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Epidemiology of Fish and Wildlife Diseases
Mammals

Samples of genetics and genomics research from the USGS Ecosystems Mission Area about the epidemiology of mammalian diseases.

White-tailed deer in a field. Photo credit: John J. Mosesso, NBII.Gov White-tailed deer in a forest. Photo credit: John J. Mosesso/NBII.Gov White-tailed deer at the top of a ridge. Photo credit: John J. Mosesso, NBII.Gov White-tailed deer in a field. Photo credit: John J. Mosesso, NBII.Gov White-tailed deer. Photo credit: John J. Mosesso, NBII.Gov
Chronic Wasting Disease: Breeding Interactions (Samuel) Chronic Wasting Disease: Genetic Selection (Samuel) Chronic Wasting Disease: Landscape Genetics (Samuel) Chronic Wasting Disease: Resistance (Samuel) Chronic Wasting Disease: Social Group Interactions (Samuel)
Black-footed ferret. Photo credit: Paul Marinari Feeding time at an elk feedground in Wyoming - March 2008

A sea otter swims in Monterey Bay, California. USGS scientists study this federally listed species in efforts to help them recover from near extinction. Photo credit: Tania Larson, USGS

Feral pig. Photo credit: USGS

Little brown bat with fungus on muzzle. Photo credit: Al Hicks, New York Department of Environmental Conservation
Prairie Dogs, Black-footed Ferrets, and Sylvatic Plague (Rocke) Predicting Parasite Spread among Greater Yellowstone Elk (Cross) Sea Otters and Gene Expression (Miles, Bodkin) Surveillance of Influenza in Wild Mammals (Hall)

White-nose Syndrome: Population Genetics of Geomyces destructans(Foster, Cuomo, Blehert)


The Role of Breeding Interactions on CWD Transmission in White-tailed Deer
White-tailed deer in a field. Photo credit: John J. Mosesso, NBII.Gov
White-tailed deer in a field. Photo credit: John J. Mosesso/NBII.Gov
Electrophoresis banding patterns for different deer at a specific microsatellite marker
Electrophoresis banding patterns for different deer at a specific microsatellite marker. Larger view

The influences of white-tailed deer behavior and social structure on chronic wasting disease (CWD) transmission are not well understood. Close, frequent contact among males and females during breeding may facilitate the transmission of CWD. The objective of our study is to evaluate the importance of CWD transmission between deer during breeding interactions. Specifically, the aims of the study are to: 1) use genetic markers to determine parental relationships among adult males, females, and fawns harvested in southwest Wisconsin, 2) determine if CWD infection is related to male-female interactions during the breeding season, and 3) determine the probability of CWD transmission between male and female deer during breeding interactions.
Muscle tissue from adult females, males and fawns collected within a 210 square-mile region of highest CWD prevalence (6-7%) will be genotyped at several microsatellite loci. Genotypes will be used to assign maternity and paternity to fawns allowing us to infer breeding interactions among adult males and females. Parentage reconstructions along with information on the infection status, stage of disease and spatial location of individuals will be used to evaluate the potential for CWD transmission between males and females during breeding interactions. Identification of the role that male-female breeding interactions play in the transmission of CWD can be used along with other CWD studies to understand rates and spread of CWD in white-tailed deer populations as well as to assist in the development of management strategies aimed at eliminating the disease.

For more information visit http://wildlife.wisc.edu/coop/CWD/CWD_Introduction.html and contact Michael D. Samuel, Wisconsin Cooperative Wildlife Research Unit.

