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Serological assessment of pathogen exposure among desert bighorn sheep in southwestern Arizona

Bighorn sheep ( Ovis canadensis ) are influenced by infectious diseases. Although Mycoplasma ovipneumoniae has been the main focus of bighorn sheep managers since early 2010, other pathogens may also influence bighorn sheep populations. We sampled desert bighorn sheep ( Ovis canadensis mexicana ) captured for a study on the Cabeza Prieta National Wildlife Refuge in southwestern Arizona, USA, 2001–2005, for a suite of pathogens: bluetongue (BT), epizootic hemorrhagic disease (EHD), parainfluenza 3, bovine respiratory syncytial virus, Clamydia , seven Leptospira serovars, bovine herpesvirus 1 (causative agent of infectious bovine rhinotracheitis), bovine viral diarrhea virus, and bovine respiratory syncytial virus. We recorded evidence of exposure to seven of these pathogens, with two Leptospira serovars ( hardjo and bratislava ), five strains of BT, and two strains of EHD detected. Seroprevalence rates of detected pathogens varied between 12–49%. We observed high levels of co-occurrence for EHD and BT. These results highlight that multiple pathogens may influence desert bighorn sheep populations. These data also provide historical context to pathogen exposure for a region where few such data are available.

Arizona

Quarantine of Aeromonas salmonicida-harboring ebonyshell mussels (Fusconaia ebena) prevents transmission of the pathogen to brook trout (Salvelinus fontinalis)

Furunculosis, caused by the bacterium Aeromonas salmonicida , was artificially induced in brook trout ( Salvelinus fontinalis ) in an experimental tank. Ebonyshells ( Fusconaia ebena ) were placed to cohabit with these fish to acquire the pathogen through siphoning. After 2 wk of cohabitation, 10 of the mussels were assayed by bacterial culture and all were found to harbor A. salmonicida . The mean cell count from soft tissue homogenates was 1.84 × 10 5 cfu/g, which comprised an average 14.41% of the total bacteria isolated from tissues. From the fluids, a mean of 2.84 × 10 5 A. salmonicida cfu/mL was isolated, which comprised an average of 17.29% of the total bacterial flora. The mussels were removed from the cohabitation tank and distributed equally among five previously disinfected tanks, 35 per tank. The F. ebena in each tank were allowed to depurate A. salmonicida for various durations: 1, 5, 10, 15 or 30 days. After each group had depurated for their assigned time, 10 were assayed for bacteria, tank water was tested, and 20 pathogen-free bioindicator brook trout were added to cohabit with the remaining mussels. Depuration was considered successful if A. salmonicida was not isolated from tank water or the mussels, and there was no infection or mortality to bioindicator fish. After 1 day of depuration, A. salmonicida was not isolated from the soft tissues; however, it was isolated from one of the paired fluids (10% prevalence). The tank water tested positive, and the bioindicator fish became infected and died. From the 5-day depuration group, A. salmonicida was not isolated from soft tissues, but was isolated from three fluids (30%; mean = 1.56 × 10 2 cfu/mL). Tank water from the 5-day group was negative, and there was no mortality among the bioindicator fish. However, A. salmonicida was isolated from 2 of 20 fish at the end of the 14-day observation period. One F. ebena fluid sample was positive for A. salmonicida from the 10-day depuration group, but none of the soft tissue homogenates. The pathogen was not isolated from 10-day tank water, but there was a 30% cumulative mortality to the bioindicator fish. Aeromonas salmonicida was not isolated from any of the soft tissue homogenates, fluids or tank water from the 15 day or 30 day depuration groups, and the bioindicator fish remained pathogen- and disease-free. Study results showed that the F. ebena were harboring a high A. salmonicida cell load going into depuration, but at 15 days and beyond, the pathogen had been depurated to the extent that the mussels did not serve as pathogen vectors.

