Michigan's First Case of Chronic Wasting Disease Detected in Kent County

Discussion in 'Whitetail Deer Disease' started by foxriver6, Aug 25, 2008.

  1. foxriver6

    foxriver6

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    FOR IMMEDIATE RELEASE
    Aug. 25, 2008

    Contacts: Bridget Patrick (MDA) 517-241-2669 or Mary Dettloff (DNR) 517-335-3014

    Michigan’s First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility

    LANSING - The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) today confirmed the state’s first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County.

    The state has quarantined all POC facilities, prohibiting the movement of all - dead or alive - privately-owned deer, elk or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans.

    DNR and MDA staff are currently reviewing records from the Kent County facility and five others to trace deer that have been purchased, sold or moved by the owners in the last five years for deer and the last seven years for elk. Any deer that may have come in contact with the CWD-positive herd have been traced to their current location and those facilities have been quarantined.

    “Michigan’s veterinarians and wildlife experts have been working throughout the weekend to complete their investigation,” said Don Koivisto, MDA director. “We take this disease very seriously, and are using every resource available to us to implement response measures and stop the spread of this disease.”

    CWD is a fatal neurological disease that affects deer, elk and moose. Most cases of the disease have been in western states, but in the past several years, it has spread to some midwestern and eastern states. Infected animals display abnormal behaviors, progressive weight loss and physical debilitation.

    Current evidence suggests that the disease is transmitted through infectious, self-multiplying proteins (prions) contained in saliva and other fluids of infected animals. Susceptible animals can acquire CWD by direct exposure to these fluids or also from contaminated environments. Once contaminated, research suggests that soil can remain a source of infection for long periods of time, making CWD a particularly difficult disease to eradicate.

    Michigan’s First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility: page 2

    “Currently, one of our top concerns is to confirm that the disease is not in free-ranging deer,” said DNR Director Rebecca Humphries. “We are asking hunters this fall to assist us by visiting check stations to allow us to take biological samples from the deer they harvest, so we can perform adequate surveillance of the free-ranging white-tailed deer herd in the area.”

    Deer hunters this fall who take deer from Tyrone, Soldon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon townships will be required to bring their deer to a DNR check station. Deer taken in these townships are subject to mandatory deer check.

    The DNR is also asking hunters who are participating in the private land five-day antlerless hunt in September in other parts of Kent County to visit DNR check stations in Kent County so further biological samples can be taken from free-ranging deer for testing. The DNR is in the process of finding additional locations for check stations in Kent County to make it more convenient for hunters.

    The deer that tested positive at the Kent County facility was a doe that had been recently culled by the owner of the facility. Michigan law requires sick deer or culled deer on a POC facility be tested for disease. The samples from the Kent County deer tested “suspect positive” last week at Michigan State University Diagnostic Center for Population and Animal Health, and were sent to the National Veterinary Services Laboratory in Ames, Iowa last Thursday for confirmatory testing. The positive results of those tests were communicated to the state of Michigan today.

    Audits of the facility by the DNR in 2004 and 2007 showed no escapes of animals from the Kent County facility were reported by the owner. Also, there were no violations of regulations recorded during the audits.

    Since 2002, the DNR has tested 248 wild deer in Kent County for CWD. In summer 2005, a number of those deer had displayed neurological symptoms similar to CWD; however, after testing it was determined the deer had contracted Eastern Equine Encephalitis.

    More information on CWD is available on Michigan’s Emerging Diseases Web site at www.michigan.gov/chronicwastingdisease
     
  2. Hamilton Reef

    Hamilton Reef Guest

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    Chronic wasting disease in Kent County deer prompts statewide quarantine

    http://www.detnews.com/apps/pbcs.dll/article?AID=/20080825/METRO/808250416/1409/METRO

    08/25/08 Gary Heinlein / Detroit News Lansing Bureau 517)371-3660 or [email protected]

    LANSING -- Michigan's first case of chronic wasting disease has been diagnosed in a white-tailed deer on a private deer farm in Kent County, officials of the state's Natural Resources and Agriculture departments said Monday.

    Chronic wasting disease is a fatal neurological disorder affecting deer, elk and moose. Most cases have been in western states, officials said, but it has spread eastward in recent years to some midwestern and eastern states. Infected animals show unusual behavior and suffer progressive weight loss and debilitation before they die.

    As a result of the newly found case, authorities have quarantined private herds and are prohibiting the movement of all privately owned deer, moose or elk in Michigan. They said they don't yet know how the animal in Kent County got the disease.

    There's no evidence, to date, the chronic wasting disease is a risk to humans.

    Natural Resources and Agriculture staff members are reviewing records of animals at the Kent County facility and five other private herds to find out how deer were purchased and moved in the last five years. They are doing the same for elk in the last seven years, officials said.

    Any deer that may have come in to contact with the diseased animal will be tracked and their current location will be quarantined, officials also said.

    "Michigan's veterinarians and wildlife experts have been working throughout the weekend to complete their investigation," said Agriculture Director Don Koivisto. "We take this disease very seriously, and are using every resource available to us to implement response measures and stop the spread of this disease."
     

  3. Hamilton Reef

    Hamilton Reef Guest

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    It doesn't matter at this point who is the first to post "I told you so!"
    A privately owned cervid (POC) operation screwed the state just as expected.
     
  4. Ninja

    Ninja Guest

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    Exactly....the greed of a few is going to radically change the management and numbers of our herd, not to mention the HUGE economic losses the people of this State will suffer.

    It burns my *** that the people responsible will be PAID for the deer that are going to be detsroyed from their herds, while many other good folks will be standing in the unemployment line.
     
  5. tommy-n

    tommy-n Banned

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    I agree, with the way the economy is it's going to put a hurting on alot of farmers ect. I know a guy that makes his living off selling all those bags of deer feed to gas stations. The tricke down effect will be huge.
     
