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White-tailed deer (WTD; Odocoileus virginianus) are a critical species for ecosystem function and wildlife management. As such, studies of cause-specific mortality among WTD have long been used to understand population dynamics. However, detailed pathological information is rarely documented for free-ranging WTD, especially in regions with a high prevalence of chronic wasting disease (CWD). This leaves a significant gap in understanding how CWD is associated with disease processes or comorbidities that may subsequently alter broader population dynamics. We investigated unknown mortalities among collared WTD in southwestern Wisconsin, USA, an area of high CWD prevalence. We tested for associations between CWD and other disease processes and used a network approach to test for co-occurring disease processes. Predation and infectious disease were leading suspected causes of death, with high prevalence of CWD (42.4%; of 245 evaluated) and pneumonia (51.2%; of 168 evaluated) in our sample. CWD prevalence increased with age, before decreasing among older individuals, with more older females than males in our sample. Females were more likely to be CWD positive, and although this was not statistically significant when accounting for age, females were significantly more likely to die with end-stage CWD than males and may consequently be an underrecognized source of CWD transmission. Presence of CWD was associated with emaciation, atrophy of marrow fat and hematopoietic cells, and ectoparasitism (lice and ticks). Occurrences of severe infectious disease processes clustered together (e.g., pneumonia, CWD), as compared to noninfectious or low-severity processes (e.g., sarcocystosis), although pneumonia cases were not fully explained by CWD status. With the prevalence of CWD increasing across North America, our results highlight the critical importance of understanding the potential role of CWD in favoring or maintaining disease processes of importance for deer population health and dynamics.

The latitudinal diversity gradient (LDG) is an established macroecological pattern, but is poorly studied in microbial organisms, particularly parasites. In this study, we tested whether latitude, elevation, and host species predicted patterns of prevalence, alpha diversity, and community turnover of hemosporidian parasites. We expected parasite diversity to decrease with latitude, alongside the diversity of their hosts and vectors. Similarly, we expected infection prevalence to decrease with latitude as vector abundances decrease. Lastly, we expected parasite community turnover to increase with latitudinal distance and to be higher between rather than within host species. We tested these hypotheses by screening blood and tissue samples of three closely related avian species in a clade of North American songbirds (Turdidae: Catharus, n = 466) across 17.5° of latitude. We used a nested PCR approach to identify parasites in hemosporidian genera that are transmitted by different dipteran vectors. Then, we implemented linear‐mixed effects and generalized dissimilarity models to evaluate the effects of latitude, elevation, and host species on parasite metrics. We found high diversity of hemosporidian parasites in Catharus thrushes (n = 44 lineages) but no evidence of latitudinal gradients in alpha diversity or prevalence. Parasites in the genus Leucocytozoon were most prevalent and lineage rich in this study system; however, there was limited turnover with latitude and host species. Contrastingly, Plasmodium parasites were less prevalent and diverse than Leucocytozoon parasites, yet communities turned over at a higher rate with latitude and host species. Leucocytozoon communities were skewed by the dominance of one or two highly prevalent lineages with broad latitudinal distributions. The few studies that evaluate the hemosporidian LDG do not find consistent patterns of prevalence and diversity, which makes it challenging to predict how they will respond to global climate change., Catharus thrushes are heavily infected by a diverse assemblage of hemosporidian parasites; however, these parasites did not follow a latitudinal diversity gradient or prevalence. Instead, we see high community turnover of Plasmodium communities with latitude and host species and moderate turnover of Leucocytozoon communities with latitude.

Bacillus anthracis , the etiological agent of anthrax, is a well-established model organism. For B. anthracis and most other infectious diseases, knowledge regarding transmission and infection parameters in natural systems, in large part, comprises data gathered from closely controlled laboratory experiments. Fatal, natural anthrax infections transmit the bacterium through new host−pathogen contacts at carcass sites, which can occur years after death of the previous host. For the period between contact and death, all of our knowledge is based upon experimental data from domestic livestock and laboratory animals. Here we use a noninvasive method to explore the dynamics of anthrax infections, by evaluating the terminal diversity of B. anthracis in anthrax carcasses. We present an application of population genetics theory, specifically, coalescence modeling, to intrainfection populations of B. anthracis to derive estimates for the duration of the acute phase of the infection and effective population size converted to the number of colony-forming units establishing infection in wild plains zebra ( Equus quagga ). Founding populations are small, a few colony-forming units, and infections are rapid, lasting roughly between 1 d and 3 d in the wild. Our results closely reflect experimental data, showing that small founding populations progress acutely, killing the host within days. We believe this method is amendable to other bacterial diseases from wild, domestic, and human systems.

