Whitetail Deer Hunting Gain a better understanding of the World's most popular big game animal and the techniques that will help you become a better deer hunter.


Old 12-11-2003, 08:20 AM
Thread Starter
Join Date: Feb 2003
Posts: 27,585
Default [Deleted]

[Deleted by Admins]
Deleted User is offline  
Old 12-11-2003, 08:24 AM
Join Date: Oct 2003
Location: Georgia
Posts: 2,032
Default RE: CWD Map

good post, lets keep it out of the southeast, looks like it is mainly in midwest
trophyhuntr is offline  
Old 12-11-2003, 08:53 AM
Join Date: Feb 2003
Location: CWD Central, WI.
Posts: 2,062
Default RE: CWD Map

good post, lets keep it out of the southeast, looks like it is mainly in midwest
Exactly how many deer has Georgia tested?
nub is offline  
Old 12-11-2003, 09:34 AM
Nontypical Buck
Strut&Rut's Avatar
Join Date: Feb 2003
Location: SW Michigan
Posts: 1,905
Default RE: CWD Map

The major concern when it reached Wisconsin and Illinois was the Mississippi River barrier.

Researches and biologists for years postulated that the disease would never spread across the Mississippi, it represented too large a natural barrier, even at its headwaters.

Guess they were wrong...

Strut&Rut is offline  
Old 12-11-2003, 11:00 AM
Join Date: Feb 2003
Location: CWD Central, WI.
Posts: 2,062
Default RE: CWD Map

Too bad they didn't have the foresight to realize it would just drive across the bridge.
nub is offline  
Old 12-11-2003, 04:45 PM
Fork Horn
Join Date: Dec 2003
Location: Wisconsin
Posts: 227
Default RE: CWD Map

it took a few thousand tests in a very small area to find first three in wi so dont count it out anywhere.
rcw280 is offline  
Old 12-11-2003, 08:33 PM
Typical Buck
Hawgnman's Avatar
Join Date: Oct 2003
Location: NC
Posts: 845
Default RE: CWD Map

On a positive note, I was surprised at the limited amount of infection in the wild.
Hawgnman is offline  
Old 12-14-2003, 03:27 PM
Fork Horn
Join Date: Dec 2003
Location: Wisconsin
Posts: 227
Default RE: CWD Map

we dont know that it is limited there has not been alot of very concentrated testing any where else other than south central WI on the wild deer
rcw280 is offline  
Old 12-15-2003, 08:21 AM
Join Date: Dec 2003
Location: http://www.vegsource.com/talk/madcow/index.html
Posts: 23
Default RE: CWD Map



INTRODUCTION. The transmissible spongiform
encephalopathies (TSEs) comprise an unusual group of
neurologic diseases of humans and animals. They are
apparently caused by proteinaceous agents called pri-
ons that are devoid of nucleic acids (Prusiner 1982).
Although debate continues (Chesebro 1998; Farquhar
et al. 1998), there is now a great deal of evidence sup-
porting the hypothesis that TSEs are caused by abnor-
mal, protease-resistant forms (PrPres) of cellular pro-
teins (PrPc) coded for and normally synthesized in
central nervous system (CNS) and lymphoid tissues
(Prusiner 1991). It is thought that these abnormal pro-
teins arise through posttranslational modifications in
tertiary structure of PrPc, resulting in decreased a-heli-
cal content and increased amounts of p-sheet (Prusiner
1997). In humans, PrPres may arise sporadically through
somatic mutations or spontaneous conversion of PrPc to
PrPres as a result of germline mutations in the PrP gene
resulting in familial disease; or they may be acquired
by infection (Prusiner 1997). In animals, TSEs are
infectious; spontaneous and familial forms have not
been identified, though they may occur.

On entering a susceptible host by some natural or
experimental process, PrPres promotes production of
species-specific PrPres from PrPc in lymphoid and CNS
tissues. The finding that PrPres catalyzes production of
PrPres from PrPc in vitro added weight to the hypothesis
that this is its mode of action in vivo (Kocisko et al.
1994; Raymond et al. 1997).

Thus, although the TSEs behave like infectious dis-
eases, the agents appear to have no inherent genetic
identity, and if this is so, the disease is more correctly
perceived and classified as a special type of toxicity.
Prions have remarkable resistance to environmental
conditions and a range of treatments that typically kill
or inactivate conventional infectious agents (Millison et
al. 1976; Taylor et al. 1995).

Prior to 1980, naturally occurring TSEs had been
reported in four species: scrapie in domestic sheep Ovis
aries and goats Capra hircus (Dickinson 1976); trans-
missible mink encephalopathy (TME) in mink Mustela
vison (Hartsough and Burger 1965); and kuru,
Creutzfeldt-Jakob disease (CJD), and Gerstmann-
Straussler-Scheinker syndrome of humans (Prusiner
and Hadlow 1979; Collnge and Palmer 1997). More
recently, chronic wasting disease (CWD) was reported
in deer Odocoileus spp. and Rocky Mountain elk
Cervus elaphus nelsoni in the United States (Williams
and Young 1980, 1982). Bovine spongiform
encephalopathy (BSE) was diagnosed in cattle Bos tau-
rus (Wells et al. 1987), in domestic cats Felis catus
(Pearson et al. 1992), and in wild mammals in or from
Great Britain (Jeffrey and Wells 1988; Kirkwood and
Cunningham 1994a) or in France (Bons et al. 1996,
1999). Bovine spongiform encephalopathy was associ-
ated with a variant of CJD (vCJD) in a few humans
beginning in 1996 (Will et al. 1996).

A disease indistinguishable from scrapie occurred In
mouflon Ovis musimon in the United Kingdom (Wood
et al. 1992). In addition, several suspect cases of TSE
were reported in albino tigers Panthera tigris (Kelly et
al. 1980) and ostriches Struthio camelus (Schoon et al.
1991), but these were not confirmed and probably were
not prion diseases.

Recent studies draw somewhat conflicting conclu-
sions about the pathogenesis of the TSEs. In part, this
may be due to variation in the different agents, differ-
ent doses and routes of exposure, and different animal
models used to study these diseases; natural hosts are
seldom employed in these studies.

Substantial evidence exists for genetic variation in
susceptibility to some prion diseases among and within
species. For example, there are differences in suscepti-
bility to scrapie among breeds of sheep (Hunter et al.
1992; O'Rourke et al. 1997b) and differences in incu-
bation period associated with genotype in mice (Bruce
et al. 1994). Genetic variation in susceptibility to spo-
radic and iatrogenic prion disease in humans is recog-
nized (Collnge and Palmer 1994). In contrast, there is
no evidence for variation in susceptibility to BSE
among cattle (Wilesmith 1994).

Studies of the pathogenesis of scrapie after intragas-
tric inoculation of mice suggested neural spread of the
agent from the gastrointestinal tract to thoracic spinal
cord via the sympathetic nervous system (Kimberlin
and Walker 1989). In hamsters orally infected with
scrapie, the route to the CNS was hypothesized to be
the vagus nerve to the parasympathetic vagal nucleus
(dorsal motor nucleus of the vagus) in the medulla
oblongata, the initial site of detection of PrPres in the
CNS (Beekes et al. 1998). Evidence of infectivity in
cattle orally infected with large doses of BSE agent was
found first in the CNS in thoracic and lumbar spinal
cord (Wells et al. 1998). Neuroinvasion in scrapie-
infected mice was linked to B lymphocytes (Klein et al
1997). There is no known immune response to TSE



agents in affected hosts; however, the lymphoreticular
system plays a role in pathogenesis of disease in rodent

Histopathologic changes in animals and humans
with TSEs are qualitatively similar and confined to the
CNS. Lesions include vacuolation of neuronal
perikarya and neurites, neuronal degeneration and loss,
gliosis (mainly astrocytic), and accumulation of PrPres
(Wells and McGill 1992; McGill and Wells 1993). The
pathogenetic mechanisms of neurodegeneration are not
understood but are under study (Sakaguchi et al. 1996;
Tobler et al. 1996; Jeffrey et al. 1997; Williams et al.
1997; Hegde et al. 1998). Scrapie-associated fibrils
(SAFs), which are fibrillar aggregates of PrPres may be
revealed by electron-microscopic examination of deter-
gent extracts of brain from affected animals (Merz et al.
1984; Hope et al. 1988; Wells and McGill 1992).