  6. terry

    terry Banned

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    Chronic Wasting disease shows up in Kent County deer


    by Howard Meyerson | The Grand Rapids Press Monday August 25, 2008, 6:16 PM A whitetail deer born and culled from a Kent County deer farm has chronic wasting disease, state wildlife officials announced Monday. It is the first time the fatal neurological disease has turned up in Michigan. It's presence is triggering big changes for hunters and deer farm owners.

    "It's triggering bait and feeding restrictions for whitetail deer in all of the Lower Peninsula, and carcass handling restrictions in the hot zone," said Becky Humphries, the Department of Natural Resources director.

    Hunters who kill deer this fall from Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield and Cannon townships will be required to bring their deer to DNR check stations. Other hunters will be strongly encouraged to do so.

    To date, there is no indication that any wild, free-ranging deer has the disease. The 3-year-old female doe with CWD is the first reported case in Michigan.

    Deer farms all over the state also are being quarantined. There are 580 in total, including breeding farms, hobby and exhibition facilities, and ranches where the deer are hunted.

    In West Michigan, there are six farms of concern, the Kent County facility where the sick deer was found and five others in Osceola and Montcalm counties, which did business with the other farm.

    Don Koivisto, the director for the Michigan Department of Agriculture, said five facilities were quarantined over the weekend. Their records are being examined to trace the sale and transfer of deer. The facilities' names were withheld pending further investigation.

    E-mail Howard Meyerson: [email protected]


    http://www.mlive.com/outdoors/index.ssf/2008/08/chronic_wasting_disease_shows.html



    ALL STORIES FROM: The Grand Rapids Press « LATEST POSTS Wasting disease shows up in Kent County deer by Howard Meyerson | The Grand Rapids Press Monday August 25, 2008, 6:16 PM A whitetail deer born and culled from a Kent County deer farm has chronic wasting disease, state wildlife officials announced Monday. It is the first time the fatal neurological disease has turned up in Michigan. It's presence is triggering big changes for hunters and deer farm owners.

    "It's triggering bait and feeding restrictions for whitetail deer in all of the Lower Peninsula, and carcass handling restrictions in the hot zone," said Becky Humphries, the Department of Natural Resources director.


    http://www.mlive.com/outdoors/index.ssf/the_grand_rapids_press/



    Wasting disease shows up in Kent County deer by Howard Meyerson | The Grand Rapids Press Monday August 25, 2008, 6:16 PM A whitetail deer born and culled from a Kent County deer farm has chronic wasting disease, state wildlife officials announced Monday. It is the first time the fatal neurological disease has turned up in Michigan. It's presence is triggering big changes for hunters and deer farm owners.

    "It's triggering bait and feeding restrictions for whitetail deer in all of the Lower Peninsula, and carcass handling restrictions in the hot zone," said Becky Humphries, the Department of Natural Resources director.

    Hunters who kill deer this fall from Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield and Cannon townships will be required to bring their deer to DNR check stations. Other hunters will be strongly encouraged to do so.

    To date, there is no indication that any wild, free-ranging deer has the disease. The 3-year-old female doe with CWD is the first reported case in Michigan.

    Deer farms all over the state also are being quarantined. There are 580 in total, including breeding farms, hobby and exhibition facilities, and ranches where the deer are hunted.

    In West Michigan, there are six farms of concern, the Kent County facility where the sick deer was found and five others in Osceola and Montcalm counties, which did business with the other farm.

    Don Koivisto, the director for the Michigan Department of Agriculture, said five facilities were quarantined over the weekend. Their records are being examined to trace the sale and transfer of deer. The facilities' names were withheld pending further investigation.

    E-mail Howard Meyerson: [email protected]


    http://www.mlive.com/outdoors/index.ssf/2008/08/chronic_wasting_disease_shows.html



    CWD MICHIGAN

    http://www.michigan.gov/dnr/1,1607,7-153-10370_12150-29070--,00.html



    P04.01

    Chronic Wasting Disease in a Captive White-Tailed Deer Farm

    Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O’Rourke, K4; Spraker, T5 1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA; 5Veterinary Diagnostic Laboratory, Colorado State University, USA

    A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006, after chronic wasting disease (CWD) had been initially discovered on the property in September 2002. Prior to the depopulation, a total of 22 positive animals had been removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29 males. Age was assessed by visual examination of teeth at the time of death and revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil, retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of animals (sixty) were found to be positive in at least one tissue; 49 were obex positive, 58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion genotype was determined for all animals. ...END...TSS



    sorry to have to report this folks.....don't flounder around with it though///


    MORE LATER...........TERRY
     
  7. terry

    terry Banned

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    Monday, June 30, 2008
    Risk behaviors in a rural community with a known point-source exposure to chronic wasting disease

    http://chronic-wasting-disease.blogspot.com/2008/06/risk-behaviors-in-rural-community-with.html


    Monday, June 23, 2008
    Persistence of Pathogenic Prion Protein during Simulated Wastewater Treatment Processes

    http://chronic-wasting-disease.blogspot.com/2008/06/persistence-of-pathogenic-prion-protein.html


    Wednesday, June 11, 2008
    Transmission and Detection of Prions in Feces

    http://chronic-wasting-disease.blogspot.com/2008/06/transmission-and-detection-of-prions-in.html



    Sunday, August 24, 2008
    HAVE ANOTHER GLASS OF CWD PRIONS COURTESY Dane County Wisconsin Mike DiMaggio, solid waste manager

    http://chronic-wasting-disease.blogspot.com/2008/08/have-another-glass-of-cwd-prions.html



