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We describe the first detection of Paranannizziopsis sp. in a wild population of vipers in Europe. Fungal infections were severe and one individual likely died from infection. Surveillance efforts are needed to better understand the threat of this pathogen to snake conservation.
Testing of ducks in Tennessee, United States, before introduction of highly pathogenic influenza A(H5N1) virus demonstrated a high prevalence of antibodies to influenza A virus but very low prevalence of antibodies to H5 (25%) or H5 and N1 (13%) subtypes. Antibody prevalence increased after H5N1 introduction.
Serum samples from wild mammals inhabiting Alaska, USA, showed that 4 species, including Ursus arctos bears and Vulpes vulpes foxes, were exposed to influenza A(H5N1) viruses. Results indicated some mammals in Alaska survived H5N1 virus infection. Surveillance efforts may be improved by incorporating information on susceptibility and detectable immune responses among wild mammals.
Wind energy generation holds the potential to adversely affect wildlife populations. Species-wide effects are difficult to study and few, if any, studies examine effects of wind energy generation on any species across its entire range. One species that may be affected by wind energy generation is the endangered Indiana bat ( Myotis sodalis ), which is found in the eastern and midwestern United States. In addition to mortality from wind energy generation, the species also faces range-wide threats from the emerging infectious fungal disease, white-nose syndrome (WNS). White-nose syndrome, caused by Pseudogymnoascus destructans , disturbs hibernating bats leading to high levels of mortality. We used a spatially explicit full-annual-cycle model to investigate how wind turbine mortality and WNS may singly and then together affect population dynamics of this species. In the simulation, wind turbine mortality impacted the metapopulation dynamics of the species by causing extirpation of some of the smaller winter colonies. In general, effects of wind turbines were localized and focused on specific spatial subpopulations. Conversely, WNS had a depressive effect on the species across its range. Wind turbine mortality interacted with WNS and together these stressors had a larger impact than would be expected from either alone, principally because these stressors together act to reduce species abundance across the spectrum of population sizes. Our findings illustrate the importance of not only prioritizing the protection of large winter colonies as is currently done, but also of protecting metapopulation dynamics and migratory connectivity.
Secondary sexual traits (e.g., horns and antlers) have ecological and evolutionary importance and are of management interest for game species. Yet, how these traits respond to emerging threats like infectious disease remains underexplored. Infectious pneumonia threatens bighorn sheep ( Ovis canadensis ) populations across North America and we hypothesized it may also reduce horn growth in male sheep. We assess the effect of pneumonia on horn size in male bighorn sheep using 12 herd datasets from across the western United States that had horn growth and disease data. Disease resulted in 12–35% reduction in increment (yearly) length and 3–13% reduction in total horn length in exposed individuals. The disease effect was prolonged when pathogens continued to circulate in sheep populations. Further, disease likely delays the age at which horns reach ¾-curl and prevents achievement of full-curl. This is further evidenced with 6 of the 12 herds experiencing an increase in average age at harvest following die-off events.
Parasitism is the most common consumer strategy among organisms, yet only recently has there been a call for the inclusion of infectious disease agents in food webs. The value of this effort hinges on whether parasites affect food-web properties. Increasing evidence suggests that parasites have the potential to uniquely alter food-web topology in terms of chain length, connectance and robustness. In addition, parasites might affect food-web stability, interaction strength and energy flow. Food-web structure also affects infectious disease dynamics because parasites depend on the ecological networks in which they live. Empirically, incorporating parasites into food webs is straightforward. We may start with existing food webs and add parasites as nodes, or we may try to build food webs around systems for which we already have a good understanding of infectious processes. In the future, perhaps researchers will add parasites while they construct food webs. Less clear is how food-web theory can accommodate parasites. This is a deep and central problem in theoretical biology and applied mathematics. For instance, is representing parasites with complex life cycles as a single node equivalent to representing other species with ontogenetic niche shifts as a single node? Can parasitism fit into fundamental frameworks such as the niche model? Can we integrate infectious disease models into the emerging field of dynamic food-web modelling? Future progress will benefit from interdisciplinary collaborations between ecologists and infectious disease biologists.