Bacillus anthracis, the causative agent of anthrax, is a considerable global health threat affecting wildlife, livestock, and the general public. In this study whole-genome sequence analysis of over 350B. anthracisisolates was used to establish a new high-resolution global genotyping framework that is both biogeographically informative, and compatible with multiple genomic assays. The data presented in this study shed new light on the diverse global dissemination of this species and indicate that many lineages may be uniquely suited to the geographic regions in which they are found. In addition, we demonstrate that plasmid genomic structure for this species is largely consistent with chromosomal population structure, suggesting vertical inheritance in this bacterium has contributed to its evolutionary persistence. This classification methodology is the first based on population genomic structure for this species and has potential use for local and broader institutions seeking to understand both disease outbreak origins and recent introductions. In addition, we provide access to a newly developed genotyping script as well as the full whole genome sequence analyses output for this study, allowing future studies to rapidly employ and append their data in the context of this global collection. This framework may act as a powerful tool for public health agencies, wildlife disease laboratories, and researchers seeking to utilize and expand this classification scheme for further investigations intoB. anthracisevolution.

Exposure and immunity to generalist pathogens differ among host species and vary across spatial scales. Anthrax, caused by a multi-host bacterial pathogen

Bacillus anthracis, the causative agent of anthrax disease, is a worldwide threat to livestock, wildlife and public health. While analyses of genetic data from across the globe have increased our understanding of this bacterium’s population genomic structure, the influence of selective pressures on this successful pathogen is not well understood. In this study, we investigate the effects of antimicrobial resistance, phage diversity, geography and isolation source in shaping population genomic structure. We also identify a suite of candidate genes potentially under selection, driving patterns of diversity across 356 globally extant B. anthracis genomes. We report ten antimicrobial resistance genes and 11 different prophage sequences, resulting in the first large-scale documentation of these genetic anomalies for this pathogen. Results of random forest classification suggest genomic structure may be driven by a combination of antimicrobial resistance, geography and isolation source, specific to the population cluster examined. We found strong evidence that a recombination event linked to a gene involved in protein synthesis may be responsible for phenotypic differences between comparatively disparate populations. We also offer a list of genes for further examination of B. anthracis evolution, based on high-impact single nucleotide polymorphisms (SNPs) and clustered mutations. The information presented here sheds new light on the factors driving genomic structure in this notorious pathogen and may act as a road map for future studies aimed at understanding functional differences in terms of B. anthracis biogeography, virulence and evolution.

Bacillus anthracis, the causative agent of anthrax disease, is a worldwide threat to livestock, wildlife and public health. While analyses of genetic data from across the globe have increased our understanding of this bacterium’s population genomic structure, the influence of selective pressures on this successful pathogen is not well understood. In this study, we investigate the effects of antimicrobial resistance, phage diversity, geography and isolation source in shaping population genomic structure. We also identify a suite of candidate genes potentially under selection, driving patterns of diversity across 356 globally extant B. anthracis genomes. We report ten antimicrobial resistance genes and 11 different prophage sequences, resulting in the first large-scale documentation of these genetic anomalies for this pathogen. Results of random forest classification suggest genomic structure may be driven by a combination of antimicrobial resistance, geography and isolation source, specific to the population cluster examined. We found strong evidence that a recombination event linked to a gene involved in protein synthesis may be responsible for phenotypic differences between comparatively disparate populations. We also offer a list of genes for further examination of B. anthracis evolution, based on high-impact single nucleotide polymorphisms (SNPs) and clustered mutations. The information presented here sheds new light on the factors driving genomic structure in this notorious pathogen and may act as a road map for future studies aimed at understanding functional differences in terms of B. anthracis biogeography, virulence and evolution.

Globally, anthrax outbreaks pose a serious threat to people, livestock, and wildlife. Furthermore, environmental change can exacerbate these outbreak dynamics by altering the host–pathogen relationship. However, little is known about how the quantitative spatial dynamics of host movement and environmental change may affect the spread of Bacillus anthracis, the causative agent of anthrax. Here, we use real‐time observations and high‐resolution tracking data from a population of common hippopotamus (Hippopotamus amphibius) in Tanzania to explore the relationship between river hydrology, H. amphibius movement, and the spatiotemporal dynamics of an active anthrax outbreak. We found that extreme river drying, a consequence of anthropogenic disturbances to our study river, indirectly facilitated the spread of B. anthracis by modulating H. amphibius movements. Our findings reveal that anthrax spread upstream in the Great Ruaha River (~3.5 km over a 9‐day period), which followed the movement patterns of infected H. amphibius, who moved upstream as the river dried in search of remaining aquatic refugia. These upstream movements can result in large aggregations of H. amphibius. However, despite these aggregations, the density of H. amphibius in river pools did not influence the number of B. anthracis‐induced mortalities. Moreover, infection by B. anthracis did not appear to influence H. amphibius movement behaviors, which suggests that infected individuals can vector B. anthracis over large distances right up until their death. Finally, we show that contact rates between H. amphibius‐ and B. anthracis‐infected river pools are highly variable and the frequency and duration of contacts could potentially increase the probability of mortality. While difficult to obtain, the quantitative insights that we gathered during a real‐time anthrax outbreak are critical to better understand, predict, and manage future outbreaks.

