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Allen Herbst

Allen Herbst is a Prion Biologist at the USGS National Wildlife Health Center.

Professional Experience

  • 2022 - Present Prion Biologist, USGS National Wildlife Health Center

  • 2014-2021 Research Associate, Centre for Prions and Protein Folding Diseases Agricultural, Food and Nutritional Sciences, University of Alberta

  • 2009-2013 Postdoctoral Fellow, Centre for Prions and Protein Folding Diseases Agricultural, Food and Nutritional Sciences, University of Alberta

  • 2013 Lecturer, University of Wisconsin

  • 2009-2010 Honorary Fellow, University of Wisconsin

  • 2008-2009 Research Associate, University of Wisconsin

  • 2001-2008 Research Assistant, University of Wisconsin

  • 1999-2001 Research Specialist, University of Wisconsin

Education and Certifications

  • Doctor of Philosophy, University of Wisconsin, Veterinary Science

  • Bachelor of Science, University of Wisconsin, Molecular Biology

  • Associate of Science, William Rainey Harper College, Chemistry

Science and Products

Susceptibility of beavers to chronic wasting disease

Chronic wasting disease (CWD) is a contagious, fatal, neurodegenerative prion disease of cervids. The expanding geographical range and rising prevalence of CWD are increasing the risk of pathogen transfer and spillover of CWD to non-cervid sympatric species. As beavers have close contact with environmental and food sources of CWD infectivity, we hypothesized that they may be susceptible to CWD pri
By
Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center