Emerging infectious pathogens are responsible for some of the most severe host mass mortality events in wild populations. Yet, effective pathogen control strategies are notoriously difficult to identify, in part because quantifying and forecasting pathogen spread and disease dynamics is challenging. Following an outbreak, hosts must cope with the presence of the pathogen, leading to host–pathogen coexistence or extirpation. Despite decades of research, little is known about host–pathogen coexistence post‐outbreak when low host abundances and cryptic species make these interactions difficult to study. Using a novel disease‐structured N‐mixture model, we evaluate empirical support for three host–pathogen coexistence hypotheses (source–sink, eco‐evolutionary rescue, and spatial variation in pathogen transmission) in a Neotropical amphibian community decimated by Batrachochytrium dendrobatidis ( Bd ) in 2004. During 2010–2014, we surveyed amphibians in Parque Nacional G. D. Omar Torríjos Herrera, Coclé Province, El Copé, Panama. We found that the primary driver of host–pathogen coexistence was eco‐evolutionary rescue, as evidenced by similar amphibian survival and recruitment rates between infected and uninfected hosts. Average apparent monthly survival rates of uninfected and infected hosts were both close to 96%, and the expected number of uninfected and infected hosts recruited (via immigration/reproduction) was less than one host per disease state per 20‐m site. The secondary driver of host–pathogen coexistence was spatial variation in pathogen transmission as we found that transmission was highest in areas of low abundance but there was no support for the source–sink hypothesis. Our results indicate that changes in the host community (i.e., through genetic or species composition) can reduce the impacts of emerging infectious disease post‐outbreak. Our disease‐structured N‐mixture model represents a valuable advancement for conservation managers trying to understand underlying host–pathogen interactions and provides new opportunities to study disease dynamics in remnant host populations decimated by virulent pathogens.
White-nose syndrome (WNS) is a fatal disease of bats that hibernate. The etiologic agent of WNS is the fungus Geomyces destructans , which infects the skin and wing membranes. Over 1 million bats in six species in eastern North America have died from WNS since 2006, and as a result several species of bats may become endangered or extinct. Information is lacking on the pathogenesis of G. destructans and WNS, WNS transmission and maintenance, individual and site factors that contribute to the probability of an outbreak of WNS, and spatial dynamics of WNS spread in North America. We considered how descriptive and analytical epidemiology could be used to fill these information gaps, including a four-step (modified) outbreak investigation, application of a set of criteria (Hill's) for assessing causation, compartment models of disease dynamics, and spatial modeling. We cataloged and critiqued adaptive-management options that have been either previously proposed for WNS or were helpful in addressing other emerging diseases of wild animals. These include an ongoing program of prospective surveillance of bats and hibernacula for WNS, treatment of individual bats, increasing population resistance to WNS (through vaccines, immunomodulators, or other methods), improving probability of survival from starvation and dehydration associated with WNS, modifying hibernacula environments to eliminate G. destructans , culling individuals or populations, controlling anthropogenic spread of WNS, conserving genetic diversity of bats, and educating the public about bats and bat conservation issues associated with WNS.
The global trade in wildlife has historically contributed to the emergence and spread of infectious diseases. The United States is the world's largest importer of wildlife and wildlife products, yet minimal pathogen surveillance has precluded assessment of the health risks posed by this practice. This report details the findings of a pilot project to establish surveillance methodology for zoonotic agents in confiscated wildlife products. Initial findings from samples collected at several international airports identified parts originating from nonhuman primate (NHP) and rodent species, including baboon, chimpanzee, mangabey, guenon, green monkey, cane rat and rat. Pathogen screening identified retroviruses (simian foamy virus) and/or herpesviruses (cytomegalovirus and lymphocryptovirus) in the NHP samples. These results are the first demonstration that illegal bushmeat importation into the United States could act as a conduit for pathogen spread, and suggest that implementation of disease surveillance of the wildlife trade will help facilitate prevention of disease emergence.
