ARIZONA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM
Chronic Wasting Disease What is Chronic Wasting Disease?
Chronic Wasting Disease (CWD) is a neurological disease affecting deer, elk
and moose that attacks the brain and is characterized by progressive weight
loss, abnormal behavior and eventual death. CWD belongs to a group of diseases
called transmissible spongiform encephalopathies (TSEs). CWD is similar to
scrapie in sheep and bovine spongiform encephalopathy (also known as mad cow
disease) in cattle as well as variant creutzfeldt-jakob disease (vCJD) in
humans, but CWD is a distinct disease known only to affect members of the deer
family. These disorders are thought to be caused by abnormal proteins or
“prions”.
Deer and elk infected with CWD during clinical stages may exhibit symptoms
including emaciation, lowered head and ears, “blank” facial stare, excessive
thirst accompanied by excessive urination,decreased food consumption leading to
poor body condition, teeth grinding, excessive salivation, wide-based stance,
and incoordination. Affected animals may be seen walking repetitive courses. The
clinical disease is often more subtle and prolonged in elk than in deer.
Can Humans be Affected with CWD?
There have been no reported cases of humans being affected with the prions
associated with CWD, either through contact with infected animals or by eating
the meat of infected animals. Studies have shown that humans living within
endemicareas have not shown any significant increase in the number of CJD or any
other documented prion disease resulting from CWD exposure. Although there has
been no identifiable risk to humans from consuming animals infected with CWD, it
cannot be said with 100% certainty that CWD will not transmit from cervids (deer
and elk) to humans so it is always important to take the proper measures to
avoid exposure to the CWD agent.
Surveillance Efforts in Arizona
Program Objectives:
To conduct hunter harvested and targeted surveillance of both deer and elk
throughout the state of Arizona. To increase surveillance efforts in areas
bordering CWD-positive states. Surveillance in Arizona has thus far shown that
CWD is not present in our deer or elk populations. The Game and Fish Department
has implemented steps to reduce the potential for this disease so that it
doesn't establish itself in Arizona. Extra efforts are being made to focus on
areas bordering CWD-positive states (CWD-positive map). Protocols have been
established should the disease find its way across our borders.
Arizona has been divided into risk areas based on proximity to states where
CWD has been found in wild cervid populations. Game Management Units (GMUs) have
been grouped based on their locations and catagorized as high risk, medium risk,
and low risk (see map below). Within each risk area, rough population estimates
of cervids (mule deer, white-tailed deer, and elk obtained from the Department’s
survey data) were used in an epidemiological model to calculate a desired sample
size that would allow for the detection of a 1% prevalence of CWD at a 95%
confidence interval.
The Department began conducting CWD surveillance in 1998 and has since
collected over 19,000 samples. Each year samples are collected from hunter
harvested and targeted deer and elk throughout the state. Hunter harvested
samples are typically collected by means of taxidermists and meat processor
participation, as well as, through check stations and regional drop-offs.
Targeted sampling consists of samples collected from roadkill and those
dispatched by Wildlife Managers due to the animal exhibiting signs consistent
with CWD.
Hunters can assist by bringing in the head of their recently harvested deer
or elk to any Game and Fish Department office between the hours of 8 a.m. and 5
p.m., Monday through Friday. Place the head in a heavy plastic garbage bag for
delivery, and keep it cool and out of the sun. If the weather is warm, it is
best to bring in the head within 1 day of harvest and keep it on ice in a cooler
before delivery.
When submitting heads for sampling, please provide accurate, up-to-date
hunter information (name and phone number) as well as hunt information (hunt#,
permit #, game management unit harvested in, state, and hunt license) as this
information is crucial should a positive CWD sample occur. Precautions
In order for Arizona to maintain its CWD-free status, hunters are advised
to take certain precautions when hunting in state or out of state. The
Department is concerned that CWD might be inadvertently brought into our state
through the transport of infected animal tissues. The Arizona Game and Fish
Commission Rule R12-4-305 allows an individual to possess, transport, or import
only the following portions of cervids lawfully taken in another state or
country:
Boneless portions of meat, or meat that has been cut and packaged; Clean
hides and capes with no skull or soft tissue attached; Antlers, clean skull
plates or skulls with antlers attached with no meat or soft tissue remaining;
Finished taxidermy mounts or products; and Upper canine teeth with no meat or
tissue attached. Do not bring the brain, intact skull, or spinal column of deer
or elk harvested in another state back into Arizona.
If you intend to hunt out of state, contact the wildlife agency in the area
you intend to hunt. Many states have regulations on carcass movement.
The following precautions should be taken when pursuing or handling deer or
elk:
Do not shoot, handle or consume any animal that is acting abnormally or
appears to be sick. Contact the Arizona Game and Fish Department at
1-800-352-0700 if you see or harvest an animal that appears sick. Wear latex or
rubber gloves when field dressing your deer or elk. Bone out the meat from your
animal. Don't saw through bone, and avoid cutting through the brain or spinal
cord (backbone). Minimize the handling of brain and spinal tissues. Wash hands
and instruments thoroughly after field dressing is completed. Avoid consuming
brain, spinal cord, eyes, spleen, tonsils and lymph nodes of harvested animals.
(Normal field dressing coupled with boning out a carcass will remove most, if
not all, of these body parts. Cutting away all fatty tissue will remove
remaining lymph nodes.) Avoid consuming the meat from any animal that tests
positive for the disease. If you have your deer or elk commercially processed,
request that your animal is processed individually, without meat from other
animals being added to meat from your animal. Contact Information
Wildlife Health Program Supervisor
Arizona Game and Fish Dept
5000 W. Carefree Hwy
Phoenix, AZ 85086
off. 623-236-7351
fax 623-236-7918
cell 623-252-7685
https://www.azgfd.com/PortalImages/files/wildlife/research/disease-CWD/ChronicWastingDisease-Web.pdf
ArizonA GAme And Fish depArtment 2015-16 Arizona Hunting Regulations
Attention hunters Game and Fish Commission Rule R12-4-305(I) was amended to
include the restriction of importing the nervous tissue of cervids (deer and
elk) from legally harvested animals from other states or countries into Arizona.
Essentially, only the meat, hides and antlers (free of brain tissue, spinal
tissue and nervous tissue) from deer and elk lawfully harvested in other states
or countries can be imported into Arizona. This Rule amendment was in response
to the prevention of Chronic Wasting Disease (CWD) in deer and elk populations
within Arizona. For more information on this rule and CWD, please see page 47.
