Chronic wasting disease (CWD) is a prion infectious disease that affects members of the deer family in North America. Concerns about the economic consequences of the presence of CWD have led management agencies to seek effective strategies to control CWD distribution and prevalence. Current mathematical models are either based on complex simulations or overly simplified compartmental models. We develop a mathematical model that includes gender structure to describe CWD in a logistically growing population. The model includes harvesting as a management strategy for the disease. We determine the stability conditions of the disease-free equilibrium for the model and calculate the basic reproduction number. We find an optimum interval of harvesting: with too little harvesting, the disease persists, whereas too much harvesting results in extinction of the population. A sensitivity analysis shows that the disease threshold is more sensitive to female than male harvesting and that harvesting has the greatest effect on the basic reproduction number. However, while harvesting may be a way to control CWD, the range of admissible harvesting rates may be very narrow, depending on other parameters. 1. Introduction Many wild animals come into contact with humans via harvesting, for meat, for pelts, or for population control. Transmissible diseases in wild populations pose a threat to ecology, the environment, and humans. Harvesting may also be a way that such disease transmission can be controlled; however, accurate harvesting of only sick animals is usually impractical or impossible. For example, many diseases have an extended latency period during which the animal is asymptomatic; as a result, targeted harvesting is not feasible. When targeted harvesting is impossible, harvesting for the sake of disease control has to be tightly balanced to ensure population survival. Mathematical models are important tools to determine optimal harvesting rates. A mathematical model should be as simple as possible to allow for easy parameterization and robust results; on the other hand, models need to include all important mechanisms of disease transmission and population behaviour. For example, if the latent period is comparable in duration to the life cycle of the animal, then incorporating population dynamics into a model becomes critical. Also, vertical transmission can sustain many diseases; in such cases, infection is passed from mother to offspring. Consequently, gender structure of the herd may play a crucial role in the life cycle of the disease. Conversely, many animals
References
[1]
E. S. Williams and S. Young, “Chronic wasting disease of captive mule deer: a spongiform encephalopathy,” Journal of wildlife diseases, vol. 16, no. 1, pp. 89–98, 1980.
[2]
S. Gilch, N. Chitoor, Y. Taguchi, M. Stuart, J. E. Jewell, and H. M. Sch?tzl, “Chronic wasting disease,” Topics in Current Chemistry, vol. 305, pp. 51–77, 2011.
[3]
C. J. Sigurdson, “A prion disease of cervids: chronic wasting disease,” Veterinary Research, vol. 39, no. 4, article no. 41, 2008.
[4]
D. O. Joly, M. D. Samuel, J. A. Langenberg et al., “Spatial epidemiology of chronic wasting disease in Wisconsin white-tailed deer,” Journal of Wildlife Diseases, vol. 42, no. 3, pp. 578–588, 2006.
[5]
C. Mathiason, A. Nalls, K. Anderson, J. Hayes-Klug, N. Haley, and E. Hoover, “Mother to offspring transmission of chronic wasting disease,” in Proceedings of the Meeting Report International Prion Congress: from Agent to Disease (PRION'10), vol. 4, no. 3, p. 158, 2010.
[6]
M. W. Miller, N. T. Hobbs, and S. J. Tavener, “Dynamics of prion disease transmission in mule deer,” Ecological Applications, vol. 16, no. 6, pp. 2208–2214, 2006.
[7]
M. W. Miller, E. S. Williams, N. T. Hobbs, and L. L. Wolfe, “Environmental sources of prion transmission in mule deer,” Emerging Infectious Diseases, vol. 10, no. 6, pp. 1003–1006, 2004.
[8]
Government of Alberta, Agriculture and Rural Development, “Chronic Wasting Disease (CWD) of Elk and Deer,” 2010, http://www.agric.gov.ab.ca/app21/rtw/index.jsp.
University of Alberta, “Border Deer Study: about CWD,” 2010, http://ursus.biology.ualberta.ca/overview.htm.
[11]
S. Kahn, C. Dubé, L. Bates, and A. Balachandran, “Chronic wasting disease in Canada: part 1,” Canadian Veterinary Journal, vol. 45, no. 5, pp. 397–404, 2004.
[12]
E. S. Almberg, P. C. Cross, C. J. Johnson, D. M. Heisey, and B. J. Richards, “Modeling routes of chronic wasting disease transmission: environmental prion persistence promotes deer population decline and extinction,” PLoS One, vol. 6, no. 5, Article ID e19896, 2011.
[13]
M. W. Miller, E. S. Williams, C. W. McCarty et al., “Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming,” Journal of Wildlife Diseases, vol. 36, no. 4, pp. 676–690, 2000.
[14]
G. Wasserberg, E. E. Osnas, R. E. Rolley, and M. D. Samuel, “Host culling as an adaptive management tool for chronic wasting disease in white-tailed deer: a modelling study,” Journal of Applied Ecology, vol. 46, no. 2, pp. 457–466, 2009.
[15]
A. Sharp and J. Pastor, “Stable limit cycles and the paradox of enrichment in a model of chronic wasting disease,” Ecological Applications, vol. 21, no. 4, pp. 1024–1030, 2011.
[16]
G. Giordano and F. Lutscher, “Predation and harvesting of an age-and sex-structured population,” Journal of Biological Dynamics, vol. 5, no. 6, pp. 600–618, 2011.