Journal of Shellfish Research

Viral pathogen detection in U.S. game-farm mallard (Anas platyrhynchos) flags spillover risk to wild birds

The threat posed by emerging infectious diseases is a major concern for global public health, animal health and food security, and the role of birds in transmission is increasingly under scrutiny. Each year, millions of mass-reared game-farm birds are released into the wild, presenting a unique and a poorly understood risk to wild and susceptible bird populations, and to human health. In particular, the shedding of enteric pathogens through excrement into bodies of water at shared migratory stop-over sites, and breeding and wintering grounds, could facilitate multi-species long-distance pathogen dispersal and infection of high numbers of naive endemic birds annually. The Mallard ( Anas platyrhynchos ) is the most abundant of all duck species, migratory across much of its range, and an important game species for pen-rearing and release. Major recent population declines along the US Atlantic coast has been attributed to game-farm and wild mallard interbreeding and the introduction maladaptive traits into wild populations. However, pathogen transmission and zoonosis among game-farms Mallard may also impact these populations, as well as wildlife and human health. Here, we screened 16 game-farm Mallard from Wisconsin, United States, for enteric viral pathogens using metatranscriptomic data. Four families of viral pathogens were identified – Picobirnaviridae (Genogroup I), Caliciviridae (Duck Nacovirus ), Picornaviridae (Duck Aalivirus ) and Sedoreoviridae (Duck Rotavirus G). To our knowledge, this is the first report of Aalivirus in the Americas, and the first report of Calicivirus outside domestic chicken and turkey flocks in the United States. Our findings highlight the risk of viral pathogen spillover from peri-domestically reared game birds to naive wild bird populations.

Frontiers Earth Science Journal

Challenges and opportunities developing mathematical models of shared pathogens of domestic and wild animals

Diseases that affect both wild and domestic animals can be particularly difficult to prevent, predict, mitigate, and control. Such multi-host diseases can have devastating economic impacts on domestic animal producers and can present significant challenges to wildlife populations, particularly for populations of conservation concern. Few mathematical models exist that capture the complexities of pathogens, yet development of such models would allow us to estimate and compare the potential effectiveness of management actions for mitigating or suppressing disease in wildlife and/or livestock host populations. We conducted a workshop in March 2014 to identify the challenges associated with developing models of pathogen transmission across the wildlife-livestock interface. The development of mathematical models of pathogen transmission at this interface is hampered by the difficulties associated with describing the host-pathogen systems including: 1) the identity of wildlife hosts, their distributions, and movement patterns, 2) the pathogen transmission pathways between wildlife and domestic animals, 3) the effects of the disease and concomitant mitigation efforts on wild and domestic animal populations, and 4) barriers to communication between sectors. To promote the development of mathematical models of transmission at this interface, we recommend further integration of modern quantitative techniques and improvement of communication among wildlife biologists, mathematical modelers, veterinary medicine professionals, producers, and other stakeholders concerned with the consequences of pathogen transmission at this important, yet poorly understood, interface.

Veterinary Sciences

Estimating occurrence, prevalence, and detection of amphibian pathogens: Insights from occupancy models

Understanding the distribution of pathogens across landscapes and their prevalence within host populations is a common aim of wildlife managers. Despite the need for unbiased estimates of pathogen occurrence and prevalence for planning effective management interventions, many researchers fail to account for imperfect pathogen detection. Instead raw data are often reported, which may lead to ineffective, or even detrimental, management actions. We illustrate the utility of occupancy models for generating unbiased estimates of disease parameters by 1) providing a written tutorial describing how to fit these models in Program PRESENCE and 2) presenting a case study with the pathogen ranavirus. We analyzed ranavirus detection data from a wildlife refuge (Maryland, US) using occupancy modeling, which yields unbiased estimates of pathogen occurrence and prevalence. We found ranavirus prevalence was underestimated by up to 30% if imperfect pathogen detection was ignored. The unbiased estimate of ranavirus prevalence in larval wood frog ( Lithobates sylvaticus ; 0.73) populations was higher than in larval spotted salamander ( Ambystoma maculatum ; 0.56) populations. In addition, the odds of detecting ranavirus in tail samples were 6.7 times higher than detecting ranavirus in liver samples. Therefore, tail samples presented a nonlethal sampling method for ranavirus that may be able to detect early (nonsystemic) infections.