Colonization of urban areas by synanthropic wildlife introduces novel and complex alterations to established ecological processes, including the emergence and spread of infectious diseases. Aggregation at urban resources can increase disease transfer, with wide-ranging species potentially infecting outlying populations. The garrison at the National Training Center, Fort Irwin, California, USA, was recently colonized by mange-infected coyotes ( Canis latrans ) that also use the surrounding Mojave Desert. This situation provided an ideal opportunity to examine the effects of urban resources on disease dynamics. We evaluated seasonal space use and determined the influence of anthropogenic subsidies, water sources, and prey density on urban resource selection. We found no difference in home range size between healthy and infected individuals, but infected residents had considerably more spatial overlap with one another than healthy residents. All coyotes selected for anthropogenic subsidies during all seasons, while infected coyotes seasonally selected for urban water sources, and healthy coyotes seasonally selected for urban areas with greater densities of natural prey. These results suggest that while all coyotes were selecting for anthropogenic subsidies, infected resident coyotes demonstrated a greater tolerance for other conspecifics, which could be facilitating the horizontal transfer of sarcoptic mange to non-resident coyotes. Conversely, healthy coyotes also selected for natural prey and healthy residents exhibited a lack of spatial overlap with other coyotes suggesting they were not reliant on anthropogenic subsidies and were maintaining territories. Understanding the association between urban wildlife, zoonotic diseases, and urban resources can be critical in determining effective responses for mitigating future epizootics.
Northern ecosystems are currently experiencing unprecedented ecological change, largely driven by a rapidly changing climate. Pathogen range expansion, and emergence and altered patterns of infectious disease, are increasingly reported in wildlife at high latitudes. Understanding the causes and consequences of shifting pathogen diversity and host-pathogen interactions in these ecosystems is important for wildlife conservation, and for indigenous populations that depend on wildlife. Among the key questions are whether disease events are associated with endemic or recently introduced pathogens, and whether emerging strains are spreading throughout the region. In this study, we used a phylogenomic approach to address these questions of pathogen endemicity and spread for Erysipelothrix rhusiopathiae , an opportunistic multi-host bacterial pathogen associated with recent mortalities in arctic and boreal ungulate populations in North America. We isolated E. rhusiopathiae from carcasses associated with large-scale die-offs of muskoxen in the Canadian Arctic Archipelago, and from contemporaneous mortality events and/or population declines among muskoxen in northwestern Alaska and caribou and moose in western Canada. Bacterial genomic diversity differed markedly among these locations; minimal divergence was present among isolates from muskoxen in the Canadian Arctic, while in caribou and moose populations, strains from highly divergent clades were isolated from the same location, or even from within a single carcass. These results indicate that mortalities among northern ungulates are not associated with a single emerging strain of E. rhusiopathiae , and that alternate hypotheses need to be explored. Our study illustrates the value and limitations of bacterial genomic data for discriminating between ecological hypotheses of disease emergence, and highlights the importance of studying emerging pathogens within the broader context of environmental and host factors.
Demographic factors are fundamental in shaping infectious disease dynamics. Aspects of populations that create structure, like age and sex, can affect patterns of transmission, infection intensity and population outcomes. However, studies rarely link these processes from individual to population-scale effects. Moreover, the mechanisms underlying demographic differences in disease are frequently unclear. Here, we explore sex-biased infections for a multi-host fungal disease of bats, white-nose syndrome, and link disease-associated mortality between sexes, the distortion of sex ratios and the potential mechanisms underlying sex differences in infection. We collected data on host traits, infection intensity and survival of five bat species at 42 sites across seven years. We found females were more infected than males for all five species. Females also had lower apparent survival over winter and accounted for a smaller proportion of populations over time. Notably, female-biased infections were evident by early hibernation and likely driven by sex-based differences in autumn mating behaviour. Male bats were more active during autumn which likely reduced replication of the cool-growing fungus. Higher disease impacts in female bats may have cascading effects on bat populations beyond the hibernation season by limiting recruitment and increasing the risk of Allee effects.
In the event of a new infectious disease outbreak, mathematical and simulation models are commonly used to inform policy by evaluating which control strategies will minimize the impact of the epidemic. In the early stages of such outbreaks, substantial parameter uncertainty may limit the ability of models to provide accurate predictions, and policymakers do not have the luxury of waiting for data to alleviate this state of uncertainty. For policymakers, however, it is the selection of the optimal control intervention in the face of uncertainty, rather than accuracy of model predictions, that is the measure of success that counts. We simulate the process of real-time decision-making by fitting an epidemic model to observed, spatially-explicit, infection data at weekly intervals throughout two historical outbreaks of foot-and-mouth disease, UK in 2001 and Miyazaki, Japan in 2010, and compare forward simulations of the impact of switching to an alternative control intervention at the time point in question. These are compared to policy recommendations generated in hindsight using data from the entire outbreak, thereby comparing the best we could have done at the time with the best we could have done in retrospect. Our results show that the control policy that would have been chosen using all the data is also identified from an early stage in an outbreak using only the available data, despite high variability in projections of epidemic size. Critically, we find that it is an improved understanding of the locations of infected farms, rather than improved estimates of transmission parameters, that drives improved prediction of the relative performance of control interventions. However, the ability to estimate undetected infectious premises is a function of uncertainty in the transmission parameters. Here, we demonstrate the need for both real-time model fitting and generating projections to evaluate alternative control interventions throughout an outbreak. Our results highlight the use of using models at outbreak onset to inform policy and the importance of state-dependent interventions that adapt in response to additional information throughout an outbreak.