With the importance of BSE and scrapie in domestic
livestock, and the heightened concern about the rela-
tionship of these diseases and human health, more
attention will certainly be focused on the TSEs in the


History and Distribution. Chronic wasting disease
(CWD) was first recognized in 1967 as a clinical syn-
drome of unknown etiology among captive mule deer
Odocoileus hemionus at wildlife research facilities in
Colorado (Williams and Young 1992). The disease was
diagnosed in 1978 as a spongiform encephalopathy by
histopathologic examination of CNS from affected ani-
mals. Shortly afterward CWD was recognized among
captive deer in Wyoming (Williams and Young 1980).
Diagnosis of CWD in Rocky Mountain elk from these
same facilities quickly followed (Williams and Young
1982). Deer and elk in a few zoological gardens in the
United States and Canada were identified with CWD in
subsequent years (Williams and Young 1992). Appar-
ently it did not persist in these locations. Chronic wast-
ing disease has recently become a concern to the game
farm industry following its diagnosis in elk in
Saskatchewan, Canada, and in South Dakota,
Nebraska, Montana, Colorado, and Oklahoma.

In 1981, CWD was recognized in a free-ranging elk
in Colorado (Spraker et al. 1997). Subsequently, it was
found in free-ranging elk in Wyoming, and in free-
ranging mule deer [1985 (M.W. Miller unpublished)]
and white-tailed deer Odocoileus virginianus [1990
(E.S. Williams unpublished)] in both states. The known
distribution of CWD currently includes captive and
free-ranging cervids in southeast Wyoming and north-
central and northeast Colorado (Miller et al. 2000) and
several game farms in the United States and Canada.

Host Range. Only three species of Cervidae are
known to be naturally susceptible to CWD: mule deer,
white-tailed deer, and Rocky Mountain elk. Subspecies
of these cervids probably are also naturally susceptible.

Pronghorn Antilocapra americanus. Rocky Moun-
tain bighorn sheep Ovis canadensis, mouflon, moun-
tain goats Oreamnos americana, moose Alces alces,
and a blackbuck Antilope cervicapra have been in con-
tact with CWD-affected deer and elk or resided in
premises where CWD had occurred but have not devel-
oped the disease. Domestic livestock are not known to
be naturally susceptible to CWD, and a few cattle,
sheep, and goats have resided in research facilities with
CWD for prolonged periods without developing the

Many species are experimentally susceptible to
CWD by intracerebral inoculation, an unnatural but
commonly used route for the study of prion disease.
Mink, domestic ferret Mustela putorius furo, squirrel
monkey Saimiri sciureus, mule deer, domestic goat
(Williams and Young 1992), and laboratory mice
(Bruce et al. 1997) are susceptible to CWD by this
route on primary passage.

Etiology. The origin of CWD is not known. Sponta-
neous development of PrPres might have occurred in
deer, with subsequent transmission to other deer and
elk. An alternate explanation is that CWD is actually
scrapie occurring in cervids. Chronic wasting disease
could also have originated by infection with an as-yet-
unrecognized prion.

Characteristics of the agent causing CWD are poorly
understood, but the agent is presumed to be a prion.
Based on mouse strain typing, it appears to differ from
the BSE agent (Bruce et al. 1997), many strains of
scrapie, and the TME agent (M.E. Bruce personal com-
munication). The marked similarity of CNS lesions and
epidemiology strongly suggests CWD agent is the
same in captive and free-ranging deer and elk.

Transmission and Epidemiology. The mode of trans-
mission of CWD is unknown. There is no evidence that
CWD is a food-borne disease associated with rendered
ruminant meat and bonemeal as was the case in BSE
(Wilesmith et al. 1988). Occurrence of the disease
among captive deer and elk, many of which were
acquired as neonates, fawns, or adults, provides strong
evidence of lateral transmission (Williams and Young
1992; Miller et al. 1998; Miller et al. 2000). Maternal
transmission may also occur; however, this has not
been definitively determined. It is likely transmission
occurred from mule deer to elk.

The scrapie agent is found in many lymphoid tissues,
including those of the digestive tract (Hadlow et al. 1980,
1982), suggesting the agent may be shed through the ali-
mentary tract. Lymphoid tissues of affected deer and elk
contain PrPres; thus, alimentary tract shedding may also
occur in CWD. The TSE agents are extremely resistant in
the environment (Brown and Gajdusek 1991); pasture
contamination has been suspected of being the source of
scrapie agent in some outbreaks of sheep scrapie (Greig
1940; Palsson 1979). Concentration of deer and elk a
captivity or by artificial feeding may increase the likeli-
hood of transmission between individuals.


The youngest animal diagnosed with natural CWD
was 17 months of age, suggesting this as an approxi-
mate minimum incubation period; however, without
knowledge of when the animal was infected, it is impos-
sible to accurately determine the incubation period.
Maximum incubation periods are not known. Most
cases of CWD among deer and elk residing in facilities
with a long history of CWD are in 3-7-year-old ani-
mals. The age of onset of clinical signs is variable in
animals brought into facilities as adults or among ani-
mals in herds newly recognized to have CWD. For
example, one elk in a presumed newly infected herd
was more than 15 years old. It is not known when dur-
ing the course of infection an animal may be infectious.

In one study, more than 90% of mule deer residing
on a premises for more than 2 years died or were eu-
thanized due to CWD (Williams and Young 1980).
Chronic wasting disease was the primary cause of adult
mortality [5 (71%) of 7 and 4 (23%) of 23] in two cap-
tive elk herds (Miller et al. 1998).

Relatively little is known about the epidemiology of
CWD in free-ranging cervids. In addition to necropsy
and examination of brains from animals showing clini-
cal signs suggestive of CWD to determine its distribu-
tion (targeted surveillance), brains from deer and elk
harvested by hunters in the CWD-endemic area have
been used to estimate prevalence. Within endemic
areas, prevalence of preclinical CWD, based on
histopathology and/or immunohistochemistry for
PrPres, is estimated at less than 1%-8% (Miller et al.
2000). Chronic wasting disease has not been found in
cervids outside the endemic areas.

Preliminary modeling suggested lateral transmission
is necessary to maintain CWD at the prevalence
observed in surveillance programs. Maternal transmis-
sion may occur, but in the model this route of trans-
mission alone was not adequate to maintain the disease
at observed levels (Miller et al. 2000).

Clinical Signs. The most striking clinical features of
CWD in deer and elk are loss of body condition and
changes in behavior. Clinical signs of CWD may be
more subtle and prolonged in elk than in mule deer.
Affected animals may increase or decrease their inter-
action with handlers or other members of the herd.
They may show repetitive behaviors, such as walking
set patterns in their pens or pastures, show periods of
somnolence or depression from which they are easily
roused, and may carry their head and ears lowered.
Affected animals continue to eat, but they consume
reduced amounts of feed, leading to gradual loss of
body condition. As the disease progresses, many
affected animals display polydipsia and polyuria;
increased salivation with resultant slobbering or drool-
ing; and incoordination, particularly posterior ataxia,
fine head tremors, and wide-based stance. Esophageal
dilatation, hyperexcitability, and syncope are, rarely
seen. Death is inevitable.

In captive herds newly experiencing CWD, sporadic
cases of prime-aged animals losing condition, being
unresponsive to symptomatic treatment, and death
from pneumonia are common. Aspiration pneumonia,
presumably from difficulty swallowing and hypersali-
vation, may lead to misdiagnosis of the condition if the
brain is not examined.

The clinical course of CWD varies from a few days
to a year, with most animals surviving a few weeks to
3-4 months. Although a protracted clinical disease is
typical, occasionally acute death may occur in white-
tailed deer (M.W. Miller unpublished). Caretakers
familiar with individual animals often recognize subtle
changes in behavior well before those not familiar with
the particular animal detect abnormalities or serious
weight loss occurs. Also, those who have seen clini-
cally affected animals are more astute at detecting early
behavioral changes than naive observers.

The clinical course of CWD in free-ranging deer and
elk is probably shorter than in captivity. Wild cervids
must forage, find water, and are susceptible to preda-
tion, all factors affecting longevity of sick animals in
the wild.

