Time Course/Persistence of Disease in a Susceptible Population

• CWD is both contagious and self-sustaining in both captive and free-living deer and elk populations in North America.
• The course of CWD within a population may be best described as an extended epidemic with a time scale of years (for confined populations) to decades or longer for free-living populations.
• Historically, natural expansion of CWD within free-living cervid populations appears to have been slow, and has probably been due mainly to dispersal and/or migratory movements of wild populations. 
• During 2002 CWD was detected in free-living populations in several areas in which it had not previously been recorded. It is not known whether the new areas have become infected due to natural movements of free-living cervids or as an expansion from the disease in captive populations or whether there are other unknown factors; some cases (e.g. in Saskatchewan) are considered highly likely to be extensions from the disease in captive cervids.
• Data from 2002 to 2003 from Colorado and Wyoming suggests the possibility of more rapid movement out of the core endemic areas to distant locations.
• In captive cervids within-herd spread of the disease is likely to be faster than in free-living populations, due to the greater density of animals and the associated increased opportunities for disease transmission by both direct and indirect transmission routes.
• Within the larger captive population, the epidemic is likely to be driven by between-herd movements of (undiagnosed) infected cervids.

Limited data on other TSE diseases is provided in literature reports below the information on CWD. Information on these diseases within the "Chronic Wasting Disease of Deer and Elk" volume of Wildpro is provided for comparative purposes and is not intended to be comprehensive.

• Onset occurs in any season. (J1.16.w10)
• Comparison of the original and later epidemic in the elk herds at one Colorado wildlife research facility found that: in both epidemics the first case occurred about three years after the herd was established, in both cases the next cases occurred two to three years after the first case and subsequent cases two to two and a half years later. (J1.34.w6)
• In captive wildlife research facilities in Colorado and Wyoming, detection of CWD in elk followed detection in mule deer by about two years. It was suggested that, if the incubation period in the two species is taken to be similar, then the mule deer transmitted the disease to the elk. (J64.11.w3)
• "CWD appears to be an emerging TSE of local [Colorado and Wyoming] and potentially broader importance." It appears that endemic CWD can be sustained in free-ranging cervid populations for decades. Epidemiological models "suggest that endemic CWD may be more properly viewed as an epidemic with a protracted time scale." It was noted that "as modelled, CWD epidemics are self-limiting because they drive affected populations to extinction." Data available and models run suggest that more intensive transmission may occur under confined conditions (i.e. captive animals) than in wild, free-ranging populations. (J1.36.w4)
• In Saskatchewan, Canada, where 39 premises (elk farms) were found to be infected in 2000-2001, it was possible to link all the farms epidemiologically, by movement of live elk between farms, to one farm which was believed to have imported infected elk from the USA. Wild mule deer found to be infected came from the vicinity of infected captive elk herds. (W43.10Apr03.CWD4)
• "Researchers who have studied CWD epidemics in both captive and free-ranging deer populations have determined that CWD is both contagious and self-sustaining (meaning that new infections occur fast enough for CWD to persist or increase over time despite the more rapid deaths of the diseased individuals; Miller et al. 1998, 2000). Supporting evidence comes from observational data (Williams and Young 1992; Miller et al. 1998, 2000) experimental data, and epidemiological models fit to observed prevalences in free-living deer (Miller et al. 2000, Gross and Miller 2001, M. W. Miller unpubl. cited in Williams et al. 2002a)." (D109.w7)
• To date, while the natural rate of expansion in free-ranging cervid populations has been slow, it appears that the disease has been spread much more widely by the movement of infected farmed elk. In at least three areas (west-central Saskatchewan, northwest Nebraska and southwest South Dakota) it is possible that an elk farm infected with CWD may have acted as a source of infection for the local populations of free-ranging cervids. (J40.66.w1)
• Natural spread has probably been due to dispersal and/or migratory movements for wild cervids from infected to uninfected subpopulations. In northeastern Colorado it appears from field data that "seasonal migration patterns may be most influential in at least one area." Observed geographic differences in the current prevalence of CWD among populations of free-ranging cervids support models of diffusion-type spread along natural migration corridors; such differences may be useful for estimation of rates of natural spread. (P40.1.w12)
• During 2001-20022 CWD was detected in several areas in which it had not previously been reported:
  • In Wisconsin (in wild white-tailed deer harvested 2001); (P40.1.w8, J40.66.w1, W27.09Mar02.cwd1)
  • In Minnesota (in a captive elk in August 2002); (W414.10Apr03.CWD4)
  • In Illinois (in wild deer; first case detected in a deer shot October 2002). (W27.02Nov02.cwd1, W411.11Apr03.CWD1)
• "In some local areas prevalence appears to be increasing at a more rapid rate than in the past, although it is not clear whether or not this is because of increased incidence or increased surveillance, reporting, and testing." (W414.10Apr03.CWD1)
• "The highest prevalence rates of CWD in Colorado have been found in wild and captive situations where deer densities were high and there was frequent congregation over artificially provided food sources such as in dense populations (M. Miller, pers. comm.)." (D109.w7)
• Data from 2002 and 2003 from Colorado and Wyoming show the presence of CWD-positive cervids some distance from the core endemic areas: as much as 100 miles from the established CWD areas. (W402.06Jan04.CWD1, W402.06Jan04.CWD2, W402.06Jan04.CWD3, W425.06Jan04.CWD2, V.w49)

Other TSE Diseases

Transmissible Mink Encephalopathy

Mustela vison - American mink:

• Animals were affected over a period of four months in 1947, nearly eight months in 1963 [no data given for 1961]. Data from three epizootics on eight or nine mink farms in Wisconsin, USA in 1947, 1961 and 1963. (J100.115.w1)
• USA: Ontario 1963. Animals were first affected in late May and continuing through the summer with one or two animals dying each week. (J14.9.w1)
• About five months. (J223.72.w1)

Scrapie:

• In many areas of the world scrapie is endemic. (W31.29Mar03.w5)

Bovine Spongiform Encephalopathy (BSE):

• This disease does not occur as an epizootic within individual herds. Epidemiological studies indicate an extended common-source epidemic for the disease in cattle in Britain. (B207)

Creutzfeldt-Jakob Disease (CJD):

• Cases of sporadic CJD occur randomly in populations worldwide. (J248.4.w1)

New variant Creutzfeldt-Jakob Disease (nvCJD):

• Onset of disease in the first cases occurred in 1994. (J98.347.w1)
• Data to the end of 2002, based on known deaths from nvCJD suggest that, at least for the codon 129 methionine/methionine homozygotes, the only genotype in which cases are known to have occurred, the epidemic has peaked. The greatest number of deaths occurred in 2000 with a decline in number of deaths during 2001 and 2002. The "best estimate" based on this data is for an additional 40 deaths, with an upper limit of 95% prediction internal of 540 cases. Using, in addition, data from testing of tissue from appendixes removed 1995-1999, in which one appendix positive for nvCJD was found out of 8318 tested, and assuming that the positive individual was homozygous for methionine and would go on to develop clinical nvCJD, would give a "best estimate" of 100 cases and an upper limit of 95% prediction internal of 2,600 cases. It was noted that, due to the absence, to date, of clinical cases in individuals with other genotypes (valine homozygotes, or heterozygotes), it was not possible to make any predictions regarding possible future cases in these genotypes. (J254.3.w1)

Kuru:

• The height of the epidemic occurred in the 1950s, with cases decreasing from the late 1950s or early 1960s onwards, since transmission ceased with the cessation of ritual cannibalism in about 1956. (B292.6.w6, J22.197.w1)
• Occasional cases still occur [2001 data]. (J246.24.w1)