Infectious diseases are increasingly recognized as an important force driving population dynamics, conservation biology, and natural selection in wildlife populations. Infectious agents have been implicated in the decline of small or endangered populations and may act to constrain population size, distribution, growth rates, or migration patterns. Further, diseases may provide selective pressures that shape the genetic diversity of populations or species. Thus, understanding disease dynamics and selective pressures from pathogens is crucial to understanding population processes, managing wildlife diseases, and conserving biological diversity. There is ample evidence that variation in the prion protein gene (PRNP) impacts host susceptibility to prion diseases. Still, little is known about how genetic differences might influence natural selection within wildlife populations. Here we link genetic variation with differential susceptibility of white-tailed deer to chronic wasting disease (CWD), with implications for fitness and disease-driven genetic selection. We developed a single nucleotide polymorphism (SNP) assay to efficiently genotype deer at the locus of interest (in the 96th codon of the PRNP gene). Then, using a Bayesian modeling approach, we found that the more susceptible genotype had over four times greater risk of CWD infection; and, once infected, deer with the resistant genotype survived 49% longer (8.25 more months). We used these epidemiological parameters in a multi-stage population matrix model to evaluate relative fitness based on genotype-specific population growth rates. The differences in disease infection and mortality rates allowed genetically resistant deer to achieve higher population growth and obtain a long-term fitness advantage, which translated into a selection coefficient of over 1% favoring the CWD-resistant genotype. This selective pressure suggests that the resistant allele could become dominant in the population within an evolutionarily short time frame. Our work provides a rare example of a quantifiable disease-driven selection process in a wildlife population, demonstrating the potential for infectious diseases to alter host populations. This will have direct bearing on the epidemiology, dynamics, and future trends in CWD transmission and spread. Understanding genotype-specific epidemiology will improve predictive models and inform management strategies for CWD-affected cervid populations.
Wildlife can be an important source of transmission of infectious disease to humans. One potential transmission route involves hunting and fishing, both common activities in the United States and worldwide. For example, during 1996, approximately 11 million Americans, about 40 percent of the total population 16 years of age and older, took part in some recreational activity relating to wildlife and fish. Another potential route of infection focuses on urban and suburban environments. These locations are of special concern because of their increasing role as wildlife habitat, the greater interface between humans and wildlife that takes place within those environments, the paucity of knowledge about disease in those wildlife populations, and the general lack of orderly management for wildlife within those environments. In the wild, several trends are contributing to the growing importance of zoonotic diseases. First, the spectrum of infectious diseases affecting wildlife today is greater than at any time during the previous century. Second, the occurrence of infectious diseases has changed, from sporadic, self-limiting outbreaks that generally resulted in minor losses to frequently occurring events that generally result in major losses of wildlife. Third, disease emergence has occurred on a worldwide scale in a broad spectrum of wildlife species and habitats. Given the scope of the problem, current disease surveillance efforts are inadequate. Few state wildlife agencies allocate personnel and resources to address wildlife disease, despite their statutory responsibility for managing nonmigratory wildlife. Some state agencies provide minimal support for regional programs based at universities. At the federal level, the primary surveillance effort is conducted by the National Wildlife Health Center, operated by the U.S. Geological Survey. Outside of government, some veterinary schools, agriculture diagnostic laboratories, and other programs provide additional information on animal diseases, primarily by examining carcasses of dead wildlife submitted for analysis, and individual university-based researchers carry out a variety of studies. Typically, information about the occurrence of disease in free-ranging wildlife is derived from surveys and mortality events in areas where wildlife observations by agencies and the public are frequent enough to detect their occurrence before carcasses are removed by scavengers and predatory animals. The result is that disease occurrence is grossly underreported, heavily biased toward mortality events, and biased toward species of special concern and interest, such as game and endangered species. Therefore, the available information should be viewed as the “proverbial tip of the iceberg” relative to disease activity within wildlife populations.