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Has CWD produced genetic selection in the Wisconsin white-tailed deer populations?
Illustration of the effects of genetic selection related to disease infection/mortality. Image credit: Stacie Robinson
Illustration of the effects of genetic selection related to disease infection/mortality. Image credit: Stacie Robinson. Larger view
White-tailed deer in a forest. Photo credit: John J. Mosesso/NBII.Gov
White-tailed deer in a forest. Photo credit: John J. Mosesso/NBII.Gov

Recent evidence indicates that prion (Prnp) genotypes in Wisconsin white-tailed deer have differential resistance to CWD infection and show differential rates of disease progression.  The most common Prnp genotype, referred to as wild-type (wt), encodes a glutamine at codon 95 (Q95Q) and glycine at codon 96 (G96G).  Other common Prnp genotypes including Q95H and G96S have been identified in the free-ranging Wisconsin white-tailed deer population.  The wt genotype (the homozygous G96G genotype) is significantly over-represented among infected deer and gene frequencies in CWD-positive and -negative deer suggests that G96S are linked to a reduced susceptibility and/or progression of CWD.  Similar patterns related to slower disease progression for the G96S genotype have been recently confirmed in laboratory challenge studies.  However, studies also indicate that 91-98% of white-tailed deer are genetically susceptible to CWD.  Similar genetic polymorphisms have been found in elk and mule deer.

The genetic basis of susceptibility and disease progression in TSE diseases is of great interest to breeding programs in domestic or captive animals and for predicting likely impacts of disease in free-ranging populations of deer which are also key stone herbivores.  Indeed, breeding for genetic resistance to scrapie has become an accepted practice in domestic sheep and has also been suggested for captive and wild deer populations.  This option is particularly important for TSE disease because there is no known treatment or vaccination.  In addition, genetic resistance is the basis from much of genetic engineering of agricultural crops.  Despite these theoretical and applied lessons from domestic animals and agricultural, there has been little investigation or evidence of genetic selection in the field of wildlife disease.  However, demonstration of such selection would have significant implications for CWD management.  In large part, many of these implications have direct bearing on the epidemiology and future trends in CWD transmission and spread.  In particular, the more resistant Prnp genotype (G96S) seems to have a long period of disease progression and thus an extended infectious period.  This longer infectious period could lead to higher CWD transmission rates in the future, both by direct contact or through environmental transmission. The goal of this project is to investigate whether there is evidence of genetic selection in the CWD affected core area of Wisconsin, where disease has been present for at least 20 years.

Related Publication:

Blanchong JA, Heisey DM, Scribner KT, Libants SV, Johnson C, Aiken JM, Langenberg JA, Samuel MD. Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: complement component C1q and Prnp polymorphisms. Infect Genet Evol. 2009 Dec;9(6):1329-35. Epub 2009 Aug 31. PMID: 19723593 (online abstract)

For more information visit http://wildlife.wisc.edu/coop/CWD/CWD_Introduction.html and contact Michael D. Samuel, Wisconsin Cooperative Wildlife Research Unit.

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Application of Landscape Genetics for Predicting Spread of CWD in Wisconsin
White-tailed deer at the top of a ridge. Photo credit: John J. Mosesso, NBII.Gov
White-tailed deer at the top of a ridge. Photo credit: John J. Mosesso/NBII.Gov
Sampling locations for landscape genetics and spread of CWD project
Sampling locations for landscape genetics and spread of CWD project

Understanding the spread of chronic wasting disease (CWD) is necessary to predict the impact of disease on deer populations and to develop effective strategies for control. Our research goal is to use a landscape genetics approach to characterize the relationship between landscape feature, spatial population genetic structure, and the distribution and potential spread of CWD in white-tailed deer in southern Wisconsin. Our research objectives are three-fold. First, characterize deer spatial genetic structure by using molecular genetic markers to assess genetic diversity and variation on the landscape. From these data we will predict distance, direction, and rates of deer dispersal. Second, identify whether landscape characteristics which explain deer spatial genetic structure over and above geographic distance. We will identify landscape features such as rivers, highways, and habitat types that are associated with genetic connectivity or discontinuity across the study region. Third, we will combine deer spatial genetic structure and landscape characteristics to develop predictive models of CWD spread. Results of this study will be used to help understand the disease dynamics of CWD, the spatial spread of disease and its relationship to deer movement and landscape features, and assist management agencies in developing appropriate management and surveillance strategies for this disease.

