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The following is a partial list of scientific evidence that suggests that baiting and feeding of wild deer
elevates the risk of CWD transmission. This list focuses almost entirely on disease risks posed by CWD
although other diseases ( Bovine Tuberculosis is an example) may pose even greater risks.
Complete literature citations are included at the end of the document for those who want to read the
original scientific articles.
Timothy R. Van Deelen, Ph.D. - Wildlife Ecology
Wisconsin Department of Natural Resources
• CWD is transmitted laterally (live diseased deer infect other deer)
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prevalences in free-living deer (Miller et al. 2000, Gross and Miller 2001, M. W. Miller unpublished in
Williams et al. 2002). These studies suggest that observed prevalences and rates of spread of CWD in
real populations could not occur without lateral transmission. For example, maternal transmission (doe to
fawn) if it occurs, is rare and cannot explain most cases where epidemiologic data are available( Miller et
al. 1998, 2000). Similarly, indirect lateral transmission (e.g. from a contaminated environment) may
require unusually high levels of contamination (see below; Williams et al. 2002). Nonetheless, emerging
research from Colorado suggests that indirect lateral transmission from environmental contamination
appears to play a role in sustained and recurrent epidemics (Miller 2002).
• Deer can get CWD by ingesting something contaminated with the disease prion
Six mule deer fawns were fed a daily dose of 2g (0.07 ounces) of brain tissue from CWD-positive
mule deer in a tightly controlled experiment for 5 days. Another three were fed the same doses using
brain tissue from CWD-negative mule deer. All deer were held separately in indoor pens that had never
before held deer. The fawns were then killed and necropsied at specific intervals 10 to 80 days postinoculation.
At 42 days and later post inoculation, all fawns dosed with CWD-positive tissue tested
positive for CWD prions in lymph tissues associated with their digestive tracts (Sigurdson et al. 1999).
Other transmissible spongiform encephalopathies (TSEs); Kuru, transmissible mink encephalopathy,
bovine spongiform encephalopathy (BSE]) appear to be transmitted through ingestion of prion-infected
tissue as well (Weissmann et al. 2002). Due to the human health crisis associated with eating BSE3
infected beef in Europe, many other researchers working with TSEs, including CWD (Sigurdson et al
1999, 2001), have traced the movements of infectious prions of orally-infected animals through the lymph
tissue embedded in the intestinal lining, into nervous tissues associated with the digestive tract (Maignien
et al 1999, Beekes and McBride 2000, Heggebo et al. 2000, Huang et al. 2002) and eventually to the brain
via the nervous system (Sigurdson et al. 2001, Weissmann et al. 2002). Experimental studies using
hamsters have shown that prions can infect through minor wounds in the skin (Taylor et al. 1996) and that
infection through minor wounds on the tongue was more efficient than infection from ingestion (Bartz et
al. 2003). These studies not only demonstrate that an oral route of infection is possible, but are beginning
to provide specific details about the pathways involved in the movement of infectious prions into the
central nervous system and other organs (Weissmann et al. 2002).
• CWD prions may be shed in feces and saliva
Following oral exposure, prions associated with many TSEs (Maignien et al 1999, Huang et al.
2002) including CWD (Sigurdson et al. 1999; Miller and Williams 2002 and Spraker et al. 2002 cited in
Williams et al. 2002) both accumulate and replicate in the lymph tissues associated with the
gastrointestinal tract – particularly in lymph tissues in contact with the mucosa lining the inside of the
intestines (e.g. Peyer’s patches, Weismann et al. 2002). In infected deer, CWD prions also accumulate in
the pancreas and various other glands of the endocrine system (Sigurdson et al 2001). Experiments with
hamsters demonstrated that infectious prions can travel from the brain to the tongue along tongueassociated
cranial nerves (Bartz et al. 2003). During digestion, the liver, pancreas, intestinal mucosa, and
other glands secrete chemicals needed for digestion (Robbins 1983) and cells lining the inner surface of
the intestine continuously die and slough off providing potential physical mechanisms for prion shedding
into the intestines (others are likely). This is evidence that infectious prions are likely shed in the feces
and saliva (Sigurdson et al. 1999).