    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 ;

    http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html





    CHRONIC WASTING DISEASE BLOG

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



    Terry S. Singeltary Sr.
    P.O. Box 42
    Bacliff, Texas USA 77518
     
  8. terry

    terry Banned

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    i did not see that other post, sorry for the double post.
    i am very sorry to see this for you Michigan hunters. it's all downhill from here, but you need to clean out these game farms now, before it's too late. test everything. quarantine them all and test. the environment in one of these places is probably nothing more than a petre dish for CWD. they should be doubled fenced off and quarantined for a decade, as to no wild animal can get in or out. just my opinion. ...TSS



    P04.01

    Chronic Wasting Disease in a Captive White-Tailed Deer Farm

    Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O’Rourke, K4; Spraker, T5 1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA; 5Veterinary Diagnostic Laboratory, Colorado State University, USA

    A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006, after chronic wasting disease (CWD) had been initially discovered on the property in September 2002. Prior to the depopulation, a total of 22 positive animals had been removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29 males. Age was assessed by visual examination of teeth at the time of death and revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil, retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of animals (sixty) were found to be positive in at least one tissue; 49 were obex positive, 58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion genotype was determined for all animals. ...END...TSS




    Monday, June 30, 2008
    Risk behaviors in a rural community with a known point-source exposure to chronic wasting disease

    http://chronic-wasting-disease.blogspot.com/2008/06/risk-behaviors-in-rural-community-with.html


    Monday, June 23, 2008
    Persistence of Pathogenic Prion Protein during Simulated Wastewater Treatment Processes

    http://chronic-wasting-disease.blogspot.com/2008/06/persistence-of-pathogenic-prion-protein.html


    Wednesday, June 11, 2008
    Transmission and Detection of Prions in Feces

    http://chronic-wasting-disease.blogspot.com/2008/06/transmission-and-detection-of-prions-in.html



    Sunday, August 24, 2008
    HAVE ANOTHER GLASS OF CWD PRIONS COURTESY Dane County Wisconsin Mike DiMaggio, solid waste manager

    http://chronic-wasting-disease.blogspot.com/2008/08/have-another-glass-of-cwd-prions.html



    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 ;

    http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html





    CHRONIC WASTING DISEASE BLOG

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



    Terry S. Singeltary Sr.
    P.O. Box 42
    Bacliff, Texas USA 77518
     
  9. terry

    terry Banned

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    please note recent paper on TSE, and CWD below and comments from Aguzzi, Sigurdson, Heikenwaelder et al. there is some interesting data on cwd there. ...tss


    Molecular Mechanisms of Prion Pathogenesis

    Adriano Aguzzi, Christina Sigurdson, and Mathias Heikenwaelder Institute of Neuropathology, University Hospital of Z¨ urich, CH-8091 Z¨ urich, Switzerland; email: [email protected], [email protected], [email protected] Annu. Rev. Pathol. Mech. Dis. 2008. 3:11-40 First published online as a Review in Advance on August 8, 2007 The Annual Review of Pathology: Mechanisms of Disease is online at pathmechdis.annualreviews.org This article's doi: 10.1146/annurev.pathmechdis.3.121806.154326 Copyright c 2008 by Annual Reviews. All rights

    Annu. Rev. Pathol. Mech. Dis. 2008. 3:11-40 First published online as a Review in Advance on August 8, 2007 The Annual Review of Pathology: Mechanisms of Disease is online at pathmechdis.annualreviews.org This article's doi: 10.1146/annurev.pathmechdis.3.121806.154326 Copyright c 2008 by Annual Reviews. All rights reserved 1553-4006/08/0228-0011$20.00

    Abstract

    Prion diseases are infectious neurodegenerative diseases occurring in humans and animals with an invariably lethal outcome. One fundamental mechanistic event in prion diseases is the aggregation of aberrantly folded prion protein into large amyloid plaques and fibrous structures associated with neurodegeneration. The cellular prion protein (PrPC) is absolutely required for disease development, and prion knockout mice are not susceptible to prion disease. Prions accumulate not only in the central nervous system but also in lymphoid organs, as shown for new variant and sporadic Creutzfeldt- Jakob patients and for some animals. To date it is largely accepted that prions consist primarily of PrPSc, a misfolded and aggregated â-sheet-rich isoform of PrPC. However, PrPSc may or may not be completely congruent with the infectious moiety. Here, we discuss the molecular mechanisms leading to neurodegeneration, the role of the immune system in prion pathogenesis, and the existence of prion strains that appear to have different tropisms and biochemical characteristics.

    snip...

