# CWD DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011



## terry (Sep 13, 2002)

Tuesday, May 31, 2011 


Chronic Wasting Disease DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011


http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-doi.html


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## ridgewalker (Jun 24, 2008)

]. However, oral or i.c. challenge with CWD of macaques did not cause disease [116]. Overall, there is no compelling evidence that CWD can be transmitted to humans with high efficiency.[

_While CJD is a horrific disease that should be eradicated from the possibility of transmission in medical facilities, the above statements are all that can be said with any certainty concerning CWD at the present time._


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## terry (Sep 13, 2002)

ridgewalker said:


> ]. However, oral or i.c. challenge with CWD of macaques did not cause disease [116]. Overall, there is no compelling evidence that CWD can be transmitted to humans with high efficiency.[
> 
> _While CJD is a horrific disease that should be eradicated from the possibility of transmission in medical facilities, the above statements are all that can be said with any certainty concerning CWD at the present time._






>>> Overall, there is no compelling evidence that CWD can be transmitted to humans with high efficiency.<<<


ridgewalker wrote;


>the above statements are all that can be said with any certainty concerning CWD at the present time.<


no it's not. maybe in your mind there ridgewalker. 


but you can't seem to see past one tree, to see the whole forest.



also, you forgot to reference from the same study ;



===============================


On the other hand, squirrel monkeys (Saimiri sciureus) were susceptible to i.c. inoculation with CWD prions [116, 117], 

and after oral exposure PrPSc was detectable in brain, spleen, and lymph nodes of 2/15 squirrel monkeys [116]. 

This shows that CWD can be transmitted to certain non-human primates, although results in Cynomolgus macaques might be of higher relevance since they are evolutionary closer relatives of humans than squirrel monkeys.


================================



key word here, and back at ya 


"might be"



see the other study on squirrel monkeys;




Discussion

As new CWD foci continue to emerge among cervid populations, the risk for CWD transmission to humans needs to be assessed. We used 2 monkey species and 2 routes of inoculation to test the susceptibility of primates to 8 different pools of CWD. 

To date, we have verified CWD in 11 of 13 intracerebrally inoculated squirrel monkeys;:SHOCKED: average incubation period was 41 months (range 33.53 months). 

Using a single CWD pool, Marsh et al. noted infection in 2 of 2 squirrel monkeys 31.34 months after intracerebral inoculation (13). Intracerebral inoculation of squirrel monkeys with other TSE agents, including agents of kuru, variant CJD, sporadic CJD, and sheep scrapie, had incubation periods of .24 months and attack rates of .100% (14,15,32). The extended incubation periods and lower attack rates for our squirrel monkeys may result from a partial species barrier to CWD.

The signs of wasting syndrome in CWD-infected monkeys were similar to those of CWD infection in cervids, in which loss of body condition is nearly always a major component of infection and neurologic deficits vary (2). The correlation of clinical signs between CWD in cervids and squirrel monkeys suggests that CWD might affect a common brain region in each species. We observed PrPres deposition in squirrel monkeys primarily in the frontal lobe of the cerebral cortex, claustrum, putamen, and thalamus. Cervids typically have the most abundant and predictable PrPres in the dorsal motor vagus nucleus (obex), olfactory cortex, and diencephalon (including thalamus, hypothalamus, metathalamus, and epithalamus) (2,33).

A plausible hypothesis could be that disruption of regions within the hypothalamus and thalamus leads to a metabolic imbalance, resulting in a severe wasting syndrome.

We did not observe a strong correlation between infectivity titer inoculated and attack incidence or incubation period (Table 1). One potential explanation is that the variation in speed of disease progression might not be relevant given the low number of animals in each group. A second possibility is that our squirrel monkeys varied at PrP alleles that may affect CWD susceptibility. However, analysis of 23 squirrel monkeys showed no PrP sequence differences correlating with susceptibility to CWD (Tables 1, 2, 4). A third possibility is that genes other than the gene for PrP might influence CWD susceptibility.