• Disease course and symptoms indicate high potential for transmission where deer are
concentrated
Appearance of CWD symptoms in an infected deer lags initial exposure by a variable time period
on the order of roughly 12 months to 24 months or more (E. S. Williams and M. W. Miller unpublished;
E. S. Williams, M. W. Miller, and T. J. Kreeger unpublished; cited in Williams et al. 2002). Once clinical
symptoms are observed, deer enter a symptomatic phase that may last on average 1 month to 4 months
before they invariably die (Williams et al. 2002). Symptoms are initially subtle but eventually include
behaviors likely to contaminate a site with bodily fluids (e.g. excess urination, excess salivation including
drooling and slobbering, and uncontrollable regurgitation, Williams et al. 2002). Deposition of feces
increases with concentration of deer activity. This is both obvious and intuitive and pellet group counts
have been used as an index of deer density since the 1940s (Bennet et al. 1940). During winter, northern
deer defecate about 22 times a day (Rogers 1987). At least one study (Shaked et al. 2001) has reported
detection of an altered form of the infectious prion in the urine of hamsters, cattle, and humans with
TSEs. This altered form, while not as virulent, produced subclinical prion infections following
experimental inoculation. Shedding of infectious prions is likely progressive during the course of disease
from infection to death (Williams et al. 2002). Replication and presence of infectious prions in gutassociated
lymph tissue early in the incubation (Sigurdson et al. 1999, Weismann et al. 2002) and
epidemiological modeling (M. W. Miller unpublished cited in Williams et al. 2002) suggest that shedding
precedes the onset of symptoms in both elk and mule deer.
In this regard, Garner (2001) documented a particularly alarming behavior among deer using
frozen feed piles. Deer used the heat from their mouths and nostrils to thaw and dislodge food such that
frozen feed piles were dented with burrows made from deer noses. He reported that “Throughout the
winter multiple numbers of deer were observed working in and around the same feed piles. I suspect that
each deer that feeds this way at a frozen feed pile leaves much of its own saliva and nasal droppings in the
field pile at which its working”(Garner 2001, p. 46).
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• Evidence from captive situations indicates that deer can get CWD from highly contaminated
environments.
In addition to direct lateral transmission, researchers suspect that deer can be infected indirectly
from contaminated environments. Contaminated pastures “appear to have served as sources in some
CWD epidemics although these observations are anecdotal and not yet corroborated by controlled
studies” (Miller et al 1998; M. W. Miller unpublished; E. S. Williams, W. E. Cook, and T. J. Kreeger
unpublished; cited in Williams et al 2002). The potential for transmission from the environment is a
function of the degree of contamination and the resistance of disease prions to chemical breakdown
(Williams et al 2001, 2002). Consequently, the highest prevalences recorded for CWD outbreaks have
been in captive situations (Williams and Young 1980; Williams et al. 2002) where because of abnormal
concentration, indirect and direct transmission likely occur together (Williams et al. 2002). At high
concentration, the persistence of the CWD prion in contaminated environments, may be a serious obstacle
to disease eradication (Williams et al. 2002).
• Baiting and Feeding causes unnatural concentration of deer
People use baiting and feeding to concentrate deer for enhanced hunter opportunity or viewing.
In northern deer, seasonal concentration in deeryards is a well-known phenomenon (Blouch 1984).
However, the potential for close animal-to-animal contact over a feed pile is fundamentally different than
the contact yarded deer experience while foraging on natural food. In deeryards, deer eat a variety of
woody browse plants and arboreal lichens (Blouch 1984) scattered across a large area. In terms of
biomass and nutrition, the best source of browse and lichens may be litter-fall rather than live plant
material growing in the understory (Ditchkoff and Servello 1998). Food sources in deeryards (litter and
understory plants) are widely distributed over a large area and they are not replaced. Moreover, browse is
typically held aloft on the plant stem such that fecal contamination is less likely. Foraging by wintering
deer is an optimization process. Energy gains associated with eating need to be balanced against energy
costs associated with travel and exposure (Moen 1976). Yarded deer with little or no access to
supplemental food maintain relatively large overlapping home ranges (e.g. 110 acres in Minnesota
[Nelson and Mech 1981], 480 acres in Michigan [Van Deelen 1995], 318 acres in Quebec [Lesage et al.
2000]) suggesting that foraging widely on a diffuse food source is normal. Garner (2001) monitored 160
radio-collared deer for 2 fall/winter periods in northern Michigan and documented their behavior over
feeding sites using both telemetry and direct observations. He demonstrated that, relative to natural
forage, supplemental feeding caused reduced home range sizes, increased overlap of home ranges in
space and time and dramatic concentrations of activity around feeding sites.
• Reduction of contact through a ban on baiting and feeding is likely very important to
eradicating or containing a CWD outbreak.