Our initial results demonstrated that landscape genetics offers a promising approach for identifying relationships between landscape features and population genetic structure for investigating wildlife disease. Genetic differentiation was correlated with CWD prevalence. The Wisconsin River had a significant influence on gene flow between study area and core-area deer. However, US Highway 18/151, which is relatively recent, did not appear to limit gene flow. Differences in landscape features such as deer density, forest cover and land use can affect deer dispersal and influence the rate at which disease establishes and increases in prevalence locally.

For more information visit http://wildlife.wisc.edu/coop/CWD/CWD_Introduction.html and contact Michael D. Samuel, Wisconsin Cooperative Wildlife Research Unit.

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Genetic Resistance to Chronic Wasting Disease (CWD) in White-tailed Deer
White-tailed deer in a field. Photo credit: John J. Mosesso, NBII.Gov
White-tailed deer in a field. Photo credit: John J. Mosesso/NBII.Gov
Potential role of complement in retention of TSEs by FDCs. Photo credit: Copyright Journal of General Virology (2001) v82. 2307
Potential role of complement in retention of TSEs by FDCs. Photo credit: Copyright Journal of General Virology (2001) v82. 2307

Increasingly, it appears that prion diseases such as chronic wasting disease (CWD) are influenced by components of the innate (non-adaptive) immune system also known as the complement system. The specific mechanisms by which prions activate the complement system are unknown. One hypothesized role of the complement system in early TSE pathogenesis is that prions are recognized and bound by complement components (C3 and C1q) that deliver prions to follicular dendritic cells where they are able to convert normal prion to the abnormal conformation, subsequently enter the central nervous system, and spread to the brain. Support for this hypothesis comes from studies in mice demonstrating that deficiencies in C3 or C1q impede the accumulation of scrapie-prion in lymph tissue and delay spread of the disease into the brain. These complement components, therefore, are natural targets to examine as factors potentially modulating CWD pathogenesis in natural populations.

The objective of our study is to investigate the association between complement gene variation and susceptibility to CWD in white-tailed deer in south-central Wisconsin. Given the important role of the complement system in immune function, free-ranging animals, unlike laboratory models, are unlikely to be completely deficient in particular components of the complement system. However, individuals within populations are often variable with respect to the specific genetic makeup of immune system genes. The goal of this study, therefore, is to examine whether genetic polymorphisms of complement components are associated with the presence or absence of CWD in a free-ranging population of white-tailed deer.

Related Publication:

Blanchong JA, Heisey DM, Scribner KT, Libants SV, Johnson C, Aiken JM, Langenberg JA, Samuel MD. Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: complement component C1q and Prnp polymorphisms. Infect Genet Evol. 2009 Dec;9(6):1329-35. Epub 2009 Aug 31. PMID: 19723593 (online abstract)


For more information visit http://wildlife.wisc.edu/coop/CWD/CWD_Introduction.html and contact Michael D. Samuel, Wisconsin Cooperative Wildlife Research Unit.

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Social Group Interactions and CWD Transmission in Female White-tailed Deer
White-tailed deer. Photo credit: John J. Mosesso, NBII.Gov
White-tailed deer. Photo credit: John J. Mosesso/NBII.Gov
Steps used in DNA genotyping of white-tailed deer and determination of relatedness among deer in different populations
Steps used in DNA genotyping of white-tailed deer and determination of relatedness among deer in different populations

Social structure and contact among white-tailed deer can greatly affect how a disease may be transmitted through the population. Our study examines how the social structure in female white-tailed deer may affect transmission of chronic wasting disease (CWD). The goals of this study are to determine how 1) CWD infection is distributed within female social units and 2) CWD infected social groups are distributed across the landscape. Females live in familial social units that exhibit high site fidelity and low dispersal. By using genetic markers, we can identify the composition of these social units based on relatedness. We can also determine the location of social units based on harvest data from the Wisconsin CWD control effort. Based on the patterns of CWD infection, we can provide clues to help discover the mechanisms of how CWD is transmitted between individuals and how it spreads on the landscape.

