Download Exotic disease focus: Chronic wasting disease

Exotic disease focus:
Chronic wasting disease
Chronic wasting disease (CWD) is a transmissible spongiform
encephalopathy of deer and elk. It is invariably fatal.
Status in New Zealand
CWD is not present in New Zealand deer and elk. It is notifiable
New Zealand deer and elk are free of chronic wasting disease
(CWD). Be aware of the clinical signs, and submit samples to the
CWD surveillance programme if appropriate. Eligibility criteria
and further information are available on the MAF Biosecurity
New Zealand (MAFBNZ) website.
under the Biosecurity Act 1993. Surveillance has been undertaken
in New Zealand and no evidence of the presence of CWD has
been found(1). Samples from animals with a clinical presentation
consistent with CWD infection are eligible to be submitted to the
CWD surveillance programme(2). Cases where the index of suspicion
is high may be investigated by the MAFBNZ incursion investigation
team.
primary means of CWD spread. Lateral transmission is sufficient
to create self-sustaining epidemics in free-living cervid populations.
Transmission is known to occur naturally within species, from elk
to mule deer and white-tailed deer, from mule deer to elk, and from
mule deer to white-tailed deer. It is also known that transmission
of CWD can occur between farmed and feral populations, most
Status overseas
likely by prolonged fence-line contact. As prions are very resistant to
CWD is widespread and an important cause of wastage in farmed
degradation, they may be transmitted directly or indirectly.
and feral deer in North America, and appears to be spreading in
A recent study found infectious prions capable of transmitting
wild deer(3). It has been found in deer imported into Korea from
CWD in saliva (oral route) and blood (transfusion) as well as
Canada(4). Surveillance in European Union countries(5) has failed to
brain (oral route)(10). These findings further reinforce the evidence
detect any evidence of the disease
. CWD could be introduced
(6)(7)(8)
that no tissue from CWD-infected cervids can be considered free
to New Zealand in live deer, some untreated deer products, or
from infectious prions. The findings also imply there is a risk of
on equipment used with deer. Importation of live deer, genetic
ectoparasites acting as vectors for CWD via haematogenous spread,
material and equipment used with deer is restricted to reduce the
and that it is less likely (although not impossible) that urine or
risk of introducing the disease. Measures applied include a ban on
faeces are the source of infectious prions. Previously described cases
importing live deer and genetic material from North America.
of suspected maternal transmission cannot be completely ruled out,
Species affected and methods of
transmission
but more likely are variants of lateral transmission.
The known natural host range is as follows:
in central nervous system and gut-associated lymphoid tissue,
Infectivity correlates with concentration of prions and is greatest
but prion is also present in the spleen and pancreas in significant
•
Mule deer (Odocoileus hemionus hemionus)
•
Black-tailed deer (Odocoileus hemionus columbianus)
•
White-tailed deer (Odocoileus virginianus)
attributed to deer having much higher levels of prions in peripheral
•
Rocky Mountain elk (Cervus elaphus nelsoni)
tissues, hence releasing more prions into the environment after
•
Mule deer x white-tailed deer hybrids.
death or from excretions.
quantities. Incubation time is inversely proportional to prion dose.
Differences in prevalence between deer and elk in the wild have been
It is expected that red deer (Cervus elaphus scotticus and Cervus
Until infectious prions can be isolated from blood, saliva, faeces or
elaphus hippelaphus), elk (Cervus elaphus canadensis and Cervus
urine of all cervid species affected by CWD, it will not be known
elaphus manitobensis) and hybrids farmed in New Zealand would be
when during the course of infection an animal become infectious.
fully susceptible if the disease were to be introduced.
Currently it is thought that shedding precedes clinical signs and is
There is no evidence of natural spread of CWD to animal families
potentially progressive throughout the course of the disease.
other than the Cervidae. There is no evidence it can infect humans,
nor have there been any confirmed cases of human disease associated
with CWD. There is evidence for a molecular barrier limiting
susceptibility of cattle, sheep and humans to CWD(9). Prion protein
homology between the source and recipient species/genotypes
appears important in controlling interspecies TSE susceptibility.
Prion proteins in general are resistant to heat, desiccation and
most disinfectants, and can persist in the environment for many
years, possibly decades. Studies of the scrapie and CWD prion
proteins show that strong bonds form between the infectious agent
and certain soil types, with subsequent retention or enhancement
of infectivity. The period of infectivity is not known, but some
The exact mechanism of transmission is still unknown, but all
infectivity remains even after being soil-bound for three years.
current research supports lateral (horizontal) transmission as the
Inoculation of soil can occur if CWD-affected carcasses, tissues
Surveillance 36 (1) 2009
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or excreta are allowed to accumulate at the surface, enabling the
•
emaciation
adsorption of prion material. Present recommendations specify that
•
oesophageal dilation (rare)
•
hyperexcitability (rare)
•
syncope (fainting/collapse on stimulation) (rarely)
Common clinical signs of disease
•
death (invariably).
Clinical signs may be present for only a few days, but typically
Aspiration pneumonia, dehydration and hypothermia are the
progress over four months and occasionally longer. Clinical signs in
sequelae most commonly associated with death in affected animals.
cervids should be excluded from CWD-contaminated facilities for at
least five years after depopulation of infected animals.
elk tend to be more subtle than in deer, and cervids with CWD are
more likely to die suddenly after handling, or after immobilisation
and misadventures.