    As an example in the field of human medicine, four cases of vCJD have been reported to be caused by blood transfusion (9- 11). This indicates that BSE prions can be recycled among humans, which has caused considerable alarm that the supply of bloodderived pharmaceuticals may be threatened (12). In particular, the report of a subclinical blood-derived vCJD infection in an individual carrying a heterozygote methionine/ valine polymorphism at codon 129 of the human PRNP gene (10) suggests that transmission of BSE prions to humans enhances their virulence and broadens the spectrum of susceptible recipients. In this respect, it has been demonstrated that polymorphisms at codon 129 of the human PRNP gene control susceptibility and incubation time in human patients (e.g., 129MM versus 129MV or 129VV drastically increases the susceptibility of humans to BSE prions). It was reported only recently that most individuals who suffered from kuru and were polymorphic at codon 129 showed incubation times longer than 50 years (13). Moreover, recent reports indicate that there is still a lot to be learned about the mechanisms of prion transmission (e.g., human to human or within scrapie-affected animal flocks) and prion tropism underlining the complex alternating distribution patterns of PrPSc (e.g., PrPSc deposition in lymphoid tissue, the CNS) and prion infectivity under varying conditions (e.g., chronic inflammation) and hosts (e.g., sheep, elk and deer, human): Chronic inflammation can alter the tropism of prion infectivity or PrPSc to organs hitherto believed prion free (e.g., liver, pancreas, kidney of mice, mammary gland of sheep, muscle of humans) (14-16). Moreover, PrPSc was reported in spleen and muscle tissue of sporadic Creutzfeldt-Jakob disease (sCJD) patients (17), and prion infectivity was demonstrated in muscle, blood, and saliva of deer suffering from CWD (18, 189). Also, prion infectivity was shown to be excreted via urine of prion-infected nephritic mice, a process defined as prionuria (19). These results emphasize the need for further assessment of possible public health risks from TSE-affected extraneural organs. It is very well possible that preexisting pathophysiological conditions of the infected host additionally contributed to unexpected distribution patterns of prion infectivity. For example, the presence of prion infectivity in the blood of sheep or deer may influence the deposition of prion infectivity in various organs previously deemed prion free. Therefore, it should be carefully reconsidered whether only organs of the CNS and the lymphoreticular system should be included in the current risk classifications of biologicals in the future. It will be important to test altered prion tropism profiles in nonlymphoid organs and body fluids (e.g., blood, urine, milk, saliva) of ruminants (e.g., sheep, goat, cattle, elk, and deer) and human patients suffering from sCJD and vCJD.

    snip...

    Recent in vivo evidence indicated that a similar phenomenon of conformational variants may occur in Alzheimer's disease (151). Here the existence of Aâ strains that can seed and accelerate aggregation and Aâ pathology was posited. These intriguing observations support the hypothesis that the pathogenetic mechanisms operating in Alzheimer's disease and in prion diseases have more in common than we often appreciate (152). Perhaps future studies will address whether different Aâ strains with distinct biochemical or neuropathological characteristics occur in humans. Can multiple prion strains coexist and effect prion replication? Two subtypes of sporadic CJD have recently been demonstrated to coexist in humans (62). Experimental studies have shown that when two strains infect the same host, one strain can impede the ability of the second strain to cause disease (153). Bartz and colleagues (154) recently suggested that this might be caused by the suppression of prion replication of the second strain. Strain features are useful for tracing prion infections between species. When transmitted to primates, BSE causes lesions strikingly similar to that of vCJD (155, 156). BSE is most likely transmissible to humans too, and strong circumstantial evidence (157-159) suggests that BSE is the cause of vCJD, which has claimed more than 200 lives in the United Kingdom (3, 160), as well as a much smaller number in some other countries (161).

    NATURAL TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: WHAT IS NEW? Cattle Prions More than a few surprises have come from further investigations of prion strains in field cases of TSEs. Until recently, BSE was believed to be associated with one single prion strain, classified by an exclusive and remarkably stable biochemical profile of PrPSc. However, distinct molecular signatures have recently been discovered through the large-scale screening of cattle mandated by European authorities in the context of BSE surveillance. These atypical profiles fall into either of two groups: H-type cases of protease-resistant fragments with a molecular weight higher than BSE, and bovine amyloidotic spongiform encephalopathy, or L type (lower) (162). To test whether these different biochemical and histopathological properties correspond to distinct strains, the Laude laboratory transmitted H-type-PrPSc isolates from French cattle into transgenic mice expressing bovine or ovine PrP (163). The recipient mice developed neurological signs exhibiting strain-specific features clearly distinct from that of the classical BSE agent, providing pivotal evidence that the underlying strains are distinct.

    Atypical Sheep Scrapie In 1998, aberrant cases of sheep scrapie were described in Norway and the strain was newly classified as Nor98 (164). Active European Union surveillance later revealed additional cases of atypical scrapie in several other countries (165, 166). Sheep infected with Nor98, or atypical scrapie, accumulated PrPSc primarily in the cerebellum and cerebral cortex rather than in the brainstem target in the classical strain (167). Additionally, on western blot analysis of atypical scrapie cases, an additional small-molecular-weight (10-12 kDa) PrP fragment appeared afterPKdigestion and was shown by epitope mapping to lack both N and C termini of PrP (167, 168). Furthermore, atypical scrapie cases occurred not only in the classical scrapie-susceptible genotypes (A136 R154 Q171), but also in genotypes associated with high resistance to classical scrapie (A136 R154 R171) (165, 166). Were these atypical scrapie cases also infectious? In 2001, atypical scrapie cases were shown to be transmissible prion diseases after inoculated ovine PrP-expressing transgenic mice developed disease and prion aggregates (169). In the meantime, several countries appear to be reporting extremely high incidences of atypical scrapie, and in fact atypical scrapie appears to be the rule rather than the exception in some geographical areas.