Maryland

Risk of invasive waterfowl interaction with poultry production: Understanding potential for avian pathogen transmission via species distribution models

Recent outbreaks of highly pathogenic avian influenza have devastated poultry production across the United States, with more than 77 million birds culled in 2022–2024 alone. Wild waterfowl, including various invasive species, host numerous pathogens, including highly pathogenic avian influenza virus (HPAIV), and have been implicated as catalysts of disease outbreaks among native fauna and domestic birds. In major poultry-producing states like Arkansas, USA, where the poultry sector is responsible for significant economic activity (>$4 billion USD in 2022), understanding the risk of invasive waterfowl interactions with domestic poultry is critical. Here, we assessed the risk of invasive waterfowl-poultry interaction in Arkansas by comparing the density of poultry production sites (chicken houses) to areas of high habitat suitability for two invasive waterfowl species, (Egyptian Goose [ Alopochen aegyptiaca ] and Mute Swan [ Cygnus olor ]), known to host significant pathogens, including avian influenza viruses. The percentage of urban land cover was the most important habitat characteristic for both invasive waterfowl species. At the 95% confidence interval, chicken house densities in areas highly suitable for both species (Egyptian Goose = 0.91 ± 0.11 chicken houses/km 2 ; Mute Swan = 0.61 ± 0.03 chicken houses/km 2 ) were three to five times higher than chicken house densities across the state (0.17 ± 0.01 chicken houses/km 2 ). We show that northwestern and western Arkansas, both areas of high importance for poultry production, are also at high risk of invasive waterfowl presence. Our results suggest that targeted monitoring efforts for waterfowl-poultry contact in these areas could help mitigate the risk of avian pathogen exposure in Arkansas and similar regions with high poultry production.

Biological Invasions

Waterfowl recently infected with low pathogenic avian influenza exhibit reduced local movement and delayed migration

Understanding relationships between infection and wildlife movement patterns is important for predicting pathogen spread, especially for multispecies pathogens and those that can spread to humans and domestic animals, such as avian influenza viruses (AIVs). Although infection with low pathogenic AIVs is generally considered asymptomatic in wild birds, prior work has shown that influenza-infected birds occasionally delay migration and/or reduce local movements relative to their uninfected counterparts. However, most observational research to date has focused on a few species in northern Europe; given that influenza viruses are widespread globally and outbreaks of highly pathogenic strains are increasingly common, it is important to explore influenza–movement relationships across more species and regions. Here, we used telemetry data to investigate relationships between influenza infection and movement behavior in 165 individuals from four species of North American waterfowl that overwinter in California, USA. We studied both large-scale migratory and local overwintering movements and found that relationships between influenza infection and movement patterns varied among species. Northern pintails ( Anas acuta ) with antibodies to avian influenza, indicating prior infection, made migratory stopovers that averaged 12 days longer than those with no influenza antibodies. In contrast, greater white-fronted geese ( Anser albifrons ) with antibodies to avian influenza made migratory stopovers that averaged 15 days shorter than those with no antibodies. Canvasbacks ( Aythya valisineria ) that were actively infected with influenza upon capture in the winter delayed spring migration by an average of 28 days relative to birds that were uninfected at the time of capture. At the local scale, northern pintails and canvasbacks that were actively infected with influenza used areas that were 7.6 and 4.9 times smaller than those of uninfected ducks, respectively, during the period of presumed active influenza infection. We found no evidence for an influence of active influenza infection on local movements of mallards ( Anas platyrhynchos ). These results suggest that avian influenza can influence waterfowl movements and illustrate that the relationships between avian influenza infection and wild bird movements are context- and species-dependent. More generally, understanding and predicting the spread of multihost pathogens requires studying multiple taxa across space and time.

