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Symbionts, including parasites, pathogens, and mutualists, can play important roles in determining whether or not invasions by host species will be successful. Loss of enemies from the native habitat, such as parasites and pathogens, can allow for higher invader fitness in the invaded habitat. The presence of mutualists (e.g., pollinators, seed dispersers, mycorrhizae, and rhizobial bacteria) in the invaded habitat can facilitate invasion success. Although there has been a great deal of research focusing on how invading hosts may benefit from enemy losses or mutualist gains, far less attention has focused on how native symbiont populations and communities respond to invasion by non-indigenous hosts and symbionts. In this paper, we present a conceptual framework examining how symbionts such as parasites, pathogens, commensals, and mutualists can influence invader success and whether these native symbionts will benefit or decline during invasion. The first major factor in this framework is the competence of the invading host relative to the native hosts. Low- or non-competent hosts that support few if any native symbionts could cause declines in native symbiont taxa. Competent invading hosts could potentially support native parasites, pathogens, commensals, and mutualists, especially if there is a closely related or similar host in the invaded range. These symbionts could inhibit or facilitate invasion or have no discernible effect on the invading host. An understanding of how native symbionts interact with competent versus non-competent invading hosts as well as various invading symbionts is critical to our understanding of invasion success, its consequences for invaded communities and how native symbionts in these communities will fare in the face of invasion.

Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow ( Passer domesticus ), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.

This article is a Commentary on Susi & Laine (2021), 230: 2447–2458.

Background In Europe, the generalist tick, Ixodes ricinus , is the main vector of several tick-borne pathogens causing diseases in humans and livestock. Understanding how different species of hosts limit the tick population is crucial for management. In general, larger ectoparasites are expected to select hosts with larger body size. Consistent with this, larval and nymphal I. ricinus can feed on a wide range of different-sized vertebrates, while the adult female stage is expected to rely on a medium–large-sized host for reproduction. However, we still have a limited understanding of whether medium-sized hosts other than roe deer can serve as hosts to adult ticks, and other factors than size may also affect host selection. Methods To increase our understanding of the suitability of the different species of medium-sized hosts for adult ticks, we sampled mainly roadkill mammals from within the questing season of ticks. We counted life stages of ticks on roe deer ( Capreolus capreolus ) ( n  = 29), red fox ( Vulpes vulpes ) ( n  = 6), badger ( Meles meles ) ( n  = 14) and red squirrel ( Sciurus vulgaris ) ( n  = 17) from spatially overlapping populations in Norway, and analysed variation between species across different body parts with a mixed-effects negative binomial model (with and without zero-inflation). Results Red squirrel hosted a high density of larval and nymphal I. ricinus , but only one individual had adult female ticks. Roe deer hosted by far the largest number of adult ticks. Badgers had very few ticks, possibly due to their thick skin. Red foxes had intermediate numbers, but a high proportion of subcutaneous, dead ticks (69.3%), suggesting they are not very suitable hosts. Body mass predicted the presence of adult I. ricinus ticks. However, species was a better predictor than body mass for number of ticks, suggesting there was species variation in host suitability beyond body mass per se. Conclusions Our study provides evidence that roe deer are indeed the main suitable reproduction host to adult I. ricinus ticks, and are likely a key to host limitation of the tick population in this northern ecosystem. Graphical Abstract

High host biodiversity is hypothesized to dilute the risk of vector‐borne diseases if many host species are ‘dead ends' that cannot effectively transmit the disease and low‐diversity areas tend to be dominated by competent host species. However, many studies on biodiversity–disease relationships characterize host biodiversity at single, local spatial scales, which complicates efforts to forecast disease risk if associations between host biodiversity and disease change with spatial scale. Here, our objective is to evaluate the spatial scaling of relationships between host biodiversity and Borrelia (the bacterial taxon which causes Lyme disease) infection prevalence in small mammals. We compared the associations between infection prevalence and small mammal host diversity for local communities (individual plots) and metacommunities (multiple plots aggregated within a landscape) sampled by the National Ecological Observatory Network (NEON), an emerging continental‐scale environmental monitoring program with a hierarchical sampling design. We applied a multispecies, spatially‐stratified capture–recapture model to a trapping dataset to estimate five small mammal biodiversity metrics, which we used to predict infection status for a subset of trapped individuals. We found that relationships between Borrelia infection prevalence and biodiversity did indeed vary when biodiversity was quantified at different spatial scales but that these scaling behaviors were idiosyncratic among the five biodiversity metrics. For example, species richness of local communities showed a negative (dilution) effect on infection prevalence, while species richness of the small mammal metacommunity showed a positive (amplification) effect on infection prevalence. Our modeling approach can inform future analyses as data from similar monitoring programs accumulate and become increasingly available through time. Our results indicate that a focus on single spatial scales when assessing the influence of biodiversity on disease risk provides an incomplete picture of the complexity of disease dynamics in ecosystems.

Domestic dogs can function as either paratenic or definitive hosts for the zoonotic raccoon roundworm Baylisascaris procyonis. However, factors leading to development of patent infections in dogs are under-studied. Here we compared infection dynamics of B. procyonis in dogs vs the natural raccoon host. Dogs and raccoons were inoculated 5000 or 500 B. procyonis eggs (n = 3 per dose) or were fed B. procyonis-infected laboratory mice (n = 3 per dose; mice inoculated with 1000 or 250 eggs). Fecal samples were analysed via flotation and a commercial coproantigen ELISA designed for detection of Toxocara spp. Two of 12 dogs (both received low dose larvae) developed patent infections; all 12 raccoons became infected with 10 developing patent infections. Compared with dogs, prepatent periods were shorter in raccoons and maximum egg outputs were much greater. Baylisascaris procyonis coproantigens were detectable via ELISA in all raccoons and the patently infected dogs. Finally, dogs spontaneously lost infections while all patently infected raccoons shed eggs until conclusion of the study. Our results demonstrate that dogs are clearly suboptimal hosts showing limited parasite establishment and fecundity vs raccoons. Despite the low competence, patently infected dogs still pose a risk for human exposure, emphasizing the importance of control measures.