Hunters can Help Monitor Arizona Deer Health – Submit Deer Heads for CWD
Testing Bring the head of your recently harvested deer to any Game and Fish
Department office between 8 a.m. and 5 p.m., Monday through Friday (office
addresses are listed on page 5). Department personnel will collect a tissue
sample for Chronic Wasting Disease (CWD) testing. Hunters that are successful in
Units 1, 2, 3, 27, 28, 29 and 30A are especially encouraged to submit heads
because these units are close to New Mexico, a state that has detected CWD in
deer and elk. It is best if the head has been kept cool and is submitted within
a day of harvest. The head may be placed in a garbage bag for delivery. You will
be asked to provide information on approximately where the animal was harvested
(within your unit) and where you can be reached (phone number) in case the test
is positive. No CWD has been detected in Arizona’s deer or elk to date. CWD
results can be found here: http://azgfdeservices.com/cwdlogin.aspx
Keep CWD out of Arizona To protect Arizona’s deer and elk herds from Chronic
Wasting Disease, new regulations have been placed on movement of animal parts
into the state. Hunters are required to take these precautions when hunting deer
or elk out-of-state (effective July 1, 2013): • Do not bring the brain, intact
skull, or spinal column into Arizona. The following elk or deer parts harvested
out-ofstate are OK to bring back into Arizona: • Boneless portions of meat, or
meat that has been cut and packaged; • Clean hides and capes with no skull or
soft tissue attached; • Antlers, clean skull plates or skulls with antlers
attached with no meat or soft tissue remaining; • Finished taxidermy mounts or
products; and • Upper canine teeth (buglers, whistlers, ivories) with no meat or
tissue attached. CWD is present in the neighboring states of Utah, Colorado, and
New Mexico, as well as many other popular hunting destinations for deer and elk.
Some states have strict regulations governing carcass movement, so we encourage
you to contact the wildlife agency where you travel for any applicable
regulations.
Hunters can Help Monitor Arizona Elk Health – Submit
Elk Heads for CWD Testing
Bring the head of your recently harvested elk to any Game and Fish
Department office between 8 a.m. and 5 p.m., Monday through Friday (office
addresses are listed on page 3). Department personnel will collect a tissue
sample for Chronic Wasting Disease (CWD) testing. Hunters that are successful in
Units 1, 2, 3, 27, 28, and 31 are especially encouraged to submit heads because
these units are close to New Mexico, a state that has detected CWD in deer and
elk.
It is best if the head has been kept cool and is submitted within a day of
harvest. The head may be placed in a garbage bag for delivery. You will be asked
to provide information about your harvested elk (hunt number, permit number,
game management unit, and date of harvest) and where you can be reached (phone
number) in case the test is positive. No CWD has been detected in Arizona’s deer
or elk to date.
CWD results can be found here:
Keep CWD out of Arizona
To protect Arizona’s deer and elk herds from Chronic Wasting Disease, new
regulations have been placed on movement of animal parts into the state.
Hunters are required to take these precautions when hunting deer or elk
out-of-state:
• Do not bring the brain, intact skull, or spinal column into
Arizona.
The following elk or deer parts harvested out-of-state are OK to bring back
into Arizona:
• Boneless portions of meat, or meat that has been cut and packaged;
• Clean hides and capes with no skull or soft tissue attached;
• Antlers, clean skull plates or skulls with antlers attached with no meat
or soft tissue remaining;
• Finished taxidermy mounts or products; and
• Upper canine teeth (buglers, whistlers, ivories) with no meat or tissue
attached.
CWD is present in the neighboring states of Utah, Colorado, and New Mexico,
as well as many other popular hunting destinations for deer and elk. Some states
have strict regulations governing carcass movement, so we encourage you to
contact the wildlife agency where you travel for any applicable regulations.
2016 Pronghorn Antelope and Elk Hunt Draw Information
File Format: PDF/Adobe Acrobat
Mar 16, 2016 ... Chronic Wasting Disease, new regulations have been placed
on movement of animal parts into the state. Hunters are required to take
these.
www.azgfd.com
ARIZONA GAME AND FISH DEPARTMENT
FY2013/2014 CHRONIC WASTING DISEASE REPORT
Wildlife and Sport Fish Restoration Act Fund
Carrington Knox
Wildlife Disease Biologist
Arizona Game and Fish Department
5000 W. Carefree Highway
Phoenix, AZ 85086
June 30, 2014
NEW CONTACT ;
Anne Justice-Allen, DVM
Wildlife Health Program Supervisor
Arizona Game and Fish Dept
5000 W. Carefree Hwy
Phoenix, AZ 85086
off. 623-236-7351
fax 623-236-7918
cell 623-252-7685
Wildlife Health Program Supervisor
Arizona Game and Fish Dept
5000 W. Carefree Hwy
Phoenix, AZ 85086
off. 623-236-7351
fax 623-236-7918
cell 623-252-7685
AZA Guidelines for Chronic Wasting Disease Surveillance Approved by the AZA
Board of Directors in 2003
In response to the concern for introduction of Chronic Wasting Disease
(CWD), and the management and regulatory implications for zoological facilities,
a set of guidelines have been drafted for AZA-accredited institutions by an ad
hoc working group of the American Association of Zoo Veterinarian's Infectious
Disease Committee in conjunction with the AZA Animal Health Committee (2003).
The objectives of these guidelines are to:
provide AZA-accredited institutions with information regarding CWD; develop
recommendations for transport of susceptible animals between institutions (both
AZA-accredited and non-accredited); develop a protocol for CWD surveillance in
AZA-accredited institutions that parallels those plan being formulated by
national regulatory authorities at this time; and recommend risk management
strategies for dealing with suspected or confirmed CWD cases in AZA-accredited
institutions should they occur. Although every individual institution needs to
establish their own acceptable level of risk with regard to this issue, the
implementation of these guidelines will show state and federal regulatory
agencies dealing with AZA-accredited institutions that our community is both
informed and proactive with regard to this issue. As USDA and state regulatory
agencies develop mandatory programs for surveillance and eradication of CWD and
cervid transport, these guidelines may require modification to comply with
regulatory requirements for each individual institution. It is strongly
encouraged that senior zoo staff establish a relationship with regulatory
personnel responsible for monitoring CWD programs in their area in order to keep
abreast of regulations being developed at both the State and Federal
levels.
Objective 1: Introduction An introduction to Transmissible Spongiform
Encephalopathies and Chronic Wasting Disease
A full review of the Transmissible Spongiform Encephalopathies (TSE) was
recently published in both the AZA Communique and the Journal of Zoo and
Wildlife Medicine. [3] The causative agents of TSE's are described as
unconventional proteinaceous infectious particles, or prions. Prions have yet to
be fully characterized but it is thought that they are abnormal proteins that
are capable of changing normal cellular prion proteins into abnormal shapes.
These abnormal shapes cause conformational changes that result in changes in
many of the properties of these proteins including: increased resistance to
heat, pH and partial resistance to proteases.
Large-scale improper folding of protein sheets in tissues of the central
nervous system is partially responsible for neurological clinical signs in all
affected species. This improper folding, when it occurs in sufficient
quantities, results in the formation of holes in brain tissue that gives it a
spongy appearance under the microscope – hence the name spongiform
encephalopathy.
