Search for: All records

Abstract Climate‐induced shifts in mosquito phenology and population structure have important implications for the health of humans and wildlife. The timing and intensity of mosquito interactions with infected and susceptible hosts are a primary determinant of vector‐borne disease dynamics. Like most ectotherms, rates of mosquito development and corresponding phenological patterns are expected to change under shifting climates. However, developing accurate forecasts of mosquito phenology under climate change that can be used to inform management programs remains challenging despite an abundance of available data. As climate change will have variable effects on mosquito demography and phenology across species it is vital that we identify associated traits that may explain the observed variation. Here, we review a suite of modeling approaches that could be applied to generate forecasts of mosquito activity under climate change and evaluate the strengths and weaknesses of the different approaches. We describe four primary life history and physiological traits that can be used to constrain models and demonstrate how this prior information can be harnessed to develop a more general understanding of how mosquito activity will shift under changing climates. Combining a trait‐based approach with appropriate modeling techniques can allow for the development of actionable, flexible, and multi‐scale forecasts of mosquito population dynamics and phenology for diverse stakeholders. 

Abstract Despite the importance of virulence in epidemiological theory, the relative contributions of host and parasite to virulence outcomes remain poorly understood. Here, we use reciprocal cross experiments to disentangle the influence of host and parasite on core virulence components—infection and pathology—and understand dramatic differences in parasite‐induced malformations in California amphibians. Surveys across 319 populations revealed that amphibians' malformation risk was 2.7× greater in low‐elevation ponds, even while controlling for trematode infection load. Factorial experiments revealed that parasites from low‐elevation sites induced higher per‐parasite pathology (reduced host survival and growth), whereas there were no effects of host source on resistance or tolerance. Parasite populations also exhibited marked differences in within‐host distribution: ~90% of low‐elevation cysts aggregated around the hind limbs, relative to <60% from high‐elevation. This offers a novel, mechanistic basis for regional variation in parasite‐induced malformations while promoting a framework for partitioning host and parasite contributions to virulence. 

A key challenge surrounding ongoing climate shifts is to identify how they alter species interactions, including those between hosts and parasites. Because transmission often occurs during critical time windows, shifts in the phenology of either taxa can alter the likelihood of interaction or the resulting pathology. We quantified how phenological synchrony between vulnerable stages of an amphibian host ( Pseudacris regilla ) and infection by a pathogenic trematode ( Ribeiroia ondatrae ) determined infection prevalence, parasite load and host pathology. By tracking hosts and parasite infection throughout development between low- and high-elevation regions (San Francisco Bay Area and the Southern Cascades (Mt Lassen)), we found that when phenological synchrony was high (Bay Area), each established parasite incurred a 33% higher probability of causing severe limb malformations relative to areas with less synchrony (Mt Lassen). As a result, hosts in the Bay Area had up to a 50% higher risk of pathology even while controlling for the mean infection load. Our results indicate that host–parasite interactions and the resulting pathology were the joint product of infection load and phenological synchrony, highlighting the sensitivity of disease outcomes to forecasted shifts in climate. 

Abstract Predation on parasites is a common interaction with multiple, concurrent outcomes. Free‐living stages of parasites can comprise a large portion of some predators' diets and may be important resources for population growth. Predation can also reduce the density of infectious agents in an ecosystem, with resultant decreases in infection rates. While predator–parasite interactions likely vary with parasite transmission strategy, few studies have examined how variation in transmission mode influences contact rates with predators and the associated changes in consumption risk.To understand how transmission mode mediates predator–parasite interactions, we examined associations between an oligochaete predatorChaetogaster limnaeithat lives commensally on freshwater snails and nine trematode taxa that infect snails.Chaetogasteris hypothesized to consume active (i.e. mobile), free‐living stages of trematodes that infect snails (miracidia), but not the passive infectious stages (eggs); it could thus differentially affect transmission and infection prevalence of parasites, including those with medical or veterinary importance. Alternatively, when infection does occur,Chaetogastercan consume and respond numerically to free‐living trematode stages released from infected snails (cercariae). These two processes lead to contrasting predictions about whetherChaetogasterand trematode infection of snails correlate negatively (‘protective predation’) or positively (‘predator augmentation’).Here, we tested how parasite transmission mode affectedChaetogaster–trematode relationships using data from 20,759 snails collected across 4 years from natural ponds in California. Based on generalized linear mixed modelling, snails with moreChaetogasterwere less likely to be infected by trematodes that rely on active transmission. Conversely, infections by trematodes with passive infectious stages were positively associated with per‐snailChaetogasterabundance.Our results suggest that trematode transmission mode mediates the net outcome of predation on parasites. For trematodes with active infectious stages, predatoryChaetogasterlimited the risk of snail infection and its subsequent pathology (i.e. castration). For taxa with passive infectious stages, no such protective effect was observed. Rather, infected snails were associated with higherChaetogasterabundance, likely owing to the resource subsidy provided by cercariae. These findings highlight the ecological and epidemiological importance of predation on free‐living stages while underscoring the influence of parasite life history in shaping such interactions. 

Abstract Classical theory suggests that parasites will exhibit higher fitness in sympatric relative to allopatric host populations (local adaptation). However, evidence for local adaptation in natural host–parasite systems is often equivocal, emphasizing the need for infection experiments conducted over realistic geographic scales and comparisons among species with varied life history traits. Here, we used infection experiments to test how two trematode (flatworm) species (Paralechriorchis syntomenteraandRibeiroia ondatrae) with differing dispersal abilities varied in the strength of local adaptation to their amphibian hosts. Both parasites have complex life cycles involving sequential transmission among aquatic snails, larval amphibians and vertebrate definitive hosts that control dispersal across the landscape. By experimentally pairing 26 host‐by‐parasite population infection combinations from across the western USA with analyses of host and parasite spatial genetic structure, we found that increasing geographic distance—and corresponding increases in host population genetic distance—reduced infection success forP. syntomentera, which is dispersed by snake definitive hosts. For the avian‐dispersedR. ondatrae, in contrast, the geographic distance between the parasite and host populations had no influence on infection success. Differences in local adaptation corresponded to parasite genetic structure; although populations ofP. syntomenteraexhibited ~10% mtDNA sequence divergence, those ofR. ondatraewere nearly identical (<0.5%), even across a 900 km range. Taken together, these results offer empirical evidence that high levels of dispersal can limit opportunities for parasites to adapt to local host populations.