Non-USGS Publications**

A. Herbst, A. Hoang, C. Kim, J. Aiken, D. McKenzie, D. Goldwater, and J. Wanagat, Metformin treatment in old rats and effects on mitochondrial integrity. Rejuvenation Res, 2021.
A. Herbst, S.J. Prior, C.C. Lee, J.M. Aiken, D. McKenzie, A. Hoang, N. Liu, X. Chen, P. Xun, D.B. Allison, and J. Wanagat, Skeletal muscle mitochondrial DNA copy number and mitochondrial DNA deletion mutation frequency as predictors of physical performance in older men and women. Geroscience, 2021.
A. Herbst, C.C. Lee, A.R. Vandiver, J.M. Aiken, D. McKenzie, A. Hoang, D. Allison, N. Liu, and J. Wanagat, Mitochondrial DNA deletion mutations increase exponentially with age in human skeletal muscle. Aging Clin Exp Res, 2020.
A. Herbst, J.M. Aiken, D. McKenzie, and J. Wanagat, Comment on: "Mitochondrial Mechanisms of Neuromuscular Junction Degeneration with Aging. Cells 2020, 9, 197". Cells, 2020. 9(8).
C.C. Lee, A. Hoang, D. Segovia, A. Herbst, F. Barthelemy, E. Gibbs, R. Crosbie, S.F. Nelson, C. Miceli, and J. Wanagat, Enhanced Methods for Needle Biopsy and Cryopreservation of Skeletal Muscle in Older Adults. J Cytol Histol, 2020. 11(2).
C. Duque Velasquez, C. Kim, T. Haldiman, A. Herbst, J. Aiken, J.G. Safar, and D. McKenzie, Chronic wasting disease (CWD) prion strains evolve via adaptive diversification of conformers in hosts expressing prion protein polymorphisms. J Biol Chem, 2020. 295(15): p. 4985-5001.
A. Herbst, A.N. Hoang, W. Woo, D. McKenzie, J.M. Aiken, R.A. Miller, D.B. Allison, N. Liu, and J. Wanagat, Mitochondrial DNA alterations in aged macrophage migration inhibitory factor-knockout mice. Mech Ageing Dev, 2019. 182: p. 111126.
A. Otero, C. Duque Velasquez, C. Johnson, A. Herbst, R. Bolea, J.J. Badiola, J. Aiken, and D. McKenzie, Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrP(CWD) deposition in orally infected white-tailed deer. BMC Vet Res, 2019. 15(1): p. 50.
T. Russell, C. Cullingham, A. Kommadath, P. Stothard, A. Herbst, and D. Coltman, Development of a Novel Mule Deer Genomic Assembly and Species-Diagnostic SNP Panel for Assessing Introgression in Mule Deer, White-Tailed Deer, and Their Interspecific Hybrids. G3 (Bethesda), 2019. 9(3): p. 911-919.
D. Gushue, A. Herbst, V. Sim, D. McKenzie, and J.M. Aiken, 14-3-3 and enolase abundances in the CSF of Prion diseased rats. Prion, 2018. 12(3-4): p. 253-260.
J. Bielas, A. Herbst, K. Widjaja, J. Hui, J.M. Aiken, D. McKenzie, R.A. Miller, S.V. Brooks, and J. Wanagat, Long term rapamycin treatment improves mitochondrial DNA quality in aging mice. Exp Gerontol, 2018. 106: p. 125-131.
A. Herbst, C.D. Velasquez, E. Triscott, J.M. Aiken, and D. McKenzie, Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion. Emerg Infect Dis, 2017. 23(9): p. 1598-1600.
A. Herbst, K. Widjaja, B. Nguy, E.B. Lushaj, T.M. Moore, A.L. Hevener, D. McKenzie, J.M. Aiken, and J. Wanagat, Digital PCR Quantitation of Muscle Mitochondrial DNA: Age, Fiber Type, and Mutation-Induced Changes. J Gerontol A Biol Sci Med Sci, 2017. 72(10): p. 1327-1333.
A. Herbst, J. Wanagat, N. Cheema, K. Widjaja, D. McKenzie, and J.M. Aiken, Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age. Aging Cell, 2016. 15(6): p. 1132-1139.
C. Duque Velásquez, C. Kim, A. Herbst, N. Daude, M.C. Garza, H. Wille, J. Aiken, and D. McKenzie, Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains. J Virol, 2015. 89(24): p. 12362-73.
N. Cheema, A. Herbst, D. McKenzie, and J.M. Aiken, Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities. Aging Cell, 2015. 14(6): p. 1085-93.
A. Herbst, A. Ness, C.J. Johnson, D. McKenzie, and J.M. Aiken, Transcriptomic responses to prion disease in rats. BMC Genomics, 2015. 16: p. 682.
A. Herbst, J.M. Aiken, and D. McKenzie, Replication of prions in differentiated muscle cells. Prion, 2014. 8(2).
A. Herbst, P. Banser, C.D. Velásquez, C.E. Mays, V.L. Sim, D. Westaway, J.M. Aiken, and D. McKenzie, Infectious prions accumulate to high levels in non proliferative C2C12 myotubes. PLoS Pathog, 2013. 9(11): p. e1003755.
A. Herbst, C.J. Johnson, K. Hynes, D. McKenzie, and J.M. Aiken, Mitochondrial biogenesis drives a vicious cycle of metabolic insufficiency and mitochondrial DNA deletion mutation accumulation in aged rat skeletal muscle fibers. PLoS One, 2013. 8(3): p. e59006.
D. Westaway, S. Genovesi, N. Daude, R. Brown, A. Lau, I. Lee, C.E. Mays, J. Coomaraswamy, B. Canine, R. Pitstick, A. Herbst, J. Yang, K.W. Ko, G. Schmitt-Ulms, S.J. Dearmond, D. McKenzie, L. Hood, and G.A. Carlson, Down-regulation of Shadoo in prion infections traces a pre-clinical event inversely related to PrP(Sc) accumulation. PLoS Pathog, 2011. 7(11): p. e1002391.
C.J. Johnson, A. Herbst, C. Duque-Velásquez, J.P. Vanderloo, P. Bochsler, R. Chappell, and D. McKenzie, Prion protein polymorphisms affect chronic wasting disease progression. PLoS One, 2011. 6(3): p. e17450.
X. Wei, A. Herbst, D. Ma, J. Aiken, and L. Li, A quantitative proteomic approach to prion disease biomarker research: delving into the glycoproteome. J Proteome Res, 2011. 10(6): p. 2687-702.
L.R. Moody, A. Herbst, and J.M. Aiken, Upregulation of interferon-gamma-induced genes during prion infection. J Toxicol Environ Health A, 2011. 74(2-4): p. 146-53.
L.R. Moody, A. Herbst, H.S. Yoo, J.P. Vanderloo, and J.M. Aiken, Comparative prion disease gene expression profiling using the prion disease mimetic, cuprizone. Prion, 2009. 3(2): p. 99-109.
A. Herbst, S. McIlwain, J.J. Schmidt, J.M. Aiken, C.D. Page, and L. Li, Prion disease diagnosis by proteomic profiling. J Proteome Res, 2009. 8(2): p. 1030-6.
X. Wei, A. Herbst, J.J. Schmidt, J. Aiken, and L. Li, Facilitating Discovery of Prion Disease Biomarkers by Quantitative Glycoproteomics. LCGC North America, 2009.
A. Herbst, J.W. Pak, D. McKenzie, E. Bua, M. Bassiouni, and J.M. Aiken, Accumulation of mitochondrial DNA deletion mutations in aged muscle fibers: evidence for a causal role in muscle fiber loss. J Gerontol A Biol Sci Med Sci, 2007. 62(3): p. 235-45.
E. Bua, J. Johnson, A. Herbst, B. Delong, D. McKenzie, S. Salamat, and J.M. Aiken, Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers. Am J Hum Genet, 2006. 79(3): p. 469-80.
J.W. Pak, A. Herbst, E. Bua, N. Gokey, D. McKenzie, and J.M. Aiken, Rebuttal to Jacobs: the mitochondrial theory of aging: alive and well. Aging Cell, 2003. 2(1): p. 9-10.
J.W. Pak, A. Herbst, E. Bua, N. Gokey, D. McKenzie, and J.M. Aiken, Mitochondrial DNA mutations as a fundamental mechanism in physiological declines associated with aging. Aging Cell, 2003. 2(1): p. 1-7.

