Thursday, May 31, 2012

Missouri MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County June 2, 2012

MDC open house on CWD next steps June 2 in Macon County


News from the Central and Northeast regions


Published on: May. 25, 2012


Posted by Joe Jerek






JEFFERSON CITY Mo. – The Missouri Department of Conservation (MDC) will hold an informational open house on Chronic Wasting Disease (CWD) in Macon County on June 2 at New Cambria High School, 501 S. Main St. The public is invited to stop by 1-4 p.m.




MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County, explain disease management actions the Department is taking, answer questions and provide information on managing private land for deer.




MDC’s disease-management steps to help contain the spread of CWD include two regulation changes to the Wildlife Code of Missouri, recommendations on transportation and disposal of deer carcasses and continuing CWD sampling of deer harvested in the area where CWD has been found.




Restriction on Feeding




The Conservation Commission approved a regulation change at its May 25 meeting that places a restriction on activities that are likely to unnaturally concentrate white-tailed deer and promote the spread of CWD. The ban on the placement of grain, salt products, minerals and other consumable natural or manufactured products is limited to the area where CWD has been found in Macon County and is comprised of Adair, Chariton, Linn, Macon, Randolph and Sullivan counties.




The regulation includes exceptions for backyard feeding of birds and other wildlife within 100 feet of any residence or occupied building, or if feed is placed in such a manner to reasonably exclude access by deer. The regulation also includes exceptions for normal agricultural, forest management, crop and wildlife food production practices.




According to MDC Deer Biologist Jason Sumners, the reason for the regulation change is that activities such as feeding and placement of minerals/salts that artificially concentrate deer greatly increase the likelihood of disease transmission from animal to animal or from soil to animal.




Removal of Antler-Point Restriction




The Conservation Commission also approved a regulation change at its May 25 meeting for a special harvest provision that rescinds the antler-point restriction (four-point rule) in Adair, Chariton, Linn, Macon, Randolph and Sullivan counties.




According to Sumners, the reason for the regulation change is that management strategies such as antler-point restrictions, which protect yearling males and promote older bucks, have been found to increase prevalence rates and further spread the disease.




Sumners explained that yearling and adult male deer have been found to exhibit CWD at much higher rates than yearling and adult females so a reduction in the number of male deer can help reduce the spread of CWD. He added that the movement of young male deer from their birth range in search of territory and mates is also a way of expanding the distribution of CWD.




Don’t Remove Carcasses from Area




MDC also encourages hunters who harvest deer in Adair, Chariton, Linn, Macon, Randolph, and Sullivan counties not to take whole deer carcasses or carcass parts out of the area where CWD has been found. Exceptions to this include meat that is cut and wrapped, meat that has been boned out, quarters or other portions of meat with no part of the spinal column or head attached, hides or capes from which all excess tissue has been removed, antlers, antlers attached to skull plates or skulls cleaned of all muscle and brain tissue, upper canine teeth and finished taxidermy products.




According to Sumners, the reason for this recommendation is that CWD can be transmitted from the environment to deer through soil and water that contain infected waste and/or infected carcasses. Deer can be infected with CWD but have no visible signs or symptoms. Moving harvested deer that still have parts known to concentrate CWD (brain, spinal cord, eyes, spleen, and lymph nodes) from the area known to have CWD can introduce the disease to other parts of the state through the improper disposal of carcasses.




He explained that hunters should make every attempt to avoid moving the head and spinal cord from the area and properly dispose of potentially infected deer carcasses, including bones and trimmings, to minimize the risk of exposure to uninfected deer. MDC advises hunters to double-bag carcass parts and take them directly to a landfill, or place them in trash cans for pick-up. Burying carcass waste deep enough to prevent scavengers from digging it up is another acceptable option. As a last resort, and only on their own land, hunters can put carcass waste back on the landscape. Carcasses should be put as close as possible to where the deer was harvested so as to not spread CWD-causing prions to new locations. If possible, put the carcass in a location where it will be inaccessible to scavengers and other deer.




Fall Harvest CWD Sampling




Sumners added that MDC will also continue to work with hunters who harvest deer this fall in Adair, Chariton, Linn, Macon, Randolph and Sullivan counties to collect samples for CWD testing. Details on these efforts are being developed and will be shared before the 2012 fall deer hunting season.






For more information on the open house, contact MDC Public Involvement Coordinator Michele Baumer at 573-522-4115, ext. 3350, or Michele.Baumer@mdc.mo.gov.










Thursday, May 31, 2012


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more






Tuesday, January 24, 2012


CWD found in two free-ranging deer from Macon County Missouri







Friday, October 21, 2011


Chronic Wasting Disease Found in Captive Deer Missouri







Friday, February 26, 2010



Chronic wasting disease found in Missouri deer








Sunday, January 22, 2012



Chronic Wasting Disease CWD cervids interspecies transmission









*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***


Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).


SNIP...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).




PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS







Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012







Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE






Saturday, February 04, 2012


Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised






Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011


The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.


snip...see full text and much more here ;







PRODUCT


Product is custom made deer feed packaged in 100 lb. poly bags. The product has no labeling. Recall # V-003-5.


CODE


The product has no lot code. All custom made feed purchased between June 24, 2004 and September 8, 2004.


RECALLING FIRM/MANUFACTURER


Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing.


REASON


Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.


VOLUME OF PRODUCT IN COMMERCE


Approximately 6 tons.


DISTRIBUTION


OH.


END OF ENFORCEMENT REPORT FOR October 20, 2004






################# BSE-L-subscribe-request@uni-karlsruhe.de #################


Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 –0500


From: "Terry S. Singeltary Sr."














