

“…When we let γ = 0 in our model, extending the duration of an infected host's life beyond the minimal time to produce an FLP burst has no value to the pathogen, since no infectious particles are shed before the host dies (Ebert and Weisser, 1997;Day 2002). Increased virulence does not impair strain competitiveness, because S* does not depend directly on υ(ξ).…”

“…Disease transmission occurs via direct contact between infectious and susceptible hosts, as well as through free-living particles. The latter may be released continuously for the duration of infection, or as a burst upon death of an infected host (Ebert and Weisser, 1997). Given the death-mediated particle burst, the endemic density of susceptibles depends on particle longevity, and increasing persistence of the free-living stage can favor increased virulence.…”

Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence

“…Because evolutionary theory is rather general, there are some obvious limitations. For example, the life cycle of parasites that need to kill their host (as is true for most parasitoids) will not match models describing transient microbial infections (Ebert & Weisser 1997). Similarly, parasites that have recently invaded a host population may not yet have been subject to coevolution as assumed by theory (Weiss 2002).…”