Ecosphere

Hosts, pathogens and hot ponds: Thermal mean and variability contribute to spatial patterns of chytrid infection

Temperature is a primary driver of heterogeneity in host–pathogen dynamics and understanding how patch-scale temperature affects landscape-scale patterns of pathogen infection is key to effective monitoring and management. In field studies, both temperature variability and mean temperature are often related to infection of ectothermic animals by fungal pathogens, and although these factors vary spatiotemporally, their contributions to infection outcomes are rarely decomposed into spatial and temporal components. We studied how patch-scale thermal conditions (mean and variability) affect infection of eastern newts Notophthalmus viridescens by Batrachochytrium dendrobatidis ( Bd ), with a special focus on disentangling spatial versus temporal contributions of thermal conditions to infection outcomes. We measured in situtemperature and Bd infection across 20 ponds in two years in southeastern Wisconsin, USA to 1) understand thermal mediation of infection and 2) quantify whether seasonal and/or among-site variation in thermal conditions drive heterogeneity in host–pathogen interactions. In our system, thermal mean and variability covaried tightly, necessitating the creation of a single index to capture both components. We found that 1) this index of thermal mean and variability was strongly and nonlinearly related to Bd infection and 2) differences among patches in thermal conditions drove this relationship, highlighting that variation in patch-level conditions can drive heterogenous host–pathogen outcomes across landscapes. Our research collectively reveals insights about the importance of local, patch-level conditions for mediating disease risk at broader scales.

Wisconsin

Pathogen transport in groundwater systems: Contrasts with traditional solute transport

Water quality affects many aspects of water availability, from precluding use to societal perceptions of fit-for-purpose. Pathogen source and transport processes are drivers of water quality because they have been responsible for numerous outbreaks resulting in large economic losses due to illness and, in some cases, loss of life. Outbreaks result from very small exposure (e.g., less than 20 viruses) from very strong sources (e.g., trillions of viruses shed by a single infected individual). Thus, unlike solute contaminants, an acute exposure to a very small amount of contaminated water can cause immediate adverse health effects. Similarly, pathogens are larger than solutes. Thus, interactions with surfaces and settling become important even as processes important for solutes such as diffusion become less important. These differences are articulated in “Colloid Filtration Theory”, a separate branch of pore-scale transport. Consequently, understanding pathogen processes requires changes in how groundwater systems are typically characterized, where the focus is on the leading edges of plumes and preferential flow paths, even if such features move only a very small fraction of the aquifer flow. Moreover, the relatively short survival times of pathogens in the subsurface require greater attention to very fast (<10 year) flow paths. By better understanding the differences between pathogen and solute transport mechanisms discussed here, a more encompassing view of water quality and source water protection is attained. With this more holistic view and theoretical understanding, better evaluations can be made regarding drinking water vulnerability and the relation between groundwater and human health.

Hydrogeology Journal

Evidence for common ancestry among viruses isolated from wild birds in Beringia and highly pathogenic intercontinental reassortant H5N1 and H5N2 influenza A viruses

Highly pathogenic clade 2.3.4.4 H5N8, H5N2, and H5N1 influenza A viruses were first detected in wild, captive, and domestic birds in North America in November&ndash;December 2014. In this study, we used wild waterbird samples collected in Alaska prior to the initial detection of clade 2.3.4.4 H5 influenza A viruses in North America to assess the evidence for: (1) dispersal of highly pathogenic influenza A viruses from East Asia to North America by migratory birds via Alaska and (2) ancestral origins of clade 2.3.4.4 H5 reassortant viruses in Beringia. Although we did not detect highly pathogenic influenza A viruses in our sample collection from western Alaska, we did identify viruses that contained gene segments sharing recent common ancestry with intercontinental reassortant H5N2 and H5N1 viruses. Results of phylogenetic analyses and estimates for times of most recent common ancestry support migratory birds sampled in Beringia as maintaining viral diversity closely related to novel highly pathogenic influenza A virus genotypes detected in North America. Although our results do not elucidate the route by which highly pathogenic influenza A viruses were introduced into North America, genetic evidence is consistent with the hypothesized trans-Beringian route of introduction via migratory birds.