Epidemiological models fit to real-world data on CWD outbreaks in mule deer predict that local
extinction of infected deer populations is likely (Gross and Miller 2001). The predicted outcomes of
these models are highly sensitive to input estimates of the amount of contact between infected and
susceptible deer meaning that small reductions in contact rates can dramatically reduce the rate at which
prevalence changes during an epidemic (Gross and Miller 2001). Garner (2001) demonstrated that
baiting and feeding was associated with deer concentration, extensive face-to-face contacts, and
increasing overlap of deer home ranges. White-tailed deer have contacts from social and grooming
behaviors apart from contact over baiting and feeding sites (Marchinton and Hirth 1984) but social groups
of whitetails tend to be small during most of the year (4 to 6 individuals, Hawkins and Klimstra 1970).
Whitetail physiology and behavior are adapted to selective foraging on nutritious plants (Putman 1988).
Moreover, social groups tend to exclude one another by using different areas or by using shared areas at
different times (Mathews 1989, Porter et al. 1991). Concentration of deer activity over feeding sites
increase both direct and indirect contact between groups by increasing home range and core area overlap
and by increasing the amount of time that unrelated deer feed in close proximity to each other (Garner
2001).
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Eliminating these contacts has added significance because CWD is a uniquely difficult disease to
manage and study. There is no treatment and no vaccine. Moreover CWD is difficult to track in a
population because of long incubation periods, subtle early clinical sign, a resistant infectious agent,
potential for environmental contamination and incomplete understanding of transmission mechanisms.
These characteristics make prevention critically important (Williams et al. 2002).
• Baiting and feeding continues to put Wisconsin’s deer herd at risk to other serious diseases
CWD is not the only infectious disease that threatens Wisconsin’s deer herd. One, Bovine Tuberculosis
(TB) warrants special attention because the link to baiting and feeding is clear. TB is an infectious
bacterial disease that is spread from animal to animal through inhalation of infectious aerosols or
ingestion of other infectious body fluids (e.g. saliva). Tuberculosis bacteria can live outside of an animal
for as long as 16 weeks on a frozen feed pile (Whipple and Palmer 2000 cited in Garner 2001) and Garner
(2001) demonstrated that supplemental food increased close contact among wild deer through a number
of mechanisms. Garner (2001) also demonstrated extensive home range overlap between a TB-positive
deer and 15 other radio-collared deer in northern Michigan. Recent epidemiological research suggests
that baiting and feeding of deer enable the TB outbreak in Michigan to persist and spread and that
declines in TB prevalence were associated with a ban on baiting and feeding (O’Brien et al. 2002).
Current attention is focused on the CWD outbreak in southwestern Wisconsin. However, should
CWD or other infectious disease show up elsewhere, baiting and feeding are likely to facilitate or enhance
an epidemic. Tuberculosis has been confirmed on six captive game farms in Wisconsin and the presence
of over 800 captive cervid farms statewide suggests that the disease risks associated with baiting and
feeding are not confined to the known CWD-infected area of southern Wisconsin.
• What do the experts say relative to artificial feeding and CWD and disease transmission?
A discussion of CWD in a review of the scientific literature on captive deer done for The Wildlife
Society (Professional society for wildlife biologists, managers, and researchers; publisher of three
premier peer-reviewed scientific journals on wildlife ecology and management)...
“Concentration of deer and elk in captivity or in the wild by artificial feeding may increase the likelihood
of transmission between individuals.” (DeMarais et al. 2002, p. 6).
In a review of the technical literature on CWD by the top CWD specialists in the world...
“Concentrating deer and elk in captivity or by artificial feed probably increases the likelihood of direct
and indirect transmission between individuals. Transmission via contact between susceptible and
infectious individuals probably requires more than just transient exposure. Thus, minimal fence-line
exposure does not pose excessive risk of transmission; however, prolonged fence-line contact increases
the possibility of transmission” (Williams et al. 2002, p.557).
In a peer-reviewed paper on the epidemiology of Bovine TB by the team of veterinarians,
epidemiologists, and wildlife researchers working to contain the outbreak in Michigan...
“Previous qualitative examinations of the origins of tested deer already suggested that TB positive
animals were more likely to come from the core area. Our new analysis quantifies that risk. The high
risk associated with the core coincides with an area of historically prevalent and intensive baiting and
supplemental feeding of deer – practices that were likely crucial to the establishment of self-sustaining
TB in the deer population” (O’Brein et al. 2002 and citations within).
In oral presentations given to the Texas chapter of the Society of Range Management (Oct. 6 2000)
and to the Southeaster Deer Study Group (Feb. 19 2001) by Dr. Robert D. Brown, Professor and
Head of the Department of Wildlife and Fisheries Sciences at Texas A&M University,
Internationally recognized expert on deer and deer nutrition...
