# Deer with chronic wasting disease found in more Alberta areas



## terry (Sep 13, 2002)

Deer with chronic wasting disease found in more Alberta areas

Documents reveal government struggled with hunter surveillance program

By Hanneke Brooymans, edmontonjournal.com September 10, 2010 1:02 PM Be the first to post a comment

Read more: http://www.vancouversun.com/life/De...lberta+areas/3507163/story.html#ixzz0zA37EjGJ

Deer with chronic wasting disease found in more Alberta areas

Documents reveal government struggled with hunter surveillance program

By Hanneke Brooymans, edmontonjournal.com September 10, 2010 1:02 PM Be the first to post a comment

Story Photos ( 1 )

Mule deer bucks Photograph by: Bruce Edwards, The Journal, Edmonton Journal EDMONTON &#8212; The Alberta government is expanding its hunter surveillance program for chronic wasting disease, as positive deer continue to turn up in an increasingly larger area.

An additional seven wildlife management units were added to the list this year, bringing the total to 26. Hunters must turn in the heads of any deer killed in this area for testing. The area began by hugging the Alberta/Saskatchewan border, but has since expanded west and south.

Tests caught 75 positive cases among the thousands of mule and white-tailed deer turned in so far. The first positive case was in an emaciated mule deer found in 2005 in a farmyard about 30 kilometres southeast of Oyen. (To view a map showing all positive cases, go to www.srd.alberta.ca/BioDiversityStew...pdates/documents/CWD-PositiveMap-Apr-2010.pdf) The disease is thought to have spread from positive cases in Saskatchewan.

&#8220;The disease appears to be spreading and new outlier cases were detected north of Jenner and northwest of Elkwater,&#8221; say documents obtained by The Journal from Alberta Sustainable Resource Development under the Freedom of Information and Protection of Privacy Act.

The documents reveal that, as the hunter surveillance program expanded, the ministry struggled to keep up with the testing and reporting of results back to hunters. One hunter complained about how long it took to get test results.

CWD is caused by a prion, similar to bovine spongiform encephalopathy, that causes deer to slowly waste away. There is no evidence that the disease can infect humans, but the World Health Organization has advised that a precautionary approach be taken and that any animal product known to be infected with any prion disease not be consumed by humans.

A briefing note to the minister and deputy minister explained that, &#8220;There are fewer wage staff working on the CWD program because of the Government of Alberta hiring freeze. This resulted in slower testing and reporting this year. It also amplified some weaknesses in the CWD data management process.

&#8220;The current process for tracking and managing data associated with hunter-killed deer was originally set up as an ad hoc means when fewer than 1,000 heads were collected per year. The program has expanded to encompass 4,000- 5,000 heads. The system is inadequate to handle that volume. The process is extremely labour-intensive and there are many places where files or data are handled manually.&#8221;

In the case of the hunter who complained, they didn&#8217;t have contact information for that person. But in general, it did take longer to get information out to hunters last season, acknowledged Darcy Whiteside, a ministry spokesman. This year they have instituted a bar code system that will track animals through the process from the time a head is turned in, on through the lab to the blood sample and test result.

The government is allowing increased hunting opportunities in areas where CWD has been found. But they are not resurrecting more aggressive, government-run winter control programs from previous years, which were regarded by experts as the only hope for preventing the disease from spreading.

David Coltman, a University of Alberta biology professor, is winding down a research program on CWD in deer in Alberta. Using collaring and monitoring of animals, in addition to genetic work, he and his team discovered that deer move a lot and in all directions and that none of the Alberta populations have any natural resistance to the disease.

&#8220;Basically, (CWD) is gradually going to creep in all directions,&#8221; he said.

[email protected]

Read more: http://www.vancouversun.com/life/De...lberta+areas/3507163/story.html#ixzz0zA3DAzls


http://www.vancouversun.com/life/De...e+found+more+Alberta+areas/3507163/story.html




Wednesday, September 08, 2010 

CWD PRION CONGRESS SEPTEMBER 8-11 2010


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html




TSS


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## Munsterlndr (Oct 16, 2004)

Hard to comprehend how CWD can be spreading in Alberta, they have not allowed baiting for years. I guess the deer didn't get the memo.


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## terry (Sep 13, 2002)

once you have a CWD hot spot, and the environment is so exposed, pretty much no amount of prevention will help. that does not mean you should just say what the heck and throw in the hat (Alberta is a hot spot for cattle bse as well). baiting, and the ban there from, is but only one part of prevention. prevention, if one is serious about it, you must defend against all routes and sources. we know that the congregation of cervids in a given area, enhances the exposure sources to cwd, and baiting enhances the congregation of cervids and other critters. we must think of rodents and exposure, infection, and further transmission there from, in that given area where baiting, feeding, plots, natural or not. it's fact, the environment is contaminated. science has proven this. now it's up to the hunters, or the DNR (if the hunters are insistent on not doing it). folks whine about to much government, but when the common folks (some) are just to stupid to understand, the government must step in and make rules and regulations and enforce them. i have update the recent link to the CWD PRION CONGRESS SEPTEMBER 8-11 2010 i had posted with more data on cwd and environmental exposure. some of you folks might be interested in it, others will probably go throw a truck load of beets or corn down somewhere so they can sit up on the porch and drink beer, while stalking their kill. just my take. ...kind regards, terry



Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, the Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisin enzyme effectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 d under conditions representative of the natural environment (pH 7.4, 22°C). Serial PMCA of treated soil samples suggests a greater than 6-log decrease in infectious titer compared with controls. We observed no apparent difference in enzyme effectiveness between bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental &#8216;hot spots&#8217; of prion infectivity.