Clinical signs are as follows and the order of clinical signs represents
the general clinical course of the disease. Some signs may not be
present, though all cases end in death:
Diagnostic approaches
Clinical signs are non-specific and provide no more than suspicion
of the presence of CWD. Histopathology is the screening test of
choice in New Zealand because it enables some of the differential
diagnoses to be considered. Any surveillance specimens in which
CWD cannot be ruled out by histopathology would be followed
•
loss of body condition due to decreased consumption of food
up with further tests – Western blot on fresh spinal cord or
•
poor hair coat
immunohistochemistry on fixed tissue, or both.
•
changes in behaviour (captive animals), such as increase or
Main endemic differential diagnoses
decreased interaction with handlers and/or repetitive behaviours
•
periods of somnolence or depression, finally resulting in
recumbency
Differential diagnoses for CWD in New Zealand deer and elk should
include common causes of wasting and nervous signs, for example:
•
lowered head and ear carriage (“drooped”)
•
Johne’s disease
•
polydipsia and polyuria
•
listeriosis
•
increased salivation with noticeable slobbering or drooling and
•
malignant catarrhal fever
bruxism
•
chronic gastrointestinal parasitism
incoordination, posterior ataxia, fine head tremors and a wide-
•
severe copper deficiency
based stance
•
sporidesmin toxicity.
•
CWD surveillance programme
MAFBNZ operates a CWD surveillance programme. Submissions
by veterinary practitioners of samples from animals which meet the
eligibility criteria are welcome.
The eligibility criteria for deer and elk are:
•
age greater than two years
•
clinical signs of progressive wasting, nervous disease, or acute,
peracute or aspiration pneumonia.
Further details regarding eligibility, the specimens required and
the submission process can be obtained from the MAFBNZ TSE
surveillance website: www.biosecurity.govt.nz/tse
Further information
www.biosecurity.govt.nz/tse
www.cwd-info.org/
www.cdc.gov/ncidod/dvrd/cwd/
www.avma.org/animal_health/brochures/cwd/cwd_brochure.asp
The emaciation, abnormal stance and low head carriage shown by this
animal are characteristic signs of chronic wasting disease. Photo: Dr.
Terry Kreeger, Wyoming Game and Fish Department.
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Surveillance 36 (1) 2009
References
(1) McIntyre L. Reports from MAF Biosecurity New Zealand – TSE programme. Surveillance 35(2),
19-20, 2008.
(2) Poland R. New Zealand’s surveillance programme for chronic wasting disease. Surveillance
29(4), 3-5, 2002.
(3) Williams ES. Chronic Wasting Disease. Veterinary Pathology 42(5), 530-549, 2005.
(4) Kim TY, Shon HJ, Joo YS, Mun UK, Kang KS, Lee YS. Additional cases of Chronic Wasting
Disease in imported deer in Korea. Journal of Veterinary Medical Science 67(8), 753-759, 2005.
(5) European Food Safety Authority. Opinion on a surveillance programme for chronic wasting
disease in the European Union. The EFSA Journal 70, 1-7, 2004. [cited 20 February 2009]
Available from: http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/opinion_
biohaz12_ch_wast_dis_ef70_en1.pdf
(6) Schettler E, Steinbach F, Eschenbacher-Kaps I, Gerst K, Meussdoerffer F, Risch K, Streich WJ,
Frohlich K. Surveillance for prion diseases in cervids, Germany. Emerging Infectious Diseases
12(2), 319-322, 2006.
(7) De Bosschere H, Saegerman C, Neukermans A, Berkvens D, Casaer J, Vanopdenbosch E, Roels
S. First chronic wasting disease (CWD) surveillance of roe deer (Capreolus calreolus) in the
northern part of Belgium. Veterinary Quarterly 28(2), 55-60, 2006.
(8) Roels S, Saegerman C, De Bosschere H, Berkvens D, Gergoire F, Hoyoux A, Mousset B,
Desmecht D, Vanopdenbosch E, Linden A. First results of chronic wasting disease (CWD)
surveillance in the south-eastern part of Belgium. Veterinary Quarterly 27(3), 98-104, 2005.
(9) Raymond GJ, Bossers A, Raymond LD, O’Rourke KI, McHolland LE, Bryant III PK, Miller MW,
Williams ES, Smits M, Caughey B. Evidence of a molecular barrier limiting susceptibility of
humans, cattle and sheep to chronic wasting disease. EMBO Journal 19(17), 4425-4430, 2000.
(10) Mathiason CK, Powers JG, Dahmes SJ, Osborn DA, Miller KV, Warren RJ, Mason GL, Hays SA,
Hayes-Klug J, Seelig DM, Wild MA, Wolfe LL, Spraker TR, Miller MW, Sigurdson CJ, Telling GC,
Hoover EA. Infectious prions in the saliva and blood of deer with chronic wasting disease.
Science 314(5796), 133-136, 2006.
Lachlan McIntyre
[email protected]
Naya Brangenberg
[email protected]
MAF Biosecurity New Zealand
PO Box 2526
Wellington
Surveillance 36 (1) 2009
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