Identifying the key vector and host species that drive the transmission of zoonotic pathogens is notoriously difficult but critical for disease control. We present a nested approach for quantifying the importance of host and vectors that integrates species’ physiological competence with their ecological traits. We apply this framework to a medically important arbovirus, Ross River virus (RRV), in Brisbane, Australia. We find that vertebrate hosts with high physiological competence are not the most important for community transmission; interactions between hosts and vectors largely underpin the importance of host species. For vectors, physiological competence is highly important. Our results identify primary and secondary vectors of RRV and suggest two potential transmission cycles in Brisbane: an enzootic cycle involving birds and an urban cycle involving humans. The framework accounts for uncertainty from each fitted statistical model in estimates of species’ contributions to transmission and has has direct application to other zoonotic pathogens.

Social interactions are required for the direct transmission of infectious diseases. Consequently, the social network structure of populations plays a key role in shaping infectious disease dynamics. A huge research effort has examined how specific social network structures make populations more (or less) vulnerable to damaging epidemics. However, it can be just as important to understand how social networks can contribute to endemic disease dynamics, in which pathogens are maintained at stable levels for prolonged periods of time. Hosts that can maintain endemic disease may serve as keystone hosts for multi-host pathogens within an ecological community, and also have greater potential to act as key wildlife reservoirs of agricultural and zoonotic diseases. Here, we examine combinations of social and demographic processes that can foster endemic disease in hosts. We synthesise theoretical and empirical work to demonstrate the importance of both social structure and social dynamics in maintaining endemic disease. We also highlight the importance of distinguishing between the local and global persistence of infection and reveal how different social processes drive variation in the scale at which infectious diseases appear endemic. Our synthesis provides a framework by which to understand how sociality contributes to the longterm maintenance of infectious disease in wildlife hosts and provides a set of tools to unpick the social and demographic mechanisms involved in any given host–pathogen system.

Disease tolerance reduces the per‐pathogen fitness costs of infection for hosts and is an important component of host adaptation to pathogens. However, how disease tolerance affects host transmission potential is not well understood, especially because there are many potential mechanisms that facilitate host tolerance. For example, tissue‐specific host tolerance leads to the reduction of host pathology, regardless of pathogen load. Hosts may also exhibit behavioral tolerance, where normal behaviors are maintained even while harboring high pathogen loads. Here, we examined the impacts that tissue‐specific and behavioral tolerance have on transmission in house finches (Haemorhous mexicanus) infected with a common and highly transmissible bacterial pathogen, Mycoplasma gallisepticum (MG). MG causes conjunctivitis in house finches and severely reduces population numbers after it arrives in a new area. Wild house finch populations differ in tissue‐specific tolerance to MG and here we assessed how this variation in tolerance influences transmission success. We inoculated wild‐captured, MG‐naïve individuals from two populations that are on the extremes of tissue‐specific tolerance to MG and determined the likelihood of these “index” individuals transmitting MG to an uninfected, susceptible cagemate. Higher tissue‐specific tolerance results in reduced conjunctivitis, which is associated with decreased deposition and spread of MG. Thus, we predicted that individuals with high tissue‐specific tolerance would be less likely to transmit MG. In contrast, we predicted that behavioral tolerance would be linked to higher transmission, as more tolerant individuals spent more time on a feeder shared with a susceptible individual despite high pathogen loads. In agreement with our prediction, individuals with high tissue‐specific tolerance were less likely to transmit MG. However, there was no effect of behavioral tolerance on the likelihood of MG transmission. Our results highlight that it is key to consider how different mechanisms of tolerance affect transmission and, therefore, host‐pathogen coevolution and epidemic dynamics. The effects of host disease tolerance on pathogen transmission are not well understood. Here, we use wild‐caught house finches to show that natural variation in tissue‐specific tolerance to a bacterial pathogen affects the transmission of this pathogen. In contrast, host behavioral tolerance does not affect the transmission of the same bacterial pathogen in house finches.

Japanese encephalitis virus (JEV) is a flavivirus that is maintained via transmission between Culex spp. mosquitoes and water birds across a large swath of southern Asia and northern Australia. Currently JEV is the leading cause of vaccine-preventable encephalitis in humans in Asia. Five genotypes of JEV (G-I–G-V) have been responsible for historical and current outbreaks in endemic regions, and G-I and G-III co-circulate throughout Southern Asia. While G-III has historically been the dominant genotype worldwide, G-I has gradually but steadily displaced G-III. The objective of this study was to better understand the phenomenon of genotype displacement for JEV by evaluating both avian host and mosquito vector susceptibilities to infection with representatives from both G-I and G-III. Since ducks and Culex quinquefasciatus mosquitoes are prevalent avian hosts and vectors perpetuating JEV transmission in JE endemic areas, experimental evaluation of virus replication in these species was considered to approximate the natural conditions necessary for studying the role of host, vectors and viral fitness in the JEV genotype displacement context. We evaluated viremia in ducklings infected with G-I and G-III, and did not detect differences in magnitude or duration of viremia. Testing the same viruses in mosquitoes revealed that the rates of infection, dissemination and transmission were higher in virus strains belonging to G-I than G-III, and that the extrinsic incubation period was shorter for the G-I strains. These data suggest that the characteristics of JEV infection of mosquitoes but not of ducklings, may have play a role in genotype displacement.