Monday, March 26, 2012





CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE








Sunday, May 27, 2012



CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE OUTBREAK, CENSORSHIP IS A TERRIBLE THING
TSS


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more

CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
 
 
 
PO-031: Aerosol transmission of chronic wasting disease to white-tailed deer


Nathaniel Denkers,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Sally Dahmes,2 David Osborn,3 Karl Miller,3 Robert Warren,3 Candace Mathiason,1 Edward Hoover1


1Colorado State University; Fort Collins, CO USA; 2WASCO Inc.; Monroe, GA USA; 3Warnell School of Forestry and Natural Resources, University of Georgia; Athens, GA USA


Purpose. A signature feature of chronic wasting disease (CWD) is its efficient lateral transmission in nature, almost surely by mucosal exposure. Our previous studies employing Tg(cerPrP) mice determined that CWD can be transmitted to a susceptible host by aerosol exposure, a route with relatively little investigation. The present study was designed to determine whether CWD is transmissible by aerosol to a native cervid host, white-tailed deer.


Materials and Methods. Nine white-tailed deer were exposed to two (2) aerosol doses of a 5% w/v CWD+ (n = 6) or CWD- (n = 3) brain homogenate, delivered via the nasal passages using a customized aerosol apparatus. At 3-month intervals post inoculation (mpi), tonsil and recto-anal mucosa-associated lymphoid tissue (RAMALT) biopsies were collected and assayed for CWD infection by protein misfolding cyclic amplification (PMCA), western blotting (WB), and immunohistochemistry (IHC).


Results. At 3 mpi and 6 mpi, tonsil and RAMALT biopsies were collected from 5 of the 6 CWD + aerosol-exposed deer. Three of the 5 (60%) tested positive for CWD by PMCA but not IHC or western blot analysis at 3 mpi. By 6 mpi, 5 of 5 (100%) were tonsil and/or RAMALT biopsy positive by at least two of the three assays. Biopsies were collected from all CWD+ aerosol-exposed deer at 9 mpi, with 6 of 6 (100%) tonsil and/ or RAMALT positive by western blot or IHC. At 10 mpi 3 of the 6 prion-exposed deer have developed early clinical signs of CWD infection (hyperphagia, polydypsia, wide leg stance and head/neck dorsi-flexion). All sham-inoculated deer are showing no clinical signs and have remained CWD negative as assessed by all three assays. Interestingly, the prion dose delivered to the deer by aerosol-exposure is estimated to be 20-fold lower than the historical oral dose that has resulted in detectable CWD infection at 6 or 12 mpi.


Conclusions. This study documents the first aerosol transmission of CWD in deer. These results further infer that aerosolized prions facilitate CWD transmission with greater efficiency than does oral exposure to a larger prion dose. Thus exposure via the respiratory mucosa may be significant in the facile spread of CWD in deer and perhaps in prion transmission overall.








PO-073: Multiple routes of prion transepithelial transport in the nasal cavity following inhalation



Anthony Kincaid, Shawn Feilmann, Melissa Clouse, Albert Lorenzo, Jason Bartz Creighton University; Omaha, NE USA


Introduction. Inhalation of either prion-infected brain homogenate or aerosolized prions has been shown to cause disease, and in the case of inhalation of infected brain homogenate, the nasal route of infection has been shown to be 10–100 times more efficient than the oral route. The cell types involved in the in vivo transport of prions across the nasal cavity epithelium have not been determined. M cells in the follicular associated epithelium have been shown to mediate transcellular transport of prions in vitro and in the gut of experimentally infected mice. We tested the hypothesis that M-cell mediated transport was responsible for prion entry across nasal cavity epithelium following inhalation.


Materials and Methods. Hamsters were inoculated extranasally with 50 or 100ul of infected (n = 31) or mock-infected (n = 13) brain homogenate. Control animals were inoculated with buffer (n = 4) or were untreated (n = 5). Following survival periods ranging from 15 to 180 min, animals were perfused, skulls were decalcified and nasal cavities were embedded in paraffin. Tissue sections were cut and processed immunohistochemically for glial fibrillary acidic protein to identify brain homogenate, or for the disease-associated form of the prion protein. Tissue sections not further than 112 um apart through the entire extent of the nasal cavity were analyzed using light microscopy; photomicrographs were obtained wherever inoculum was observed on the surface of, within, or deep to the nasal mucosa for each animal.


Results. Infected or uninfected brain homogenate was identified within the nasal cavities of animals at all time points and was seen crossing the nasal cavity epithelium within minutes of inoculation; the transepithelial transport of brain homogenate continued for up to 3 h after inoculation. Infected or uninfected brain homogenate was seen adhering to, or located within, M cells at all time points. However, larger volumes of infected or uninfected brain homogenate were identified crossing between cells of the olfactory and respiratory epithelia in multiple locations. In addition, infected or uninfected brain homogenate was identified within the lumen of lymphatic vessels in the lamina propria beneath the nasal mucosa at all time points.


Conclusion. Transepithelial transport of prions across nasal cavity mucosa begins within minutes of inhalation and can continue for up to 3 h. While M cells appear to transport prions across the follicular associated epithelium, larger amounts of prions are transported between the cells of the respiratory and olfactory epithelia, where they immediately enter the lymphatic vessels in the lamina propria. Thus, inhaled prions can be spread via lymph draining the nasal cavity and have access to somatic and autonomic nerves in the lamina propria of the nasal cavity. The increased efficiency of the nasal cavity route of infection compared with the oral route may be due to the rapid and prolonged transport of prions between cells of the respiratory and olfactory epithelia.






PO-033: Replication efficiency of soil-bound prions varies with soil type


Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA; 2Creighton University; Omaha, NE USA


Prion sorption to soil is thought to play an important role in the transmission of scrapie and chronic wasting disease (CWD) via the environment. Sorption of PrP to soil and soil minerals is influenced by the strain and species of PrPSc and by soil characteristics. However, the ability of soil-bound prions to convert PrPc to PrPSc under these wide-ranging conditions remains poorly understood. We developed a semiquantitative protein misfolding cyclic amplification (PMCA) protocol to evaluate replication efficiency of soil-bound prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy (TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log decrease in PMCA replication efficiency with a corresponding 1.3-log reduction in titer. The increased binding of PrPSc to soil over time corresponded with a decrease in PMCA replication efficiency. The PMCA efficiency of bound prions varied with soil type, where prions bound to clay and organic surfaces exhibited significantly lower replication efficiencies while prions bound to sand exhibited no apparent difference in replication efficiency compared to unbound controls. PMCA results from hamster and CWD agent-infected elk prions yielded similar findings. Given that PrPSc adsorption affinity varies with soil type, the overall balance between prion adsorption affinity and replication efficiency for the dominant soil types of an area may be a significant determinant in the environmental transmission of prion diseases.