Pathogenesis. The pathogenesis of CWD is not specif-
ically known, though considerable research is currently
under way to better understand the dynamics of the dis-
ease in deer and elk. Based on similarities in clinical
course, neuropathology, and distribution of PrPres, patho-
genesis of CWD is likely similar to scrapie (Hadlow et
al. 1980,1982) The CWD agent probably enters the ani-
mal by ingestion, perhaps from environmental contami-
nation or direct interaction with animals shedding the
agent. In mule deer fawns experimentally infected with
CWD, PrPres was detected in retropharyngeal and ileoce-
cal lymph nodes, tonsil, and Peyer's patches by 42 days
after inoculation (Sigurdson et al. 1999).

The parasympathetic vagal nucleus in the medulla
oblongata is the site of the most severe and consistent
lesions in deer (Williams and Young 1993) and is the site
of PrPres accumulation, prior to development of spongi-
form changes (E.S. Williams unpublished; T.R. Spraker
personal communication). Distribution of lesions in the
brain (Williams and Young 1993) may explain clinical
signs. Emaciation may be associated with hypothalamic
damage, and polydipsia may reflect damage to the par-
aventricular and supraoptic nuclei and subsequent dia-
betes insipidus (Williams and Young 1992).

Pathology. Alterations in clinical chemistry and
hematology may occur in CWD-affected animals, but
the alterations are not diagnostic. In captive deer, low
urine specific gravity (1.002-1.010) reflects polydipsia
and possibly inability to concentrate urine (Williams
and Young 1980). In free-ranging animals, urine spe-
cific gravity may not be as low because they may not
have ready access to water and may be dehydrated at
death. Other nonspecific changes in clinical pathology
reflect emaciation or intercurrent diseases.

The gross lesions of CWD are nonspecific. Car-
casses may be in poor nutritional state or emaciated
but may be in fair condition if the animal died of aspi-


ration pneumonia or after only a short clinical course.
Aspiration pneumonia with or without fibrinous pleuri-
tis may be present in some animals. Rumen contents
contain excessive water in those animals displaying
polydipsia; sometimes the contents appear frothy. Sand
and gravel are often abundant in the forestomachs.

Microscopic lesions of CWD have been described in
mule deer and elk (Williams and Young 1993; Hadlow
1996). The lesions are qualitatively typical of TSEs.
Distribution of lesions is similar in deer and elk, with
some minor differences in degree. In all cases of clini-
cal CWD, lesions are in the parasympathetic vagal
nucleus in the dorsal portion of the medulla oblongata
at the obex, in hypothalamus and thalamus, and in
olfactory tracts and cortex. Other regions of the brain,
in particular, thalamus and cerebellum, show typical
spongiform changes with varying degrees of severity.
Lesions are usually mild in the cerebral cortex, hip-
pocampus, and basal ganglia.

Plaques composed of PrPres can be appreciated on
routine hematoxylin-eosin staining in most clinically
affected white-tailed deer and in a few mule deer but
are not obvious in elk (Bahmanyar et al. 1985;
Williams and Young 1992). In white-tailed deer,
plaques are often surrounded by vacuoles in the neu-
ropil, which allows them to be easily visualized. The
plaques stain strongly on immunohistochemistry for
PrPres by using a variety of polyclonal and monoclonal
antibodies (Guiroy et al. 1991a,b; Williams and Young
1992; Liberski et al. 1993; O'Rourke et al. 1998b). Pat-
terns of immunostaining in CWD include granularity
and amorphous clumps on neuronal membranes,
perivascular aggregates, and large, apparently extracel-
lular accumulations of PrPres.

Scrapie-associated fibrils are found in brains and
spleen of deer and elk with CWD (Williams and Young
1992; Spraker et al. 1997). The ultrastructural lesions
of CWD are typical of lesions found in the other TSEs
(Guiroy et al. 1993, 1994; Liberski et al. 1993).

Diagnosis. Clinical signs of CWD are not specific, and
currently diagnosis is based on examination of the brain
for spongiform lesions and/or accumulation of PrPres.
The parasympathetic vagal nucleus in the dorsal portion
of the medulla oblongata at the obex is the most impor-
tant site to be examined for diagnosis of CWD
(Williams and Young 1993) and should be submitted for
histopathologic examination on every animal suspected
of having CWD. The whole head or whole brain can be
submitted to the diagnostic laboratory to ensure that the
correct portion of the brain is examined. Supplemental
tests include negative-stain electron microscopy for
SAP or Western blotting for detection of PrPres in brain
(Williams and Young 1992; Spraker et al. 1997).

Demonstration of PrPres in lymph nodes, tonsil, and
conjunctival lymphoid tissues is useful in antemortem
diagnosis of sheep scrapie (Ikegami et al. 1991;
Schreuder et al. 1996, 1998; O'Rourke et al. 1998a).
These techniques are currently being tested in deer and
elk to determine their sensitivity and specificity.

Differential Diagnoses. Differential diagnoses of
CWD in deer and elk include a wide variety of diseases
that cause CNS disease and emaciation. Animals with
brain abscesses, traumatic injuries, encephalitis,
meningitis, peritonitis, pneumonia, arthritis, starvation,
nutritional deficiencies, and dental attrition have been
submitted to laboratories as CWD suspects. Aspiration
pneumonia is often seen as a terminal event in deer and
elk with CWD and, when it is recognized in a prime-
aged cervid, CWD should be considered.

Immunity. There is no known immune response to the
CWD agent. In sheep and mice, PrP genotype plays a
major role in development of scrapie. There is marked
homology between mule deer, white-tailed deer, and
elk PrP gene sequences (Cervenakova et al. 1997; K.
O'Rourke personal communication). Polymorphism
was detected in mule deer (codon 138, serine or
asparagine) (Cervenakova et al. 1997; O'Rourke et al.
1997a), white-tailed deer (K. O'Rourke personal com-
munication), and elk [codon 132 (129), methionine or
leucine] (Cervenakova et al. 1997; Schatzl et al. 1997;
O'Rourke et al. 1998b). It is not yet known whether
particular PrP genotypes confer resistance or increase
susceptibility to CWD; however, codon 132 methio-
nine homozygotes were overrepresented in free-rang-
ing and captive CWD-affected elk when compared to
unaffected elk (O'Rourke et al. 1999).

Control and Treatment There is no known treatment
for animals affected with CWD, and it is considered
100% fatal once clinical signs develop. If an affected
animal develops pneumonia, treatment with antibiotics
might prolong the course of illness but will not alter the
fatal outcome.

Control of CWD is problematic. In the face of long
incubation periods, subtle early clinical signs, absence of
reliable antemortem diagnostic tests, extremely resistant
infectious agent, possible environmental contamination,
and lack of understanding of transmission, designing
methods for control or eradication of CWD is extremely
difficult. Management currently involves quarantine or
depopulation of CWD-affected herds. Two attempts to
eradicate CWD from captive cervid facilities failed,
though the cause of the failure was not determined;
residual environmental contamination following facility
cleanup was possible (Williams and Young 1992).

Management of CWD in free-ranging animals is
even more problematic. Long-term active surveillance
to determine distribution and prevalence of CWD has
been instituted to assist in evaluating changes over time
and effect of management intervention. Translocation
and artificially feeding cervids in the endemic areas has
been banned in an attempt to limit range expansion and
to decrease transmission of CWD. Localized popula-
tion reduction in areas of high CWD prevalence is
being considered.

Public Health Concerns. No cases of human disease
have been associated with CWD. There is a long history


of human exposure to scrapie through handling and
eating sheep tissues, including brain, yet there is no
evidence that this presents a risk to human health.
However, in the absence of complete information and
in consideration of the similarities of animal and
human TSEs, hunters harvesting deer and elk in the
endemic areas or meat processors and taxidermists
handling cervid carcasses should take some common-
sense measures to avoid exposure to the agent and to
other zoonotic pathogens. Sick animals should not be
harvested for consumption; hunters, game-meat
processors, and taxidermists should wear latex or rub-
ber gloves when dressing a deer or elk from these
areas; and the brain, spinal cord, lymph nodes, spleen,
tonsils, and eyes should be discarded and not con-
sumed, because these organs probably contain the
greatest amount of CWD agent. Since TSE agents have
never been demonstrated in skeletal muscle, boning
game meat is an effective way to reduce the potential
for exposure.