Here we present a developing probabilistic simulation model and tool to assess likely lead times from emergence to detection and arrival for new emerging infectious diseases (EIDs). Key aspects include combining real-world data available on multiple scales with a flexible underlying disease model. As demonstrated by the SARS-CoV-2 pandemic and other emerging infectious diseases, there is a need for scenario exploration for mitigation, surveillance and preparedness strategies. Existing simulation engines have been assessed but found to offer an insufficient set of features with regards to flexibility and control over processes, disease model structure and data sets incorporated for a wider enough range of diseases, circumstances, cofactors and scenarios (Heslop et al. 2017) to suit our aims. We are therefore developing the first version of a simulation model designed to be able to incorporate a diverse range of disease models and data sources including multiple transmission and infectivity stages, multiple host species, varying and evolving virulence, socioeconomic differences, climate events and public health countermeasures. It is designed to be flexible with respect to implementing both improvements in the model structure and data as they become available. It is based on a discrete-time (daily) structure where spatial movement and transition between categories and detection are stochastic rates dependent on spatial data and past states in the model, while being informed by the most suitable data available (Fig. 1). The probability of detection is in itself treated as a probabilistic process and treated as a variable dependent on socioeconomic factors and parameterized by past performance, yet open for manipulation in scenario exploration regarding surveillance and reporting effectiveness. Pathogen hotspot data are sourced from literature and included as a probabilistic assessment of emergence as well as a source of cofactor data (Allen et al. 2017), population data are adressed (Leyk et al. 2019) for utility and combined with data on local connectivity (Nelson et al. 2019) and transnational movement patterns (Recchi et al. 2019Fig. 1), as well as an increasing set of ecological and socioeconomic candidate variables. Model parameterization relies on a machine learning framework with matching to the often partial data available for known relevant disease cases as the training data, and assessing them for plausible ranges of input for new, hypothetical EIDs. As parameterizations improve, the range of scenarios to explore will incorporate effects of climate change and multiple stressors. When a suitable version becomes available it will be shared under a MIT license.

The persistence of a parasite species in an ecological community is determined both by its environmental tolerance and host breadth. The relative contribution of these niche characteristics to parasite community structure is challenging to parse because host persistence is also a consequence of extrinsic environmental factors. We investigated haemosporidian parasites (genera Plasmodium, Leucocytozoon, and Haemoproteus) in a clade of avian hosts in eastern North America. Species in this clade of Catharus thrushes occupy specific elevational bands in a non‐phylogenetically determined manner. This allowed us to tease apart the effects of host relatedness and elevation on parasite community structure, diversity, and infection prevalence. We screened blood and tissue samples from 414 adult birds from four mountain ranges in the Appalachian Highlands for blood parasites using a cytochrome‐b‐nested PCR protocol and identified parasite lineages by sequencing. We found an overall infection prevalence of 88.4% and identified a total of 38 parasite lineages including six novel lineages. Parasite community patterns varied by genus. Host relatedness rather than elevational zone predicted the beta turnover and phylobeta turnover of Leucocytozoon parasites, indicating that closely related rather than geographically proximate host species had more similar parasites. This pattern was not seen in Plasmodium parasites because the diversity of this parasite genus varied considerably in the high elevational zones among mountain ranges, that is, a sky‐island effect. Haemoproteus parasites were rare in this study system. Our study suggests that the mechanisms that underlie community structuring vary between haemosporidian genera due to differences in the degree of host sharing among lineages.

The relationship between parasite virulence and transmission is a pillar of evolutionary theory that has implications for public health. Part of this canon involves the idea that virulence and free-living survival (a key component of transmission) may have different relationships in different host&ndash, parasite systems. Most examinations of the evolution of virulence-transmission relationships&mdash, Theoretical or empirical in nature&mdash, Tend to focus on the evolution of virulence, with transmission being a secondary consideration. Even within transmission studies, the focus on free-living survival is a smaller subset, though recent studies have examined its importance in the ecology of infectious diseases. Few studies have examined the epidemic-scale consequences of variation in survival across different virulence&ndash, survival relationships. In this study, we utilize a mathematical model motivated by aspects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) natural history to investigate how evolutionary changes in survival may influence several aspects of disease dynamics at the epidemiological scale. Across virulence&ndash, survival relationships (where these traits are either positively or negatively correlated), we found that small changes (5% above and below the nominal value) in survival can have a meaningful effect on certain outbreak features, including R0, and on the size of the infectious peak in the population. These results highlight the importance of properly understanding the mechanistic relationship between virulence and parasite survival, as the evolution of increased survival across different relationships with virulence may have considerably different epidemiological signatures.