**Disclaimer: The views expressed in Non-USGS publications are those of the author and do not represent the views of the USGS, Department of the Interior, or the U.S. Government.

link
Mule deer munching on a shrub in the midst of a winter snow

Assessing the Ability of Incineration to Inactivate CWD Prions from Carcasses

Chronic wasting disease (CWD), a fatal neurologic disease of cervids, presents a monumental management challenge, in part because the etiological agent, an infectious prion, is extremely difficult to inactivate and can be transmitted directly or indirectly to hosts. Due to these attributes of prions, proper disposal of CWD-infected carcasses is an important consideration for management agencies to...
By
Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
link

Assessing the Ability of Incineration to Inactivate CWD Prions from Carcasses

Chronic wasting disease (CWD), a fatal neurologic disease of cervids, presents a monumental management challenge, in part because the etiological agent, an infectious prion, is extremely difficult to inactivate and can be transmitted directly or indirectly to hosts. Due to these attributes of prions, proper disposal of CWD-infected carcasses is an important consideration for management agencies to...
Learn More
link
A white-tailed deer fawn taking refuge in vegetation.

Advancing the Use of RT-QuIC for Applications in CWD Management

Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. The development of the real-time quaking-induced conversion (RT-QuIC) assay has the potential to transform laboratory research of prions and provide new opportunities for improved surveillance and management.
By
Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
link

Advancing the Use of RT-QuIC for Applications in CWD Management

Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. The development of the real-time quaking-induced conversion (RT-QuIC) assay has the potential to transform laboratory research of prions and provide new opportunities for improved surveillance and management.
Learn More
link
Mule deer in Wyoming with snow covered mountains in the distance

Chronic Wasting Disease

Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. CWD is one member of a family of diseases called transmissible spongiform encephalopathies (TSEs), and is thought to be caused by prions. CWD is the only TSE known to affect free-ranging wildlife.
By
Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
link