Our results suggest a hierarchy of CWD transmission within social groups based on familial relationships. Direct (deer-to-deer) transmission of CWD likely occurs between closely related female deer. CWD transmission also appears to occur among spatially proximate females. However, we cannot determine whether occasional direct contact or contact with a contaminated environment is responsible for increased infection among proximate females. It is likely that direct and environmental (deer-environment-deer) transmission occurs in this epidemic. The influence of spatially proximate females and close female kin on CWD infection does not extend beyond a 2-3 km radius. In addition, the spatial relationship between infected females and among infected males and females suggests that CWD transmission operates on a local scale of 20-30 km2.

Related Publication:

Daniel A. Grear, Michael D. Samuel, Kim T. Scribner, Byron V. Weckworth and Julie A. Langenberg. Influence of genetic relatedness and spatial proximity on chronic wasting disease infection among female white-tailed deer. Journal of Applied Ecology 2010; Volume 47 Issue 3, Pages 532 - 540. Journal compilation 2010 British Ecological Society. DOI: 10.1111/j.1365-2664.2010.01813.x (online abstract)

For more information visit http://wildlife.wisc.edu/coop/CWD/CWD_Introduction.html and contact Michael D. Samuel, Wisconsin Cooperative Wildlife Research Unit.

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Prairie Dogs, Black-footed Ferrets, and Sylvatic Plague
Black-footed ferret. Photo credit: Paul Marinari
Black-footed ferret. Photo credit: Paul Marinari.
Black-tailed prairie dog. Photo credit: Lisa Zolly, NBII.Gov
Black-tailed prairie dog. Photo credit: Lisa Zolly/NBII.Gov

Plague, caused by the bacterium Yersinia pestis, is a disease of wild rodents that can afflict humans and other mammals.  Prairie dogs in western U.S., are susceptible to plague, (> 90% mortality in afflicted colonies).   Prairie dogs play a critical role,  maintaining biodiversity and integrity of western grasslands stretching from southern Canada to northern Mexico.  The black-tailed prairie dog (once the most abundant mammal in North America) has declined to less than 2% of its former population and sylvatic plague is one of the most serious threats to its continued existence.  The endangered black-footed ferret (Mustela nigripes) depends on prairie dogs as both food sources and to provide habitat (prairie dog burrows).  A captive breeding and recovery program was established for ferrets in 1987 after disease outbreaks nearly eradicated the last known wild population.  Management and recovery of this species is tightly linked to prairie dog survival.  The black-footed ferret is also highly susceptible to plague and may suffer high mortality rates upon infection.  Limiting the incidence of plague infections in prairie dogs and other wild rodents would reduce the incidence and potential of zoonotic transmission of the disease and enhance recovery potential of the black-footed ferret.  One method for controlling disease in free-ranging wildlife is to prevent infection through a targeted oral immunization program.   Recombination techniques were used to insert several antigens of Y. pestis into an attenuated form of raccoon pox virus, a vaccine vector.   This vaccine was incorporated into baits and voluntarily consumed by prairie dogs.   Experimental exposure to 70,000 Y. pestis bacteria, a realistic dose encountered by prairie dogs in a plague outbreak, resulted in a 94% survival rate of vaccinated animals, whereas only 6% of non-vaccinated controls survived the infection.  Research to develop a feasible baiting system for mass immunization programs of prairie dogs are ongoing.

For more information view Protecting Black-Footed Ferrets and Prairie Dogs Against Sylvatic Plague (PDF, 699 KB) Acrobat and contact Tonie E. Rocke, National Wildlife Health Center.