[17]
M. Kot, Elements of Mathematical Ecology, Cambridge University Press, 2001.
[18]
J.-M. Gaillard, M. Festa-Bianchet, and N. G. Yoccoz, “Population dynamics of large herbivores: variable recruitment with constant adult survival,” Trends in Ecology and Evolution, vol. 13, no. 2, pp. 58–63, 1998.
[19]
C. Castillo-Chavez and W. Huang, “The logistic equation revisited: the two-sex case,” Mathematical Biosciences, vol. 128, no. 1-2, pp. 299–316, 1995.
[20]
M. R. Miller, A. White, K. Wilson, and M. Boots, “The population dynamical implications of male-biased parasitism in different mating systems,” PLoS One, vol. 2, no. 7, article no. e624, 2007.
[21]
J. M. Heffernan, R. J. Smith, and L. M. Wahl, “Perspectives on the basic reproductive ratio,” Journal of the Royal Society Interface, vol. 2, no. 4, pp. 281–293, 2005.
[22]
J. Li, D. Blakeley, and R. J. Smith?, “The Failure of R0,” Computational and Mathematical Methods in Medicine, vol. 2011, Article ID 527610, 17 pages, 2011.
[23]
J. Carr, Applications of Centre Manifold Theory, Springer, New York, NY, USA, 1981.
[24]
C. Castillo-Chavez and B. Song, “Dynamical models of tuberculosis and their applications,” Mathematical Biosciences and Engineering, vol. 1, no. 2, pp. 361–404, 2004.
[25]
O. Diekmann, J. A. Heesterbeek, and J. A. Metz, “On the definition and the computation of the basic reproduction ratio R0 in models for infectious diseases in heterogeneous populations,” Journal of Mathematical Biology, vol. 28, no. 4, pp. 365–382, 1990.
[26]
P. van den Driessche and J. Watmough, “Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission,” Mathematical Biosciences, vol. 180, pp. 29–48, 2002.
[27]
M. J. Pybus, “Alberta's Chronic Wasting Disease Management Programs in 2006 and upcoming surveillance,” 2010, http://www.srd.alberta.ca/FishWildlife/WildlifeDiseases/ChronicWastingDisease/documents/Alberta2006CWDManagementAndUpcomingSurveillance.pdf.
[28]
J. E. Gross and M. W. Miller, “Chronic wasting disease in mule deer: disease dynamics and control,” Journal of Wildlife Management, vol. 65, no. 2, pp. 205–215, 2001.
[29]
J. Binfet and D. W. Lutz, “Deer and Elk population status and harvest structure in Western North America: a summary of state and provincial status surveys,” in Proceedings of the Western States and Provinces Deer and Elk Workshop, vol. 5, pp. 48–68, 2003, http://www.muledeerworkinggroup.com/Docs/Proceedings/.
[30]
A. N. Hamir, J. A. Richt, J. M. Miller et al., “Experimental transmission of Cchronic Wasting Disease (CWD) of Elk (Cervus elaphus nelsoni), white-tailed Deer (Odocoileus vivginianus), and Mule Deer (Odocoileus hemionus) to white-tailed Deer by intracerebral route,” Veterinary Pathology, vol. 45, no. 3, pp. 297–306, 2008.
[31]
C. W. Clark and D. E. Tait, “Sex-selective harvesting of wildlife populations,” Ecological Modelling, vol. 14, no. 3-4, pp. 251–260, 1982.
[32]
M. M. Conner, J. E. Gross, P. C. Cross, M. R. Ebinger, R. R. Gillies, and M. D. Samuel, “Scale-dependent approaches to modeling spatial epidemiology of chronic wasting disease,” Special Report, 2007, http://www.cwd-info.org/index.php/fuseaction/resources.newresearch.
[33]
S. M. Blower and H. Dowlatabadi, “Sensitivity and uncertainty analysis of complex models of disease transmission: an HIV model, as an example,” International Statistics Review, vol. 62, no. 2, pp. 229–243, 1994.
[34]
J. M. Gaillard, M. Festa-Bianchet, and N. G. Yoccoz, “Population dynamics of large herbivores: variable recruitment with constant adult survival,” Trends in Ecology and Evolution, vol. 13, no. 2, pp. 58–63, 1998.
[35]
J. O. Lloyd-Smith, P. C. Cross, C. J. Briggs et al., “Should we expect population thresholds for wildlife disease?” Trends in Ecology and Evolution, vol. 20, no. 9, pp. 511–519, 2005.
[36]
M. M. Conner, M. R. Ebinger, J. A. Blanchong, and P. C. Cross, “Infectious disease in cervids of North America,” Annals of the New York Academy of Sciences, vol. 1134, pp. 146–172, 2008.
[37]
M. Begon, M. Bennett, R. G. Bowers, N. P. French, S. M. Hazel, and J. Turner, “A clarification of transmission terms in host-microparasite models: numbers, densities and areas,” Epidemiology and Infection, vol. 129, no. 1, pp. 147–153, 2002.
[38]
T. J. Habib, E. H. Merrill, M. J. Pybus, and D. W. Coltman, “Modelling landscape effects on density-contact rate relationships of deer in eastern Alberta: implications for chronic wasting disease,” Ecological Modelling, vol. 222, no. 15, pp. 2722–2732, 2011.