For humans, eating infected or contaminated tissue is a likely route of CWD exposure. In other animal models, oral transmission of TSE is generally 1,000-fold less effective than direct intracerebral challenge and results in longer incubation periods and lower efficiency of disease transmission. In our oral transmission experiments, we found evidence of CWD infection in 3 monkeys; 2 at 69 mpi had abundant PrPres in brain and lower levels in spleen and lymph nodes, and 1 euthanized at 39 mpi had PrPres in lymphatic tissues only. Thus, transmission seems to be slower by the oral route than by the intracerebral route, and other orally infected monkeys may be affected in the future.

Cynomolgus macaques are evolutionarily closer to humans than are squirrel monkeys (17). At nearly 6 years postinoculation, no macaques have shown clinical signs of CWD. Intracerebral inoculation of cynomolgus macaques with BSE causes disease in 3 years; human variant CJD requires 23 years, and human sporadic CJD requires 5 years (16,34). However, oral inoculation of cynomolgus macaques with BSE agent required a minimum of 5 years before clinical disease was observed (35). There-fore, we cannot rule out CWD transmission to cynomolgus macaques.

The PrP gene sequence can influence cross-species transmission of prion disease. Therefore, we compared squirrel monkey and cynomolgus macaque PrP gene sequences to look for differences that might account for different susceptibilities of these monkeys to CWD. In the PrP gene excluding the signal peptide, deer differed from squirrel monkeys at 17 residues and from cynomolgus macaques at 16 residues, but 14 of these differing residues were identical in squirrel monkeys and macaques (Figure 4). Therefore, there are only 2 residues in cynomolgus macaques (100 and 108) and 3 residues in squirrel monkeys (56, 159 and 182) at which these monkeys differ from deer and also from each other. These residues might play a role in susceptibility differences seen in our study.

Human exposure to CWD-infected cervids in past decades is likely. The highest levels of prion infectivity are present in the central nervous system and lymphatic tissues of CWD-infected cervids; contamination of knives, saws, and muscles with these tissues can easy occur when processing game. Despite the likelihood of exposures, epidemiologic studies of humans living in CWD-endemic areas of Colorado and Wyoming during 19792001 have not shown any increases in human TSE cases (36,37). Ongoing studies by the Colorado Department of Public Health and Environmental Human Prion Disease Surveillance Program, in conjunction with the University of Colorado School of Medicine, have also concluded that no convincing cases of CWD transmission to humans have been detected in Colorado (38).

However, if CWD in humans appears like a wasting syndrome similar to that observed in the squirrel monkeys in our study, affected persons might receive a diagnosis of a metabolic disorder and never be tested for TSE. Fortunately, additional laboratory data are consistent with the epidemiologic data, and these results support the conclusion that a species barrier protects humans from CWD infection (1113,20,36,37).


http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1158&context=zoonoticspub&sei-redir=1#search="genetic+code+human+to+Cynomolgus+macaques"



don't get me wrong, i hope and pray you are correct, i wish that none of this would transmit to humans, but i can't ignore what science shows to date.



everybody is entitled to their opinions, everybody can interpret these studies in their own way. i interpret this study as a warning shot across the bow of the boat. same as with what the CDC have been saying across the past decade. i know you did not read all the source data supplied there ridgewalker, so you probably did not read ;



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





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: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

snip...

full text ;


http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html




FDA is not 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


http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html


see full text ;


http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html



CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.


http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf





again there ridgewalker, we can kindly agree to disagree. 


have a nice day. ...


kind regards, 
terry


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## ridgewalker (Jun 24, 2008)

I did take a considerable amount of time reading those studies. However I found no evidence that equated CJD and CWD. Also I found nothing that documented transfer of CWD, by any route, from deer to human. The numbers from Colorado just say to me that the probability of transmission of CWD to human must be extremely low if the possibility exists at all. If I am wrong I will be the first to be devastated.

Yes, we can honestly disagree. I really do wish you well in your quest to find resolution. Wishing you good health and peaceful days.


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