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


Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. The purpose of these experiments was to determine susceptibility of white-tailed deer (WTD) to scrapie and to compare the resultant clinical signs, lesions, and molecular profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate.


All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer that was necropsied at 15.6 months had widespread distribution of PrPSc highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues prior to the onset of clinical signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues.


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.




PO-041: Susceptibility of domestic cats to CWD infection


Amy Nalls, Jeanette Hayes-Klug, Kelly Anderson, Davis Seelig, Kevin Carnes, Susan Kraft, Edward Hoover, Candace Mathiason


Colorado State University; Fort Collins, CO USA


Domestic and non-domestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE); very likely due to 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 domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain homogenate.


Between 40 and 43 months two IC-inoculated cats developed slowly progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors, and ataxia”’ultimately mandating euthanasia. PrPCWD was detected in the brains of these animals by western blot, immunohistochemistry (IHC), and quaking-induced conversion (RT-QuIC) assays. No clinical signs of TSE were detected in the remaining primary passage cats at 86 months pi. Feline-adapted CWD (FelCWD) was sub-passaged into groups (n = 4 or 5) of cats by IC, PO, and IP/SQ routes.


All 5 IC inoculated cats developed symptoms of disease 20–24 months pi (approximately half the incubation period of primary passage). Additional symptoms in these animals included increasing aggressiveness and hyper responsiveness. FelCWD was demonstrated in the brains of all the affected cats by western blot and IHC. Currently, 3 of 4 IP/SQ, and 1 of 4 PO inoculated cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. Magnetic resonance imaging (MRI) has been performed on 11 cats (6 clinically ill, 2 asymptomatic, and 3 age-matched negative controls). Abnormalities were detected in 4 of 6 clinically ill cats and included multifocal signal changes consistent with inflammation, ventricular size increases, more prominent sulci, and white matter tract cavitation.


These results demonstrate that CWD can be transmitted and adapted to the domestic cat, and raise the potential for cervid-to-feline transmission in nature.




PO-055: Transgenetic modeling of the CWD species barrier to humans


Eri Saijo,1 Sehun Kim,2 Claudio Soto,3 Glenn Telling2 1University of Kentucky College of Medicine; Fort Collins, CO USA; 2Department of Microbiology, Immunology and Pathology; Colorado State University; Fort Collins, CO USA ; 3Department of Neurology; University of Texas Houston Medical School; Houston, TX USA


Our recent studies raise significant concerns about the zoonotic potential of CWD. First, we showed that tissues consumed by humans derived from deer or elk with CWD, including skeletal muscle and antler velvet, harbor infectious prions. In other studies, cervid PrPSc converted human PrPC after CWD prions were stabilized by successive passages in vitro or in vivo.


We also identified at least two distinct strains of CWD, referred to as CWD1 and CWD2, the host-range properties of which are currently undefined. Other studies showed that codon 129, and the corresponding 132 residue in elk, significantly influenced the transmission of BSE and CWD prions respectively in transgenic (Tg) mouse models.


We inoculated Tg mice expressing human PrP encoding either methionine (M) or valine (V) at codon 129 with deer or elk CWD prions that previously produced disease in Tg mice expressing deer PrP with characteristics typical of CWD1 and CWD2 strains, as well as CWD prions that had been passaged multiple times in Tg mice expressing deer PrP.


While most Tg mice remained free of signs of prion disease for >260 days, small numbers of inoculated mice developed multiple, progressive neurological signs, that were consistent with prion disease. However, examination of brain materials from diseased mice failed to confirm the presence of protease-resistant human PrP. These preliminary results are consistent with a significant species barrier in humans to these CWD strains, and indicate that the 129 polymorphism does not modulate susceptibility.


PO-056: PrPCWD profiling of white-tailed deer (Odocoileus virginianus) with different Prnp genotypes following experimental oral infection


Camilo Duque Velasquez,1 Allen Herbst,1 Chad Johnson,2 Judd Aiken,1 Debbie McKenzie1 1Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, AB Canada; 2Department of Soil Science; University of Wisconsin; Madison, WI USA


Chronic wasting disease (CWD) affects captive and free-ranging cervid populations in North America and farmed cervids of South Korea. CWD and scrapie are the only prion diseases in which the transmission occurs horizontally. The cervid Prnp gene is polymorphic at various positions. The effect of these changes on infection is influenced by the sequence and structure compatibility between the host and the infectious source. Prion strains have been described virtually in every prion disease and strongly impact disease characteristics (clinical symptoms, neuropathological profiles, incubation periods, species tropism as well as biochemical and biophysical properties of the abnormally folded prion protein). Prion protein sequence differences can result, upon subsequent infection, in the generation of novel strains as documented in sheep scrapie. We have previously shown that Prnp polymorphisms influence susceptibility to CWD in free-ranging white-tailed deer. In CWD-positive deer populations, alleles Q95G96 (wt) were over-represented compared to the H95G96 and Q95S96 alleles. Experimental oral infection of white-tailed deer with known Prnp genotypes (with inoculum from CWDpositive wt/wt deer) confirmed the link between prion protein primary sequence and the progression of disease. Heterozygous interference occurred in varying degrees as evidenced by the difference in the extension of the incubation period as an effect of alleles Q95S96 and H95G96. Interestingly, the biochemical profiles of the wt/Q95S96 and wt/H95G96 isolates resemble the wt/wt, differing only in the amount of protease resistant PrPCWD present suggesting that the wt allele is preferentially converted. PrPCWD profiling revealed differences between deer with at least one wt allele and the H95G96/Q95S96 deer suggesting that this PrPCWD is unique compared to the PrPCWD from wt/wt animals.