Management Implications. The presence of CWD in
captive and free-ranging cervids is a serious manage-
ment problem. Captive populations are quarantined,
which limits usefulness and value of the animals for
research or commerce. Indemnity for depopulated
cervids currently is not available. Guidelines for man-
agement of captive herds with CWD are being devel-
oped by federal, state, and provincial animal health

Implications for free-ranging populations of deer
and elk are significant. Deer and elk are not translo-
cated from CWD-endemic areas, surveillance pro-
grams are expensive for wildlife management agencies,
and the impact of the disease on the population dynam-
ics of deer and elk is not currently known. Preliminary
modeling suggests that CWD could detrimentally
affect populations in endemic areas (M.W. Miller
unpublished). Public and agency concerns and percep-
tions about human health risks associated with all the
TSEs may ultimately influence management of herds
of free-ranging cervids in the endemic areas.


Distribution and Host Range. Cases of TSE, now rec-
ognized as caused by the BSE agent, were diagnosed in
ten species of Bovidae and Felidae (Table 17.1) at or
from zoological collections in the British Isles (Kirk-
wood and Cunningham 1994a). Cases occurred in
cheetah Acinonyx jubatus exported to Australia (Peel
and Curran 1992) and France (Baron et al. 1997). A
possible case of TSE associated with BSE agent was
reported in a rhesus macaque Macaco mulatto (Bons et
al. 1996); however, this diagnosis has been questioned
(Baker et al. 1996). Recently, spongiform encephalopa-
thy associated with oral exposure to the BSE agent was
confirmed in captive brown lemurs Eulemurfluvus and

TABLE 17.1—Wild mammals reported with naturally occurring transmissible
spongiform encephalopathies

Scientific name Common Name Disease(a) References

Taurotragus oryx Eland(b) BSE Fleetwood and Furley 1990; Kirkwood and Cunningham 1994a

Tragelaphus strepsiceros Greater kudu' BSE Kirkwood et al. 1990; Kirkwood and and Cunningham 1994a

Tragelaphus angasii Nyala(b) BSE Jeffrey and Wells 1988

Oryx dammah Scimitar-homed oryx(b) BSE Kirkwood and Cunningham 1994a

Oryx gazella Gemsbok(b) BSE Jeffrey and Wells 1988

Oryx leucoryx Arabian oryx(b) BSE Kirkwood et al. 1990

Bison bison Bison BSE R. Bradley, personal communication

Ovis musimon Mouflon(b) Scrapie Wood et al. 1992

Odocoileus hemionus Mule deer(b,c) CWD Williams and Young 1980

Odocoileus virginianus White-tailed deer(b,c) CWD Spraker et al. 1997

Cervus elaphus nelsoni Rocky Mountain elk(b,c) CWD Williams and Young 1982

Felis concolor Cougar(b) BSE Willoughby et al. 1992

Felis pardalis Ocelot(b) BSE Kirkwood and Cunningham 1994b

Panthera tigris Tiger(b) BSE Kirkwood and Cunningham 1999

Acinonyx jubatus Cheetah(b) BSE Peet and Curran 1992; Kirkwood and Cunningham 1994b; Kirkwood et al. 1995; Baron et al. 1997

Mustela vison Mink (b) TME Hartsough and Burger 1965; Hadlow and Karstad 1968; Hartung et al. 1970

(a) BSE, bovine spongiform encephalopathy; CWD, chronic wasting disease;
TME, transmissible mink encepalopathy.
(b) Captive animals.
(c) Free-ranging animals.


a mongoose lemur Eulemur mongw in France (Bons et
al. 1999).

Transmission and Epidemiology. The epidemiology
of BSE in zoo animals in Great Britain is similar to that
of BSE in cattle. The epidemic in cattle arose through
the practice of including ruminant-derived protein in
cattle feeds (Wilesmith et al. 1988, 1991). It was
thought that changes in rendering procedures used in
preparing this material resulted in failure to inactivate
the agent, which was hypothesized to be a strain of
scrapie from sheep. The first clinical cases were diag-
nosed in cattle in 1986. Subsequent analysis of the epi-
demic in cattle revealed there must have been wide-
spread exposure to the agent via proprietary feeds
starting during the winter of 1980-81 (Wilesmith et al.

The cases in zoo animals are thought to have been
caused by the BSE agent for three reasons: their tem-
poral and geographic coincidence with the BSE epi-
demic in cattle; affected zoo animals were either
known, or suspected, to have been exposed to contam-
inated feeds; and the pathology and incubation period
of the disease in various strains of mice inoculated with
brain homogenates from an affected nyala Tragelaphus
angasii and a greater kudu Tragelaphus strepsicems
were nearly identical to those occurring when mice
were inoculated with BSE from cattle (Jeffrey et al.
1992; Bruce et al. 1994). The ungulates were exposed
to feeds containing ruminant-derived protein, and the
carnivores were exposed to tissues, probably including
CNS, from cattle incubating BSE that were considered
unfit for human consumption (Kirkwood and Cunning-
ham 1994a,b).

The question of whether BSE is laterally or mater-
nally transmissible in cattle has received vigorous
investigation. At present, there is some indication that
it is transmissible vertically or by other routes at a low
rate (Donnelly et al. 1997a; Wilesmith et al. 1997). The
occurrence of cases in greater kudu that were born after
the July 1988 ban on inclusion of ruminant-derived
protein in ruminant feeds [Her Majesty's Stationery
Office (HMSO) 1988] and that were not thought to
have been exposed via the diet raised the possibility
that lateral transmission might have occurred in this
species (Kirkwood et al. 1992, 1994; Cunningham et
al. 1993; Kirkwood and Cunningham 1994a). How-
ever, the pattern of the epidemic in cattle has since
revealed that some degree of feed contamination was
present for a considerable period after the July 1988
ban, and the possibility that the kudu were exposed to
these feeds cannot be excluded. Because of this, and
the fact that no further cases have occurred in this
species since 1992, which exceeds the apparent aver-
age incubation period of 31 months, it is possible that
all the kudu cases could, as in cattle, have been due to
ingestion of contaminated feeds.

It seems reasonable that the cases in eland Taurotra-
gus oryx (Fleetwood and Furley 1990) and scimitar-
homed orvx Orvx dammah, bom, like some of the
kudu, quite long after the July 1988 feed ban, were due
to exposure to contaminated feeds. Measures to ensure
the exclusion of ruminant-derived protein from feeds
were subsequently tightened in the United Kingdom,
and there has been a marked decline in the number of
cases among cattle, indicating the efficacy of these
measures (Donnelly et al. 1997b). Decline in the num-
ber of new cases in zoo ungulates during recent years
supports this and, although no firm conclusions can be
drawn at this stage, provides no evidence for natural
transmission between antelope.

Because dates of infection of affected zoo animals
were not known, incubation periods of the disease
could not be determined precisely. However, data on
age at death suggest that incubation periods vary
between species, and they are clearly longer in Felidae
(62-84 months) than in Bovidae (28-48 months).

Clinical Signs. Clinical signs in zoo animals have
been reviewed by Kirkwood and Cunningham (1994a),
and a detailed description of clinical signs in one
greater kudu has been published (Kirkwood et al.
1994). These include various signs of CNS dysfunc-
tion, including ataxia, abnormal head and ear posture,
fine muscle tremors, myoclonus, dullness, behavioral
changes, excessive lip and tongue movements, and
weight loss. In most cases, the disease progressed over
weeks, and there was gradual progression of severity
but, in some cases, the disease appeared to have a rapid
onset and a course of only a few days.

Pathogenesis. The specific pathogenesis of BSE in
zoo animals has not been studied. The route of spread
of the agent after oral exposure to central nervous and
other tissues remains unclear. Although infectivity has
been detected in several tissues other than CNS in
sheep with scrapie and cattle with BSE, lesions have
been observed only in the CNS.

Pathology. The comparative pathology of BSE and the
recent cases of spongiform encephalopathy in greater
kudu and domestic cats have been reviewed (Wells et al.
1993). In cheetah, spongiform changes involved the
entire brain axis, and vacuolation of tha neuropil was
the most prominent feature (Kirkwood et al. 1995). All
the zoo animals that were examined for SAP were pos-
itive (Kirkwood and Cunningham 1994a).