Infection, Genetics and Evolution

Ecological and socioeconomic factors associated with the human burden of environmentally mediated pathogens: A global analysis

Background Billions of people living in poverty are at risk of environmentally mediated infectious diseases—that is, pathogens with environmental reservoirs that affect disease persistence and control and where environmental control of pathogens can reduce human risk. The complex ecology of these diseases creates a global health problem not easily solved with medical treatment alone. Methods We quantified the current global disease burden caused by environmentally mediated infectious diseases and used a structural equation model to explore environmental and socioeconomic factors associated with the human burden of environmentally mediated pathogens across all countries. Findings We found that around 80% (455 of 560) of WHO-tracked pathogen species known to infect humans are environmentally mediated, causing about 40% (129 488 of 359 341 disability-adjusted life years) of contemporary infectious disease burden (global loss of 130 million years of healthy life annually). The majority of this environmentally mediated disease burden occurs in tropical countries, and the poorest countries carry the highest burdens across all latitudes. We found weak associations between disease burden and biodiversity or agricultural land use at the global scale. In contrast, the proportion of people with rural poor livelihoods in a country was a strong proximate indicator of environmentally mediated infectious disease burden. Political stability and wealth were associated with improved sanitation, better health care, and lower proportions of rural poverty, indirectly resulting in lower burdens of environmentally mediated infections. Rarely, environmentally mediated pathogens can evolve into global pandemics (eg, HIV, COVID-19) affecting even the wealthiest communities. Interpretation The high and uneven burden of environmentally mediated infections highlights the need for innovative social and ecological interventions to complement biomedical advances in the pursuit of global health and sustainability goals. Funding Bill & Melinda Gates Foundation, National Institutes of Health, National Science Foundation, Alfred P. Sloan Foundation, National Institute for Mathematical and Biological Synthesis, Stanford University, and the US Defense Advanced Research Projects Agency.

The Lancet Planetary Health

Application of a microfluidic quantitative polymerase chain reaction technique to monitor bacterial pathogens in beach water and complex environmental matrices

Microfluidic quantitative polymerase chain reaction (MFQPCR) and conventional quantitative polymerase chain reaction methods were compared side by side in detecting and quantifying 19 genetic markers associated with Escherichia coli and select bacterial pathogens in algae, beach sand, and water from Lake Michigan. Enteropathogenic E. coli (EPEC), Shiga toxin-producing E. coli , Salmonella spp., Campylobacter jejuni , and Clostridium perfringens were among the pathogens tested. Of the pathogenic markers, eaeA that encodes intimin in EPEC was detected in all sample types: water (5%), detached/floating algae (42%), exposed/stranded algae (43%), sand below exposed algae (27%), and nearshore sand with no algae (22%). Other pathogenic markers, however, were detected sporadically. Despite comparable results from the two methods for the genetic markers tested in this study, the MFQPCR method may be superior, with the advantage of detecting and quantifying multiple pathogens simultaneously in environmental matrices.

Indiana

Prey choice and habitat use drive sea otter pathogen exposure in a resource-limited coastal system

The processes promoting disease in wild animal populations are highly complex, yet identifying these processes is critically important for conservation when disease is limiting a population. By combining field studies with epidemiologic tools, we evaluated the relationship between key factors impeding southern sea otter ( Enhydra lutris nereis ) population growth: disease and resource limitation. This threatened population has struggled to recover despite protection, so we followed radio-tagged sea otters and evaluated infection with 2 disease-causing protozoal pathogens, Toxoplasma gondii and Sarcocystis neurona , to reveal risks that increased the likelihood of pathogen exposure. We identified patterns of pathogen infection that are linked to individual animal behavior, prey choice, and habitat use. We detected a high-risk spatial cluster of S. neurona infections in otters with home ranges in southern Monterey Bay and a coastal segment near San Simeon and Cambria where otters had high levels of infection with T. gondii . We found that otters feeding on abalone, which is the preferred prey in a resource-abundant marine ecosystem, had a very low risk of infection with either pathogen, whereas otters consuming small marine snails were more likely to be infected with T. gondii . Individual dietary specialization in sea otters is an adaptive mechanism for coping with limited food resources along central coastal California. High levels of infection with protozoal pathogens may be an adverse consequence of dietary specialization in this threatened species, with both depleted resources and disease working synergistically to limit recovery.