PO-057: Host factors influence prion strain adaptation


Crystal Meyerett Reid, Mark Zabel Colorado State University; Fort Collins, CO USA


Background. Chronic Wasting disease (CWD) is one of many prion-mediated diseases known as transmissible spongiform encephalopathies (TSEs). There is ever-increasing biological and biochemical evidence that prion pathogenesis is caused by the conversion of the normal host protein (PrPC) into an abnormal disease causing conformation (PrPRES). How prions encipher heritable strain properties without nucleic acid remains unclear. Previously we have shown that host factors have contributed to the adaptation of an original deer CWD prion strain to transgenic mice.


Materials and Methods. We assessed strain differences using biological and biochemical assays and found that amplified cervid prions and serial-passaged cervid prions were significantly different than that of the original cervid strain. It is possible that prion mutation and adaptation can broaden the host range. Previous reports, however, indicate that there is a strict species barrier preventing CWD infection in wildtype mice.


Results. Here we show the generation of a mouse-adapted strain of CWD upon serial passage into transgenic cervidized mice and then subsequent passage into wildtype mice. All wildtype mice remained non-clinical upon first passage but became completely susceptible after second passage with similar incubation times to those of mice terminally ill from a mouse adapted scrapie strain. Inoculation of our mouse adapted CWD strain back into cervidized mice delayed progression to terminal disease.


Conclusion. We conclude that prion strain adaptation and mutation is highly dependent upon host factors and host encoded PrPC primary sequence. Upon serial passage the adapted prion strain shares more characteristics with prion strains from the new host rather than the original species.








OR-12: Chronic wasting disease transmission and pathogenesis in cervid and non-cervid Species


Edward A. Hoover, Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, Davis M. Seelig, Nathaniel D. Denkers, Amy V. Nalls, Mark D. Zabel, and Glenn C. Telling


Prion Research Program, Department of Microbiology, Immunology, and Pathology; Colorado State University; Fort Collins, CO USA


Since its recognition as a TSE in the late 1970s, chronic wasting disease (CWD) of cervids has been distinguished by its facile spread and is now recognized in 18 states, 2 Canadian provinces, and South Korea. The efficient horizontal spread of CWD reflects a prion/host relationship that facilitates efficient mucosal uptake, peripheral lymphoid amplification, and dissemination by exploiting excretory tissues and their products, helping to establish indirect/environmental and well as direct (e.g., salivary) transmission. Recent studies from our group also support the likelihood of early life mother to offspring and aerosol CWD prion transmission. Studies of cervid CWD exposure by natural routes indicate that incubation period for detection of overt infection, while still uncertain, may be much longer than originally thought.


Several non-cervid species can be infected by CWD experimentally (e.g., ferrets, voles, cats) with consequent species-specific disease phenotypes. The species-adapted prions so generated can be transmitted by mucosal, i.e., more natural, routes. Whether non-cervid species sympatric with deer/elk can be infected in nature, however, remains unknown. In vitro CWD prion amplification studies, in particular sPMCA, can foreshadow in vivo susceptibility and suggest the importance of the PrPC rigid loop region in species barrier permissiveness. Trans-species CWD amplification appears to broaden the host range/strain characteristics of the resultant prions. The origins of CWD remain unknown, however, the existence of multiple CWD prion strains/ quasi-species, the mechanisms of prion shedding/dissemination, and the relationship between sheep scrapie and CWD merit further investigation.






PO-060: Transmission of chronic wasting disease from mother to offspring


Candace Mathiason, Amy Nalls, Stephenie Fullaway, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley, Edward Hoover


Colorado State University; Fort Collins, CO USA


To investigate the role mother to offspring transmission plays in chronic wasting disease (CWD) we have developed a cervid model employing the Reeve’s muntjac deer (Muntiacus reevesi). Eight muntjac doe were orally inoculated with CWD and tested PrPCWD lymphoid positive by 4 mo post infection. Twelve fawns were born to these eight CWD-infected doe, 3 were born viable, 6 were born non-viable, and 3 were harvested as fetuses (1 each from first, second or third trimester of pregnancy) from CWDinfected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry (IHC) performed on serial tonsil and rectal lymphoid tissue biopsies. One fawn that was IHC PrPCWD positive at 40 d of age is now, at 28 mo of age, showing early clinical signs associated with CWD infection. Moreover, CWD prions have been detected by sPMCA in placenta, brain, spleen and mesenteric lymphoid tissue harvested from 5 full-term non-viable fawns, and in fetal placenta and brain tissue harvested in utero from the second and third trimester fetuses. Additional tissues and pregnancy related fluids from doe and offspring are being analyzed for CWD prions. In summary, using the muntjac deer model we have demonstrated CWD clinical disease in an offspring born to a CWD-infected doe, and in utero transmission of CWD from mother to offspring. These studies provide basis to further investigate the mechanisms of maternal transfer of prions.








PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)


Davis Seelig, Amy Nalls, Maryanne Flasik, Victoria Frank, Candace Mathiason, Edward Hoover Colorado State University; Fort Collins, CO USA


Background and Introduction. Chronic wasting disease (CWD) is an efficiently transmitted prion disease of cervids with an as yet to be fully defined host range. Moreover, the risk that CWD poses to feline predators and scavangers, through crossspecies consumption and subsequent transmission, is unknown. Previous and ongoing studies in our laboratory evaluating the susceptibility of domestic cats (Felis catus) to CWD (Mathiason et. al., NeuroPrion 2011, Nalls et. al., NeuroPrion 2012) have documented the susceptibility of domestic cats to CWD following intracerebral (IC) inoculation. However, many of the pathologic features of feline-adapted CWD, including the neural and systemic patterns of PrPCWD accumulation and neuropathology, remain unknown.