Diagnosis. Clinical signs are not specific, but the dis-
ease may be strongly suspected in animals that show
progressive behavioral changes or ataxia, postural
abnormalities, and abnormal muscle movements; the
suspect animals reside in or were imported from the
United Kingdom or other European countries with
endemic BSE; and where there is potential exposure to
BSE-contaminated feeds. The disease cannot be con-
firmed during life, and diagnosis depends on detection
of characteristic histopathologic changes and other
analyses of CNS material collected at postmortem
examination. In addition to detection of SAP, these


analyses include immunostaining and immunoblotting
techniques for PrPres (Scott et al. 1990). Further confir-
mation and, possibly, some information about strain
type can be obtained by inoculating brain homogenates
into panels of various genotypes of mice and studying
the incubation periods and lesion profiles (Jeffrey et al.
1992; Bruce et al. 1994, 1997).

Immunity. There is no known immune response to
TSE agents. Patchiness of the distribution of cases
among taxa in zoo animals suggested variation in sus-
ceptibility to the BSE agent among species (Kirkwood
and Cunningham 1994a; Kirkwood et al. 1995). How-
ever, this remains to be confirmed.

Treatment and Control. No treatment is available to
halt, reverse, or delay the development of these dis-
eases. Control of BSE in zoo animals has been dis-
cussed (Cunningham 1991; Kirkwood and Cunning-
ham 1992, 1994a). Measures to prevent inclusion of
rendered products in feeds (HMSO 1988) for zoo rumi-
nants should effectively control the disease unless ver-
tical or horizontal transmission occurs.

Since September 1990, there has been a statutory
ban in the United Kingdom on feeding specified offal
(brain, spinal cord, spleen, thymus, tonsils, and intes-
tines) from cattle older than 6 months to any animals
(HMSO 1990). This legislation did not preclude feed-
ing tissues from zoo ungulates, but Kirkwood and Cun-
ningham (1994a) considered it advisable not to feed to
animals the offals of any species that could have been
exposed to BSE. Furthermore, in the absence of infor-
mation about tissue distribution of the agent in zoo
animals, they considered that it would be prudent to
avoid using any tissues of zoo animals in BSE-endemic
countries as food for others.

Public Health Concerns. There is no known human
health risk from zoo ungulates or felids with BSE,
because these animals are not part of the human food
chain. Contact with clinically affected animals is not
considered a health risk, but appropriate protective mea-
sures should be taken during postmortem examinations.

Management Concerns. Management implications
depend on whether BSE is naturally transmissible among
zoo animals. If it is, then introduction of an incubating
animal into a population of captive or free-living wild
animals is likely to have serious consequences (Cunning-
ham 1991; Kirkwood and Cunningham 1994a). The dis-
ease may therefore severely compromise movements
between zoological collections for breeding management
or for rcintroduction to the wild. Animals that could have
been exposed to the BSE agent, their offspring, or con-
tacts should not be moved into populations that have not
been exposed, unless the damage that this would cause to
a conservation breeding program outweighs the risk of
introduction of a TSE (Kirkwood and Cunningham
1994a). However, even if there is no risk of spread to con-
specifics during life, tissues from affected or carrier ani-
mals could present a risk if eaten by other animals. For
this reason, it has been recommended that no animal
that could have been exposed to the BSE or other TSE
agent should be used in reintroduction programs (Cun-
ningham 1991; Kirkwood and Cunningham 1994a).


Transmissible mink encephalopathy is a rare TSE of
ranched mink (Marsh and Hanson 1979); it has never
been diagnosed in free-ranging mink. Only a few out-
breaks have occurred in North America and Europe
(Marsh 1976). The disease is thought to be associated
with inadvertently incorporating sheep with scrapie into
mink feed (Marsh and Hanson 1979); however, several
TME outbreaks were associated with feeding cattle and
not sheep (Marsh et al. 1991). This has led to the hypoth-
esis that an unidentified spongiform encephalopathy
may be circulating in cattle in the United States (Marsh
et al. 1991; Robinson 1996). Neither BSE nor any other
bovine TSE has been identified in the United States.

Transmissible mink encephalopathy causes 60%-
100% morbidity within a population and 100% mortal-
ity of affected mink during outbreaks (Robinson 1996).
Animals show behavioral changes and become aggres-
sive, ataxic, and carry their tail over their backs, until
they become somnolent, moribund, and die. The dis-
ease is not transmissible among affected animals
except occasionally by bite wounds or cannibalism
(Marsh and Hanson 1979). The microscopic lesions are
qualitatively typical of the TSEs, but the lesions tend to .
be more severe in the rostral portions of the brain in
comparison to the distribution of lesions in ruminants
(Eckroade et al. 1979). Transmissible mink enceph-
alopathy has been experimentally transmitted by
intracerebral inoculation to cattle (Robinson et al.
1995) and to sheep, goats, and a variety of laboratory
species, including primates (Marsh 1976; Hadlow et al.
1987). Striped skunks Mephitis mephitis and raccoons
Procyon lotor were also experimentally susceptible to
TME (Eckroade et al. 1973). Transmissible mink
encephalopathy, may be considered of greatest impor-
tance as a model of the TSEs, primarily through the
carefully crafted studies of Marsh, Hadlow, and col-
leagues, rather than as a significant disease of domestic
animals or humans. It is of potential management con-
cern to those raising mink but is of no known concern
to free-ranging species.


Bahmanyar, S., E.S. "Williams, F.B. Johnson, S. Young, and
D.C. Gajdusek. 1985. Amyloid plaques in spongiform
encephalopathy of mule deer. Journal of Comparative
Pathology 95:1-5.

Baker, H.F., R.M. Ridley, G.A. Wells, and J.W. Ironside. 1996.
Spontaneous spongiform encephalopathy in a monkey.
Lancet 348:955-956.

Baron, T., P. Belli, J.Y. Madec, P. Moutou, C. Vitaud, and M.
Savey. 1997. Spongiform encephalopathy in an imported
cheetah in France. Veterinary Record 141:270-271.


Beekes, M., P.A. McBride, and E. Baldauf. 1998. Cerebral tar-
geting indicates vagal spread of infection in hamsters fed
with scrapie. Journal of General Virology 79:601-607.

Bons, N., N. Mestre-Frances, Y. Chamay, and F. Tagliavini.
1996. Spontaneous spongifonn encephalopathy in a
young adult rhesus monkey. Lancet 348:55.

Bons, N., N. Mestre-Frances, P. Belli, P. Cathala, D.C. Gaj-
dusek, and P. Brown. 1999. Natural and experimental
oral infection of nonhuman primates by bovine spongi-
fonn encephalopathy agents. Proceedings of the National
Academy of Sciences USA 96:4046-4051.

Brown, P., and D.C. Gajdusek. 1991. Survival of scrapie virus
after 3 years' interment. Lancet 337:269-70.

Bruce, M.E., A. Chree, I. McConnell, J. Foster, G. Pearson,
and H. Praser. 1994. Transmission of bovine spongifonn
encephalopathy and scrapie to mice: Strain variation and
species barrier. Philosophical Transactions of the Royal
Society of London [B] 343:405^11.

Bruce, M.E., R.G. Will, J.W. Ironside, I. McConnell, D.
Drummond, A. Suttie, L. McCardle, A. Chree, J. Hope,
C. Birkett, S. Cousens, H. Fraser, and C.J, Bostock. 1997.
Transmission to mice indicate that 'new variant' CJD is
caused by the BSE agent. Nature 389:498-501.

Cervenakova, L., R. Rohwer, E.S. Williams, P. Brown, and
D.C. Gajdusek. 1997. High sequence homology of the
PrP gene in mule deer and Rocky Mountain elk. Lancet

Chesebro, B. 1998. BSE and prions: Uncertainties about the
agent. Science 279:42-43.

Collinge, J., and M.S. Palmer. 1994. Molecular genetics of
human prion diseases. Philosophical Transactions of the
Royal Society of London [B] 343:371-378.

———. 1997. Human prion diseases. In Prion diseases, ed. J.
Collinge and M.S. Palmer. New York: Oxford University
Press, pp. 18-56.