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Predicting Disease Spread among Greater Yellowstone Elk using DNA Markers for Elk and their Parasites
Feeding time at an elk feedground in Wyoming - March 2008. Photo credit: Vicki Patrek, USGS
Feeding time at an elk feedground in Wyoming - March 2008. Photo credit: Vicki Patrek, USGS

There is a growing need to understand connectivity and movement patterns among elk herds and their parasites across the Greater Yellowstone Ecosystem (GYE). We are developing microsatellite and mitochondrial (mt) deoxyribonucleic acid (DNA) makers to assess connectivity among elk from nine study areas. So far, we have sequenced 695 base pairs (bp) of mtDNA control region from 407 elk. Statistical analyses revealed moderately-high mtDNA differentiation, suggesting limited female-mediated gene flow among study areas. We also genotyped 11 nuclear DNA microsatellites from 80 elk on four study areas. Statistical analyses revealed relatively low genetic differentiation, suggesting moderately high gene flow. The nearly 10-fold higher mtDNA differentiation suggests relatively limited female-mediated gene flow, possibly due to female philopatry. One microsatellite locus in a disease-related gene (IFNG) had relatively high FST (FST = 0.07), suggesting a possible adaptive function of IFNG. Five additional microsatellites were optimized, including three loci in genes with disease-related functions. All 16 microsatellite, mtDNA, and base line data represent important tools for long term, noninvasive monitoring of elk population connectivity across the GYE. To study helminth parasites, we noninvasively sampled 554 fecal deposits during 2007 and 2008 from elk, bison, bighorn sheep, pronghorn, and cattle from across the GYE. We developed an internal transcribed spacer region 2 (ITS-2) nuclear gene sequencing assay for parasite species identification, and a cytochrome oxidase-1 (CO1) mitochondrial assay for assessing parasite gene flow. We produced ITS-2 polymerase chain reaction (PCR) products from 345 individual nematode parasites of ungulate hosts, and identified 223 (88%) to species. Dictyocaulus viviparous lungworms were at moderate prevalence (10-50%) in elk and bison. The most prevalent gastrointestinal (GI) parasite in elk was Spiculopteragia spp., with ~5-10% prevalence. Bison in the GYE appear to commonly be infected with both Cooperia oncophora and Ostertagia ostertagi. Bighorn sheep are commonly infected with Protostrongylus lungworms and Marshallagia GI worms, which were not shared with other wild ungulates in the GYE. These DNA markers and preliminary data provide valuable tools for noninvasive monitoring of parasite transmission across the GYE.

For more information view Viral Tracking of Wildlife Corridors across the Rocky Mountains (PDF, 374 KB) Acrobat and contact Paul C. Cross at the Northern Rocky Mountain Science Center; Gordon Luikart, Marty Kardos, or Vanessa Ezenwa at the University of Montana, Missoula; or P.J. White at the National Park Service.

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Expression of Genes (as Novel Biomarkers) in Sea Otter Populations as Indicators of Exposure to Organic Pollutants, Metals, Parasites, Bacterial Infection, Viral Infection, and Thermal Stress
A sea otter swims in Monterey Bay, California. USGS scientists study this federally listed species in efforts to help them recover from near extinction. Photo credit: Tania Larson, USGS
A sea otter swims in Monterey Bay, California. USGS scientists study this federally listed species in efforts to help them recover from near extinction. Photo credit: Tania Larson, USGS

Sea otters are present in geographically separate populations that span over 30 degrees of latitude and vary in status from rapidly increasing to declining, and include two listed as Threatened under the Endangered Species Act.  Recognized constraints to sea otter populations include food limitation, predation, harvest, disease, and contaminants.  Here, we propose to use coastal ecosystems from highly urbanized California to relatively pristine Alaska, as a large-scale laboratory to understand the factors that currently influence these systems, and to provide the critical data and tools needed to establish how coastal ecosystems will respond to future environmental change.  We will use the sea otter, an apex consumer and sentinel of ecosystem health, to identify the mechanisms, pathways and expressions of response to physical and biological ecosystem perturbations.