California

Season of death, pathogen persistence and wildlife behaviour alter number of anthrax secondary infections from environmental reservoirs

An important part of infectious disease management is predicting factors that influence disease outbreaks, such as R , the number of secondary infections arising from an infected individual. Estimating R is particularly challenging for environmentally transmitted pathogens given time lags between cases and subsequent infections. Here, we calculated R for Bacillus anthracis infections arising from anthrax carcass sites in Etosha National Park, Namibia. Combining host behavioural data, pathogen concentrations and simulation models, we show that R is spatially and temporally variable, driven by spore concentrations at death, host visitation rates and early preference for foraging at infectious sites. While spores were detected up to a decade after death, most secondary infections occurred within 2 years. Transmission simulations under scenarios combining site infectiousness and host exposure risk under different environmental conditions led to dramatically different outbreak dynamics, from pathogen extinction ( R < 1) to explosive outbreaks ( R > 10). These transmission heterogeneities may explain variation in anthrax outbreak dynamics observed globally, and more generally, the critical importance of environmental variation underlying host–pathogen interactions. Notably, our approach allowed us to estimate the lethal dose of a highly virulent pathogen non-invasively from observational studies and epidemiological data, useful when experiments on wildlife are undesirable or impractical.

Etosha National Park

Comparison of filters for concentrating microbial indicators and pathogens in lake-water samples

Bacterial indicators are used to indicate increased health risk from pathogens and to make beach closure and advisory decisions; however, beaches are seldom monitored for the pathogens themselves. Studies of sources and types of pathogens at beaches are needed to improve estimates of swimming-associated health risks. It would be advantageous and cost-effective, especially for studies conducted on a regional scale, to use a method that can simultaneously filter and concentrate all classes of pathogens from the large volumes of water needed to detect pathogens. In seven recovery experiments, stock cultures of viruses and protozoa were seeded into 10-liter lake water samples, and concentrations of naturally occurring bacterial indicators were used to determine recoveries. For the five filtration methods tested, the highest median recoveries were as follows: glass wool for adenovirus (4.7%); NanoCeram for enterovirus (14.5%) and MS2 coliphage (84%); continuous-flow centrifugation (CFC) plus Virocap (CFC+ViroCap) for Escherichia coli (68.3%) and Cryptosporidium (54%); automatic ultrafiltration (UF) for norovirus GII (2.4%); and dead-end UF for Enterococcus faecalis (80.5%), avian influenza virus (0.02%), and Giardia (57%). In evaluating filter performance in terms of both recovery and variability, the automatic UF resulted in the highest recovery while maintaining low variability for all nine microorganisms. The automatic UF was used to demonstrate that filtration can be scaled up to field deployment and the collection of 200-liter lake water samples.

Michigan, New York, Ohio, Wisconsin

Characterization of low-pathogenicity H5N1 avian influenza viruses from North America

Wild-bird surveillance in North America for avian influenza (AI) viruses with a goal of early identification of the Asian H5N1 highly pathogenic AI virus has identified at least six low-pathogenicity H5N1 AI viruses between 2004 and 2006. The hemagglutinin (HA) and neuraminidase (NA) genes from all 6 H5N1 viruses and an additional 38 North American wild-bird-origin H5 subtype and 28 N1 subtype viruses were sequenced and compared with sequences available in GenBank by phylogenetic analysis. Both HA and NA were phylogenetically distinct from those for viruses from outside of North America and from those for viruses recovered from mammals. Four of the H5N1 AI viruses were characterized as low pathogenicity by standard in vivo pathotyping tests. One of the H5N1 viruses, A/MuteSwan/MI/451072-2/06, was shown to replicate to low titers in chickens, turkeys, and ducks. However, transmission of A/MuteSwan/MI/451072-2/06 was more efficient among ducks than among chickens or turkeys based on virus shed. The 50% chicken infectious dose for A/MuteSwan/MI/451072-2/06 and three other wild-waterfowl-origin H5 viruses were also determined and were between 10 5.3 and 107.5 50% egg infective doses. Finally, seven H5 viruses representing different phylogenetic clades were evaluated for their antigenic relatedness by hemagglutination inhibition assay, showing that the antigenic relatedness was largely associated with geographic origin. Overall, the data support the conclusion that North American H5 wild-bird-origin AI viruses are low-pathogenicity wild-bird-adapted viruses and are antigenically and genetically distinct from the highly pathogenic Asian H5N1 virus lineage. Copyright ?? 2007, American Society for Microbiology. All Rights Reserved.