The relationship between parasite virulence and transmission is a pillar of evolutionary theory that has specific implications for public health. Part of this canon involves the idea that virulence and free-living survival (a key component of transmission) may have different relationships in different host-parasite systems. Most examinations of the evolution of virulence-transmission relationships—theoretical or empirical in nature—tend to focus on the evolution of virulence, with transmission a secondary consideration. And even within transmission studies, the focus on free-living survival is a smaller subset, though recent studies have examined its importance in the ecology of infectious diseases. Few studies have examined the epidemic-scale consequences of variation in survival across different virulence-survival relationships. In this study, we utilize a mathematical model motivated by aspects of SARS-CoV-2 natural history to investigate how evolutionary changes in survival may influence several aspects of disease dynamics at the epidemiological scale. Across virulence-survival relationships (where these traits are positively or negatively correlated), we found that small changes (5% above and below the nominal value) in survival can have a meaningful effect on certain outbreak features, including theR0, and the size of the infectious peak in the population. These results highlight the importance of properly understanding the mechanistic relationship between virulence and parasite survival, as evolution of increased survival across different relationships with virulence will have considerably different epidemiological signatures.

Significance This study applies coalescence modeling to a “slowly evolving” bacterial pathogen, Bacillus anthracis, to derive estimates of infection durations and founding population sizes from natural anthrax mortalities. Although coalescence modeling has been applied to highly mutable chronic pathogens (i.e., HIV), to date, methodological hurdles have prevented its wider application. Our findings show it is possible to obtain pathological data from infections, post hoc, which may be applicable to other pathogens and settings, including clinical. Given their higher resolution, microsatellites will remain useful in shorter evolutionary timeframe studies., Bacillus anthracis, the etiological agent of anthrax, is a well-established model organism. For B. anthracis and most other infectious diseases, knowledge regarding transmission and infection parameters in natural systems, in large part, comprises data gathered from closely controlled laboratory experiments. Fatal, natural anthrax infections transmit the bacterium through new host−pathogen contacts at carcass sites, which can occur years after death of the previous host. For the period between contact and death, all of our knowledge is based upon experimental data from domestic livestock and laboratory animals. Here we use a noninvasive method to explore the dynamics of anthrax infections, by evaluating the terminal diversity of B. anthracis in anthrax carcasses. We present an application of population genetics theory, specifically, coalescence modeling, to intrainfection populations of B. anthracis to derive estimates for the duration of the acute phase of the infection and effective population size converted to the number of colony-forming units establishing infection in wild plains zebra (Equus quagga). Founding populations are small, a few colony-forming units, and infections are rapid, lasting roughly between 1 d and 3 d in the wild. Our results closely reflect experimental data, showing that small founding populations progress acutely, killing the host within days. We believe this method is amendable to other bacterial diseases from wild, domestic, and human systems.

Environmentally transmitted diseases are comparatively poorly understood and managed, and their ecology is particularly understudied. Here we identify challenges of studying environmental transmission and persistence with a six-sided interdisciplinary review of the biology of anthrax (Bacillus anthracis). Anthrax is a zoonotic disease capable of maintaining infectious spore banks in soil for decades (or even potentially centuries), and the mechanisms of its environmental persistence have been the topic of significant research and controversy. Where anthrax is endemic, it plays an important ecological role, shaping the dynamics of entire herbivore communities. The complex eco-epidemiology of anthrax, and the mysterious biology of Bacillus anthracis during its environmental stage, have necessitated an interdisciplinary approach to pathogen research. Here, we illustrate different disciplinary perspectives through key advances made by researchers working in Etosha National Park, a long-term ecological research site in Namibia that has exemplified the complexities of the enzootic process of anthrax over decades of surveillance. In Etosha, the role of scavengers and alternative routes (waterborne transmission and flies) has proved unimportant relative to the long-term persistence of anthrax spores in soil and their infection of herbivore hosts. Carcass deposition facilitates green-ups of vegetation to attract herbivores, potentially facilitated by the role of anthrax spores in the rhizosphere. The underlying seasonal pattern of vegetation, and herbivores' immune and behavioural responses to anthrax risk, interact to produce regular 'anthrax seasons' that appear to be a stable feature of the Etosha ecosystem. Through the lens of microbiologists, geneticists, immunologists, ecologists, epidemiologists, and clinicians, we discuss how anthrax dynamics are shaped at the smallest scale by population genetics and interactions within the bacterial communities up to the broadest scales of ecosystem structure. We illustrate the benefits and challenges of this interdisciplinary approach to disease ecology, and suggest ways anthrax might offer insights into the biology of other important pathogens. Bacillus anthracis, and the more recently emerged Bacillus cereus biovar anthracis, share key features with other environmentally transmitted pathogens, including several zoonoses and panzootics of special interest for global health and conservation efforts. Understanding the dynamics of anthrax, and developing interdisciplinary research programs that explore environmental persistence, is a critical step forward for understanding these emerging threats.