Sea otter diet and nutrition will be determined through direct estimates of caloric intake rates.  Concurrently, we will evaluate the health of the ecosystem as reflected in the expression of genes (as novel biomarkers) in each sea otter population specific to: 1) organic pollutants, 2) metals, 3) parasites, 4) bacterial infection, 5) viral infection, and 6) thermal stress.  The combined data sets on: 1) nearshore productivity and inputs from land and sea, 2) sea otter diet and nutrition, and 3) gene expression will support a multivariate analysis of empirical factors likely responsible for directing the status and trend within and among geographically distinct sea otter populations.  Analytical outcomes will be used to determine the present magnitude and scale of human influences from watersheds, which can then be used to forecast coastal ecosystem responses to anticipated environmental change such as increasing temperature, sea level rise, ocean acidification, contaminants, and disease.

For more information view the Sea Otter Studies at the Western Ecological Research Center and the Sea Otter Studies at the Alaska Science Center, and contact A. Keith Miles, Western Ecological Research Center, and James L. Bodkin, Alaska Science Center.

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Surveillance of Influenza in Wild Mammals
Feral pig. Photo credit: USGS
A sea otter swims in Monterey Bay, California. USGS scientists study this federally listed species in efforts to help them recover from near extinction. Photo credit: Tania Larson, USGS

Feral swine have been shown to have exposure histories to AI and may have important roles in AI disease ecology. Other mammalian species are also exposed to and potentially infected by AI. These include javalina, skunks, and raccoons. As many of these species frequently come into contact with human populations and livestock, the roles of mammalian species in regards to AI need to be investigated. The NWHC has the expertise and experience to develop surveillance systems that could be applied to geographic areas with strategic importance. Initial efforts will focus on establishing a robust and meaningful surveillance system in Mexico, Southwest US, and Central America. Enlisting local, national, and international agencies in countries of interest, training personnel to safely capture, handle, and sample mammalian species, and designing a system of sampling, testing and reporting will be required. Experts in mammalian behavior, capture, and sampling will be enlisted to train and educate personnel involved in local sampling efforts. Viral isolates uncovered in mammals will be characterized genetically to recover their evolutionary history and interactions with other reservoirs of influenza. Surveillance efforts in mammalian species will enable determination of which animals are important in AI ecology and define what the risks of AI in those species are to human health and agriculture.

For more information contact Jeffrey S. Hall, National Wildlife Health Center.

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Population Genetics of Geomyces destructans from Whole Genome Sequences
Little brown bat with fungus on muzzle. Photo credit: Al Hicks, New York Department of Environmental Conservation
Little brown bat with fungus on muzzle. Photo credit: Al Hicks, New York Department of Environmental Conservation

Genome sequencing of Geomyces destructans, the fungus causative of the skin infection that is hallmark of White-nose Syndrome (WNS), is completed. This genome will provide the basis for research into the genetics of the fungus, including population genetics, phylogenetics, and comparative genomics. Because of the recent emergence and rapid spread of WNS, little genetic differentiation among isolates is expected. Thus, we will use whole genome comparisons from resequencing of 15-20 G. destructans isolates from diseased bats collected throughout the current range of the disease in the US. For each resequenced genome, we anticipate coverage of at least 100X, enabling in depth comparison of isolates to assess genetic changes across the landscape. We will also compare these genomes to three isolates from Europe to evaluate differentiation among intercontinental isolates and the potential for the fungus to have emerged from European bats. The ultimate goal of this project is to use genomics to assess spread, source populations, transmission, pathogenicity, detection, and evolutionary history of G. destructans.

For more information contact Jeffrey Foster (Center for Microbial Genetics & Genomics, Northern Arizona University), Christina Cuomo (Broad Institute of MIT and Harvard), and David Blehert, National Wildlife Health Center. For more information, visit: http://www.broadinstitute.org/news/1516

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