    Chronic Wasting Disease Among all animal prion diseases, CWD of cervids is likely the most efficiently transmitted. CWD infections occur in mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), Rocky Mountain elk (Cervus elaphus nelsoni) (170), and moose (Alces alces shirasi) (171). Prevalence can reach as high as 30% in dense, free-ranging deer populations and nearly 100% in captive animals (171). Hypotheses for CWD transmission range from spread via direct contact to exposure through grazing in areas contaminated by prion-infected secretions, excretions (saliva, urine, feces), tissues (placenta), or decomposed carcasses. Insightful experimental studies have recently revealed two key findings: (a) Saliva from CWD-infected deer can transmit disease (18), and (b) CWD-infected carcasses allowed to decay naturally in confined pastures can lead to CWD infections in captive deer (172). Additionally, the abundant CWD-prion accumulation within lymphoid tissues may also lead to CWD prion buildup in nonlymphoid organs with lymphoid follicles, as was recently shown in kidney, potentially shifting shedding routes (173). It is unknown whether other types of inflammation, such as the granulomatous inflammation in the intestine seen in Johne's disease (Mycobacterium avium subsp. paratuberculosis; affects ruminants, including deer and elk) or parasitic inflammation, could lead to or perhaps increase prion excretion by fecal routes. The environmental prion contamination in CWD underscores the difficulties of CWD disease management.Within North America,CWDinfected deer and elk have been detected in 14 states and two Canadian provinces (170, 174, 175). CWD surveillance in Europe has been more limited. However, in Germany, a total of 7300 captive and free-ranging cervids were tested forCWDwith no sign of infection (176). Reindeer or caribou (Rangifer tarandus), from North America or Northern Europe respectively, have a highly homologous prion sequence compared with mule deer and thus are likely susceptible to CWD. Other European cervids such as moose and red deer (C. elaphus) are also expected to be CWD susceptible. The deer and elk primary protein structures are highly conserved, as seen in other mammals. Interestingly, a polymorphism at codon 225S/F may influence CWD susceptibility in mule deer. When comparing the frequency of genotypes among CWDnegative and -positive deer (n = 1482), the odds that a CWD-infected animal was 225SS was 30 times greater when compared with 225SF, whereas the frequency of 225SF/FF genotypes in CWD-negative deer was 9.3%, but only 0.3% in CWD-positive deer (177).

    Additionally, elk have a polymorphism at codon 132 (M/L) of Prnp, corresponding to polymorphic codon 129 (M/V) in humans. Elk expressing 132ML and 132LL Prnp were reported to be overrepresented among elk with CWD when compared with uninfected controls (178), and 132LL elk experimentally infected with CWD have resisted infection for at least four years, whereas 132MM or 132ML elk (n = 2 each) developed terminal clinical prion disease by 23 or 40 months post inoculation, respectively, confirmed by immunohistochemistry and western blotting for PrPSc (179). White-tailed deer also have Prnp polymorphisms that may affect their CWD susceptibility. A reduced susceptibility to CWD was linked to a G96S and a Q95H polymorphism in a study comparing allelic frequencies from CWD-positive and CWDnegative free-rangingWisconsin white-tailed deer (180).

    snip...end

    http://arjournals.annualreviews.org/doi/pdf/10.1146/annurev.pathmechdis.3.121806.154326

    http://chronic-wasting-disease.blogspot.com/2008/08/have-another-glass-of-cwd-prions.html


    p.s. also see ;


    P02.42

    Characterization of CWD Prion Strains Uding Transgenic Mice

    Angers, RC1; Browning, SR1; Seward, TS2; Miller, MW3; Balachandran, A4; McKenzie, D5; Hoover, EA6; Telling, GC2 1University of Kentucky, Microbiology, Immunology and Molecular Genetics, USA; 2University of Kentucky, Sanders Brown Center on Aging, USA; 3Wildlife Research Center, Colorado Division of Wildlife, USA; 4Canadian Food Inspection Agency, Animal Diseases Research Institute, Canada; 5University of Wisconsin, School of Veterinary Medicine, USA; 6Colorado State University, Microbiology, Immunology and Pathology, USA

    Although the distribution and host range of chronic wasting disease (CWD) is increasing, whether or not different CWD strains occur in various geographic locations or in different cervid species remains unclear. To address this we used cervidized transgenic mice (Tg(CerPrP)1536) to analyze CWD prions isolated from mule deer, white-tailed deer and elk from various geographic locations in North America. Isolates were characterized on the basis of incubation times in Tg(CerPrP)1536 mice. In all cases serial transmissions were performed in Tg(CerPrP)1536 mice. The biochemical properties of CerPrPSc produced in the brains of diseased mice were assessed by western blotting and conformational stability assays. We also used histoblot analysis to obtain a global portrait of the neuroanatomical distribution of CerPrPSc in the brains of diseased Tg(CerPrP)1536 mice in conjunction with immunohistochemical staining and hematoxylin and eosin staining to more fully characterize neuropathology. The glycosylation ratios of CerPrPSc were similar for all samples analyzed with the diglycosylated species of CerPrPSc being chiefly represented. Additionally, the stability of CerPrPSc, assessed by treatment with increasing concentrations of guanidine hydrochloride, demonstrated that the various CWD isolates were associated with similar conformations of CerPrPSc. Consistent with these results, there was little variation in the mean incubation times of CWD samples originating from different locations or species. However, while most inoculated Tg(CerPrP)1536 mice developed prion disease around 200 days post-inoculation, occasionally the incubation time of CWD prions approached 300 days. The neuropathological profile of mice Tg(CerPrP)1536 mice with more rapid incubation times consisted of extensive CerPrPSc deposition in the corpus callosum and frequently the hippocampus with corresponding neuronal vacuolation. In contrast, Tg(CerPrP)1536 mice with longer incubation times profiles displayed an unsystematic pattern of CerPrPSc deposition and vacuolation with irregular large plaques scattered throughout the brain and no CerPrPSc accumulation in the corpus callosum. Our data suggest the existence of one prevailing CWD strain in the United States and Canada, and raise the possibility of a co-existing second strain in some cases. ...end

    TSS
     
  10. pjslyfox

    pjslyfox Guest

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    I have to agree with anyone who feels that these game farms should be shut down. It should have been done as soon as CWD was first reported in this country. Perhaps now we can get baiting AND game farms out of here! The risk is too high for wildlife. Let's pray that none of this disease is found anywhere else in our state or country.
     
  11. PahtridgeHunter

    PahtridgeHunter

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    Unfortunately, I sort of figured it was inevitable. Now I just hope we're able to contain it and prevent the spread of CWD any further. This one hits a little too close to home for me as I now do 90% of my deer hunting near the Kent County border...although CWD found ANYWHERE over our borders is a tragedy.:nono:

    For those in the know, can the soil at these facilities be burned to kill off any remaining pathogens?
     