Transmissible spongiform encephalopathies consist of numerous diseases in
man and animals. [3] Those TSE's of concern to zoo and wildlife practitioners
include scrapie (sheep and goats), bovine spongiform encephalopathy (BSE),
transmissible mink encephalopathy (TME), feline spongiform encephalopathy (FSE),
and chronic wasting disease (CWD) in deer (Odocoileus sp.) and elk (Cervus
elaphus nelsoni). Kuru, classical Creutzfeld-Jakob disease (CJD),
Gerstmann-Straussler syndrome (GSS), fatal familial insomnia, and variant
Creutzfeld-Jakob disease (vCJD) are TSEs that affect humans.
All are characterized by a long incubation period, up to forty years in
kuru, without the presence of clinical symptoms. The clinical phase results in a
progressive degenerative neuropathy without the presence of an identifiable
inflammatory process or specific signs of chronic viral infection. In addition,
no virus-like or other micro-organism-like structure is present in the brains or
CNS fluid of infected patients. All infections result in death in the species in
which they occur. There is currently no vaccine or treatment for any of these
diseases.
Chronic Wasting Disease (CWD) is a progressive, debilitating and invariably
fatal disease of deer and elk. [1] It was first recognized in 1967 and clinical
signs include progressive weight loss, behavior changes, and listlessness. It is
classified as a transmissible spongiform encephalopathy (TSE) or "prion"
disease. The disease has been found in greatest numbers among free-ranging deer
and elk in north central Colorado and southeastern Wyoming; but cases have been
found in free-ranging deer and/or elk in Nebraska, South Dakota, New Mexico,
Utah, Illinois, and Wisconsin. In addition, CWD has been diagnosed in farmed elk
and/or deer herds in several states including Colorado, Kansas, Minnesota,
Montana, Nebraska, Oklahoma, South Dakota, and Wisconsin. In Canada, CWD has
been identified in both free-ranging deer and privately owned elk in
Saskatchewan, and farmed elk in Alberta.
CWD has affected mule deer (Odocoileus hemionus), white-tailed deer (O.
virginianus), and elk (Cervus elaphus nelsoni). Other ruminants housed near
infected cervids have not been naturally infected. It is not known whether other
cervid species (North American or exotic) are susceptible to infection.
Transmission between animals is most likely to occur through animal-to-animal
contact and/or contamination of feed or water sources with saliva, urine or
feces from a diseased animal. The route of transmission has not been
definitively determined. It does not appear that CWD is transmitted to other
ruminant species in contact with infected cervids.
Diagnosis is confirmed by immunohistochemical staining of the obex portion
of the brainstem after death. Recently, three ELISA-based CWD diagnostic test
kits have been approved by the USDA; these tests can be applied to lymph node,
and are licensed for use in deer and elk. Although these will be used for
surveillance of free-ranging cervids, they are not currently approved for use in
captive cervid regulatory programs.
Current information indicates that CWD does not cause illness in people.
The known prion diseases of humans and domestic animals appear to be caused by
prions unrelated to CWD. It is unknown whether consumption of infected tissue
may present a risk. Risk avoidance recommendations for those with close contact
to susceptible animals (hunters, wildlife biologists, pathologists)
include:
Do not consume meat from any deer or elk that looks or acts sick. Wear
gloves when field dressing/performing necropsy on carcasses and wash hands and
instruments thoroughly when complete. Do not consume brain, spinal cord, eyes,
spleen, tonsils, and lymph nodes from deer and elk. The USDA and some states
have a voluntary herd-certified status program. A federal program for
surveillance and eradication of CWD is currently being developed by the USDA.
Several states have placed moratoria on imports and transport of cervids at the
time of this writing. Check with your State Veterinarian for current
information.
Objective 2: Acquisition and Disposition Recommendations for acquiring and
dispositioning susceptible animals in AZA-accredited facilities Introduction of
CWD into a zoological institution may occur through:
Acquisition of infected asymptomatic animals;
Unintended contact between susceptible collection cervids and free-ranging
cervids;
Contamination of the exhibit/facility, feed, or bedding. Regulations for
interstate transport of cervids are currently being developed by the USDA and
many states. Due to the rapid changes in state and federal regulations
pertaining to cervid movement, it is critical that a designated staff member
obtain current information from the appropriate regulatory agencies.
Jurisdiction over captive cervids varies between states but is assigned to
either the State's Department of Agriculture (DOA), or equivalent, and/or
Department of Fish and Game, or equivalent.
The currently proposed USDA program will be designed to restrict interstate
movement in order to provide basic minimum standards for the federal programs
(Plan for Assisting State, Federal Agencies, and Tribes in Managing Chronic
Wasting Disease in Wild and Captive Cervids, USDA-APHIS, June 26, 2002). State
regulatory programs may implement additional controls if deemed necessary.
We recommend that the following guidelines and definitions be applied to
cervid and other ungulate species:
High Risk species
Known CWD susceptible cervid species (O. hemoinus, O. virginianus, C.
elaphus nelsoni, and subspecies);
At Risk species
Other cervid species that have unknown susceptibility to CWD;
Low / No Risk species
Non-cervid ungulates Movement of cervids from a non-accredited source into
an AZA-accredited institution: Source area
All incoming cervids ("high" and "at risk" species) should originate from
facilities in non-endemic areas. This includes cervids originating from the
wild. These areas may change as increased surveillance occurs. Source
history
Obtain "high risk" animals from sources that have met the criteria for a
"CWD accredited-free herd" (surveillance program in place without detection of
CWD for a minimum of 5 years). "At risk" cervids and other ungulates should be
acquired from facilities without a history of CWD or undiagnosed cases of
wasting or neurologic disease. State regulations may only allow importation or
intrastate transport of cervids from herds with surveillance data; therefore,
this restriction may differ between states. Cervids that are obtained from
free-ranging herds must be from non-endemic areas and/or less than 12 months of
age. Movement between AZA-accredited institutions: Documentation of a disease
surveillance program (based on the AZA requirements for medical records and
necropsies) and provisions to exclude wildlife may suffice to meet the same
criteria established for "CWD accredited free herds" of farmed cervids.
Discussion with regulatory agencies may allow AZA institutions to transfer
cervids between institutions (similar to the exemption for TB testing of cervids
transferred between AZA facilities). As the federal program is developed, AAZV
will continue to work with the USDA on behalf of AZA member institutions.
However, it is expected that program species (Odocoileus hemionus, O.
virginianus, Cervus elaphus nelsoni) will be required to meet all federal
requirements, regardless of source.
Movement from an AZA-accredited institution to a non-accredited facility:
Only those AZA-accredited institutions that have documentation meeting standards
for a "CWD accredited free herd" should ship cervids to non-accredited
facilities. Receiving facilities should meet all institutional and AZA
requirements for disposition.