Chronic Wasting Disease

Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. CWD is one member of a family of diseases called transmissible spongiform encephalopathies (TSEs), and is thought to be caused by prions. CWD is the only TSE known to affect free-ranging wildlife.
Learn More

Science and Products

  • Publications

    Susceptibility of beavers to chronic wasting disease

    Chronic wasting disease (CWD) is a contagious, fatal, neurodegenerative prion disease of cervids. The expanding geographical range and rising prevalence of CWD are increasing the risk of pathogen transfer and spillover of CWD to non-cervid sympatric species. As beavers have close contact with environmental and food sources of CWD infectivity, we hypothesized that they may be susceptible to CWD pri
    By
    Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center

    Non-USGS Publications**

    A. Herbst, A. Hoang, C. Kim, J. Aiken, D. McKenzie, D. Goldwater, and J. Wanagat, Metformin treatment in old rats and effects on mitochondrial integrity. Rejuvenation Res, 2021.
    A. Herbst, S.J. Prior, C.C. Lee, J.M. Aiken, D. McKenzie, A. Hoang, N. Liu, X. Chen, P. Xun, D.B. Allison, and J. Wanagat, Skeletal muscle mitochondrial DNA copy number and mitochondrial DNA deletion mutation frequency as predictors of physical performance in older men and women. Geroscience, 2021.
    A. Herbst, C.C. Lee, A.R. Vandiver, J.M. Aiken, D. McKenzie, A. Hoang, D. Allison, N. Liu, and J. Wanagat, Mitochondrial DNA deletion mutations increase exponentially with age in human skeletal muscle. Aging Clin Exp Res, 2020.
    A. Herbst, J.M. Aiken, D. McKenzie, and J. Wanagat, Comment on: "Mitochondrial Mechanisms of Neuromuscular Junction Degeneration with Aging. Cells 2020, 9, 197". Cells, 2020. 9(8).
    C.C. Lee, A. Hoang, D. Segovia, A. Herbst, F. Barthelemy, E. Gibbs, R. Crosbie, S.F. Nelson, C. Miceli, and J. Wanagat, Enhanced Methods for Needle Biopsy and Cryopreservation of Skeletal Muscle in Older Adults. J Cytol Histol, 2020. 11(2).
    C. Duque Velasquez, C. Kim, T. Haldiman, A. Herbst, J. Aiken, J.G. Safar, and D. McKenzie, Chronic wasting disease (CWD) prion strains evolve via adaptive diversification of conformers in hosts expressing prion protein polymorphisms. J Biol Chem, 2020. 295(15): p. 4985-5001.
    A. Herbst, A.N. Hoang, W. Woo, D. McKenzie, J.M. Aiken, R.A. Miller, D.B. Allison, N. Liu, and J. Wanagat, Mitochondrial DNA alterations in aged macrophage migration inhibitory factor-knockout mice. Mech Ageing Dev, 2019. 182: p. 111126.
    A. Otero, C. Duque Velasquez, C. Johnson, A. Herbst, R. Bolea, J.J. Badiola, J. Aiken, and D. McKenzie, Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrP(CWD) deposition in orally infected white-tailed deer. BMC Vet Res, 2019. 15(1): p. 50.
    T. Russell, C. Cullingham, A. Kommadath, P. Stothard, A. Herbst, and D. Coltman, Development of a Novel Mule Deer Genomic Assembly and Species-Diagnostic SNP Panel for Assessing Introgression in Mule Deer, White-Tailed Deer, and Their Interspecific Hybrids. G3 (Bethesda), 2019. 9(3): p. 911-919.
    D. Gushue, A. Herbst, V. Sim, D. McKenzie, and J.M. Aiken, 14-3-3 and enolase abundances in the CSF of Prion diseased rats. Prion, 2018. 12(3-4): p. 253-260.
    J. Bielas, A. Herbst, K. Widjaja, J. Hui, J.M. Aiken, D. McKenzie, R.A. Miller, S.V. Brooks, and J. Wanagat, Long term rapamycin treatment improves mitochondrial DNA quality in aging mice. Exp Gerontol, 2018. 106: p. 125-131.
    A. Herbst, C.D. Velasquez, E. Triscott, J.M. Aiken, and D. McKenzie, Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion. Emerg Infect Dis, 2017. 23(9): p. 1598-1600.