    Last edited: Aug 26, 2008
  12. Nick Adams

    Nick Adams

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    Could be. Probably. We suspect it to be the case. We don't know this for a fact.

    Appears to me that deer at these facilities are tested much more intensively for CWD than wild deer. If that is the case it's not surprising that the first CWD positive deer was found in one of these facilities. I suspect we will have to wait for more comprehensive CWD testing of the wild deer population in the area before we know whether it originated inside or outside of the fence.

    -na
     
  13. terry

    terry Banned

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    Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility Contact: Bridget Patrick (MDA) or Mary Dettloff (DNR) 517-241-2669 or 517-335-3014 Agency: Natural Resources

    August 25, 2008 LANSING - The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) today confirmed the state's first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County.

    The state has quarantined all POC facilities, prohibiting the movement of all - dead or alive - privately-owned deer, elk or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans.

    DNR and MDA staff are currently reviewing records from the Kent County facility and five others to trace deer that have been purchased, sold or moved by the owners in the last five years for deer and the last seven years for elk. Any deer that may have come in contact with the CWD-positive herd have been traced to their current location and those facilities have been quarantined.

    "Michigan's veterinarians and wildlife experts have been working throughout the weekend to complete their investigation," said Don Koivisto, MDA director. "We take this disease very seriously, and are using every resource available to us to implement response measures and stop the spread of this disease."

    CWD is a fatal neurological disease that affects deer, elk and moose. Most cases of the disease have been in western states, but in the past several years, it has spread to some midwestern and eastern states. Infected animals display abnormal behaviors, progressive weight loss and physical debilitation.

    Current evidence suggests that the disease is transmitted through infectious, self-multiplying proteins (prions) contained in saliva and other fluids of infected animals. Susceptible animals can acquire CWD by direct exposure to these fluids or also from contaminated environments. Once contaminated, research suggests that soil can remain a source of infection for long periods of time, making CWD a particularly difficult disease to eradicate.

    Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility: "Currently, one of our top concerns is to confirm that the disease is not in free-ranging deer," said DNR Director Rebecca Humphries. "We are asking hunters this fall to assist us by visiting check stations to allow us to take biological samples from the deer they harvest, so we can perform adequate surveillance of the free-ranging white-tailed deer herd in the area."

    Deer hunters this fall who take deer from Tyrone, Soldon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon townships will be required to bring their deer to a DNR check station. Deer taken in these townships are subject to mandatory deer check.

    The DNR is also asking hunters who are participating in the private land five-day antlerless hunt in September in other parts of Kent County to visit DNR check stations in Kent County so further biological samples can be taken from free-ranging deer for testing. The DNR is in the process of finding additional locations for check stations in Kent County to make it more convenient for hunters.

    The deer that tested positive at the Kent County facility was a doe that had been recently culled by the owner of the facility. Michigan law requires sick deer or culled deer on a POC facility be tested for disease. The samples from the Kent County deer tested "suspect positive" last week at Michigan State University Diagnostic Center for Population and Animal Health, and were sent to the National Veterinary Services Laboratory in Ames, Iowa last Thursday for confirmatory testing. The positive results of those tests were communicated to the state of Michigan today.

    Audits of the facility by the DNR in 2004 and 2007 showed no escapes of animals from the Kent County facility were reported by the owner. Also, there were no violations of regulations recorded during the audits.

    Since 2002, the DNR has tested 248 wild deer in Kent County for CWD. In summer 2005, a number of those deer had displayed neurological symptoms similar to CWD; however, after testing it was determined the deer had contracted Eastern Equine Encephalitis.

    More information on CWD is available on Michigan's Emerging Diseases Web site at www.michigan.gov/chronicwastingdisease.


    http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806-198865--,00.html


    MICHIGAN SURVEILLANCE AND RESPONSE PLAN FOR
    CHRONIC WASTING DISEASE OF FREE-RANGING AND
    PRIVATELY-OWNED/CAPTIVE CERVIDS


    http://www.michigan.gov/documents/CWD_ContingencyPlan_41755_7.pdf


    http://www.michigan.gov/documents/dnr/CWDexecsumm_246633_7.pdf


    TSS
     
  14. Hamilton Reef

    Hamilton Reef Guest

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    FOR IMMEDIATE RELEASE

    Aug. 26, 2008

    Contact: Mary Dettloff 517-335-3014

    DNR Acts to Implement CWD Surveillance and Response Plan

    In the wake of Monday’s announcement that Chronic Wasting Disease (CWD) has been confirmed in a three-year old privately-owned white-tailed deer in Kent County, the Michigan Department of Natural Resources is acting immediately to implement provisions of the state’s Surveillance and Response Plan for CWD.

    Among the provisions is an immediate ban on all baiting and feeding of deer and elk in the Lower Peninsula. DNR conservation officers will step up surveillance and enforcement efforts on baiting. Baiting and feeding
    unnaturally congregate deer into close contact, thus increasing the transmission of contagious diseases such as CWD and bovine tuberculosis. Bait and feed sites increase the likelihood that those areas will
    become contaminated with the feces of infected animals, making them a source of CWD infection for years to come.

    Additionally, the provisions include a mandatory deer check for hunters who take a deer within Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon townships, which contain the surveillance area or “hot zone.” All hunters who take a deer during any deer hunting season this fall within the “hot zone” will be required to visit a DNR deer check station so that their deer can be tested for CWD.
    The DNR currently is seeking locations for additional deer checkstations in the area to make it more convenient for hunters. To prevent unintentional spread of CWD, the only parts of deer harvested in the
    surveillance zone that will be allowed to be transported out will be boned meat, capes, and antlers cleaned of all soft tissues.