Journal of Virology

Three pathogens in sympatric populations of pumas, bobcats, and domestic cats: Implications for infections disease transmission

Anthropogenic landscape change can lead to increased opportunities for pathogen transmission between domestic and non-domestic animals. Pumas, bobcats, and domestic cats are sympatric in many areas of North America and share many of the same pathogens, some of which are zoonotic. We analyzed bobcat, puma, and feral domestic cat samples collected from targeted geographic areas. We examined exposure to three pathogens that are taxonomically diverse (bacterial, protozoal, viral), that incorporate multiple transmission strategies (vector-borne, environmental exposure/ingestion, and direct contact), and that vary in species-specificity. Bartonella spp., Feline Immunodeficiency Virus (FIV), and Toxoplasma gondii IgG were detected in all three species with mean respective prevalence as follows: puma 16%, 41% and 75%; bobcat 31%, 22% and 43%; domestic cat 45%, 10% and 1%. Bartonella spp. were highly prevalent among domestic cats in Southern California compared to other cohort groups. Feline Immunodeficiency Virus exposure was primarily associated with species and age, and was not influenced by geographic location. Pumas were more likely to be infected with FIV than bobcats, with domestic cats having the lowest infection rate. Toxoplasma gondii s eroprevalence was high in both pumas and bobcats across all sites; in contrast, few domestic cats were seropositive, despite the fact that feral, free ranging domestic cats were targeted in this study. Interestingly, a directly transmitted species-specific disease (FIV) was not associated with geographic location, while exposure to indirectly transmitted diseases – vector-borne for Bartonella spp. and ingestion of oocysts via infected prey or environmental exposure for T. gondii – varied significantly by site. Pathogens transmitted by direct contact may be more dependent upon individual behaviors and intra-specific encounters. Future studies will integrate host density, as well as landscape features, to better understand the mechanisms driving disease exposure and to predict zones of cross-species pathogen transmission among wild and domestic felids.

PLoS ONE

Exposing extinction risk analysis to pathogens: Is disease just another form of density dependence?

In the United States and several other countries, the development of population viability analyses (PVA) is a legal requirement of any species survival plan developed for threatened and endangered species. Despite the importance of pathogens in natural populations, little attention has been given to host-pathogen dynamics in PVA. To study the effect of infectious pathogens on extinction risk estimates generated from PVA, we review and synthesize the relevance of host-pathogen dynamics in analyses of extinction risk. We then develop a stochastic, density-dependent host-parasite model to investigate the effects of disease on the persistence of endangered populations. We show that this model converges on a Ricker model of density dependence under a suite of limiting assumptions, including a high probability that epidemics will arrive and occur. Using this modeling framework, we then quantify: (1) dynamic differences between time series generated by disease and Ricker processes with the same parameters; (2) observed probabilities of quasi-extinction for populations exposed to disease or self-limitation; and (3) bias in probabilities of quasi-extinction estimated by density-independent PVAs when populations experience either form of density dependence. Our results suggest two generalities about the relationships among disease, PVA, and the management of endangered species. First, disease more strongly increases variability in host abundance and, thus, the probability of quasi-extinction, than does self-limitation. This result stems from the fact that the effects and the probability of occurrence of disease are both density dependent. Second, estimates of quasi-extinction are more often overly optimistic for populations experiencing disease than for those subject to self-limitation. Thus, although the results of density-independent PVAs may be relatively robust to some particular assumptions about density dependence, they are less robust when endangered populations are known to be susceptible to disease. If potential management actions involve manipulating pathogens, then it may be useful to model disease explicitly. ?? 2005 by the Ecological Society of America.

Ecological Applications