Range shifts of infectious plant disease are expected under climate change. As plant diseases move, emergent abiotic-biotic interactions are predicted to modify their distributions, leading to unexpected changes in disease risk. Evidence of these complex range shifts due to climate change, however, remains largely speculative. Here, we combine a long-term study of the infectious tree disease, white pine blister rust, with a six-year field assessment of drought-disease interactions in the southern Sierra Nevada. We find that climate change between 1996 and 2016 moved the climate optimum of the disease into higher elevations. The nonlinear climate change-disease relationship contributed to an estimated 5.5 (4.4–6.6) percentage points (p.p.) decline in disease prevalence in arid regions and an estimated 6.8 (5.8–7.9) p.p. increase in colder regions. Though climate change likely expanded the suitable area for blister rust by 777.9 (1.0–1392.9) km 2 into previously inhospitable regions, the combination of host-pathogen and drought-disease interactions contributed to a substantial decrease (32.79%) in mean disease prevalence between surveys. Specifically, declining alternate host abundance suppressed infection probabilities at high elevations, even as climatic conditions became more suitable. Further, drought-disease interactions varied in strength and direction across an aridity gradient—likely decreasing infection risk at low elevations while simultaneously increasing infection risk at high elevations. These results highlight the critical role of aridity in modifying host-pathogen-drought interactions. Variation in aridity across topographic gradients can strongly mediate plant disease range shifts in response to climate change.
Increasing risk of pathogen spillover coupled with overall declines in wildlife population abundance in the Anthropocene make infectious disease a relevant concern for species conservation worldwide. While emerging molecular tools could improve our diagnostic capabilities and give insight into mechanisms underlying wildlife disease risk, they have rarely been applied in practice. Here, employing a previously reported gene transcription panel of common immune markers to track physiological changes, we present a detailed analysis over the course of both acute and chronic infection in one wildlife species where disease plays a critical role in conservation, bighorn sheep ( Ovis canadensis ). Differential gene transcription patterns distinguished between infection statuses over the course of acute infection and differential correlation (DC) analyses identified clear changes in gene co-transcription patterns over the early stages of infection, with transcription of four genes—TGFb, AHR, IL1b and MX1—continuing to increase even as transcription of other immune-associated genes waned. In a separate analysis, we considered the capacity of the same gene transcription panel to aid in differentiating between chronically infected animals and animals in other disease states outside of acute disease events (an immediate priority for wildlife management in this system). We found that this transcription panel was capable of accurately identifying chronically infected animals in the test dataset, though additional data will be required to determine how far this ability extends. Taken together, our results showcase the successful proof of concept and breadth of potential utilities that gene transcription might provide to wildlife disease management, from direct insight into mechanisms associated with differential disease response to improved diagnostic capacity in the field.
Oral vaccination is an emerging management strategy to reduce the prevalence of high impact infectious diseases within wild animal populations. Plague is a flea-borne zoonosis of rodents that often decimates prairie dog ( Cynomys spp.) colonies in the western USA. Recently, an oral sylvatic plague vaccine (SPV) was developed to protect prairie dogs from plague and aid recovery of the endangered black-footed ferret ( Mustela nigripes ). Although oral vaccination programs are targeted toward specific species, field distribution of vaccine-laden baits can result in vaccine uptake by non-target animals and unintended indirect effects. We assessed the impact of SPV on non-target rodents at paired vaccine and placebo-treated prairie dog colonies in four US states from 2013 to 2015. Bait consumption by non-target rodents was high (70.8%, n = 3113), but anti-plague antibody development on vaccine plots was low (23.7%, n = 266). In addition, no significant differences were noted in combined deer mice ( Peromyscus maniculatus ) and western harvest mouse ( Reithrodontomys megalotis ) abundance or community evenness and richness of non-target rodents between vaccine-treated and placebo plots. In our 3-year field study, we could not detect a significant positive or negative effect of SPV application on non-target rodents.