Spatial localization of an obligate-killing, free-living pathogen generates a landscape of patches where new infections occur. As an infectious patch ages, both pathogen exposure at the patch and the probability of lethal infection following exposure can decline. We model stage-structured infectious patches, where non-lethal exposure can naturally "vaccinate" susceptible hosts. We let the between-stage difference in pathogen transmission, and then the between-stage difference in patch virulence, increase independently of other parameters. Effects of increasing either between-stage difference (about a fixed mean) depend on the probability a patch transitions from the first to second stage, i.e., the chance that a killer patch becomes a vaccinator. For slower stage transition, greater between-stage differences decreased susceptibles, and increased both resistant-host and killer patch numbers. But our examples reveal that each effect can be reversed when between-stage transition occurs more rapidly. For sufficiently rapid stage transition, increased between-stage virulence differences can lead to pathogen extinction, and leave the host at disease-free equilibrium. The model's general significance lies in demonstrating how epidemiological variation among sites of environmentally transmitted disease can strongly govern host-parasite dynamics.

When a transmission hotspot for an environmentally persistent pathogen establishes in otherwise high-quality habitat, the disease may exert a strong impact on a host population. However, fluctuating environmental conditions lead to heterogeneity in habitat quality and animal habitat preference, which may interrupt the overlap between selected and risky habitats. We evaluated spatio-temporal patterns in anthrax mortalities in a plains zebra ( Equus quagga ) population in Etosha National Park, Namibia, incorporating remote-sensing and host telemetry data. A higher proportion of anthrax mortalities of herbivores was detected in open habitats than in other habitat types. Resource selection functions showed that the zebra population shifted habitat selection in response to changes in rainfall and vegetation productivity. Average to high rainfall years supported larger anthrax outbreaks, with animals congregating in preferred open habitats, while a severe drought forced animals into otherwise less preferred habitats, leading to few anthrax mortalities. Thus, the timing of anthrax outbreaks was congruent with preference for open plains habitats and a corresponding increase in pathogen exposure. Given shifts in habitat preference, the overlap in high-quality habitat and high-risk habitat is intermittent, reducing the adverse consequences for the population.

How a disease is transmitted affects our ability to determine R0, the average number of new cases caused by an infectious host at the onset of an epidemic. R0 becomes progressively more difficult to compute as transmission varies from directly transmitted diseases to diseases that are vector-borne to environmentally transmitted diseases. Pathogens responsible for diseases with environmental transmission are typically maintained in environmental reservoirs that exhibit a complex spatial distribution of local infectious zones (LIZs). Understanding host encounters with LIZs and pathogen persistence within LIZs is required for an accurate R0 and modeling these contacts requires an integrated geospatial and dynamical systems approach. Here we review how interactions between host and pathogen populations and environmental reservoirs are driven by landscape-level variables, and synthesize the quantitative framework needed to formulate outbreak response and disease control.

How a disease is transmitted affects our ability to determine R0, the average number of new cases caused by an infectious host at the onset of an epidemic. R0 becomes progressively more difficult to compute as transmission varies from directly transmitted diseases to diseases that are vector-borne to environmentally transmitted diseases. Pathogens responsible for diseases with environmental transmission are typically maintained in environmental reservoirs that exhibit a complex spatial distribution of local infectious zones (LIZs). Understanding host encounters with LIZs and pathogen persistence within LIZs is required for an accurate R0 and modeling these contacts requires an integrated geospatial and dynamical systems approach. Here we review how interactions between host and pathogen populations and environmental reservoirs are driven by landscape-level variables, and synthesize the quantitative framework needed to formulate outbreak response and disease control.

This research was conducted as part of a Ph.D. dissertation at the University of California, Berkeley.