Summary of General Management Recommendations for Zoos Obtain a herd
history of source of captive elk or deer that may be acquired for the
collection.
Sources of captive elk or deer should ideally be from another
AZA-accredited institution or herd that is certified as CWD-free.
Minimize potential contact between collection and wild cervids.
Submit brain for CWD surveillance to the National Veterinary Services
Laboratory (NVSL) from any cervid that dies or is euthanized over the age of 12
months.
Check with state veterinarian's office regarding current restrictions in
movement of cervids. Objective 3: Surveillance Plan Recommended surveillance
plan for AZA-accredited institutions Herd Certification Herd "CWD-free"
certification programs will vary between states, and may be more stringent than
the USDA federal program. Currently, there is no officially approved antemortem
(performed on living animal) test for CWD. Diagnosis is based on histopathologic
changes in brain tissue using immunohistochemical (IHC) staining of the obex
(brainstem). There are approximately 26 veterinary diagnostic laboratories
certified by USDA to perform CWD testing (contact your state veterinarian for
details). In 2003, the USDA approved three ELISA-based CWD diagnostic test kits
(Bio-Rad, VMRD, IDEXX).
Although these tests are incorporated into surveillance of free-ranging
cervids, they are not currently approved for captive cervid regulatory programs.
In order to align with planned federal certification status for captive cervids,
AZA institutions should maintain cervid herds for a minimum of 5 years with no
evidence of CWD on necropsy using approved testing methods.
The national surveillance plan for farmed cervids (USDA) includes mandatory
death reporting and CWD testing (by a certified laboratory) of all animals,
except calves, that are slaughtered or die on the premises. It is not known at
this time whether these plans will be applied to zoos in a regulatory fashion.
Record keeping requirements for AZA accreditation should be adequate to meet
inventory requirements; however, additional diagnostic testing may need to be
implemented.
Experimental studies have indicated that IHC staining of lymphoid tissue
obtained via tonsil biopsy may provide an antemortem test for CWD. [2] It
appears that this may be useful to detect early infection in deer but may not be
sensitive in elk, due to differences in CWD pathogenesis in this species.
Therefore, lymphoid tissue (especially from tonsils) should be considered for
testing from "high risk" or "at risk" species to contribute to the database.
Details of collection and submission procedures should be obtained directly from
the designated laboratory.
Necropsy surveillance AZA accreditation standards require member
institutions to perform necropsy examinations on all collection animals to
determine the cause of death (see www.aza.org/accreditation). This does not
always require removal and examination of the brain (specifically, the obex). It
is strongly recommended that all zoo cervids over the age of 12 months that die
or are euthanized should have the head (specifically, obex of the brain)
submitted to NVSL, or a certified laboratory for CWD testing. In addition,
tonsil and retropharyngeal lymph nodes should be collected for possible future
testing.
Management and Surveillance of Free-Ranging Cervids on Zoo Grounds
Free-ranging cervids pose a potential risk to zoo collection animals. Although
the actual risk cannot be quantified at this time, it is real. Therefore, every
effort should be made to exclude these animals from zoo grounds. Maintenance of
appropriate wildlife exclusion methods such as perimeter fences should be used
to minimize contact between wildlife and collection animals. Any free-ranging
cervids that die or are euthanized around the zoo grounds or surrounding areas
should be screened for CWD.
Objective 4: Risk Management Risk management, response and control USDA and
State regulatory eradication programs The USDA began its CWD eradication program
for farmed elk and deer herds in fiscal year 2003 (Plan for Assisting States,
Federal Agencies, and Tribes in Managing Chronic Wasting Disease in Wild and
Captive Cervids, USDA-APHIS, June 26, 2002). The National Park Service will
continue its targeted surveillance and removal of cervids exhibiting clinical
signs of CWD. The Department of the Interior will work with states in hunter
surveillance programs. Although enrollment of captive cervid herds is voluntary,
herds that have program species (red deer, elk, mule deer, white-tailed deer)
will not be permitted to move animals interstate if they are not
certified.
If enrolled from initiation of the program, interstate transport will be
permitted after the first year of surveillance if no cases of CWD have been
detected. Herds that are enrolled at later dates will be required to meet the
full 5-year surveillance period before moving animals interstate. Interstate and
intrastate movement of non-program cervid species will be subject to state
regulations. It is strongly recommended that all AZA institutions comply with
voluntary requirements for CWD certification for any cervid herds in their
collection, including non-program cervid species.
If an institution participates in a voluntary herd certification program,
remember that CWD is a reportable disease and results of CWD positive cases will
be communicated through a network of certified testing laboratories to the USDA.
Therefore, cervids from AZA institutions that test positive will be reported by
the testing laboratory. In addition, veterinarians at the specific institutions
will be responsible for contacting the appropriate state agencies (as designated
by the state; this could include the state veterinarian, department of fish and
wildlife, board of animal health, etc.) should a positive be found. Those
institutions with CWD positive cervids will fall under the jurisdiction of
federal and state eradication programs; we recommend creating a relationship
with your regulatory authorities now to enhance communication should a suspect
or positive case be found.
Currently, the USDA defines a positive case of CWD as any animal found
positive by IHC staining of appropriate tissues. Suspects include any animal
from a "high risk" species with compatible clinical signs. "Trace back" and
"trace forward" investigations would be conducted by regulatory personnel to
determine source and possibly exposed animals. Based on documentation already
present in AZA-accredited institutions, sources and dispositions of animals can
be identified, including enclosures and animal contacts.
Options for herds with a positive case include depopulation or quarantine
and surveillance. Depopulation may not be desirable in the case of genetically
valuable individuals. However, quarantine would result in restrictions on
movements of cervids to and from, and possibly within, the institution.
Additional restrictions on use of the premises, surveillance and testing, and
quarantine for at least 60 months from the last known case would be imposed on
the institution.
Individual institutions will need to determine the most appropriate plan
with their regulatory agencies. Herd management plans are required for CWD
positive and exposed herds. These plans include provisions for depopulation or
quarantine, disposition of carcasses, decontamination, and future use of the
premises (Plan for Assisting States, Federal Agencies, and Tribes in Managing
Chronic Wasting Disease in Wild and Captive Cervids, USDA-APHIS, June 26,
2002).
Carcass disposal and decontamination Carcass disposal of cervids may be
regulated by state or local municipalities. Methods for handling CWD positive
carcasses include incineration, tissue digestion, and burial using an engineered
landfill (USAHA CWD Workshop, St. Louis, Missouri, October 22, 2002). Zoos are
encouraged to discuss changes in current procedures with their local and state
regulatory agencies. Wisconsin has developed a CWD carcass disposal risk
assessment document. Guidelines for farm clean-up and disinfection have been
created for use in Saskatchewan.
