Disease-driven mass mortality event leads to widespread extirpation and variable recovery potential of a marine predator across the eastern Pacific.

The prevalence of disease-driven mass mortality events is increasing, but our understanding of spatial variation in their magnitude, timing and triggers are often poorly resolved. Here, we use a novel range-wide dataset comprised 48 810 surveys to quantify how sea star wasting disease affected Pycnopodia helianthoides, the sunflower sea star, across its range from Baja California, Mexico to the Aleutian Islands, USA. We found that the outbreak occurred more rapidly, killed a greater percentage of the population and left fewer survivors in the southern half of the species's range. Pycnopodia now appears to be functionally extinct (greater than 99.2% declines) from Baja California, Mexico to Cape Flattery, Washington, USA and exhibited severe declines (greater than 87.8%) from the Salish Sea to the Gulf of Alaska. The importance of temperature in predicting Pycnopodia distribution rose more than fourfold after the outbreak, suggesting latitudinal variation in outbreak severity may stem from an interaction between disease severity and warmer waters. We found no evidence of population recovery in the years since the outbreak. Natural recovery in the southern half of the range is unlikely over the short term. Thus, assisted recovery will probably be required to restore the functional role of this predator on ecologically relevant time scales.

Infection burdens and virulence under heat stress: ecological and evolutionary considerations.

As a result of global change, hosts and parasites (including pathogens) are experiencing shifts in their thermal environment. Despite the importance of heat stress tolerance for host population persistence, infection by parasites can impair a host's ability to cope with heat. Host-parasite eco-evolutionary dynamics will be affected if infection reduces host performance during heating. Theory predicts that within-host parasite burden (replication rate or number of infecting parasites per host), a key component of parasite fitness, should correlate positively with virulence-the harm caused to hosts during infection. Surprisingly, however, the relationship between within-host parasite burden and virulence during heating is often weak. Here, we describe the current evidence for the link between within-host parasite burden and host heat stress tolerance. We consider the biology of host-parasite systems that may explain the weak or absent link between these two important host and parasite traits during hot conditions. The processes that mediate the relationship between parasite burden and host fitness will be fundamental in ecological and evolutionary responses of host and parasites in a warming world. This article is part of the theme issue 'Infectious disease ecology and evolution in a changing world'.