# Michigan decides to scale down cwd testing as disease continues it's spread



## terry (Sep 13, 2002)

CWD Surveillance 

Since 1996, the DNR has tested over 34,000 white-tailed deer, 1,590 elk and 70 moose for CWD. All of these animals have tested negative for the disease. With the finding of the positive privately- owned white-tailed deer in Kent County in 2008, surveillance efforts were increased in this county and in the 9 townships surrounding the location of this deer. Over 4,000 free-ranging white-tailed deer have been tested from Kent County, with all of these being negative for CWD. 

After 8 years of extensive statewide surveillance, and over 3 years of surveillance in Kent County, the DNR will focus CWD testing for 2012 only on those animals displaying signs of a neurological disorder, consistent with CWD.



:SHOCKED: :help:


CWD Signs 


Although other diseases or injuries can cause similar signs, the DNR will perform a full necropsy and submitt samples for CWD testing from any animal displaying these signs.





http://www.michigan.gov/emergingdiseases/0,4579,7-186-25806_26404-271871--,00.html





> All but three of the 43 positive animals detected since 2005 were asymptomatic, meaning 40 animals did not show any symptoms of CWD at the time of collection.



http://chronic-wasting-disease.blogspot.com/2012/02/three-kansas-deer-confirmed-positive-in.html





a foolish move $$$, in my opinion.


there is no fool-proof way to determine if even an ostensibly healthy deer has the disease.


this is like sticking your head in the sand, and wishing it away, or just flat refusing to want to know. 


this is exactly what the USDA did with the june 2004 enhanced BSE surveillance program. they screwed it up so bad, they had to literally confirm a mad cow or two. then when the atypicals starting to show up, and after the GAO and OIG had proven the testing for BSE was rigged, yes I mean literally rigged, as in FRAUD. they shut mad cow testing down to where the numbers were so low, it would be almost impossible to find BSE i.e. testing 40,000 out of 100 MILLION.


is this what kind of CWD surveillance Michigan wants ???



good luck with that. ...





SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. daaa.




http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm






*** 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






http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm





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...





CWD Zoonotic Potential, Species Barriers, and Strains



Current Understanding of the CWD Species Barrier




Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence.




Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29).







Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern.







Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).







CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.







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...






*** 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



http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm






see much more here ;




http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html






Tuesday, February 14, 2012


White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease


http://transmissiblespongiformencep...2/white-house-budget-proposes-cuts-to-ag.html







Thursday, February 16, 2012 


Bovine Spongiform Encephalopathy BSE 


31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012 


http://transmissiblespongiformencep.../bovine-spongiform-encephalopathy-bse-31.html









50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD 




2012 


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. 


Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years. 


However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil. 


Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < < 




http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf






SNIP...SEE FULL TEXT ; 



http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html





Thursday, February 09, 2012 


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE 


http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html





kind regards,
terry


----------



## terry (Sep 13, 2002)

A cautionary tale against stopping surveillance too soon is provided by past CWD developments in Michigan. CWD surveillance in Michigan had continued since 1998 with 23,739 white-tailed deer, 887 elk, and 46 moose tested as of October 21, 2008 (Daniel OBrien, Michigan Department of Natural Resources, oral commun). In addition, 8,452 captive cervids have been tested by the Michigan Department of Agriculture. Even with 10 years of surveillance effort, the first positive case was discovered in a captive animal in fall of 2008. Thus, even with a reasonable level of surveillance effort for a considerable period of time, a new case may be detected where a jurisdiction was previously believed to be CWD-free when the probability of introduction is greater than zero. 

http://pubs.usgs.gov/of/2012/1036/pdf/ofr2012_1036.pdf 



TSS


----------