Based on other prion diseases and the link between contaminated pastures
and CWD outbreaks, environmental contamination presents a major risk factor.
Whether environments can be completely disinfected is questionable. Until
effective cleaning and disinfection protocols can be identified, it is
recommended that cervids should not be introduced to facilities or exhibits
where CWD has occurred for at least 5 years. It is also critical that
free-ranging cervids and other wildlife be excluded from these areas.
Other considerations Other biosecurity measures that should be addressed
for AZA-accredited institutions include staff education addressing zoonotic
concerns, carcass disposal methods, and exhibit and facility contamination and
decontamination. Currently, CWD has not been linked to human disease, despite
recent media reports. AAZV has developed a Chronic Wasting Disease Fact Sheet
(in PDF) that outlines general precautions that should be followed to minimize
risks.
For Additional Information Chronic Wasting Disease Alliance APHIS Chronic
Wasting Disease Information State of WY State of CO State of NE State of MN
State of WI APHIS: Scrapie Information APHIS: Bovine Spongiform Encephalopathy
Information UK Department for Environment Food and Rural Affairs: Bovine
Spongiform Encephalopathy Information Acknowledgements We (M. Miller, D. Travis)
wish to thank AAZV, Disney's Animal Programs, and Lincoln Park Zoo for support
to attend the USAHA meetings and for time to keep current on diseases of concern
to the zoo veterinary community. We also wish to thank Drs. Robyn Barbiers,
Julie Langenberg, Bob Cook, Wilbur Amand, Don Janssen, and Bruce Rideout for
their advice and comments on this manuscript. We especially appreciate the
discussions with Drs. Michael Gilsdorf and Dean Goeldner (USDA NAHP) regarding
CWD and zoos.
Literature Williams, E.S., M.W. Miller, T.J. Kreeger, R.H. Kahn, and E.T.
Thorne. 2002. Chronic wasting disease of deer and elk. J. Wildl. Managem. 66(3):
551-563.
Wolfe, L.L., M.M. Conner, T.H. Baker, V.J. Dreitz, K.P. Burnham, E.S.
Williams, N.T. Hobbs, and M.W. Miller. 2002. Evaluation of tonsillar biopsy data
for estimating chronic wasting disease prevalence in free-ranging mule deer.
Proc. Wildl. Dis. Confer. Arcata, California. p. 126.
Travis, D.A. and M. Miller. 2003. A Review of the transmissible spongiform
encephalopathies and recommendations for surveillance of chronic wasting disease
in zoos. Journal of Zoo and Wildlife Medicine 34(2): 125-133.
Importation requirements for Deer include: The word "Cervidae" refers to a
family of animals that includes a number of different species of deer. The
Arizona Game and Fish Department has regulatory jurisdiction over the following
species of Cervidae: Moose, Whitetailed Deer, Mule Deer, Red Deer, and Elk (also
known as Wapiti). For further information about these species, contact the
Arizona Game and Fish Department at (602) 942-3000. For all other species of
Cervidae including Reindeer, Axis Deer, Sitka Deer, and Fallow Deer, the Arizona
Department of Agriculture has restrictions on their importation. The
requirements for these types of Cervidae include:
Prior import permit; issued by telephone; call (602) 542-4293 from 8 a.m.
to 5 p.m. Arizona time Monday through Friday. An original health certificate
issued by an accredited veterinarian within 30 days prior to entry. Photocopies
of health certificates must have an original veterinarian signature. Individual
identification by USDA eartag listed on the health certificate. Tuberculosis
testing:
Accredited-free herd – no testing required. Qualified or monitored herd –
one negative tuberculosis test within 90 days before entry. Non-status herd –
two negative tuberculosis tests no less than 90 days apart with the second test
conducted within 90 days before entry. Brucellosis testing:
Certified-free herd – no testing required. Monitored herd – one negative
test on all sexually intact animals 6 months of age or older within 90 days
before entry. Non-status herd - one negative test on all sexually intact animals
6 months of age or older within 30 days before entry and a retest conducted
within 90 days after entry.
ARIZONA GAME AND FISH DEPARTMENT
Chronic Wasting Disease Prevention, Detection, Response, and Management
Plan
July 12, 2010
Notice of Public Information Arizona Game and Fish Commission Statewide
ban on cervid importation Effective May 18, 2002, the Arizona Game and Fish
Department, under direction from the Arizona Game and Fish Commission and under
the authority of R12-4-409(G), has instituted an emergency statewide ban on the
importation of cervids designated as restricted live wildlife under
R12-4-406(A)(9)(b). The purpose of the emergency importation ban is to prevent
the movement of captive cervids into Arizona to protect against the introduction
of chronic wasting disease to free-ranging or captive wildlife.
The emergency importation ban applies to cervids of the genus Alces, common
name: moose; cervids of the genus Odocoileus, common name: white-tailed and mule
deer; and cervids of the genus Cervus, common name: red deer and wapiti (elk),
except that the species Cervus nippon, Nippon deer, is not restricted.
Chronic wasting disease (CWD) was first recognized by biologists in the
1960s as a disease syndrome of captive deer held in wildlife research facilities
in Ft. Collins, Colorado, but was not recognized as a transmissible spongiform
encephalopathy until the late 1970s. This disease was subsequently recognized in
captive deer, and later in captive elk, from wildlife research facilities near
Ft. Collins, Kremmling, and Meeker, Colorado, and Wheatland, Wyoming, as well as
in at least two zoological collections. More recently, CWD has been diagnosed in
privately owned elk residing on game ranches in several Western states and
provinces. Although CWD was first diagnosed in captive research cervids, the
original source (or sources) of CWD in either captive cervids or free-ranging
cervids is unknown; whether CWD in research animals really preceded CWD in the
wild, or vice versa, is equally uncertain.
Much of the information we have on this disease comes from the endemic area
of northeastern Colorado and southeastern Wyoming where it appears that, on
average, CWD probably infects about 5-15 percent of the deer in the area.
Modeling of the impact of this disease indicates that this rate of infection is
sufficient to suppress deer population levels in this area.
In addition to cases in captive research and free-ranging deer and elk, CWD
has been diagnosed in privately owned elk on game farms in several states
beginning in 1996. Infection has been particularly severe in a group of
interconnected facilities near Rapid City, South Dakota, that appear to be the
original source of infection for other South Dakota game farms as well as the
Saskatchewan epidemic. In contrast, infected elk in two of three Nebraska farms
originated in Colorado, and infected elk in Oklahoma apparently originated in
Montana; CWD has been confirmed in the Montana and Colorado source herds.