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“One of the major points of this paper is the concern over transmission of disease. It amazes me that we
have not done more studies in Texas on disease transmission at food plots and deer feeders, whether they
be for supplementing the deer or for baiting. We know that in 1994 tuberculosis (TB) was first detected
in wild deer in Michigan. It is now in a 5-county area, and has spread to carnivores and dairy herds”...”In
Wyoming and around Yellowstone Park, brucellosis is wide spread among cattle, elk, and bison, the latter
two species being concentrated on feeding grounds in the winter. Likewise, Chronic Wasting Disease
(CWD) has now been observed in free-ranging elk and mule deer in several western states. Since CWD
is passed animal to animal, concentrations caused by supplemental feeding is believed to increase the
spread of the disease” (Brown Unpublished).
In a report issued by a panel of internationally recognized wildlife disease experts who reviewed
Colorado’s CWD management program...
“Regulations preventing...feeding and baiting of cervids should be continued” (Peterson et al. 2002).
In a comprehensive review of the ecological and human social effects of artificial feeding and
baiting of wildlife prepared by the Canadian Cooperative Wildlife Health Centre, Department of
Veterinary Pathology, University of Saskatchewan...
“Significant ecological effects of providing food to wildlife have been documented through observation
and experimentation at the individual, population, and community levels. The increased potential for
disease transmission and outbreak is perhaps of greatest and immediate concern; recent outbreaks of
bovine tuberculosis and chronic wasting disease in Canada and the United States giving credence to this
point. Nevertheless, even if disease is prevented, other significant ecological concerns exist” (Dunkley
and Cattet 2003, p. 22).
Review
To insure that this document accurately reflects the scientific knowledge of prion disease, CWD, and deer
biology, this document was reviewed by the following specialists (position and expertise follows each
name):
• Judd Aiken Ph.D. (Professor of animal health and biomedical sciences, UW-Madison; prion diseases)
• Valerius Geist Ph.D (Professor Emeritus, Department of Environmental Science, University of
Calgary; ecology behavior and management of deer)
• Julia Langenberg DVM (Wildlife Veterinarian, Wisconsin DNR; CWD, wildlife diseases)
• Nohra Mateus-Pinilla DVM, Ph.D. (Research Epidemiologist, Illinois Natural History Survey,
University of Illinois; wildlife diseases, epidemiology)
• Nancy Mathews Ph.D. (Assoc. Professor of wildlife ecology, UW-Madison; deer ecology and
behavior)
• Keith McCaffery M.S. (Deer specialist, Wisconsin DNR, retired; deer ecology and management)
• Robert Rolley Ph.D. (Population Ecologist, Wisconsin DNR; population dynamics, deer
management)
 

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“One of the major points of this paper is the concern over transmission of disease. It amazes me that we have not done more studies in Texas on disease transmission at food plots and deer feeders, whether they be for supplementing the deer or for baiting. We know that in 1994 tuberculosis (TB) was first detected in wild deer in Michigan. It is now in a 5-county area, and has spread to carnivores and dairy herds”...”In
Wyoming and around Yellowstone Park, brucellosis is wide spread among cattle, elk, and bison, the latter two species being concentrated on feeding grounds in the winter. Likewise, Chronic Wasting Disease (CWD) has now been observed in free-ranging elk and mule deer in several western states. Since CWD is passed animal to animal, concentrations caused by supplemental feeding is believed to increase the
spread of the disease” (Brown Unpublished). In a report issued by a panel of internationally recognized wildlife disease experts who reviewed Colorado’s CWD management program... “Regulations preventing...feeding and baiting of cervids should be continued” (Peterson et al. 2002). In a comprehensive review of the ecological and human social effects of artificial feeding and baiting of wildlife prepared by the Canadian Cooperative Wildlife Health Centre, Department of Veterinary Pathology, University of Saskatchewan... “Significant ecological effects of providing food to wildlife have been documented through observation and experimentation at the individual, population, and community levels. The increased potential for disease transmission and outbreak is perhaps of greatest and immediate concern; recent outbreaks of bovine tuberculosis and chronic wasting disease in Canada and the United States giving credence to this
point. Nevertheless, even if disease is prevented, other significant ecological concerns exist”

I agree. Both food plots and baitng should be treated equally in dieases transmition but both WI and MI only banned baiting thuse even further privatizing the hered to private land owners.
 

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Rancid,

The DNR Director banned both baiting and feeding. I am sure food plots will have some restrictions coming down in the future as well.
 

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I agree. I dont forsee a ban on bait plots but like other things, the government can regulate it to death to make it more hassle than it's worth.
 
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