The chief objectives of this work were:


(1) to design a sensitive, enhanced immunohistochemical (E-IHC) protocol for the detection of CWD prions (PrPCWD) in feline tissues;


(2) to document the systemic distribution of PrPCWD in CWD-infected cats through E-IHC;


(3) to utilize single and multiple-label immunostaining and laser scanning confocal microscopy (LSCM) to provide insights into the subcellular patterns of PrPCWD accumulation and neuropathologic features of CWD-infected cats; and


(4) to compare feline CWD to the other known feline TSE Materials and Methods. Periodate-lysine-paraformaldehyde (PLP)-fixed, paraffin-embedded (PLP-PE) from terminal, IC-inoculated (n = 9) and sham-inoculated (n = 2), 1st and 2nd passage, CWD-infected cats were examined by E-IHC for the presence of PrPCWD and its association with markers of cell phenotype and organelles.


Results. The most sensitive E-IHC technique for the detection of PrPCWD in feline tissues incorporated a combination of slide pretreatment with proteinase-K (PK) in concert with tyramide signal amplification (TSA). With this protocol, we identified PrPCWD deposits throughout the CNS, which, in the 1st passage cats was primarily restricted to the obex, but increased in distribution and severity upon 2nd passage to include a number of midbrain nuclei, cortical gray matter, the thalamus and hypothalamus, and the hippocampus. Peripheral PrPCWD deposits were detected only in the 2nd passage cats, and included the enteric nervous system, the Peyer’s patches, and the retropharyngeal and mesenteric lymph nodes. PrPCWD was not detected in the sham-inoculated cats.


Moreover, using multi-label analysis, intracellular PrPCWD aggregates were seen in association with neurofilament heavy chain (NFH)-positive neurons and GFAP-positive astrocytes. In addition, large aggregates of intracellular PrPCWD were identified within LAMP1-positive lysosomes.


Conclusions. Feline PrPCWD is present in CNS neurons, astrocytes and LAMP-1-positive lysosomes. The morphologic overlap between the PrPCWD deposits in feline CWD and BSE-origin feline spongiform encephalopathy (FSE), implicates the importance of the host as a key determinant in the development of prion neuropathology and suggest a signature for detection of potential spontaneous feline prion disease.






PO-099: Estimating the risk of CWD transmission to humans—An interim report of a comprehensive study in non-human primates


Ann-Christin Schmaedicke DPZ; Goettingen, Germany


Chronic Wasting Disease (CWD) is a transmissible prion disease that occurs primarily among North American cervid species. CWD has emerged as a prion disease in captive as well as freeranging cervids with rising incidence. Continuous consumption of cervid-derived products in conjunction with increasing CWD prevalence suggests a risk for human exposure to CWD prions.


Although surveillance data collected in the North American population did not provide epidemiological evidence for CWD transmissions to humans it remains unclear whether a biological risk for such transmissions exists or can be excluded. In order to gauge the potential transmissibility of CWD to humans, a comprehensive CWD risk assessment in cynomolgus macaques has been initiated. To test for the CWD interspecies transmission to humans, we used a primate species previously shown to mimic the BSE susceptibility of humans. In addition, this species is phylogenetically close to humans with a homologous amino acid sequence of the prion protein. When we assessed the genotype of macaque PrP, the homozygosity for methionine at codon 129 was confirmed in all animals.


The zoonotic potential of CWD is evaluated by challenging groups of animals via different inoculation routes. General transmissibility of CWD to macaques is tested by intracerebral (i.c.) inoculation of brain homogenate from CWD-infected white-tailed deer (WTD) and elk. This was either done by direct injection of 10 mg CWDWTD to two animals (> 880 dpi) or by surgical implantation of CWD-WTD or CWD-elk contaminated steel wires in two animals (> 750 dpi) or three animals (> 400 dpi), respectively.


To address the risk of hunters while field dressing carcasses, we inoculated two animals with CWD-WTD by dermal scarification (> 920 dpi). To simulate human consumption of CWDinfected food products, we orally challenged three animals with 10 g CWD-WTD brain (> 820 dpi) and three animals with 3 kg CWD muscle tissue from different cervid species (> 950 dpi) by repeated feeding. Mock-inoculated macaques are co-housed in the same cage allowing exposure to saliva and faeces of CWDinoculated macaques.


To date, all inoculated animals remain asymptomatic. Cerebrospinal fluid and blood from all animals were and are going to be collected bimonthly, processed and stored in a repository. Analysis of these samples using ultrasensitive prion detection methods has been initiated. Oral challenge of 50 mg BSE to cynomolgus macaques can lead to fatal disease only after more than 5 y of incubation time (1952 dpi).


Thus, to estimate whether CWD could be transmitted to macaques or not, we assume that observation of challenged animals would be necessary for at least 8–10 y.




PO-248: TSE infectivity survives burial for five years with little reduction in titer


Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and R(D)SVS; University of Edinburgh; Edinburgh, UK


BSE infected animals, BSE-contaminated materials and other sources of TSE (prion) infection, such as carcasses from scrapie infected sheep, CWD infected deer and cadavers of individuals infected with CJD may all end up in the environment through burial or other methods of disposal. They may continue to act as a reservoir of TSE infectivity if cattle or other susceptible animals were to be exposed to these sources in the future. In order to address these concerns, we performed two large scale demonstration experiments under field conditions which were designed to mimic some of the ways by which TSE infected materials may have been disposed of. The project examined the fate of TSE infectivity over a period of five years in two scenarios; when the infectivity was contained within bovine heads and when the infectivity was buried without any containment. Two soil types were compared: a sandy loam and a clay loam. We used the 301V TSE strain which was derived by serial passage of BSE in VM mice.