At this time, the detection of CWD in new areas is expanding rapidly as
there have been detection in free-ranging deer in additional areas of Nebraska,
Alberta, Wisconsin and South Dakota during 2002. In addition to the problems
associated with this disease on wild populations, there is also a significant
economic impact with the detection of the disease in both free ranging and
captive cervids. As an example, Saskatchewan has spent approximately $30 million
in attempts at eradicating the disease in infected game farms. In Colorado, a
supplemental appropriation of $300,143 was made in December 2001, and an
additional appropriation of $430,750 is being considered for the fiscal year
beginning on July 1, 2002.
One of the problems with this disease is that it is virtually impossible to
eradicate once it enters into a jurisdiction. This conclusion is based on the
fact that there is no live animal test for the disease, so an agency cannot
implement testing and elimination of only infected animals. Second, there is a
long incubation period associated with the disease. Some of the research that
has been completed suggests that the incubation period may exceed 36 months, and
perhaps even longer. Another problem is that the epidemiological links from one
positive herd to 38 other infected captive elk herds in Saskatchewan and the
shipment of exposed elk from one infected captive elk operation in Colorado to
facilities in 19 states indicate the potential for the spread of CWD via the
captive cervid industry. This means that from a few herds, the disease has the
potential to have been spread to as many as 19 other states. Finally, a
significant issue with this disease is that one of the measures considered to
control its spread is extreme reduction of animal density. This entails removal
of a large number of deer that otherwise could be harvested by hunters, which in
turn equates to a potential economic loss to not only the Department but also to
local businesses such as restaurants and hotels that are supported by hunters.
Although chronic wasting disease (CWD) is not a new disease, there are a
number of factors that have escalated the importance of this disease in the last
three months. Until recently, this disease was largely thought of as a disease
of the 11-county region comprised of southeastern Wyoming, northeastern
Colorado, and the panhandle region of Nebraska. However, recently, this disease
has been detected in free-ranging wildlife in South Dakota, the West Slope
region of Colorado, and in Wisconsin. This signals to the wildlife health
community that the disease has the capacity to expand to outside what was
thought to be the endemic area. The economic consequences of these new
detections are immense as is evidenced from the experience in Wisconsin. Within
the first month after detection, the Wisconsin wildlife management agency
expended approximately $250,000 in control and public information efforts. This
has proven to be the tip of the iceberg as the agency has announced plans to
kill approximately 15,000 animals in the focal area. This will also cost the
agency considerable money.
At this time, the most effective management approach is to take measures to
ensure, to the greatest extent possible, that the disease does not enter into
Arizona. Therefore, effective May 18, 2002, the Arizona Game and Fish Department
has imposed an emergency statewide ban on the importation of cervids designated
as restricted live wildlife under R12-4-406(A)(9)(b). The Department is also
initiating Emergency and Regular rulemaking on this issue to permanently
implement the ban on cervid importation.
If you have any questions, or need any additional information on the
emergency importation ban, please contact:
Chasa O'Brien, Research Branch Chief Arizona Game and Fish Department WMRS
5000 W. Carefree Highway Phoenix, AZ 85086-5000 (623) 236-7247
*** Chronic Wasting Disease CWD TSE Prion Roundup March 30, 2016 ***
Tuesday, March 29, 2016
ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM?
Tuesday, March 29, 2016
Maryland Department of Natural Resources Five Deer Test Positive for
Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
Thursday, March 24, 2016
ARKANSAS FIRST BATCH OF TARGET TESTS REVEALS 19 ADDITIONAL CWD-POSITIVE
CERVIDS
Friday, March 18, 2016
Michigan confirms additional CWD-positive free-ranging, white-tailed deer,
bringing the total to seven
Wednesday, March 16, 2016
Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting
Disease TSE Prion
Tuesday, March 08, 2016
Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance, Testing,
and Preparedness ???
Sunday, March 06, 2016
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases
mounting
TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al
should take up Arkansas reporting of test results to the public and open
discussion. ...
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Thursday, March 10, 2016
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING
RODEO FOR CWD VIDEO
CHRONIC WASTING DISEASE: The Final Epidemic
Wednesday, March 02, 2016
Kansas Chronic Wasting Disease CWD TSE Prion 52 cases 2015 updated report
'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Friday, February 26, 2016
Pennsylvania Monitoring the Growing Threat of Chronic Wasting Disease CWD
TSE Prion
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Friday, January 29, 2016
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
Friday, November 20, 2015
ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer
Herd
Friday, October 23, 2015
Ohio Wildlife Council Passes Rule to Help Monitor CWD
Wednesday, August 05, 2015
Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases
to date
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Friday, March 18, 2016 CFSAN
Constituent Update: FDA Announces Final Rule on Bovine Spongiform
Encephalopathy BSE MAD COW TSE PRION Center for Food Safety and Applied
Nutrition - Constituent Update
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Saturday, February 6, 2016
Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
MAD COW DISEASE HAS BEEN IN THE USA FOR DECADES, AND I BELIEVE IT WAS IN
THE USA FIRST, PLEASE SEE ;
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult
mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer
or dead dairy cattle...
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
Veterinary Pathology Onlinevet.sagepub.com Published online before print
February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February
27, 2014 0300985814524798
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1
E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado
State University, Fort Collins, CO, USA 2Department of Biomedical Sciences,
Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of
Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS,
6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email
address: dseelig@umn.edu
Abstract
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and
progressive prion disease of cervids with an as yet to be fully clarified host
range. While outbred domestic cats (Felis catus) have recently been shown to be
susceptible to experimental CWD infection, the neuropathologic features of the
infection are lacking. Such information is vital to provide diagnostic power in
the event of natural interspecies transmission and insights into host and strain
interactions in interspecies prion infection. Using light microscopy and
immunohistochemistry, we detail the topographic pattern of neural spongiosis
(the “lesion profile”) and the distribution of misfolded prion protein in the
primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular
and subcellular associations between misfolded prion protein (PrPD) and central
nervous system neurons and glial cell populations. From these studies, we (1)
describe the novel neuropathologic profile of FelCWD, which is distinct from
either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide
evidence of serial passage-associated interspecies prion adaptation. In
addition, we demonstrate through confocal analysis the successful
co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and
synaptophysin, which, in part, implicates each of these in the neuropathology of
FelCWD. In conclusion, this work illustrates the simultaneous role of both host
and strain in the development of a unique FelCWD neuropathologic profile and
that such a profile can be used to discriminate between FelCWD and FSE.
prion chronic wasting disease immunohistochemistry interspecies cat feline
spongiform encephalopathy transmissible spongiform encephalopathy adaptation
species barrier
Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Docket
No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with
Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil
Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
Greetings FDA et al, I kindly would like to make comment submission to
;
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
A Notice by the Food and Drug Administration on 03/04/2016
This document has a comment period that ends in 54 days (05/03/2016)
Action Notice; Request For Comments And For Scientific Data And
Information.