Environmentally Transmitted Diseases Are Comparatively Poorly Understood And Managed, And Their Ecology Is Particularly Understudied. Here We Identify Challenges Of Studying Environmental Transmission And Persistence With A Six-Sided Interdisciplinary Review Of The Biology Of Anthrax (Bacillus Anthracis). Anthrax Is A Zoonotic Disease Capable Of Maintaining Infectious Spore Banks In Soil For Decades (Or Even Potentially Centuries), And The Mechanisms Of Its Environmental Persistence Have Been The Topic Of Significant Research And Controversy. Where Anthrax Is Endemic, It Plays An Important Ecological Role, Shaping The Dynamics Of Entire Herbivore Communities. The Complex Eco-Epidemiology Of Anthrax, And The Mysterious Biology OfBacillus AnthracisDuring Its Environmental Stage, Have Necessitated An Interdisciplinary Approach To Pathogen Research. Here, We Illustrate Different Disciplinary Perspectives Through Key Advances Made By Researchers Working In Etosha National Park, A Long-Term Ecological Research Site In Namibia That Has Exemplified The Complexities Of Anthrax’S Enzootic Process Over Decades Of Surveillance. In Etosha, The Role Of Scavengers And Alternate Routes (Waterborne Transmission And Flies) Has Proved Unimportant, Relative To The Long-Term Persistence Of Anthrax Spores In Soil And Their Infection Of Herbivore Hosts. Carcass Deposition Facilitates Green-Ups Of Vegetation To Attract Herbivores, Potentially Facilitated By Anthrax Spores’ Role In The Rhizosphere. The Underlying Seasonal Pattern Of Vegetation, And Herbivores’ Immune And Behavioral Responses To Anthrax Risk, Interact To Produce Regular “Anthrax Seasons” That Appear To Be A Stable Feature Of The Etosha Ecosystem. Through The Lens Of Microbiologists, Geneticists, Immunologists, Ecologists, Epidemiologists, And Clinicians, We Discuss How Anthrax Dynamics Are Shaped At The Smallest Scale By Population Genetics And Interactions Within The Bacterial Communities Up To The Broadest Scales Of Ecosystem Structure. We Illustrate The Benefits And Challenges Of This Interdisciplinary Approach To Disease Ecology, And Suggest Ways Anthrax Might Offer Insights Into The Biology Of Other Important Pathogens.Bacillus Anthracis,And The More Recently EmergedBacillus CereusBiovarAnthracis, Share Key Features With Other Environmentally-Transmitted Pathogens, Including Several Zoonoses And Panzootics Of Special Interest For Global Health And Conservation Efforts. Understanding The Dynamics Of Anthrax, And Developing Interdisciplinary Research Programs That Explore Environmental Persistence, Is A Critical Step Forward For Understanding These Emerging Threats.

The outbreak and transmission of disease-causing pathogens are contributing to the unprecedented rate of biodiversity decline. Recent advances in genomics have coalesced into powerful tools to monitor, detect, and reconstruct the role of pathogens impacting wildlife populations. Wildlife researchers are thus uniquely positioned to merge ecological and evolutionary studies with genomic technologies to exploit unprecedented “Big Data” tools in disease research; however, many researchers lack the training and expertise required to use these computationally intensive methodologies. To address this disparity, the inaugural “Genomics of Disease in Wildlife” workshop assembled early to mid-career professionals with expertise across scientific disciplines (e.g., genomics, wildlife biology, veterinary sciences, and conservation management) for training in the application of genomic tools to wildlife disease research. A horizon scanning-like exercise, an activity to identify forthcoming trends and challenges, performed by the workshop participants identified and discussed 5 themes considered to be the most pressing to the application of genomics in wildlife disease research: 1) “Improving communication,” 2) “Methodological and analytical advancements,” 3) “Translation into practice,” 4) “Integrating landscape ecology and genomics,” and 5) “Emerging new questions.” Wide-ranging solutions from the horizon scan were international in scope, itemized both deficiencies and strengths in wildlife genomic initiatives, promoted the use of genomic technologies to unite wildlife and human disease research, and advocated best practices for optimal use of genomic tools in wildlife disease projects. The results offer a glimpse of the potential revolution in human and wildlife disease research possible through multi-disciplinary collaborations at local, regional, and global scales.

NIH GM083863 (to Wayne Getz). Ivan Horak was funded by the University of Pretoria and the National Research Foundation of South Africa.

Background Anthrax is a globally distributed disease affecting primarily herbivorous mammals. It is caused by the soil-dwelling and spore-forming bacterium Bacillus anthracis. The dormant B. anthracis spores become vegetative after ingestion by grazing mammals. After killing the host, B. anthracis cells return to the soil where they sporulate, completing the lifecycle of the bacterium. Here we present the first study describing temporal microbial soil community changes in Etosha National Park, Namibia, after decomposition of two plains zebra (Equus quagga) anthrax carcasses. To circumvent state-associated-challenges (i.e. vegetative cells/spores) we monitored B. anthracis throughout the period using cultivation, qPCR and shotgun metagenomic sequencing. Results The combined results suggest that abundance estimation of spore-forming bacteria in their natural habitat by DNA-based approaches alone is insufficient due to poor recovery of DNA from spores. However, our combined approached allowed us to follow B. anthracis population dynamics (vegetative cells and spores) in the soil, along with closely related organisms from the B. cereus group, despite their high sequence similarity. Vegetative B. anthracis abundance peaked early in the time-series and then dropped when cells either sporulated or died. The time-series revealed that after carcass deposition, the typical semi-arid soil community (e.g. Frankiales and Rhizobiales species) becomes temporarily dominated by the orders Bacillales and Pseudomonadales, known to contain plant growth-promoting species. Conclusion Our work indicates that complementing DNA based approaches with cultivation may give a more complete picture of the ecology of spore forming pathogens. Furthermore, the results suggests that the increased vegetation biomass production found at carcass sites is due to both added nutrients and the proliferation of microbial taxa that can be beneficial for plant growth. Thus, future B. anthracis transmission events at carcass sites may be indirectly facilitated by the recruitment of plant-beneficial bacteria. Electronic supplementary material The online version of this article (10.1186/s12866-017-1111-6) contains supplementary material, which is available to authorized users.