PPo3-26:

Identification of Renal Origin for CWD Urinary Prion Excretion in Deer

Davis M. Seelig,1 Nicholas J. Haley,1 Jan P. Langeveld and Edward A. Hoover1 1Colorado State University; Department of Microbiology, Immunology and Pathology; Fort Collins, CO USA; 2Central Institute for Animal Disease Control (CIDC-Lelystad); Lelystad, The Netherlands

Chronic wasting disease (CWD) is an efficiently transmitted prion disease of cervids. Although bioassays have confirmed the presence of infectious prions in urine and other body fluids of infected deer, origin and mechanisms of prion transfer to and shedding in excreta remains unknown. To address these questions, we have developed enhanced immunohistochemistry (IHC) methods employing tyramide signal amplification (TSA) on formalin-fixed, paraffin-embedded (FFPE) tissues of n = 20 CWD-infected white-tailed deer. Using these methods we have demonstrated PrPCWD present granular to clumped aggregates both within the cytoplasm of renal tubule cells and in the interstitium. Cytoplasmic PrPCWD aggregates were detected most commonly in proximal convoluted tubule epithelial cells. PrPCWD was not identified in the lower urinary tract (ureters or bladder) of any CWD-infected animal. In summary, we present evidence for PrPCWD accumulation within the renal tubule cells, which may identify a proximate tissue source and explain the manner by which infectious prions are excreted in the urine of infected deer, thereby leading to the high degree of direct and indirect horizontal transmission of chronic wasting disease.

PPo8-21:

Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification

Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA

Key words: CWD, feces, PMCA, elk

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC.

PPo3-20:

Transmission and Adaptation of Chronic Wasting Disease to North American Voles

Christina M. Carlson,1,2 Jay R. Schneider,1 Dennis M. Heisey,1 Joel A. Pedersen2 and Christopher J. Johnson1 1Prion Research Laboratory; USGS National Wildlife Health Center; Madison, Wisconsin USA; 2Program in Cellular and Molecular Biology; University of Wisconsin; Madison, Wisconsin USA

We previously demonstrated efficient transmission of cervid chronic wasting disease (CWD) to four species of native North American cricetid rodents (which include hamsters, voles and New World rats and mice) via intracerebral inoculation: meadow vole (Microtus pennsylvanicus), red-backed vole (Myodes gapperi), white-footed mouse (Peromyscus leucopus), and deer mouse (Peromyscus maniculatus). Onset of clinical disease was faster and median survival times shorter in the two vole species than the two Peromyscus species. To investigate CWD adaptation in a new host, we performed five serial passages in meadow voles, starting with CWD positive white-tailed deer inoculum. Initial challenge resulted in a median survival time of 280 days, progressively shortening to 67 days by fifth passage. Western blot analysis demonstrated the presence of PrPTSE in brain tissue throughout all passages, and suggested stability of the glycosylation site occupancy ratios as diglycosylated > monoglycosylated > unglycosylated, despite ongoing adaptation. This glycosylation pattern was consistent with those observed in other cricetid rodents challenged with CWD, scrapie, or mouse-adapted 139A scrapie and contrasts with the Muridae (Old World rodents) 139A pattern of monoglycosylated>diglycosylated>unglycosylated. Similarly, the molecular mass of proteinase K-cleaved PrPTSE was indistinguishable throughout all passages, indicating adaptation may result in more subtle changes to the PrPTSE protein than can be resolved by western blotting. Immunohistochemical staining of brain sections revealed punctate PrPTSE staining and spongiosis, especially in the thalamus. The results of this study show that CWD can be intracerebrally transmitted and adapted to meadow voles, suggesting this species could be a potential bridge species or reservoir for CWD.

PPo3-40: Mother to Offspring Transmission of Chronic Wasting Disease

Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA

Key words: Chronic wasting disease, vertical transmission, muntjac deer

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam. Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.

PPo3-35:

Susceptibility of Domestic Cats to CWD Infection

Amy V. Nalls, Candace K. Mathiason, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly R. Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft and Edward A. Hoover Colorado State University; Fort Collins, CO USA 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 or orally with CWD deer brain homogenate. Between 40 and 43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors, and ataxia&#8212;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 any of the 5 cats orally inoculated or the 2 remaining intracerebrally inoculated cats after 73 months pi. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.


http://www.prion2010.org/bilder/pri...39&PHPSESSID=a30a38202cfec579000b77af81be3099



Greetings,

A disturbing study indeed, but even more disturbing, the fact that this very study shows the potential for transmission of the TSE agent into the wild of yet another species in the USA. Science has shown that the feline is most susceptible to the TSE agent. Will CWD be the demise of the mountain lions, cougars and such in the USA? How many have ever been tested in the USA? I recall there is a study taking place ;

Review A prion disease of cervids: Chronic wasting disease Christina J. Sigurdson et al ;

Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).

snip...see full text ;


http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html



Thursday, December 25, 2008

Lions and Prions and Deer Demise


http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html


http://chronic-wasting-disease.blogspot.com/2010/07/comments-sought-on-revised-plan-to.html


http://chronic-wasting-disease.blogspot.com/2009/09/experimental-oral-transmission-of.html


http://chronic-wasting-disease.blogspot.com/2009/08/susceptibilities-of-nonhuman-primates.html


http://chronic-wasting-disease.blogspot.com/




see more here, UPDATED URL ;



Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





kind regards, terry


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