Summary The Food and Drug Administration (FDA or we) is requesting
scientific data, information, and comments that would assist the Agency in its
plan to develop a risk assessment for produce grown in fields or other growing
areas amended with untreated biological soil amendments of animal origin
(including raw manure). The risk assessment will evaluate and, if feasible,
quantify the risk of human illness associated with consumption of produce grown
in fields or other growing areas amended with untreated biological soil
amendments of animal origin that are potentially contaminated with enteric
pathogens, such as Escherichia coli O157:H7 or Salmonella. The risk assessment
also will evaluate the impact of certain interventions, such as use of a time
interval between application of the soil amendment and crop harvest, on the
predicted risk. The risk assessment is intended to inform policy decisions with
regard to produce safety.
Table of Contents Back to Top DATES: ADDRESSES: Electronic Submissions
Written/Paper Submissions FOR FURTHER INFORMATION CONTACT: SUPPLEMENTARY
INFORMATION: I. Background A. What are the food safety concerns related to
untreated biological soil amendments of animal origin? B. How did FDA's rule on
produce safety address BSAAO? II. FDA's Risk Assessment III. Issues for
Consideration IV. Reference DATES: Back to Top Submit either electronic or
written comments and scientific data and information by May 3, 2016.
ADDRESSES: Back to Top You may submit comments and scientific data and
information as follows:
SNIP...
SUPPLEMENTARY INFORMATION: Back to Top
I. Background Back to Top A. What are the food safety concerns related to
untreated biological soil amendments of animal origin? Biological soil
amendments of animal origin (BSAAO) can be a source of contamination of produce
with pathogens that can cause human illness. Human pathogens in BSAAO, once
introduced to the growing environment, may be inactivated at a rate that is
dependent upon a number of environmental, regional, and other agricultural and
ecological factors. The rate of pathogen population decline over time is also
influenced by the types of BSAAO and application methods. Furthermore, the types
of produce and whether or not BSAAO may come into contact with a harvestable
portion of the crop influences the likelihood of pathogen transfer from the
amended soil to produce (Ref. 1).
Some produce farms use untreated BSAAO for various reasons, including that
they are inexpensive, readily available, and rich nutrient sources for growing
crops. Whether it is feasible for a farm to use untreated BSAAO as a principal
nutrient source depends on numerous factors, including whether there is a
required time interval between application and harvest and the length of such an
interval (which may affect the nutrients retained or available from BSAAO), and
crop nutrient demand (i.e., the nutrients needed to support crop growth).
Typical examples of untreated BSAAO are raw cattle manure, poultry litter, swine
slurry, and horse manure. FDA acknowledges that required application intervals
for certain uses of untreated BSAAO could influence the number of crop cycles a
farm is able to undertake each year and/or the choices farms make regarding
which type of amendment to apply (e.g., raw manure, composted manure, or other
nutrient sources).
B. How did FDA's rule on produce safety address BSAAO? In January 2013,
based in part upon authority provided by the FDA Food Safety Modernization Act,
we published a proposed Produce Safety Rule entitled “Standards for the Growing,
Harvesting, Packing, and Holding of Produce for Human Consumption” (78 FR 3504,
January 16, 2013). Among other provisions related to BSAAO, the proposed rule
included at § 112.56(a)(1)(i) (21 CFR 112.56(a)(1)(i)) a 9-month minimum
application interval for untreated BSAAO applied in a manner that does not
contact covered produce during application and minimizes the potential for
contact with covered produce after application (78 FR 3504 at 3637). In response
to public comments, we withdrew this proposed 9-month minimum application
interval in a supplemental proposed rulemaking that we published on September
29, 2014 (79 FR 58434 at 58457 through 58461). In the supplemental proposed
rule, we acknowledged the limited body of currently available scientific
evidence relating to the proposed 9-month interval and the need for additional
research in this area, and described our planned risk assessment and research
agenda (79 FR 58434 at 58460 through 58461). Accordingly, we deferred our
decision on an appropriate minimum application interval.
On November 27, 2015, we published a final Produce Safety Rule entitled
“Standards for the Growing, Harvesting, Packing, and Holding of Produce for
Human Consumption,” (80 FR 74354). The final rule is now codified at 21 CFR part
112. In the preamble to the final rule, we restated our decision with respect to
the appropriate minimum BSAAO application interval (80 FR 74354 at 74463). We
reserved one of the provisions in the final rule's Subpart F (Biological Soil
Amendments of Animal Origin and Human Waste) because we continue to believe that
a quantitative application interval standard is necessary and anticipate
locating such a future standard in that provision. As finalized, the Produce
Safety Rule establishes that there is no minimum application interval required
when untreated BSAAO are applied in a manner that does not contact covered
produce during or after application (§ 112.56(a)(1)(ii)), and the minimum
application interval is [reserved] when applied in a manner that does not
contact produce during application and minimizes the potential for contact with
produce after application (§ 112.56(a)(1)(i)).
II. FDA's Risk Assessment Back to Top FDA, in consultation with the U.S.
Department of Agriculture, is conducting a risk assessment to evaluate the risk
of human illness associated with the consumption of produce grown in growing
areas amended with untreated BSAAO that are potentially contaminated with
enteric pathogens such as E. coli O157:H7 or Salmonella. The risk assessment
will evaluate the impact of different agricultural and ecological conditions and
certain interventions, such as use of a time interval or intervals between
application of untreated BSAAO and crop harvest, on the predicted risk. The risk
assessment will take into account available data and information on relevant
steps in the produce food safety continuum including: The initial prevalence and
levels of pathogens in untreated BSAAO; the methods used to apply untreated
BSAAO to soils; pathogen survival (and growth) in untreated BSAAO and soils
amended with untreated BSAAO; pathogen transfer to produce grown in amended
soils; pathogen survival and growth on produce; and pathogen survival, growth,
and cross-contamination during storage and other steps in the supply chain
(e.g., washing). The risk assessment will include characterization of the
variability and uncertainty of pathogen survival and growth under different
agricultural and ecological conditions (e.g., soil types, application methods,
or geographic locations/climatic factors) and time intervals between application
of untreated BSAAO and crop harvest. The risk assessment is intended to inform
policy decisions with regard to produce safety.
III. Issues for Consideration Back to Top FDA is requesting comments and
scientific data and other information relevant to this risk assessment. We are
particularly interested in scientific data and information concerning, but not
limited to, the following factors that may affect the risk of human illness
associated with the consumption of produce grown in fields or other growing
areas amended with untreated BSAAO (including raw manure):
1. Data on the prevalence and levels of pathogens.
a. The frequency of detecting the presence of pathogens in untreated BSAAO
and soil amended with BSAAO, such as Salmonella in poultry litter, and E. coli
O157:H7 and other pathogenic Shiga-toxin producing E. coli in cattle manure.