Cunningham, A.A. 1991. Bovine spongifonn encephalopathy
and British zoos. Journal of Zoo and Wildlife Medicine

Cunningham, A.A., G.A.H. Wells, A.C. Scott, J.K. Kirkwood,
and J.E.F. Bamett. 1993. Transmissible spongifonn
encephalopathy in greater kudu (Tragelaphus strep-
siceros). Veterinary Record 132:68.

Dickinson, A.G. 1976. Scrapie in sheep and goats. In Slow
virus diseases of animals and man, ed. R.H. Kimbcrlin.
Amsterdam: North Holland, pp. 209-241.

Donnelly, C.A., N.M. Perguson, A.C. Ghani, J.W. Wilesmith,
. and R.M. Anderson. 1997a. Analysis of dam-calf pairs of
BSE cases: Confirmation of a maternal risk enhance-
ment. Proceedings of the Royal Society of London [B]

Donnelly, C.A., A.C. Ghani, N.M. Ferguson, and R.M. Ander-
son. 1997b. Recent trends in the BSE epidemic. Nature

Eckroade, R.J., G.M. Zu Rhein, and R.P. Hanson. 1973. Trans-
missible mink encephalopathy in carnivores: Clinical,
light and electron microscopic studies in raccoons, skunks
and ferrets. Journal of Wildlife Diseases 9:229-240.

•———. 1979. Experimental transmissible mink encephalopa-
thy: Brain lesions and their sequential development. In
Slow transmissible diseases of the nervous system, vol. I,
ed. S.B. Prusiner and W.J. Hadlow. New York: Academic,

Farquhar, C.F., R.A. Somerville, and M.E. Bruce. 1998.
Straining the prion hypothesis. Nature 391:345-346.

Fleetwood, A.J., and C.W. Purley. 1990. Spongiform
encephalopathy in an eland. Veterinary Record

Greig, J.R. 1940. Scrapie: Observations on the transmission of
the disease by mediate contact. Veterinary Journal

Guiroy, D.C., E.S. Williams, R. Yanagihara, and D.C. Gaj-
dusek. 199 la. Immunolocalization of scrapie amyloid
(PrP27-30) in chronic wasting disease of Rocky Moun-
tain elk and hybrids of captive mule deer and white-tailed
deer. Neuroscience Letters 126:195-198.

———. 199 1b. Topographic distribution of scrapie amyloid-
immunoreactive plaques in chronic wasting disease in
captive mule deer (Odocoileus hemionus hemionus).
Acta Neuropathologica (Berlin) 81:475-478.

Guiroy, D.C., E.S. Williams, P.P. Liberski, I. Wakayama, and
D.C. Gajdusek. 1993. Ultrastructural neuropathology of
chronic wasting disease in captive mule deer. Acta Neu-
ropathologica (Berlin) 85:437-444.

Guiroy, D.C., P.P. Liberski, E.S. Williams, and D.C. Gajdusek.
1994. Electron microscopic findings in brain of Rocky
Mountain elk with chronic wasting disease. Folia Neu-
ropathology 32:171-173.

Hadlow, W.J. 1996. Differing neurohistologic images of
scrapie, transmissible spongifonn encephalopathy, and
chronic wasting disease of mule deer and elk. In
Bovine spongifonn encephalopathy: The BSE dilemma,
ed. C.J. Gibbs Jr. New York: Springer-Verlag,
pp. 122-137.

Hadlow, W.J., and L. Karstad. 1968. Transmissible
encephalopathy of mink in Ontario. Canadian Veterinary
Journal 9:193-196.

Hadlow, W.J., R.C. Kennedy, R.E. Race, and C.M. Ekiund.
1980. Virologic and neurohistologic findings in dairy
goats affected with natural scrapie. Veterinary Pathology

Hadlow, W.J., R.C. Kennedy, and R.E. Race. 1982. Natural
infection of Suffolk sheep with scrapie virus. Journal of
Infectious Disease 146:657-664.

Hadlow, W.J., R.E. Race, and R.C. Kennedy. 1987. Experi-
mental infection of sheep and goats with transmissible
mink encephalopathy virus. Canadian Journal of Veteri-
nary Research 51:135-144.

Hartsough, G.R., and D. Burger. 1965. Encephalopathy of
mink: I. Epizootiologic and clinical observations. Jour-
nal of Infectious Diseases 115:387-392.

Hartung, J., H. Zimmermann, and U. Johannsen. 1970. Infec-
tious encephalopathy in the mink: I. Clinical, epizootio-
logical and experimental studies. Monatshefte fur Veteri-
narmedivn 15:385-388.

Hegde, R.S., J.A. Mastrianni, M.R. Scott, K.A. de Fea, P.
Tremblay, M. Torctua, S.J. de Annond, S.B. Prusiner,
and V.R. Lingappa. 1998. A transmembrane form of the
prion protein in neurodegenerative disease. Science

Her Majesty's Stationery Office (HMSO). 1988. The bovine
spongifonn encephalopathy order 1988. Statutory Instru-
ment Number 1039. London: HMSO.

————. 1990. Bovine spongifonn encephalopathy (No. 2).
Amendment Order 1990. London: HMSO.

Hope, J., L.J. Reekie, N. Hunter, G. Multhaup, K. Beyreuther,
H. White, A.C. Scott, M.J. Stack, M. Dawson, and G.A.
Wells. 1988. Fibrils from brains of cows with new cattle
disease contain scrapie-associated protein. Nature

Hunter, N., J.D. Foster, and J. Hope. 1992. Natural scrapie in
British sheep: Breeds, ages and PrP gene polymor-
phisms. Veterinary Record 130:389-392.

Ikegami. Y., M. Ito, H. Isomura, E. Momotani, K. Sasaki, Y.
Muramatsu, N. Ishiguro, and M. Shinagawa. 1991. Pre-
clinical and clinical diagnosis of scrapie by detection of
PrP protein in tissues of sheep. Veterinary Record

Jeffrey, M., and G.A.H. Wells. 1988. Spongiform
encephalopathy in a nyala (Tragelaphus angasi). Veteri-
nary Pathology 25:398-399.


Jeffrey, M., J.R. Scott, A. Williams, and H. Fraser. 1992.
Ultrastructural features of spongifonn encephalopathy
transmitted to mice from three species of Bovidae. Ada
Neuropalhologica (Berlin) 84:559-569.

Jeffrey, M., C.M. Goodsir, M.E. Bruce, P.A. McBride, and
J.R. Fraser. 1997. In vivo toxicity of prion protein in
murine scrapie: Ultrastructural and immunogold stud-
ies. Neuropathology and Applied Neurobiology

Kelly, D.F, H. Pearson, A.I. Wright, and L.W. Greenham.
1980. Morbidity in captive white tigers. In The compar-
ative pathology of zoo animals, ed. RJ. Montali and G.
Migaki. Front Royal, VA: Smithsonian Institution, pp.

Kimberiin, R.H., and C.A. Walker. 1989. Pathogenesis of
scrapie in mice after intragastric infection. Virus
Research 12:213-220.

Kirkwood, J.K., and A.A. Cunningham. 1992. Spongifonn
encephalopathy in zoo ungulates: Implications for
translocation and reintroduction. In Proceedings of the
conference'of the American Association of Zoo Veteri-
narians and the American Association of Wildlife Veteri-
narians, Oakland, California, ed. R.E. Junge. Oakland,
CA: American Association of Zoo Veterinarians, pp.

————. 1994a. Epidemiological observations on spongiform
encephalopathies in captive wild animals in the British
Isles. Veterinary Record 135:296-303.

——. 1994b. Patterns of incidence of spongiform
encephalopathy in captive wild animals in the British
Isles. In Wildlife Disease Association, European Divi-
sion, Symposium. Paris, pp. 28.

1999. Scrapie-like spongiform encephalopathies
(prion diseases) in nondomesticated species. In Zoo and
wild animal medicine, ed. M.E. Fowler and R.E. Miller.
Philadelphia: W.B. Saunders, pp. 662-668.

Kirkwood, J.K., G.A.H. Wells, J.W. Wilesmith, A.A. Cun-
ningham, and S.I. Jackson. 1990. Spongiform
encephalopathy in an Arabian oryx (Oryx leucoryx) and
a greater kudu (Tragelaphus strepsiceros). Veterinary
Record 127:418-420.