The use of camera traps is now widespread and their importance in wildlife studies is well understood. Camera trap studies can produce millions of photographs and there is a need for a software to help manage photographs efficiently. In this paper, we describe a software system that was built to successfully manage a large behavioral camera trap study that produced more than a million photographs. We describe the software architecture and the design decisions that shaped the evolution of the program over the study's three year period. The software system has the ability to automatically extract metadata from images, and add customized metadata to the images in a standardized format. The software system can be installed as a standalone application on popular operating systems. It is minimalistic, scalable and extendable so that it can be used by small teams or individual researchers for a broad variety of camera trap studies.

Bacillus anthracis strains K1 and K2 were isolated from two plains zebra anthrax carcasses in Etosha National Park, Namibia. These are draft genomes obtained by Illumina MiSeq sequencing of isolates collected from culture of blood-soaked soil from each carcass.

To mitigate the effects of zoonotic diseases on human and animal populations, it is critical to understand what factors alter transmission dynamics. Here we assess the risk of exposure to lethal concentrations of the anthrax bacterium, Bacillus anthracis, for grazing animals in a natural system over time through different transmission mechanisms. We follow pathogen concentrations at anthrax carcass sites and waterholes for five years and estimate infection risk as a function of grass, soil or water intake, age of carcass sites, and the exposure required for a lethal infection. Grazing, not drinking, seems the dominant transmission route, and transmission is more probable from grazing at carcass sites 1–2 years of age. Unlike most studies of virulent pathogens that are conducted under controlled conditions for extrapolation to real situations, we evaluate exposure risk under field conditions to estimate the probability of a lethal dose, showing that not all reservoirs with detectable pathogens are significant transmission pathways.

Host-parasite dynamics can be strongly affected by seasonality and age-related host immune responses. We investigated how observed variation in the prevalence and intensity of parasite egg or oocyst shedding in four co-occurring ungulate species may reflect underlying seasonal variation in transmission and host immunity. This study was conducted July 2005–October 2006 in Etosha National Park, Namibia, using indices of parasitism recorded from 1,022 fecal samples collected from plains zebra (Equus quagga), springbok (Antidorcas marsupialis), blue wildebeest (Connochaetes taurinus), and gemsbok (Oryx gazella). The presence and intensity of strongyle nematodes, Strongyloides spp. and Eimeria spp. parasites, were strongly seasonal for most host-parasite combinations, with more hosts infected in the wet season than the dry season. Strongyle intensity in zebra was significantly lower in juveniles than adults, and in springbok hosts, Eimeria spp. intensity was significantly greater in juveniles than adults. These results provide evidence that acquired immunity is less protective against strongyle nematodes than Eimeria spp. infections. The seasonal patterns in parasitism further indicate that the long dry season may limit development and survival of parasite stages in the environment and, as a result, host contact and parasite transmission.

Anthrax in herbivorous wildlife and livestock is generally assumed to be transmitted via ingestion or inhalation of Bacillus anthracis spores. Although recent studies have highlighted the importance of the ingestion route for anthrax transmission, little is known about the inhalational route in natural systems. Dust bathing could aerosolize soilborne pathogens such as B. anthracis, exposing dust-bathing individuals to inhalational infections. We investigated the potential role of dust bathing in the transmission of inhalational anthrax to herbivorous wildlife in Etosha National Park, Namibia, an area with endemic seasonal anthrax outbreaks. We 1) cultured soils from dust-bathing sites for the presence and concentration of B. anthracis spores, 2) monitored anthrax carcass sites, the locations with the highest B. anthracis concentrations, for evidence of dust bathing, including a site where a zebra died of anthrax on a large dust bath, and 3) characterized the ecology and seasonality of dust bathing in plains zebra ( Equus quagga), blue wildebeest ( Connochaetes taurinus), and African savanna elephant ( Loxodonta africana) using a combination of motion-sensing camera traps and direct observations. Only two out of 83 dust-bath soils were positive for B. anthracis, both with low spore concentrations (≤20 colony-forming units per gram). We also detected no evidence of dust baths occurring at anthrax carcass sites, perhaps due to carcass-induced changes in soil composition that may deter dust bathing. Finally, despite observing some seasonal variation in dust bathing, preliminary evidence suggests that the seasonality of dust bathing and anthrax mortalities are not correlated. Thus, although dust bathing creates a dramatic cloud of aerosolized soil around an individual, our microbiologic, ecologic, and behavioral results in concert demonstrate that dust bathing is highly unlikely to transmit inhalational anthrax infections.

