Mike said:
Mike - thanks for posting the more detailed article. I have been in Texas and missed recent scientific postings
I understand completely. News in Texas is hard to come by. :lol:
They should be getting TV, Telephone, and the internet soon.
That Telegraph is not very thorough. :lol:
TEXAS, home of where they dont test cows for BSE, they just render them ;-)
Subject: Infectious Prions in the Saliva and Blood of Deer with Chronic Wasting Disease
Date: October 5, 2006 at 1:45 pm PST
Infectious Prions in the Saliva
and Blood of Deer with Chronic
Wasting Disease
Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A. Osborn,5 Karl V. Miller,5
Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1 Davis M. Seelig,1
Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6 Christina J. Sigurdson,1
Glenn C. Telling,7 Edward A. Hoover1*
A critical concern in the transmission of prion diseases, including chronic wasting disease (CWD)
of cervids, is the potential presence of prions in body fluids. To address this issue directly, we
exposed cohorts of CWD-nai¨ve deer to saliva, blood, or urine and feces from CWD-positive deer.
We found infectious prions capable of transmitting CWD in saliva (by the oral route) and in blood
(by transfusion). The results help to explain the facile transmission of CWD among cervids and
prompt caution concerning contact with body fluids in prion infections.
SNIP...
Deer cohorts 1 (blood), 2 (saliva), and 3
(urine and feces) were electively euthanized at
18 months pi to permit whole-body examination
for PrPCWD. The greatest scrutiny was directed
toward those tissues previously established
to have highest frequency of PrPCWD deposition
in infected deer and generally regarded
as the most sensitive indicators of infection—
medulla oblongata and other brainstem regions,
tonsil, and retropharyngeal lymph node. We
found unequivocal evidence of PrPCWD in brain
and lymphoid tissue of all six tonsil biopsy–
positive deer in cohorts 1 (blood) and 2 (saliva),
whereas all deer in cohorts 3 and 5 were negative
for PrPCWD in all tissues (Table 2 and
Figs. 1 and 2).
The transmission of CWD by a single blood
transfusion from two symptomatic and one
asymptomatic CWDþ donor is important in at
least three contexts: (i) It reinforces that no tissue
from CWD-infected cervids can be considered
free of prion infectivity; (ii) it poses the
possibility of hematogenous spread of CWD,
such as through insects; and (iii) it provides a
basis for seeking in vitro assays sufficiently
sensitive to demonstrate PrPCWD or alternate
prion protein conformers in blood—one of the
grails of prion biology and epidemiology.
The identification of blood-borne prion
transmission has been sought before with mixed
results (9–11). Bovine spongiform encephalopathy
and scrapie have been transmitted to naBve
sheep through the transfer of 500 ml of blood
or buffy coat white blood cells from infected
sheep (12, 13). In addition, limited but compelling
evidence argues for the transmission of variant
Creutzfeldt-Jakob disease (vCJD) through blood
from asymptomatic donors (14–16). Even in
sporadic CJD, PrPres has been found in periph-
eral organs of some patients (17). The present
work helps establish that prion diseases can be
transmitted through blood.
The presence of infectious CWD prions in
saliva may explain the facile transmission of
CWD. Cervid-to-cervid interactions (SOM text),
especially in high density and captive situations,
would be expected to facilitate salivary crosscontact
(11, 18, 19). Salivary dissemination of
prions may not be limited to CWD. Proteaseresistant
prion protein has been demonstrated in
the oral mucosa, taste buds, lingual epithelium,
vomeronasal organ, and olfactory mucosa of
hamsters infected with transmissible mink
encephalopathy (19) and ferrets infected with
CWD (20). Although no instance of CWD
transmission to humans has been detected, the
present results emphasize the prudence of using
impervious gloves during contact with saliva or
blood of cervids that may be CWD-infected.
Environmental contamination by excreta
from infected cervids has traditionally seemed
the most plausible explanation for the dissemination
of CWD (21). However, we could not
detect PrPCWD in cohort 3 deer inoculated repeatedly
with urine and feces from CWDþ deer and examined up to 18 months pi (Table 2).
There are several reasons to view this negative
finding cautiously, including small sample size,
elective preclinical termination, and potential
variation in individual susceptibility that may
be associated with the 96 G/S polymorphism in
the PRNP gene (7, 22). Although no genotype
of white-tailed deer is resistant to CWD infection,
PRNP genotypes S/S or G/S at codon 96
appear to have reduced susceptibility manifest
by longer survival (7). Both deer in cohort 3
(urine and feces) were subsequently shown to
be of the PRNP 96 G/S genotype. Thus, it is
possible, although we think unlikely, that these
deer had a prolonged incubation period (918
months pi) before the amplification of PrPCWD
became detectable in tissues. Recent studies
have shown that PrPres is poorly preserved
after incubation with intestinal or fecal content
(23, 24). Further research using cervid and surrogate
cervid PrP transgenic mice (25) are indicated
to continue to address the presence of
infectious CWD prions in excreta of CWDþ deer and to provide a more substantial basis for
reconsideration of the assumption that excreta
are the chief vehicle for CWDdissemination and
transmission.
