# CWD AND ENVIRONMENTAL FACTORS i.e. saliva, fecal shedding and fecal-oral transmission



## terry (Sep 13, 2002)

##################### Bovine Spongiform Encephalopathy #####################


Subject: CWD AND ENVIRONMENTAL FACTORS i.e. saliva, fecal shedding and fecal-oral transmission is likely
Date: October 1, 2006 at 6:31 pm PST

CWD Annual Report  2005

To date, we have developed a reliable, non-lethal method for detecting chronic wasting disease in

mule deer that represented a significant breakthrough in improving the ability to monitor

prevalence of the disease over time and space. We also have demonstrated that chronic wasting

disease can be transmitted indirectly, and that fecal shedding and fecal-oral transmission is likely.

We also have developed epidemic models for chronic wasting disease in captive mule deer that

align well with the independent empirical findings on transmission processes, underscoring the

likely importance of indirect transmission in the ecology of chronic wasting disease in natural

populations.


full text ;


http://www.nrel.colostate.edu/projects/cwd/papers/CWD_ann_rpt_2005_w_figs.pdf

Vet Pathol 42:530549 (2005)

REVIEW ARTICLE

Chronic Wasting Disease

E. S. WILLIAMS1

Department of Veterinary Sciences, University of Wyoming, Laramie, WY

Abstract. Chronic wasting disease (CWD) is a unique transmissible spongiform encephalopathy (TSE) of

mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus

nelsoni). The natural history of CWD is incompletely understood, but it differs from scrapie and bovine spongiform

encephalopathy (BSE) by virtue of its occurrence in nondomestic and free-ranging species. CWD has

many features in common with scrapie, including early widespread distribution of disease-associated prion

protein (PrPd) in lymphoid tissues, with later involvement of central nervous system (CNS) and peripheral

tissues. This distribution likely contributes to apparent efficiency of horizontal transmission and, in this, is

similar to scrapie and differs from BSE. Clinical features and lesions of CWD are qualitatively similar to the

other animal TSEs. Microscopically, marked spongiform lesions occur in the central nervous system (CNS)

after a prolonged incubation period and variable course of clinical disease. During incubation, PrPd can be

identified in tissues by antibody-based detection systems. Although CWD can be transmitted by intracerebral

inoculation to cattle, sheep, and goats, ongoing studies have not demonstrated that domestic livestock are

susceptible via oral exposure, the presumed natural route of exposure to TSEs. Surveillance efforts for CWD

in captive and free-ranging cervids will continue in concert with similar activities for scrapie and BSE. Eradication

of CWD in farmed cervids is the goal of state, federal, and industry programs, but eradication of CWD

from free-ranging populations of cervids is unlikely with currently available management techniques.


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Transmission

Although the exact method of transmission of CWD

is not known, horizontal and indirect transmission appear

to be the most important routes of spread.99 Epidemiologic

observations suggest that in addition to

transmission within species, CWD can be transmitted

from elk to mule deer and white-tailed deer, from mule

deer to elk, and from mule deer to white-tailed deer.156

Maternal transmission, if it occurs, does not appear to

play a significant role in the epidemiology of the disease.

99 To date, PrPd and infectivity have not been

identified in placentas of deer and elk. This is in contrast

to scrapie, in which high levels of infectivity reside

in the placenta,5,122,143,144 and epidemiologic investigations

have found that transmission at the time of

lambing appears to be important in maintaining scrapie

in flocks.

Results of a series of studies investigating CWD

transmission have recently been published.102 Direct

transmission of CWD between animals occurred, although

the exact mechanism was not determined. The

role of environmental contamination in maintaining infectivity

is not entirely understood; however, controlled

studies showed infectivity remained on pastures

in which CWD-affected deer resided approximately 2

years previously. These studies were conducted in pastures

presumed to be highly contaminated. Thus, extrapolation

to field situations should be done with care,

but these data suggest caution in managing pastures or

paddocks that have housed CWD-affected cervids. In

addition, mule deer were infected by contact with skeletal

remains of CWD-affected deer and surrounding

ground and vegetation. This information bolsters the

need for caution when moving portions of harvested

cervids that contain the highest amount of infectivity,

such as the head and the spine, to areas where CWD

does not exist.


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full text ;


http://www.vetpathology.org/cgi/reprint/42/5/530.pdf


DRAFT 

WYOMING GAME AND FISH DEPARTMENT 

CHRONIC WASTING DISEASE MANAGEMENT PLAN 

February 17, 2006 


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6. Epidemiology of CWD: detection, shedding, and environmental contamination. 
Thirty elk were orally inoculated with elk CWD prion in May 2005. Every six weeks, elk are individually housed in metabolic cages for three days. Feces, urine, saliva, and blood are collected. These samples are used to develop and validate an assay capable of detecting minute concentrations of the CWD prion in a variety of substrates. Additional samples for testing are collected from insects, rabbits, rodents, and soil where the CWD-infected elk are housed. This study could determine: 1) how the CWD prion is shed from infected animals; 2) the temporal pattern of such shedding; and 3) the degree and extent of environmental contamination with the CWD prion. 


http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf


Experimental CWD Infection and Bioassay in the Ferret
Edward A. Hoover', Christina J. Sigurdson', Candace K. Mathiason', Michael W. Miller2, Matthew R. Perroti', Gwyneth A. Eliason', Terry R. Spraker3, and Jason C. Bartz4
'Prion Research Laboratory, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; 2Colorado Division of Wildlife, Fort Collins, CO 80526; 3Colorado State Veterinary Diagnostic Laboratory, Fort Collins, CO 80523;4Department of Medical Microbiology and Immunology, Creighton University, Omaha, NB 68178