Kirkwood, J.K., G.A.H. Wells, A. A. Cunningham, S.I. Jack-
son, A.C. Scott, M. Dawson, and J.W. Wilesmith. 1992.
Scrapie-like encephalopathy in a greater kudu (Tragela-
phus strepsiceros) which had not been fed ruminant-
derived protein. Veterinary Record 130:365-367.

Kirkwood, J.K., A.A. Cunningham, A.R. Austin, G.A.H.
Wells, and A.W. Sainsbury. 1994. Spongiform
encephalopathy in a greater kudu (Tragelaphus strep-
siceros) introduced into an affected group. Veterinary
Record 134:167-168.

Kirkwood, J.K., A.A. Cunningham, E.J. Flach, S.M. Thorn-
ton, and G.A.H. Wells. 1995. Spongiform encephalopa-
thy in another captive cheetah (Acinonyx jubatus): Evi-
dence for variation in susceptibility or incubation periods
between species? Journal of Zoo and Wildlife Medicine

Klein, M.A., R. Prigg, E. Flechsig, A.J. Raeber, U. Kalinke, H.
Bluethmann, F. Bootz, M, Suter, R.M. Zinkemagel, and
A. Aguzzi. 1997. A crucial role for B cells in neuroinva-
sive scrapie. Nature 390:687-690.

Kocisko, D.A., J.H. Come, S.A. Priola, B. Chesebro, G.J.
Raymond, P.T. Lansbury, and B. Caughley. 1994. Cell-
free formation of protease-resistant prion protein. Nature

Liberski, P.P., D.C. Guiroy, E.S. Williams, R. Yangihara, P.
Brown, and D.C. Gajdusek. 1993. The amyloid plaque.
In Light and microscopic neuropathology of slow virus
disorders, ed. P.P. Uberski. Boca Raton, FL: CRC, pp.

Marsh, R.F. 1976. The subacute spongiform encepha-
lopathies. Frontiers of Biology 44:359-380.

Marsh, R.F, and R.P. Hanson. 1979. On the origin of trans-
missible mink encephalopathy. In Slow transmissible dis-
eases of the nervous system, vol. 1, ed. S.B. Prusiner and
W.J. Hadlow. New York: Academic, pp. 451-460.

Marsh, R.F., R.A. Bessen, S. Lehmann, and G.R. Hartsough.
1991. Epidemiological and experimental studies on a
new incident of transmissible mink encephalopathy.
Journal of General Virology 72:589-594.

McGill, I.S., and G.A. Wells. 1993. Neuropathological find-
ings in cattle with clinically suspect but histologically
unconfirmed bovine spongifonn encephalopathy (BSE).
Journal of Comparative Pathology 108:241-260.

Merz, P.A., R.G. Rohwer, K. Kascsak, H.M. Wisniewiski,
R.A. Somerville, C.J. Gibbs Jr., and D.C. Gajdusek.
1984. Infection-specific particle from the unconventional
slow virus diseases. Science 225:437-440.

Miller, M.W, M.A. Wild, and E.S. Williams. 1998. Epidemi-
ology of chronic wasting disease in Rocky Mountain elk.
Journal of Wildlife Diseases 34:532-538.

Miller, M.W., E.S. Williams, C.W. McCarty, T.R. Spraker, T.J.
Kreeger, C.T. Larsen, and E.T. Thoroe. 2000. Epidemiol-
ogy of chronic wasting disease in free-ranging cervids.
Journal of Wildlife Diseases. 36:676-690.

Millison, G.C., G.D. Hunter, and R.H. Kimberiin. 1976. The
physico-chemical nature of the scrapie agent. In Slow
virus diseases of animals and man, ed. R.H. Kimberiin.
Amsterdam: North Holland, pp. 243-266.

O'Rourke, K., T.R. Spraker, M.W. Miller, and E.S. Williams.
1997a. Three alleles of the prion protein gene in mule
deer (Odocoileus hemionus hemionus) with chronic
wasting disease. GenBank, Accession nos. 2213811,
2213938, 2213936, http://www.ncbi.nlm.gov/Entrez/

O'Rourke, K., G.R. Holyoak, W.W. dark, J.R. Mickelson, S.
Wang, R.P. Meico, T.E. Besser, and W.C. Foote. 1997b.
PrP genotypes and experimental scrapie in orally inocu-
lated Suffolk sheep in the United States. Journal of Gen-
eral Virology 78:975-978.

O'Rourke, K., TV. Baszler, S.M. Parish, and D.P. Knowles.
1998a. Preclinical detection of PrPsc in nictitating mem-
brane lymphoid tissue of sheep. Veterinary Record

O'Rourke, K., TV. Baszler, J.M. Miller, T.R. Spraker, I.
Sadler-Riggleman, and D.P. Knowles. 1998b. Mono-
clonal antibody F89/160.1.5 defines a conserved epitope
on the ruminant prion protein. Journal of Clinical Micro-
biology 36:1750-1755.

O'Rourke, K.I;, T.E. Besser, M.W. Miller, T.P. Cline, T.R.
Spraker, A.L. Jenny, M.A. Wild, G.L. Zebarth, and E.S.
Williams. 1999. PrP genotypes of captive and free-rang-
ing Rocky Mountain elk (Cervus elaphus nelsoni) with
chronic wasting disease. Journal of General Virology

Palsson, P.A. 1979. Rida (scrapie) in Iceland and its epidemi
ology. In Slow transmissible diseases of the nervous system,
vol. 1, ed. S.B. Prusiner and W.J. Hadlow. New
York: Academic, pp. 357-366.

Pearson, G.R., J.M. Wyatt, T.J. Gruffydd-Jones, J. Hope, A
Chong, R.J. Higgins, A.C. Scott, and G.A. Wells. 1992
Feline spongifonn encephalopathy: Fibril and PrP stud
ies. Veterinary Record 131:307-310.

Peet, R.L., and J.M. Curran. 1992. Spongiform encephalopathy
in an imported cheetah (Acinonyx jubatus). Australian
Veterinary Journal 69:117.

Prusiner, S.B. 1982. Novel proteinaceous infectious particle
cause scrapie. Science 216:136-144.

————. 1991. Molecular biology of prion diseases. Selene


1997. Prion diseases and the BSE crisis. Science

Prusiner, S.B., and W.J. Hadlow, eds. 1979. Slow transmissi-
ble diseases of the nervous system, vol. 1. New York:
Academic, 472 pp.

Raymond, G.J., J. Hope, D.A. Kocisko, S.A. Priola, L.D. Ray-
mond, A. Bossers, J. Ironside, R.G. Will, S.G. Chen, R.B.
Petersen, P. Gambetti, R. Rubenstein, M.A. Smits, P.T.
Lansbury Jr., and B. Caughey. 1997. Molecular assess-
ment of the potential transmissibilities of BSE and
scrapie to humans. Nature 388:285-288.

Robinson, M.M. 1996. An assessment of transmissible mink
encephalopathy as an indicator of bovine scrapie in U.S.
cattle. In Bovine spongiform encephalopathy: The BSE
dilemma, ed. C.J. Gibbs Jr. New York: Springer-Verlag,
pp. 97-107.

Robinson, M.M., W.J. Hadlow, D.P. Knowles, T.P. Huff, P.A.
Lacy, R.F. Marsh, and J.R. Gorham. 1995. Infection of
cattle with the agents of TME and scrapie. Journal of
Comparative Pathology 113:241-251.

Sakaguchi, S., S. Katamine, N. Nishida, R. Moriuchi, K.
Shigematsu, T. Sugimoto, A. Nakatani, Y. Kataoka, T.
Houtani, S. Shirabe, H. Okada, S' Hasegawa, T.
Miyamoto, and T. Noda. 1996. Loss of cerebellar Purk-
inje cells in aged mice homozygous for a disrupted PrP
gene. Nature 380:528-531.

Schatzl, H.M., F. Wopmer, S. Gilch, A. von Brunn, and G.
Jager. 1997. Is codon 129 of prion protein polymorphic
in human beings but not in animals? Lancet

Schoon, H.-A., D. Brunckhorst, and J. Pohlenz. 1991. Spongi-
form encephalopathy in a red-necked ostrich [in Ger-
man]. Tierwritliche Praxis 19:263-265. Abstract.

Schreuder, B.E.C., L.J.M. van Keulen, M.E.W. Vromans,
J.P.M. Langeveld, and M.A. Smits. 1996. Preclinical test
for prion diseases. Nature 381:563.