The results reported here provide a plausible
basis for the efficient transmission of CWD in
nature. We demonstrate that blood and saliva in
particular are able to transmit CWD to naBve deer
and produce incubation periods consistent with
those observed in naturally acquired infections
(3, 26). The time from exposure to first detection
of PrPCWD by tonsil biopsy was variable—as
short as 3 months but as long as 18 months (likely
underestimates due to sampling frequency).
The results also reinforce a cautious view of the
exposure risk presented by body fluids, excreta,
and all tissues from CWDþ cervids. ...
SNIP...END
http://www.sciencemag.org/cgi/content/abstract/314/5796/133
http://www.sciencemag.org/
##################### Bovine Spongiform Encephalopathy #####################
Prion protein in cardiac muscle of elk (Cervus elaphus nelsoni) and white-tailed deer (Odocoileus virginianus) infected with chronic wasting disease
Jean E. Jewell1, Jeremy Brown1, Terry Kreeger2 and Elizabeth S. Williams1,
1 Department of Veterinary Sciences, University of Wyoming, Wyoming State Veterinary Laboratory (WSVL), 1174 Snowy Range Road, Laramie, WY 82070, USA
2 Veterinary Services Branch, Wyoming Game and Fish Department (WGFD), Wheatland, WY 82201, USA
Correspondence
Jean E. Jewell
[email protected]
To investigate the possible presence of disease-associated prion protein (PrPd) in striated muscle of chronic wasting disease (CWD)-affected cervids, samples of diaphragm, tongue, heart and three appendicular skeletal muscles from mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi) were examined by ELISA, Western immunoblot and immunohistochemistry (IHC). PrPd was detected in samples of heart muscle from seven of 16 CWD-infected white-tailed deer, including one free-ranging deer, and in 12 of 17 CWD-infected elk, but not in any of 13 mule deer samples, nor in the single CWD-infected moose. For white-tailed deer, PrPd was detected by Western blot at multiple sites throughout the heart; IHC results on ventricular sections of both elk and white-tailed deer showed positive staining in cardiac myocytes, but not in conduction tissues or nerve ganglia. Levels of PrPd in cardiac tissues were estimated from Western blot band intensity to be lower than levels found in brain tissue. PrPd was not detected in diaphragm, triceps brachii, semitendinosus, latissiumus dorsi or tongue muscles for any of the study subjects. This is the first report of PrPd in cardiac tissue from transmissible spongiform encephalopathy-infected ruminants in the human food chain and the first demonstration by immunological assays of PrPd in any striated muscle of CWD-infected cervids.
Deceased 29 December 2004.
http://vir.sgmjournals.org/cgi/content/abstract/87/11/3443?ct
TSS
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##################### Bovine Spongiform Encephalopathy #####################
Patterns of PrPCWD accumulation during the course of chronic wasting disease infection in orally inoculated mule deer (Odocoileus hemionus)
Karen A. Fox1,2, Jean E. Jewell3, Elizabeth S. Williams3, and Michael W. Miller1
1 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA
2 College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
3 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA
Correspondence
Michael W. Miller
[email protected]
Patterns of abnormal prion protein (PrP) accumulation during the course of chronic wasting disease (CWD) infection were studied and the distribution and timing of disease-associated PrP (PrPCWD) deposition and lesions in 19 mule deer (Odocoileus hemionus) 90–785 days after oral inoculation were described. PrPCWD deposition occurred relatively rapidly and widely in lymphoid tissues, later in central and peripheral nervous tissues and sporadically in a variety of tissues and organs in terminal disease stages. Development of spongiform encephalopathy lagged behind PrPCWD deposition in the central nervous system (CNS), but occurred in the same neuroanatomical locations. PrPCWD deposition in the lymphatic and nervous systems tended to be consistent and progressive in specific organs and tissues. Locations of PrPCWD deposition were similar between deer of two PrP genotypes (225SS and 225SF), but the time course differed between genotypes: in 225SF deer, PrPCWD accumulated more slowly in lymphatic tissues than in 225SS animals, but that disparity was small in comparison to the disparity between genotypes in timing of deposition in CNS tissue. These data confirm retropharyngeal lymph node and medulla oblongata at the level of the obex as early sites of PrPCWD accumulation in mule deer with CWD. Data on the relative time frames for and genetic influences on PrPCWD accumulation may also offer insights about epidemic dynamics and potential control strategies.
Deceased 29 December 2004.
http://vir.sgmjournals.org/cgi/content/abstract/87/11/3451
TSS
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CWD AND ENVIRONMENTAL FACTORS i.e. saliva, fecal shedding and fecal-oral transmission is likely
http://p079.ezboard.com/fwolftracksproductionsfrm2.showMessage?topicID=592.topic
TSS
THE SEVEN 1/2 SCIENTIST REPORT ***
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle
03-025IFA
03-025IFA-2
Terry S. Singeltary
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518