Based on the work of Bartz et al., we have developed the ferret model of CWD infection and employed this system to: (1) compare brain lesions and PrPcwd distribution in brain and lymphoid tissues in ferrets with those in deer, and (2) assay secretions/excretions from deer for CWD prion infectivity. Groups of ferrets were inoculated via the oral or intracerebral (i.c.) route with CWD + vs. CWD- deer brain homogenates, white blood cells, or saliva. Inoculated ferrets were monitored clinically and either sacrificed at pre-determined intervals from 3 to 24 months post inoculation (pi) or when terminal symptoms developed. Ferrets inoculated ic with CWD+ brain developed clinical neurologic disease and were euthanized between 14 and 19 months. Tissues were examined by histopathology, and by immunohistochemical staining, ELISA, and western blotting for Histopathologic lesions indicative of TSE included spongiform vacuolation and neuronal necrosis. PrPcwd was demonstrated in ferret brain by ELISA and western blot assays. In addition, dual immunofluorescent staining revealed PrPcwd localized at astrocyte surface membranes and within neurons. Results to date from ferret bioassay of saliva and blood cells from CWD+ deer will be reported. These studies confirm the susceptibility of the ferret to CWD infection and pose the potential that CWD infectivity can be assayed in this small animal model.


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Based on epidemiological studies there

is evidence that the disease is transmitted horizontally from infected to susceptible cervids

(Miller and Williams, 2003). Maternal transmission may also occur but seems to play a

subordinate role. Accumulation of PrPres in gut-associated lymphoid tissues during the disease

course suggests agent shedding in faeces and/or saliva as plausible transmission routes

(Sigurdson et al., 1999). Residual infectivity in contaminated environments, either from

excreta or from decomposed carcasses of infected animals, may also be important in

sustaining epidemics.


http://www.efsa.europa.eu/etc/media...nion_biohaz12_ch_wast_dis_ef70_report_en1.pdf


CWD

3.4.2 Evidence for lateral transmission 


The CWD agent has been demonstrated in lymphoid tissues of the alimentary tract that suggests that the agent may be shed through the alimentary tract (faeces and saliva).

see Annexe 1 on distribution of tissue infectivity (old data)...tss


http://ec.europa.eu/food/fs/sc/ssc/out324_en.pdf

http://72.14.209.104/search?q=cache...+DISEASE+AND+TISSUE&hl=en&gl=us&ct=clnk&cd=11



and secondly the possibility of a sylvatic reservoir...


http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


Observations of deer and elk in captivity indicate that CWD is contagious though the

exact mechanism(s) of transmission are not yet known. Based on pathogenesis of the disease

it is plausible that the CWD agent exits the body in saliva and feces. The contribution of

82

environmental contamination to the epidemiology of CWD is not specifically known but

observations of cohorts of elk and deer in captivity strongly suggest it is important in areas of

high CWD prevalence and high densities of susceptible species. This is an area of

considerable ongoing research.


http://www.blackwellpublishing.com/products/journals/suppmat/nan/nan477/NAN477sm.pdf


CHRONIC WASTING DISEASE

Review of research published since November 2004


SNIP...


7) EPIDEMIOLOGY AND TRANSMISSION

From enclosures previously used by infected animals

28. Research reviewed in the WIN report showed that healthy cervids could be

infected with CWD by grazing on pastures contaminated with excreta from

infected cervids or with the carcases of diseased cervids. This provided

evidence for environmental transmission of CWD.

29. A more recent experimental study examined the potential for soil to serve as

a reservoir for TSEs by examining the interaction of PrPSc (from an adapted

transmissible mink encephalopathy agent) with common soil minerals

(Johnson et al, 2006). It was demonstrated that substantial PrPSc could be

adsorbed by the clay minerals, kaolinite and montmorillonite as well as

quartz. In addition, significant adsorption to whole soil samples was found.

Furthermore, there was a strong interaction between PrPSc and

montmorillonite. To determine whether prions remained infectious in soil,

clay samples experimentally contaminated with an inoculum were ic

inoculated into hamsters. Symptoms developed in these animals at

approximately the same time as those injected with directly with the inoculum.

The study suggests that TSE infectivity released into soil may be preserved in

a bioavailable form which may contribute to disease transmission. The

authors suggest this study adds to the evidence for environmental

transmission of CWD.


http://www.seac.gov.uk/papers/CWD-review.pdf



Prions Adhere to Soil Minerals and Remain Infectious
Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4* 

1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America 

An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.

Funding. This work was supported by USEPA grant 4C-R070-NAEX (JAP) and DOD grant DAMD170310369 (JMA).

Competing interests. The authors have declared that no competing interests exist.

Editor: David Westaway, University of Toronto, Canada

Received: December 20, 2005; Accepted: March 8, 2006; Published: April 14, 2006

DOI: 10.1371/journal.ppat.0020032

Copyright: © 2006 Johnson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abbreviations: BH, brain homogenate; BSE, bovine spongiform encephalopathy; CWD, chronic wasting disease; dpi, days postinoculation; Kte, kaolinite; Mte, montmorillonite; PK, proteinase K; PrPC, normal cellular isoform of the prion protein; PrPSc, disease-associated prion protein; TSE, transmissible spongiform encephalopathy

* To whom correspondence should be addressed. E-mail: [email protected]

Citation: Johnson CJ, Phillips KE, Schramm PT, McKenzie D, Aiken JM, et al. (2006) Prions Adhere to Soil Minerals and Remain Infectious. PLoS Pathog 2(4): e32


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Discussion....SNIP.....too long for this board, FULL TEXT ;



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