TSE infectivity was recovered from all the heads exhumed annually for five years from both types of soil, with little reduction in the amount of infectivity throughout the period of the experiment. Small amounts of infectivity were found in the soil immediately surrounding the heads, but not in samples remote from them. Similarly there was no evidence of significant lateral movement of infectivity from the buried bolus. However large amounts of TSE infectivity were recovered at the site of burial of both boluses. There was limited vertical upward movement of infectivity from the bolus buried in clay soil and downward movement from the bolus buried in sandy soil.


Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.






see more here ;




Epidemiology Update March 23, 2006


As of today, 13 locations and 32 movements of cattle have been examined with 27 of those being substantially completed. Additional investigations of locations and herds will continue. In addition, state and federal officials have confirmed that a black bull calf was born in 2005 to the index animal (the red cow). The calf was taken by the owner to a local stockyard in July 2005 where the calf died. The calf was appropriately disposed of in a local landfill and did not enter the human or animal food chain. http://www.aphis.usda.gov/newsroom/hot_issues/bse/bse_al_epi-update.shtml




> The calf was appropriately disposed of in a local


> landfill and did not enter the human or animal food chain.




Wednesday, May 30, 2012


PO-248: TSE infectivity survives burial for five years with little reduction in titer






TSS

Friday, May 25, 2012

Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota

News Release


For immediate release: Friday, May 25, 2012


Contact: Malissa Fritz, BAH Communications Director, 651-201-6830


Chronic Wasting Disease found in a farmed red deer from Ramsey County


Mandatory surveillance program leads to detection of the disease


St. Paul, Minn – The Minnesota Board of Animal Health today announced that a farmed red deer from a Ramsey County herd tested positive for Chronic Wasting Disease (CWD).


The brain stem from a two-year-old female red deer was submitted for testing at the University of Minnesota Veterinary Diagnostic Laboratory, where preliminary results were positive for CWD. The National Veterinary Services Laboratory today confirmed the positive test. The Board of Animal Health has placed the herd under quarantine and is working with the owners to determine the herd’s future.


The red deer died on the farm on May 10. The animal was tested for the disease as part of Minnesota’s mandatory CWD surveillance program, which has been in place since 2003. Farmed cervidae producers in Minnesota must CWD test all deer and elk over 16 months of age that die or are slaughtered.


This herd has been registered with the Board of Animal Health since 2000. “This herd is an example of farmers who take great care in the management of their animals,” said Dr. Paul Anderson, assistant director of the Board of Animal Health. “In their 12 years of herd registration with the Board, this producer has met all of the requirements.”


The Board of Animal Health is coordinating with the Minnesota Department of Natural Resources (DNR). The DNR is currently evaluating the situation and will likely test wild white-tailed deer in the area this fall.


CWD is a fatal brain and nervous system disease found in cervidae in certain parts of North America. The disease is caused by an abnormally shaped protein called a prion, which can damage brain and nerve tissue. Infected animals may show signs of the disease including progressive loss of body weight, behavioral changes, staggering, increased water consumption and drooling. In later stages of the disease, animals become emaciated (thus “wasting” disease).


According to state health officials and the federal Centers for Disease Control and Prevention, there is no evidence that CWD can be transmitted to humans.


For more information on CWD and the Board of Animal Health, visit www.bah.state.mn.us.


--30--










Chronic wasting disease found in a red deer from North Oaks farm herd


By Dennis Lien






Posted: 05/25/2012 12:01:00 AM CDT


May 26, 2012 1:45 AM GMTUpdated: 05/25/2012 08:45:21 PM CDT




A farmed red deer from a large northern Ramsey County herd has tested positive for chronic wasting disease.


The Minnesota Board of Animal Health said the 2-year-old female deer died on the farm May 10, and a required examination of its brain stem tested positive for the fatal brain and nervous system disease affecting elk and deer.


The 500-head North Oaks herd remains under quarantine, and officials are trying to figure out how the disease got there and what to do with the rest of the red deer, a large species native to Europe and Asia.


It marks the fifth case of farmed cervids testing positive in Minnesota for chronic wasting disease, according to Dr. Paul Anderson, a board veterinarian. Three were elk; the fourth, a white-tailed deer.


In those instances, including the most recent one in Olmsted County in 2009, all other herd members were slaughtered and tested for the disease.


"It's way too early to tell (in this case),'' said Anderson, noting the investigation will take weeks.


"The one thing I will say, this particular operation has had absolutely perfect surveillance for CWD,'' he added. "They have never missed an animal they needed to test, and all the animals have tested negative. This farm is one of the best-run in the state, and it's going to take some work to see if we can figure out where this came from.''


A man answering a telephone number listed at northoaksfarms.com declined to comment.


"I would refer you to the Board of Animal Health. We're working closely with them. Goodbye,'' he said and hung up.

That herd of red deer has been registered with the Board of Animal Health since 2000.


Chronic wasting disease, which is found in elk and deer in parts of North America, is caused by an abnormally shaped protein called a prion, which can damage brain and nerve tissue. Infected animals show progressive loss of body weight with accompanying behavioral changes, including staggering, drinking large amounts of water, excessive urinating and drooling.


There is no evidence the disease can be transmitted to humans or other animals such as cattle or sheep, according to federal and state health experts. Authorities believe it most likely is transmitted by animal-to-animal contact or exposure to contaminated habitat.


The disease can have a long incubation period, making it difficult to figure out how animals became infected.


In the North Oaks case, the brain stem from the red deer was submitted to the University of Minnesota Veterinary Diagnostic Laboratory, where preliminary results were positive. The U.S. Department of Agriculture's National Veterinary Services Laboratory in Ames, Iowa, confirmed the positive test Friday, May 25.


The deer was tested as part of the state's mandatory CWD surveillance program.


Since 2003, Minnesota has required registration and chronic wasting disease surveillance programs for farmed cervid herds. When animals 16 months or older die or are slaughtered, herd owners must submit brain samples for testing.