    In addition, all transport of live wild deer, elk and moose will be prohibited statewide, including transport for rehabilitation purposes. Currently, there is no live animal test for CWD, and infected animals often show no signs of illness for years in spite of being infectious for other animals. Movement for rehabilitation purposes may speed geographic spread of the disease.

    The DNR will act immediately to test an additional 300 deer within the “hot zone” in Kent County. The DNR will be cooperating with local officials to collect fresh road-killed deer, and will be urging deer hunters participating in the early antlerless season on private land in September to comply with the mandatory deer check. Landowners in Kent County “hot zone” who would like to obtain disease control permits to cull deer from their property and assist with the collection of deer for testing should contact the DNR’s Wildlife
    Disease Lab at 517-336-5030. Permits will be available immediately upon request. Landowners who do not want to cull deer, but want to participate in the collection of deer for testing, can obtain assistance
    from the DNR in culling deer.

    DNR officials reminded citizens that, to date, there is no evidence that CWD poses a risk to humans, nor has there been verified evidence that the disease can be transmitted to humans.

    CWD is a fatal neurological disease that affects deer, elk and moose. Most cases of the disease have been in western states, but in the past several years, it has spread to Midwestern and eastern states. Infected
    animals display abnormal behaviors, loss of bodily functions and a progressive weight loss. Current evidence suggests that the disease is transmitted through infectious, self-multiplying proteins (prions).
    Prions are normal cell proteins whose shape has been transformed, causing CWD. The disease is transmitted by exposure to saliva of infected animals. Susceptible animals can also acquire CWD by eating
    feces from an infected animal, or soil contaminated by them. Once contaminated, soil can remain a source of infection for many years, making CWD a particularly difficult disease to manage.

    More information about CWD is available on the State of Michigan’s Emerging Diseases Web site at www.michigan.gov/chronicwastingdisease.

    The DNR is committed to the conservation, protection, use and enjoyment of the state’s natural resources for current and future generations.
     
  15. terry

    terry Banned

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    greetings Michigan hunters,

    i know that by removing top soil yearly, by two foot or more, after several years, the disease was still there (scrapie research). once it is in the environment, it will take years to get out. i dont know if by burning the topsoil would do it or not? you probably would have to burn everything that had come into contact with those deer/elk/feed/fencelines/ etc.


    HERE IS some research that is ongoing, and some other research that has been completed on soil and TSE. ...TSS



    P04.08 Environmental Persistence of TSEs - Extraction of PrPSc from Soil Smith, A; Fernie, Karen; Somerville, R Neuropathogenesis Unit, UK Background: There are concerns about the potential spread of transmissible spongiform encephalopathies (TSEs) by environmental routes following, for example, burial of infected carcasses or the disposal of waste water. The extent to which TSE infectivity survives or is disseminated within soil and soil water is unclear as is the likelihood of ensuing infection. Aim: As part of this environmental project, soil samples are being collected from lysimeters containing either infected bovine heads or boluses of infectivity. The aim of this experiment is to devise a method for the extraction of PrPSc from soil and examines the interaction between soil and its components and TSE infectivity. Methods: Samples from two soil types (clay and sandy loam) were spiked with known amounts of TSE infected brain homogenate and subjected to various extraction methods including combinations of freeze/thaw, boiling, sonication and mixing with various solvents and detergents. Any recovery was determined on western blot using PrPSc as a surrogate marker for the presence of TSE infectivity. Results: These experiments have shown that PrPSc binds strongly to both sandy and clay soil, and to pure sand (quartz). Elution from quartz and the soils was only achieved in the presence of the detergent sarkosyl, and in the case of clay soil, satisfactory elution was only achieved if PrPSc was digested with proteinase K. This finding suggests that components in clay soil may bind differently to PrP than those of sandy soil, and that the N-terminal domain of PrP is involved in this binding. Conclusion: These results form the basis of a method for the extraction of PrPSc from soil and will be used to assay samples from a large scale lysimeter experiment. Samples testing positive for the presence of PrPSc will be selected for bioassay in mice. Results to date suggest that TSE infectivity may bind strongly to soil components and could therefore persist in the environment for long periods of time.


    P04.61

    Survival of PrPSc during Simulated Wastewater Treatment Processes

    Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3 1University of Wisconsin, Soil Science/Civil and Environmental Engineering, USA; 2University of Wisconsin, Civil and Environmental Engineering, USA; 3University of Wisconsin, Comparative Biosciences, USA


    Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.


    P04.71 Oral Transmission of Prion Disease Is Enhanced by Binding to Soil Particles Johnson, C; Pedersen, J; Chappell, R; McKenzie, D; Aiken, J University of Wisconsin - Madison, USA A long-unanswered question in prion biology is how certain transmissible spongiform encephalopathies (TSEs), such as sheep scrapie and cervid chronic wasting disease, spread from animal to animal. Anecdotal evidence and controlled field experiments have suggested the presence of an environmental TSE reservoir. We, and others, have speculated that soil may harbor TSE agent in the environment and allow its transfer to naïve hosts. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and that prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. We assessed the oral infectivity of Mte- and soil-bound prions and found that prions bound to Mte are orally bioavailable and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces incubation period relative to unbound agent. Cox proportional hazards modelling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy and organic carbon content, and found soil-bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third soil was equivalent to that of unbound agent. Enhanced infectivity of soilbound prions may explain the environmental transmission of some TSEs despite the presumably low levels shed into the environment.