Samples may be obtained at different stages of untreated BSAAO storage prior to
application, or after application. If available, for each data point, we also
invite information regarding the following:
The type of untreated BSAAO (e.g., animal origin and content);
how the untreated BSAAO, including raw manure, was sampled and handled
prior to analysis;
the size of the analytical unit (i.e., detection limit) and test
method;
the number of positives, the total number of samples, and the time period
in which the testing was conducted; and
sampling protocol (e.g., simple random, stratified random, targeted).
b. The pathogen concentration, i.e., the number of pathogen cells per
amount (unit volume or weight), in contaminated untreated BSAAO or soil amended
with untreated BSAAO, especially cattle manure and poultry litter. If available,
for each data point, we ask that the data be provided in unaggregated form and
that Most Probable Number (MPN) patterns as well as raw data (e.g., number of
positive and negative tubes per serial dilution) be provided.
2. Data and information on survival of pathogens (e.g., Salmonella, E. coli
O157:H7), and pathogen transfer to produce.
a. Kinetic data that describe the survival (or inactivation) or growth of
pathogens in untreated BSAAO, especially cattle manure and poultry litter;
b. Kinetic data that describe the survival (or inactivation) or growth of
pathogens in soil amended with untreated BSAAO, especially cattle manure and
poultry litter, as influenced by soil type, untreated BSAAO type, application
method, geographic locations/climatic factors (e.g., temperature, days of
sunlight, intensity of solar irradiation, moisture, rainfall) and other
factors;
c. The mechanisms for pathogen transfer from soils to specific types or
categories of produce, such as leafy greens, or to produce generally, and
associated transfer coefficients, including irrigation and rain water splash,
direct contact between produce and soil, machinery or people or animals
contaminated by soil and directly contacting produce during growth and harvest
of produce;
d. Pathogen transfer rates (i.e., transfer coefficients) from amended soils
to specific types or categories of produce, such as leafy greens, or to produce
generally, as influenced by soil type, untreated BSAAO type, application method,
climate factors, commodity type or any other pertinent factors not listed
here;
e. The survival of pathogens on produce in the field or other growing area
before harvest; and
f. The variability in the survival of different Salmonella serotypes,
different subtypes of E. coli O157:H7, or other pathogens of public health
significance in amended soils under field, greenhouse, or laboratory
conditions.
3. On-farm practices with regard to the use of untreated BSAAO, including,
but not limited to, the following aspects.
a. The extent to which untreated BSAAO are used in different regions in the
United States, as well outside the United States in regions that export produce
to the United States;
b. The types of untreated BSAAO and the soil type, and associated physical
and chemical parameters (including but not exclusive to nutrient content,
moisture and pH); and the crops typically grown in each BSAAO-amended soil
type;
c. Characterization of the proportion of produce farms that have one or
more soil types per geographical location;
d. The amount of untreated BSAAO applied per unit surface (e.g., per acre)
or the ratio of untreated BSAAO/soil, including typical ratio and variability by
commodity type, including, for example, row crops such as leafy greens;
e. The time of year, number of applications, and amount of untreated BSAAO
that are applied;
f. The method of application (e.g., surface, incorporated), and whether or
not the amended soil is covered (e.g., with plastic mulch);
g. Produce commodity type and cropping cycles;
h. Climate conditions and irrigation practices after soil is amended,
before and after planting; and
i. The crop density (e.g., the number of rows per bed, and the distance
between adjacent rows in a bed), distance between two crop beds (furrow width),
and the influence of such factors on pathogen transfer.
4. Harvesting, handling, and storage conditions that may affect pathogen
detection and levels, survival, growth, or inactivation between harvest and
retail sale along the farm-to-fork continuum.
a. The harvesting practices and the average conditions as well as the range
of climactic conditions prior to harvesting (e.g., time and temperature, rain
events) under which produce is handled in the field and in packing
operations;
b. The survival, growth, or inactivation of pathogens on produce
(including, for example, specific commodities or categories such as leafy
greens, or produce generally) during transportation and storage;
c. Typical storage conditions (e.g., time, temperature) for produce
(including, for example, specific commodities or categories, such as leafy
greens, or produce generally), from harvest until consumer purchase and whether
and how those storage conditions affect pathogen levels; and
d. The types and concentration of antimicrobial chemicals or other
treatments, if any, applied to the water used for wash or transport of produce
during farm or other distribution operations prior to retail, and the efficacy
of these treatments in reducing pathogen levels, as well as the likelihood of
cross-contamination during wash or transport.
5. Storage conditions such as times and temperatures that may affect
pathogen growth and/or survival during transportation and storage of produce in
the consumer's home, and consumer handling practices with respect to produce
after purchase, including data and information on consumer washing
practices.
We are also interested in other comments concerning, but not limited to,
the types of untreated BSAAO, produce commodities, relevant agricultural and
ecological conditions, and appropriate mitigation strategies that the Agency
should consider in the risk assessment.
IV. Reference Back to Top The following reference is on display in the
Division of Dockets Management (see ADDRESSES) and is available for viewing by
interested persons between 9 a.m. and 4 p.m., Monday through Friday; they are
also available electronically at http://www.regulations.gov. FDA
has verified the Web site address, as of the date this document publishes in the
Federal Register, but Web sites are subject to change over time.
1. Food and Drug Administration, 2015. “Final Qualitative Assessment of
Risk to Public Health from On-Farm Contamination of Produce.” Available at: http://www.fda.gov/downloads/Food/FoodScienceResearch/RiskSafetyAssessment/UCM470780.pdf.
Accessed January 20, 2016. Show citation box
Dated: February 29, 2016.
Leslie Kux,
Associate Commissioner for Policy.
COMMENT
Greetings FDA et al,
I kindly would like to make comment submission to Docket No.
FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens
from Produce Grown in Fields Amended with Untreated Biological Soil Amendments
of Animal Origin; Request for Comments, Scientific Data, and Information
MY comment as follows,
There has been proven documented risk for Untreated Biological Soil
Amendments of Animal Origin and risk of transmitting Transmissible Spongiform
Encephalopathy TSE Prion disease aka mad cow type disease such as the typical
and atypical Bovine Spongiform Encephalopathy strains, typical and atypical
Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and
even the Transmissible Mink Encephalopathy TME Prion disease.
Science has shown that infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces thereby leading to
transmission by direct contact and environmental contamination.
Ingestion of prion contaminated leaves and roots produced disease with a
100% attack rate and an incubation period not substantially longer than feeding
animals directly with scrapie brain homogenate.
Plants can uptake prions from contaminated soil and transport them to
different parts of the plant tissue (stem and leaves) [please see data from Soto
et al Prion2015 Conference below in Science reference data].
Also, Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area is very concerning.
Science has shown that soil plays a role in the spreading and transmission
of the CWD and Scrapie TSE prion agent.
For these reason and more (see reference materials) I urge the FDA to stop
this practice of Untreated Biological Soil Amendments of Animal Origin,
including blood, for use on our produce grown in fields, for the following
reasons ;
snip...
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
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