The Minnesota Department of Natural Resources plans to meet with the board soon and likely will test wild white-tailed deer in the area.


"We haven't had any reports of sick deer in the area,'' said Lou Cornicelli, DNR wildlife research manager.


Although the other farmed herds have been destroyed, Anderson said decisions are made on a case-by-case basis.


"Whenever something like this happens, we do what is best for the herd and figure out a way to make sure this disease is eradicated,'' Anderson said.


Dennis Lien can be reached at 651-228-5588.









CHRONIC WASTING DISEASE UPDATE September 6, 2002



Minnesota has announced the finding of CWD in a captive elk in Aitkin County. The animal was a five-year-old male. It had been purchased from a captive facility in Stearns County in August of 2000. The herd where the elk was found has been placed under quarantine as has two additional facilities where the infected elk had resided prior to it coming to the farm in Aitkin County. Minnesota DNR officials will test wild deer in the area to determine if there is any sign of CWD in the free-ranging population. This is the first case of CWD in either captive or freeranging cervids in Minnesota. Several more states have passed bans on the importation of deer and elk carcasses from states where CWD has been found in wild animals. Previously the states of Colorado, Illinois and Iowa and the province of Manitoba had passed such bans. The states of Vermont, Oregon and Missouri have enacted similar bans. Numerous states have issue voluntary advisories to their out-of-state hunters encouraging them not to bring the carcass or carcass parts of deer and elk into their state. The bans do permit the importation of boned out meat, hides or cape with no meat attached, clean skull cap with antler attached, finished taxidermy heads or the ivories of elk. The state of Georgia has recently banned the importation of live cervids into that state also. Some citizens of Colorado have formed a new political action group called Colorado Wildlife Defense (just happens that the acronym is CWD). The stated goal of this group are; Elimination of big game diseases, especially CWD; promotion of healthy wildlife habitat; promotion of scientifically sound wildlife research; promotion of a discussion of the ethics of hunting and wildlife management; education of the hunting and non hunting public. Their action plan calls for; requiring double fencing of all game farms at owners expense; all game farmers provide annual proof of bonding; prohibit new licenses for deer and elk farms; prohibit expansion in acreage of existing game farms; prohibit the transfer of game farm licenses; prohibit charging for hunting behind high wire; prohibit blocking of traditional migratory paths by high fences; requiring game farms to maintain environmental controls and prohibit the escape of contaminated water or soil; requiring immediate reporting of missing deer or elk from game farms; and requiring all game farm deer and elk to be tested for brucellosis and TB. Wisconsin has announced that 7 more free-ranging deer have tested positive for CWD. They have expanded their eradication zone by an additional 15 square miles to cover these findings. The total number of free-ranging CWD positive in Wisconsin is now 31 white-tail deer.


In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in Colorado. At that time, the farmer advised the Wisconsin Department of Agriculture that both animals from the exposed herd in Colorado were dead. He has now advised Wisconsin Ag. that he was mistaken and that one of the animals is still alive in his herd. The second draft of the implementation documents for the National CWD Plan was distributed to committee members and others on Friday, August 30. The final documents are due to APHIS and USFWS on Friday, September 13. The herd of captive elk in Oklahoma that had been exposed to CWD will be destroyed this week. This herd had an elk test positive for CWD in 1997 but the depopulation of the herd was not agreed to by the owners and federal representatives until this week. Since the discovery of CWD in the herd, the remaining animals have been under quarantine, however, in the meantime the herd has dropped from 150 animals to 74. Due to a lack of communication, not all of the 76 animals that died in the interim were tested for CWD. All remaining animals will be tested but the true degree of infection rate of the herd will never be known.


The owners of the facility will not be permitted to restock the area with cervids for a period of five years. A New York based organization, BioTech Research Fund I LLC has committed a $1 million line of credit to fund commercialization of tests for brain-wasting disorders and production of various vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three years developing new ways not only to diagnose CWD, but create vaccines for mad cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD have been successful in more than 100 samples from Colorado and Wisconsin according to company officials. Gene-Thera plans to license and market some o fits disease test kits by the end of the year, then begin volume distribution by mid-2003. The abstracts of the presentations from the CWD Conference in Denver August 6 and 7 have been posted on the Colorado Division of Wildlife web site. You will need adobe acrobat reader to read them.






If you don’t have adobe acrobat, you can download it free at http://www.adobe.com/products/acrobat/readstep.html









Minnesota: Second case in a game farmed elk discovered in Stearns Co.



This is a trace forward from the previously affected game farm in Aitkins Co. An additional game farm in Benton Co is under quarantine.


snip...


Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study- Wildlife officials call W. Slope move a mistake Date: January 17, 2003 Source: Denver Post Contacts: Theo Stein Environment Writer