    P04.104 Survival of Prion Proteins in Environmental Matrices Maluquer de Motes, C1; Torres, JM2; Pumarola, M3; Girones, R1 1University of Barcelona, Spain; 2Centro de Investigacion en Sanidad Animal, Spain; 3Autonomous University of Barcelona, Spain Several publications have suggested the environment as a possible route of transmission, especially for sheep scrapie and cervid Chronic Wasting Disease (CWD). The role of the environment as a reservoir for these disorders is difficult to prove and faces a considerable lack of information. In this work, different methodologies have been developed to evaluate the survival and inactivation of TSE agents in environmental matrices. Different slaughterhouse and urban sewage samples were spiked with diverse strains of either scrapie or BSE agents and kept under controlled conditions for extended periods of time. Aliquots of every experiment were sequentially collected and concentrated according to a methodology specifically selected for each type of matrix. Sensitivity of the methods developed was estimated among 2-10 ƒÊg of infected tissue. PrPres was finally detected by western blot. Films were then transformed into digital pictures, signal intensities were quantified and regression models were computed. According to the results obtained, scrapie agent showed higher stability than BSE in all the environments studied. However, no significant differences were observed among mouse-passaged scrapie strains and sheep scrapie. The regression models provided t90 and t99 values (times of incubation necessaries for 90% and 99% reduction of PrPres levels). In urban sewage, i.e., t99 was estimated as about 50 and 22 days for scrapie and BSE respectively. In general, the effect of the matrix was clearly observed in all the experiments, showing up to a 6-8 fold higher reduction of PrPres levels in comparison to PBS controls. As some of the inocula were titrated in terms of infectious doses, we approximated the decay of PrPres levels to the reduction of infectivity for both agents. In slaughterhouse wastewater, i.e., two-log reduction was observed for both agents after 30-35 days of incubation. Data on infectivity will be confirmed by a series of bioassay experiments.



    P04.125 Environmental Persistence of TSE Infectivity: Field Studies Fernie, K; Smith, A; Somerville, R Neuropathogenesis Unit, Roslin Institute, UK Background: There is concern about the consequences of contamination of the environment with TSE infectivity. Infectivity may enter the environment by various routes, persist in the ground and spread from the original source to contaminate an extended area and groundwater. Aims: We are studying this problem by addressing the following questions: 1. Does infectivity with some containment (e.g. in a carcass) survive in the carcass over time; 2. Does infectivity without containment survive, and is it disseminated into the surrounding soil and water? 3. Do the environmental conditions, e.g. soil type and pH, affect the survival and/or transport of infectivity through soil? Methods: To address these questions, we are performing two field experiments (with appropriate containment) each using two soil types. Air temperature, rainfall, soil temperature and moisture content are being monitored. In one experiment a series of 10 bovine heads have been spiked with the BSE derived TSE strain 301V and buried in the two soils, contained within individual lysimeters, for exhumation and analysis at yearly intervals. Rainwater flowing through and collected as groundwater is also being analysed. In the second experiment a bolus of infected brain is buried at the centre of two 3 meter diameter lysimeters and soil samples taken from them at regular intervals. Water flow-through is also analysed. Results: To date, the first two bovine heads have been exhumed and the surrounding soil sampled. Both of the exhumed heads were apparently largely decomposed but on examination of the brain cavity were found to contain significant amounts of brain tissue. These have been sampled and are presently being analysed. The soil samples taken from around the heads and five sets of core samples taken from the soil surrounding the buried brain in the two large lysimeters are presently being analysed for PrPSc, the abnormal protein associated with the TSEs and for infectivity. Water samples have also been collected for analyses. Discussion: We will use the acquired data to build a predictive model of TSE behaviour in the environment which will inform future risk assessments.


    snip...end....NEUROPRION 2007...TSS


    Public release date: 11-Aug-2008

    Contact: Dr. Björn Seidel
    [email protected]
    49-297-230-2330
    Fraunhofer-Gesellschaft

    Resistant prions


    A flock of sheep at pasture – a seemingly idyllic scene. But appearances can be deceptive: If the animals are suffering from scrapie, entire flocks may perish. Scrapie is an infectious disease in which prions destroy the animal's brain, rather like BSE. The brain becomes porous, the sheep lose their orientation, they suffer from strong itching sensations and scrape off their fleece. Eventually, the infected animals die.

    It is difficult to contain the disease – all too often, scrapie will break out again on the same farm several months or years after it has apparently been eradicated. Are the prions transmitted not only by direct contact, but also by the environment – perhaps by the pastures? How long do prions that get into the pasture via the saliva and excrements of the sick animals, persist in the ground?

    Together with fellow-scientists from the Robert Koch Institute in Berlin and the Friedrich Loeffler Institute (Federal Research Institute for Animal Health) on the island of Riems, research scientists from the Fraunhofer Institute for Molecular Biology and Applied Ecology IME in Schmallenberg investigated these questions on behalf of the German Ministry for Environment, Nature Conservation and Nuclear Safety BMU. "We mixed soil samples with scrapie pathogens to find out how long the pathogens would survive," says Dr. Björn Seidel, who headed the investigations at IME. "Even after 29 months, in other words more than two years, we were still able to detect prions in the soil." But are these prions still infectious? "The soil actually seems to increase the infectiousness of the pathogens. The incubation period – the time it takes for the disease to break out – is exceedingly short even after the prions have persisted in the soil for 29 months. All of the animals that were given contaminated soil became sick within a very short time.

    These results indicate that fresh incidences of scrapie among sheep are due to contaminated pastures," says Seidel in summary. The results of the study reveal that sheep may even become infected from the surface water, though the risk of infection is much lower in this case. There is no danger to humans, however: scrapie pathogens seem unable to affect them.

    Another cause for concern is chronic wasting disease (CWD). Like BSE and scrapie, this is caused by prions, but it mainly affects deer. The numbers of infected animals in North America are rising steeply. How long do BSE and CWD prions survive in the ground? "To find this out, we urgently need to carry out further tests. The appropriate research applications have already been submitted," says Seidel.


    http://www.eurekalert.org/pub_releases/2008-08/f-rp081108.php#



    continued