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Host sex is an important source of heterogeneity in the severity of epidemics. Pinpointing the mechanisms causing this heterogeneity can be difficult because differences in behaviour among sexes (e.g. greater territorial aggression in males) can bias exposure risk, obfuscating the role of immune function, which can lead to differences in pathology, in driving differential susceptibility between sexes. Thus, sex‐biased transmission driven by differences in immune function independent of behaviour is poorly understood, especially in non‐mammalian systems.

Urbanization can influence local richness (alpha diversity) and community composition (beta diversity) in numerous ways. For instance, reduced connectivity and land cover change may lead to the loss of native specialist taxa, decreasing alpha diversity. Alternatively, if urbanization facilitates nonnative species introductions and generalist taxa, alpha diversity may remain unchanged or increase, while beta diversity could decline due to the homogenization of community structure. Wetlands and ponds provide critical ecosystem services and support diverse communities, making them important systems in which to understand the consequences of urbanization. To determine how urban development shapes pond community structure, we surveyed 68 ponds around Madison, Wisconsin, USA, which were classified as urban, greenspace, or rural based on surrounding land use. We evaluated how landscape and local pond factors were correlated with the alpha diversity of aquatic plants, macroinvertebrates, and aquatic vertebrates. We also analyzed whether surrounding land use was associated with changes in community composition and the presence of specific taxa. We found a 23% decrease in mean richness (alpha diversity) from rural to urban pond sites and a 15% decrease from rural to greenspace pond sites. Among landscape factors, adjacent developed land, mowed lawn cover, and greater distances to other waterbodies were negatively correlated with observed pond richness. Among pond level factors, habitat complexity was associated with increased richness, while nonnative fishes were associated with decreased richness. Beta diversity was relatively high for all ponds due to turnover in composition between sites. Urban ponds supported more nonnative species, lacked a subset of native species found in rural ponds, and had slightly higher beta diversity than greenspace and rural ponds. Our results suggest that integrating ponds into connected greenspaces, maintaining riparian vegetation, preventing nonnative fish introductions, and promoting habitat complexity may mitigate the negative effects of urbanization on aquatic richness. While ponds are small in size and rarely incorporated into urban conservation planning, the high beta diversity of distinct pond communities emphasizes their importance for supporting urban biodiversity.

Predators can increase the biomass of their prey, particularly when prey life stages differ in competitive ability and predation is stage specific. Akin to predators, parasites influence host population sizes and engage in stage‐structured interactions, yet whether parasites can increase host population biomass remains relatively unexplored. Using a stage‐structured consumer–resource model and a mesocosm experiment with snails and castrating trematodes, we examined responses of host biomass to changes in infection prevalence under variation in host pathology and resource competition. Equilibrium adult host biomass increased with infection prevalence in the model when parasites castrated hosts and adults were superior competitors to juveniles. Juvenile biomass increased with infection prevalence whether parasites caused mortality or castration, but only when juveniles were superior competitors. In mesocosms, increases in infection by castrating trematodes reduced snail egg production, juvenile abundance, and adult survival. At high competition, juvenile growth and total biomass increased with infection prevalence due to competitive release. At low competition, juvenile biomass decreased with infection due to reduced reproduction. These results highlight how disease‐induced biomass overcompensation depends on infection pathology, resource availability, and competitive interactions within and between host life stages. Considering such characteristics may benefit biocontrol efforts using parasites.

Non‐native freshwater snails can play important roles as consumers, hosts, and prey. Despite their potential ecological importance, global patterns in non‐native snail taxonomy, geography, and ecology have not been documented. Our objectives were to use a semi‐quantitative systematic review to describe non‐native freshwater snail global diversity, distribution, mechanisms of introduction, and interactions with natural enemies, including parasites and predators.

Host behaviour is known to influence disease dynamics. Additionally, hosts often change their behaviours in response to pathogen detection to resist and avoid disease. The capacity of wildlife populations to respond to pathogens using behavioural plasticity is critical for reducing the impacts of disease outbreaks. However, there is limited information regarding the ability of ectothermic vertebrates to resist diseases via behavioural plasticity.

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Disease outbreaks among wildlife have surged in recent decades alongside climate change, although it remains unclear how climate change alters disease dynamics across different geographic regions. We amassed a global, spatiotemporal dataset describing parasite prevalence across 7346 wildlife populations and 2021 host-parasite combinations, compiling local weather and climate records at each location. We found that hosts from cool and warm climates experienced increased disease risk at abnormally warm and cool temperatures, respectively, as predicted by the thermal mismatch hypothesis. This effect was greatest in ectothermic hosts and similar in terrestrial and freshwater systems. Projections based on climate change models indicate that ectothermic wildlife hosts from temperate and tropical zones may experience sharp increases and moderate reductions in disease risk, respectively, though the magnitude of these changes depends on parasite identity.