The Colorado Division of Wildlife knowingly used a herd of captive elk exposed to chronic wasting disease in a grazing study on the Western Slope in January 1990, possibly introducing the disease to the elk-rich area. "It was a bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny it." About 150 wild elk were allowed to graze in the same pens near Maybell after the research herd was removed and may have picked up the abnormal protein that causes the disease from the feces and urine left by the captive elk. While the Division of Wildlife has expressed concern before that its animals might have helped spread CWD, this is the first time the agency has acknowledged it knowingly moved elk exposed to CWD deep into an area where the disease was not known to already exist. Studies that could help determine the source of CWD on the Western Slope are incomplete, and officials say what data that do exist are so new and so spotty they may not provide all the answers. So far, it appears that less than 1 percent of deer and elk in the area are infected, compared with as much as 15 to 20 percent in hotspots in northeastern Colorado. But as wildlife officials grapple with CWD's appearance in northwestern Colorado, officials now admit the decision to continue the grazing study over the objections of some biologists was an error. At the time, biologists wanted to see whether elk grazing on winter range depleted forage that ranchers wanted for fattening cattle in spring. "I think in hindsight a lot of good people probably did some dumb things, myself included," said Bruce Gill, a retired wildlife manager who oversaw research efforts and remembers the debate over the project. "Had we known CWD would explode into such a potentially volatile ecologic and economic issue, we wouldn't have done it." Elk ranchers, who have been blamed for exporting the disease from its stronghold on the Colorado and Wyoming plains to seven states and two Canadian provinces, say the agency's belated disclosure smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker and rancher who is now demanding a legislative inquiry. "If I'd have moved animals I knew to be infected around like that, I'd be in jail." Grand Junction veterinarian and sportsman Dick Steele said he faults the agency for not disclosing information about CWD-exposed research animals before October, when information was posted on the Division of Wildlife website. "This went way beyond poor judgment," he said. "My main concern is that this has been hidden for the last 12 years. It would have been real important to our decision-making process on how to deal with CWD." While the Maybell information is new, Perkins and other ranchers have long suspected Division of Wildlife research facilities near Meeker and Kremmling, which temporarily housed mule deer kept in heavily infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of an outbreak led the agency to sample 450 deer around the Meeker and Kremmling facilities. None tested positive, but the sample size was only large enough to detect cases if the infection rate was greater than 1 percent. This fall, tests on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases north of Interstate 70 and west of the Continental Divide. Biologists believe the infection rate in that area, which includes the Maybell, Meeker and Kremmling sites, is still well below 1 percent. But CWD has never been contained in a wild population, so experts fear the problem will grow worse.


The Division of Wildlife says it will be months before a statistical analysis of the fall's sampling results can be completed, an exercise that may shed light on the disease's origin on the Western Slope. "We're just not going to speculate at this point," said Ver Steeg of the possible Maybell connection. "This is one possibility, but certainly not the only possibility." Some biologists think a defunct elk ranch near Pagoda, which had dozens of unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects. "It may be inconclusive to them," said Perkins. "It isn't inconclusive to us."








To date, 19 CWD-positive animals have been found on six Wisconsin farms. All have been white-tailed deer except for one elk imported from a Minnesota herd later found to be infected. More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring program.






Subject: CWD disease detected on Lac qui Parle County cervid farm southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST


Chronic wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The Board of Animal Health announced today that chronic wasting disease (CWD) has been detected in one domestic white-tailed deer on a cervid farm in Lac qui Parle County, which is located in southwestern Minnesota.


Immediately, DNR officials will conduct a local deer survey to determine the number of wild deer in the area. It is expected that not many deer will be found because the area is highly agricultural, with little deer habitat surrounding the farm. DNR will conduct opportunistic sampling of deer, like road kills, in the immediate area now and will conduct intensive hunter-harvested surveillance during the 2006 firearm deer season.


Although this positive animal is a captive deer, DNR has conducted surveillance for CWD in wild deer in the area. The farm is located near the northern boundary of deer permit area 447, where wild deer surveillance for CWD last occurred in 2003.


Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. In total, we collected 392 samples from those permit areas during the regular firearm deer season and CWD was not detected."


The sampling of wild deer was designed statistically to have a 95 percent confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, DNR wildlife programs manager.


"This situation is very similar to the positive elk farm discovered in Stearns County in 2003, which followed the first discovery of CWD in an Aitkin County elk farm," DonCarlos said. “The DNR response will be similar to the Stearns County action and will include an initial assessment of wild deer populations in the area and development of a surveillance program for next fall."


From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide and no disease found in the wild herd.


"The intensive surveillance conducted in 2003 indicated CWD was not present in wild deer," Cornicelli said. “In addition, all indications are that this positive captive deer has not contacted any wild deer, but we will conduct additional surveillance this fall to be sure."












Subject: CWD disease detected on Lac qui Parle County cervid farm southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST Chronic wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The Board of Animal Health announced today that chronic wasting disease (CWD) has been detected in one domestic white-tailed deer on a cervid farm in Lac qui Parle County, which is located in southwestern Minnesota.


Immediately, DNR officials will conduct a local deer survey to determine the number of wild deer in the area. It is expected that not many deer will be found because the area is highly agricultural, with little deer habitat surrounding the farm. DNR will conduct opportunistic sampling of deer, like road kills, in the immediate area now and will conduct intensive hunter-harvested surveillance during the 2006 firearm deer season.


Although this positive animal is a captive deer, DNR has conducted surveillance for CWD in wild deer in the area. The farm is located near the northern boundary of deer permit area 447, where wild deer surveillance for CWD last occurred in 2003.


Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. In total, we collected 392 samples from those permit areas during the regular firearm deer season and CWD was not detected."


The sampling of wild deer was designed statistically to have a 95 percent confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, DNR wildlife programs manager.


"This situation is very similar to the positive elk farm discovered in Stearns County in 2003, which followed the first discovery of CWD in an Aitkin County elk farm," DonCarlos said. “The DNR response will be similar to the Stearns County action and will include an initial assessment of wild deer populations in the area and development of a surveillance program for next fall."


From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide and no disease found in the wild herd.


"The intensive surveillance conducted in 2003 indicated CWD was not present in wild deer," Cornicelli said. “In addition, all indications are that this positive captive deer has not contacted any wild deer, but we will conduct additional surveillance this fall to be sure."















*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***




Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012



CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).



SNIP...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).




SNIP...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).

SNIP...



Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, SNIP...SEE FULL TEXT ;




SNIP...SEE FULL TEXT ;



*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***




WHICH CAME FIRST, THE CART OR THE HORSE $$$



PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS








please see full text ;





Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012







see much more here ;











Thursday, February 09, 2012



50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE







Saturday, February 04, 2012



Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised







Tuesday, December 20, 2011



CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011




The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.



RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.





snip...see full text and much more here ;









SNIP...SEE FULL TEXT ;











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.








THIRD CJD REPORT UK 1994


snip...


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. These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...










PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;


Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.







NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;




Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II







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 ;







Saturday, March 5, 2011


MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA






Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas








TSS