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Disease Transmission
Transmission Modes

Transmission Modes

Disease transmission is typically modeled using functional forms reflecting assumptions of whether the transmission modes are density dependent (DD), frequency dependent (FD) or intermediate. In density dependent disease transmission contact rates increase as density increases, therefore disease transmission also increases. Frequency dependent disease transmission occurs when there is no relationship between contact rates (or transmission events) and density of a population. Intermediate transmission modes can occur when environmental transmission or time lags due to the long progression and slow signs of CWD can lead to non-linearities.

Introduction

Epidemiological models of CWD transmission in deer demonstrate that observed patterns of prevalence are best described by frequency-dependent transmission, although density dependent or intermediate transmission may still be occurring [5,6,9,10,11,18]. Frequency dependence, where the per capita infection rate is independent of host density, changes linearly with disease prevalence rather than with the density of infected animals [8]. Frequency dependence likely arises because contact among deer are limited by patterns of social interactions and seasonal movements [3,5,6,9,11,13,14]. Female white-tailed deer in the mid-western and eastern United States are highly philopatric and maintain matrilineal groups formed by female offspring that remain close to their mothers’ home ranges [2,12]. Elevated risk of transmission arises from familial interactions within these groups or by environmental contamination from overlapping home ranges [4,6,7,11,14-17]. These associations also constrain between-group social interactions, leading to contact rates independent of population density [14]. Density dependent transmission, where the per capita infection rate changes linearly with the density of infected animals [7], could still be occurring depending on the spatial scale [1,16], population density [16], or season [10,11] when disease transmission occurs.

Literature Cited

1. Almberg ES, Cross PC, Johnson CJ, Heisey DM, Richards BJ. Modeling routes of chronic wasting disease transmission: environmental prion persistence promotes deer population decline and extinction. PLOS ONE. 2011 May;6(5):e19896.

2. Cullingham CI, Merrill EH, Pybus MJ, Bollinger TK, Wilson GA, Coltman DW. Broad and fine‐scale genetic analysis of white‐tailed deer populations: estimating the relative risk of chronic wasting disease spread. Evolutionary Applications. 2010;4(1):116–31.

3. Grear DA, Luong LT, Hudson PJ. Network transmission inference: Host behavior and parasite life cycle make social networks meaningful in disease ecology. Ecological Applications. 2013;23(8):1906–14.

4. Grear DA, Samuel MD, Scribner KT, Weckworth BV, Langenberg JA. Influence of genetic relatedness and spatial proximity on chronic wasting disease infection among female white-tailed deer. Journal of Applied Ecology. 2010;47(3):532–540.

5. Gross JE, Miller MW. Chronic wasting disease in mule deer: Disease dynamics and control. The Journal of Wildlife Management. 2001;65(2):205–215.

6. Jennelle CS, Henaux V, Wasserberg G, Thiagarajan B, Rolley RE, Samuel MD. Transmission of chronic wasting disease in Wisconsin white-tailed deer: implications for disease spread and management. PLOS ONE. 2014 Mar;9(3):e91043.

7. Magle SB, Kardash LH, Rothrock AO, Chamberlin JC, Mathews NE. Movements and habitat interactions of white-tailed deer: implications for chronic wasting disease management. The American Midland Naturalist. 2015 Apr 1;173(2):267–82.

8. McCallum H, Barlow N, Hone J. How should pathogen transmission be modelled? Trends in Ecology & Evolution. 2001 Jun;16(6):295–300.

9. Miller MW, Hobbs NT, Tavener SJ. Dynamics of prion disease transmission in mule deer. Ecological Applications. 2006;16(6):2208–2214.

10. Oraby T, Vasilyeva O, Krewski D, Lutscher F. Modeling seasonal behavior changes and disease transmission with application to chronic wasting disease. Journal of Theoretical Biology. 2014 Jan 7;340:50–9.

11. Potapov A, Merrill E, Pybus M, Coltman D, Lewis MA. Chronic wasting disease: possible transmission mechanisms in deer. Ecological Modelling. 2013 Feb 10;250:244–57.

12. Porter WF, Mathews NE, Underwood HB, Sage RW, Behrend DF. Social organization in deer: implications for localized management. Environmental Management. 1991 Nov 1;15(6):809–14.

13. Samuel MD, Storm DJ. Chronic wasting disease in white-tailed deer: infection, mortality, and implications for heterogeneous transmission. Ecology. 2016 Nov;97(11):3195–3205.

14. Schauber EM, Nielsen CK, Kjaer LJ, Anderson CW, Storm DJ. Social affiliation and contact patterns among white-tailed deer in disparate landscapes: implications for disease transmission. J Mammal. 2015 Feb;96(1):16–28.

15. Silbernagel ER, Skelton NK, Waldner CL, Boolinger TK. Interaction among deer in a chronic wasting disease endemic zone. The Journal of Wildlife Management. 2011;75(6):1453–61.

16. Storm DJ, Samuel MD, Rolley RE, Shelton P, Keuler NS, Richards BJ, et al. Deer density and disease prevalence influence transmission of chronic wasting disease in white-tailed deer. Ecosphere. 2013;4(1):1–14.

17. Tosa MI, Schauber EM, Nielsen CK. Localized removal affects white‐tailed deer space use and contacts. The Journal of Wildlife Management. 2016 Sep 30;81(1):26–37.

18. Wasserberg G, Osnas EE, Rolley RE, Samuel MD. Host culling as an adaptive management tool for chronic wasting disease in white-tailed deer: A modelling study. Journal of Applied Ecology. 2009;46(2):457–466.

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