    A. Herbst, K. Widjaja, B. Nguy, E.B. Lushaj, T.M. Moore, A.L. Hevener, D. McKenzie, J.M. Aiken, and J. Wanagat, Digital PCR Quantitation of Muscle Mitochondrial DNA: Age, Fiber Type, and Mutation-Induced Changes. J Gerontol A Biol Sci Med Sci, 2017. 72(10): p. 1327-1333.
    A. Herbst, J. Wanagat, N. Cheema, K. Widjaja, D. McKenzie, and J.M. Aiken, Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age. Aging Cell, 2016. 15(6): p. 1132-1139.
    C. Duque Velásquez, C. Kim, A. Herbst, N. Daude, M.C. Garza, H. Wille, J. Aiken, and D. McKenzie, Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains. J Virol, 2015. 89(24): p. 12362-73.
    N. Cheema, A. Herbst, D. McKenzie, and J.M. Aiken, Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities. Aging Cell, 2015. 14(6): p. 1085-93.
    A. Herbst, A. Ness, C.J. Johnson, D. McKenzie, and J.M. Aiken, Transcriptomic responses to prion disease in rats. BMC Genomics, 2015. 16: p. 682.
    A. Herbst, J.M. Aiken, and D. McKenzie, Replication of prions in differentiated muscle cells. Prion, 2014. 8(2).
    A. Herbst, P. Banser, C.D. Velásquez, C.E. Mays, V.L. Sim, D. Westaway, J.M. Aiken, and D. McKenzie, Infectious prions accumulate to high levels in non proliferative C2C12 myotubes. PLoS Pathog, 2013. 9(11): p. e1003755.
    A. Herbst, C.J. Johnson, K. Hynes, D. McKenzie, and J.M. Aiken, Mitochondrial biogenesis drives a vicious cycle of metabolic insufficiency and mitochondrial DNA deletion mutation accumulation in aged rat skeletal muscle fibers. PLoS One, 2013. 8(3): p. e59006.
    D. Westaway, S. Genovesi, N. Daude, R. Brown, A. Lau, I. Lee, C.E. Mays, J. Coomaraswamy, B. Canine, R. Pitstick, A. Herbst, J. Yang, K.W. Ko, G. Schmitt-Ulms, S.J. Dearmond, D. McKenzie, L. Hood, and G.A. Carlson, Down-regulation of Shadoo in prion infections traces a pre-clinical event inversely related to PrP(Sc) accumulation. PLoS Pathog, 2011. 7(11): p. e1002391.
    C.J. Johnson, A. Herbst, C. Duque-Velásquez, J.P. Vanderloo, P. Bochsler, R. Chappell, and D. McKenzie, Prion protein polymorphisms affect chronic wasting disease progression. PLoS One, 2011. 6(3): p. e17450.
    X. Wei, A. Herbst, D. Ma, J. Aiken, and L. Li, A quantitative proteomic approach to prion disease biomarker research: delving into the glycoproteome. J Proteome Res, 2011. 10(6): p. 2687-702.
    L.R. Moody, A. Herbst, and J.M. Aiken, Upregulation of interferon-gamma-induced genes during prion infection. J Toxicol Environ Health A, 2011. 74(2-4): p. 146-53.
    L.R. Moody, A. Herbst, H.S. Yoo, J.P. Vanderloo, and J.M. Aiken, Comparative prion disease gene expression profiling using the prion disease mimetic, cuprizone. Prion, 2009. 3(2): p. 99-109.
    A. Herbst, S. McIlwain, J.J. Schmidt, J.M. Aiken, C.D. Page, and L. Li, Prion disease diagnosis by proteomic profiling. J Proteome Res, 2009. 8(2): p. 1030-6.
    X. Wei, A. Herbst, J.J. Schmidt, J. Aiken, and L. Li, Facilitating Discovery of Prion Disease Biomarkers by Quantitative Glycoproteomics. LCGC North America, 2009.
    A. Herbst, J.W. Pak, D. McKenzie, E. Bua, M. Bassiouni, and J.M. Aiken, Accumulation of mitochondrial DNA deletion mutations in aged muscle fibers: evidence for a causal role in muscle fiber loss. J Gerontol A Biol Sci Med Sci, 2007. 62(3): p. 235-45.
    E. Bua, J. Johnson, A. Herbst, B. Delong, D. McKenzie, S. Salamat, and J.M. Aiken, Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers. Am J Hum Genet, 2006. 79(3): p. 469-80.
    J.W. Pak, A. Herbst, E. Bua, N. Gokey, D. McKenzie, and J.M. Aiken, Rebuttal to Jacobs: the mitochondrial theory of aging: alive and well. Aging Cell, 2003. 2(1): p. 9-10.
    J.W. Pak, A. Herbst, E. Bua, N. Gokey, D. McKenzie, and J.M. Aiken, Mitochondrial DNA mutations as a fundamental mechanism in physiological declines associated with aging. Aging Cell, 2003. 2(1): p. 1-7.