Estimates of parasite intensity within host populations are essential for many studies of host–parasite relationships. Here we evaluated the seasonal, age- and sex-related variability in faecal water content for two wild ungulate species, springbok (Antidorcas marsupialis) and plains zebra (Equus quagga). We then assessed whether or not faecal water content biased conclusions regarding differences in strongyle infection rates by season, age or sex. There was evidence of significant variation in faecal water content by season and age for both species, and by sex in springbok. Analyses of faecal egg counts demonstrated that sex was a near-significant factor in explaining variation in strongyle parasite infection rates in zebra (P = 0.055) and springbok (P = 0.052) using wet-weight faecal samples. However, once these intensity estimates were re-scaled by the percent of dry matter in the faeces, sex was no longer a significant factor (zebra, P = 0.268; springbok, P = 0.234). These results demonstrate that variation in faecal water content may confound analyses and could produce spurious conclusions, as was the case with host sex as a factor in the analysis. We thus recommend that researchers assess whether water variation could be a confounding factor when designing and performing research using faecal indices of parasite intensity.

Patterns of association in many ungulate species vary throughout the year, with males periodically segregating from females. Sexual segregation can occur if males and females use different habitats (habitat segregation), occupy exclusive ranges (spatial segregation) or occur in separate social groups (social segregation). Previous studies on social segregation in ungulates have focused mostly on non-reproductive periods and species in temperate systems with short mating seasons. This study examined social segregation in African buffalo Syncerus caffer at Hluhluwe-iMfolozi Park, South Africa, during their 6-month mating season. During this period, mature male buffalo alternated between joining mixed-sex herds which comprise females and young, and small all-male groups. Activity patterns of male buffalo in both group types were examined to determine if differences in time allocation or activity asynchrony could explain the observed segregation. Mature males foraged for less time than both adult females and younger males when they were with mixed herds. Mature male buffalo differed in how their active time was apportioned to foraging and reproductive activities between the two group types. Females maintained group cohesion despite only low synchrony in activity, therefore segregation of male buffalo could not be explained by the activity budget hypothesis. For males in mixed-sex herds, reproductive activities were apparently at the expense of foraging time. The high time and energy costs of reproductive activities were probably responsible for the periodic separation of male buffalo from mixed herds during the extended mating period.

We tested the fertility announcement hypothesis, whereby male song during a female’s fertile period functions as both a paternity guard and an advertisement for extra-pair copulations, in an eastern population of song sparrows Melospiza melodia over two broods within a breeding season. Our results did not support one of its main predictions: male song rate was not significantly higher in the female’s fertile period than in her post-fertile period. Song rate peaked prior to pairing, when males were establishing territories and trying to attract females. Once paired, song rate dropped by a factor of about ten, and was consistently low through all stages of the nesting cycle. Males who failed to pair continued singing at high rates throughout the breeding season. Our results do not support the fertility announcement hypothesis, therefore song rate is not used primarily as a paternity assurance strategy by song sparrows.

Background Most vertebrates experience coinfections, and many pathogen-pathogen interactions occur indirectly through the host immune system. These interactions are particularly strong in mixed micro-macroparasite infections because of immunomodulatory effects of helminth parasites. While these trade-offs have been examined extensively in laboratory animals, few studies have examined them in natural systems. Additionally, many wildlife pathogens fluctuate seasonally, at least partly due to seasonal host immune changes. We therefore examined seasonality of immune resource allocation, pathogen abundance and exposure, and interactions between infections and immunity in plains zebra (Equus quagga) in Etosha National Park (ENP), Namibia, a system with strongly seasonal patterns of gastrointestinal (GI) helminth infection intensity and concurrent anthrax outbreaks. Both pathogens are environmentally transmitted, and helminth seasonality is driven by environmental pressures on free living life stages. The reasons behind anthrax seasonality are currently not understood, though anthrax is less likely directly driven by environmental factors. Results We measured a complex, interacting set of variables and found evidence that GI helminth infection intensities, eosinophil counts, IgE and IgGb antibody titers, and possibly IL-4 cytokine signaling were increased in wetter seasons, and that ectoparasite infestations and possibly IFN-γ cytokine signaling were increased in drier seasons. Monocyte counts and anti-anthrax antibody titers were negatively associated with wet season eosinophilia, and monocytes were negatively correlated with IgGb and IgE titers. Taken together, this supports the hypothesis that ENP wet seasons are characterized by immune resource allocation toward Th-2 type responses, while Th1-type immunity may prevail in drier seasons, and that hosts may experience Th1-Th2 trade-offs. We found evidence that this Th2-type resource allocation is likely driven by GI parasite infections, and that these trade-offs may render hosts less capable of concurrently mounting effective Th1-type immune responses against anthrax. Conclusions This study is one of the first to examine laboratory-demonstrated Th1-Th2 trade-offs in a natural system. It provides evidence that seasonally bound pathogens may affect, through immunology, transmission dynamics of pathogens that might otherwise not be seasonally distributed. It suggests that, by manipulating the internal host ecosystem, GI parasites may influence the external ecosystem by affecting the dynamics of another environmentally transmitted pathogen. Electronic supplementary material The online version of this article (doi:10.1186/s12898-014-0027-3) contains supplementary material, which is available to authorized users.