————. 1998. Tonsillar biopsy and PrPsc detection in the pre-
clinical diagnosis of scrapie. Veterinary Record

Scott, A.C., G.A.H. Wells, M.J. Stack, H. White, and M. Daw-
son. 1990. Bovine spongiform encephalopathy: Detec-
tion and quantitation of fibrils, fibril protein (PrP) and
vacuolation in brain. Veterinary Microbiology

Sigurdson, C.J., E.S. Williams, M.W. Miller, T.R. Spraker,
K.I. O'Rouike, and E.A. Hoover. 1999. Oral transmis-
sion and early lymphoid tropism of chronic wasting dis-
ease PrPres in mule deer fawns (Odocoileus hemionus).
Journal of General Virology 80:2757-2764.

Spraker, T.R., M.W. Miller, E.S. Williams, D.M. Getzy, W.J.
Adrian, G.G. Schoonveld, R.A. Spowart, K.I. O'Rourke,
J.M. Miller, and P.A. Merz. 1997. Spongiform
encephalopathy in free-ranging mule deer (Odocoileus
hemionus), white-tailed deer (Odocoileus virginianus),
and Rocky Mountain elk (Cervus elaphus nelsoni) in
northcentral Colorado. Journal of Wildlife Diseases

Taylor, D.M., S.L. Woodgate, and M.J. Atkinson. 1995. Inac-
tivation of the bovine spongiform encephalopathy agent
by rendering procedures. Veterinary Record

Tobler, I., S.E. Gaus, T. Deboer, P. Achermann, M. Fischer, T.
Rulicke, M. Moser, B. Oesch, P.A. McBride, and J.C.
Manson. 1996. Altered circadian activity rhythms and
sleep in mice devoid of prion protein. Nature

Wells, G.A., and I.S. McGill. 1992. Recently described
scrapie-like encephalopathies of animals: Case defini-
tions. Research in Veterinary Science 53:1-10.

Wells, G.A., A.C. Scott, C.T. Johnson, R.F. Gunning, R.D.
Hancock, M. Jeffrey, M. Dawson, and R. Bradley. 1987.
A novel progressive spongiform encephalopathy in cat-
tle. Veterinary Record 121:419-420.

Wells, G.A., S.A.C. Hawkins, A.A. Cunningham, W.H.
Blamire, J.W. Wilesmith, A.R. Sayers, and P. Hams.
1993. Comparative pathology of the new transmissible
spongiform encephalopathies. In Transmissible spongi-
form encephalopathies, ed. R. Bradley and B. Marchant.
Brussels: European Commission, pp. 327—345.

Wells, G.A., S.A.C. Hawkins, R.B. Green, A.R. Austin, I.
Dexter, Y.I. Spencer, M.J. Chaplin, M.J. Stack, and M.
Dawson. 1998. Preliminary observations on the patho-
genesis of experimental bovine spongiform encephalopa-
thy (BSE): An update. Veterinary Record 142:103-106.

Wilesmith, J.W. 1994. An epidemiologist's view of bovine
spongiform encephalopathy. Philosophical Transactions
of the Royal Society of London [B] 343:357-361.

Wilesmith, J.W, G.A.H. Wells, M.P. Cranwell, and J.B.M.
Ryan. 1988. Bovine spongiform encephalopathy: Epi-
demiological studies. Veterinary Record 123:638-644.

Wilesmith, J.W., J.B.M. Ryan, and M.J. Atkinson. 1991.
Bovine spongiform encephalopathy: Epidemiological
studies on the origin. Veterinary Record 128:199-203.

Wilesmith, J.W, G.A. Wells, J.B. Ryan, D. Gavier-Widen, and
M.M. Simmons. 1997. A cohort study to examine mater-
nally-associated risk factors for bovine spongiform
encephalopathy. Veterinary Record 141:239-43.

Will, R.G., J.W. Ironside, M. Zeidler, S.N. Cousens, K.
Estibeiro, A. Alperovitch, S. Poser, M. Pocchiari, A. Hof-
man, and P.G. Smith. 1996. A new variant of Creutzfeldt-
Jakob disease in the UK. Lancet 347:921-925.

Williams, A., P.J. Lucassen, D. Ritchie, and M. Bruce. 1997.
PrP deposition, microglial activation, and neuronal apop-
tosis in murine scrapie. Experimental Neurology

Williams, E.S., and S. Young. 1980. Chronic wasting disease
of captive mule deer: A spongiform encephalopathy.
Journal of Wildlife Diseases 16:89-98.

————. 1982. Spongiform encephalopathy of Rocky Moun-
tain elk. Journal of Wildlife Diseases 18:465-471.
——. 1992. Spongiform encephalopathies of Cervidae. Sci-
entific and Technical Review Office of International Epi-
wotics 11:551-567.
-. 1993. Neuropathology of chronic wasting disease of
mule deer (Odocoileus hemionus) and elk (Cervus ela-
phus nelsoni). Veterinary Pathology 30:36-45.

Willoughby, K., D.F. Kelly, D.G. Lyon, and G.A.H. Wells.
1992. Spongiform encephalopathy in a captive puma
(Felis concolor). Veterinary Record 131:431-434.

Wood, J.L.N., L.J. Lund, and S.H. Done. 1992. The natural
occurrence of scrapie in moufflon. Veterinary Recora

a few things to ponder...TSS

What state officials aren't telling you about chronic wasting disease -- the politics and blunders behind its spread and the true dangers.


No case of mad cow disease has ever been confirmed in the United States,
but Marsh urged the USDA to ban the practice of feeding processed bone
and blood meal made from rendered sheep, cows and deer to other
ruminants. His suggestion would have cost the agricultural industry
dearly in substitute protein, and the USDA took no action. Frustrated,
in 1993, Marsh repeated his concern in the state Ag Review, warning
Wisconsin dairy farmers they were feeding cattle to cattle. He also
talked to The New York Times. Marsh's published comments ignited such a
torrent of complaints from the state's agri-business industry, which
underwrites much of the UW Agriculture School's research, that the
college's dean tried to silence Marsh. Marsh was harassed and threatened
with lawsuits, and the university sponsored a symposium "whose only
purpose seemed to be arguing there was no need to change animal feeding
patterns," recalls Aiken, then a Marsh colleague, as was Olander. (Both
joined Marsh in pushing for a broad ruminant-to-ruminant feeding ban.)

Marsh was "not allowed to speak, while everyone discredited his work,"
says John Stauber, executive director of the Madison-based Center for
Media and Democracy, who dedicated his book, Mad Cow, USA, to Marsh.
Despite the humiliation inflicted by the university, Marsh would be
vindicated. When protein feed from rendered downer cows and scrapie
sheep was identified as the cause of mad cow disease in Britain in 1996,
the university lionized Marsh in its Wisconsin Alumni Magazine as the
scientist who'd predicted the disaster and tried to stop it.

"We were inundated. We had over 200 phone messages from CBS, NBC and
other people in the media who wanted to talk to Dick," remembers
professor Bruce Christenson, Marsh's successor as chair of the
department of animal health and biomedical sciences. But by then, Marsh,
58, had cancer, recalls Christenson. "He was a warrior even when he knew
he was dying."





The summary does tend to give a particular slant to the epidemiology of
BSE which is not totally sound. It is a possibility that the agent of
BSE may be in the cattle population in a number of countries already
apart from the USA and that clinical cases are occurring on rare
occasions. It is also important to off the possibility of the
relationship between BSE and certain low-temperature rendering systems.
For that reason a number of other countries apart from the USA and
France are at risk and, in particular, the Netherlands, Denmark,
Germany and Belgium. For these reasons it would be wise to move to an
international ban on the feeding of ruminant protein to rumi
MADCOW is offline  
Old 12-15-2003, 08:45 AM
Thread Starter
Join Date: Feb 2003
Posts: 27,585
Default [Deleted]

[Deleted by Admins]
Deleted User is offline  

Quick Reply: [Deleted]

Contact Us - Archive - Advertising - Cookie Policy - Privacy Statement - Terms of Service - Do Not Sell My Personal Information -

Copyright © 2021 MH Sub I, LLC dba Internet Brands. All rights reserved. Use of this site indicates your consent to the Terms of Use.