    **Disclaimer: The views expressed in Non-USGS publications are those of the author and do not represent the views of the USGS, Department of the Interior, or the U.S. Government.

  • Science
    link
    Mule deer munching on a shrub in the midst of a winter snow

    Assessing the Ability of Incineration to Inactivate CWD Prions from Carcasses

    Chronic wasting disease (CWD), a fatal neurologic disease of cervids, presents a monumental management challenge, in part because the etiological agent, an infectious prion, is extremely difficult to inactivate and can be transmitted directly or indirectly to hosts. Due to these attributes of prions, proper disposal of CWD-infected carcasses is an important consideration for management agencies to...
    By
    Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
    link

    Assessing the Ability of Incineration to Inactivate CWD Prions from Carcasses

    Chronic wasting disease (CWD), a fatal neurologic disease of cervids, presents a monumental management challenge, in part because the etiological agent, an infectious prion, is extremely difficult to inactivate and can be transmitted directly or indirectly to hosts. Due to these attributes of prions, proper disposal of CWD-infected carcasses is an important consideration for management agencies to...
    Learn More
    link
    A white-tailed deer fawn taking refuge in vegetation.

    Advancing the Use of RT-QuIC for Applications in CWD Management

    Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. The development of the real-time quaking-induced conversion (RT-QuIC) assay has the potential to transform laboratory research of prions and provide new opportunities for improved surveillance and management.
    By
    Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
    link

    Advancing the Use of RT-QuIC for Applications in CWD Management

    Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. The development of the real-time quaking-induced conversion (RT-QuIC) assay has the potential to transform laboratory research of prions and provide new opportunities for improved surveillance and management.
    Learn More
    link
    Mule deer in Wyoming with snow covered mountains in the distance

    Chronic Wasting Disease

    Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. CWD is one member of a family of diseases called transmissible spongiform encephalopathies (TSEs), and is thought to be caused by prions. CWD is the only TSE known to affect free-ranging wildlife.
    By
    Ecosystems Mission Area, Biological Threats and Invasive Species Research Program, National Wildlife Health Center
    link

    Chronic Wasting Disease

    Chronic wasting disease (CWD) is an emerging infectious disease that is fatal to free-ranging and captive animals in Cervidae, the deer family. CWD is one member of a family of diseases called transmissible spongiform encephalopathies (TSEs), and is thought to be caused by prions. CWD is the only TSE known to affect free-ranging wildlife.
    Learn More