Environmental
Impact Statements; Availability, etc.: Animal Carcass Management This Notice
document was issued by the Animal and Plant Health Inspection Service
(APHIS)
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Show agency attachment(s) DEPARTMENT OF AGRICULTURE Animal and Plant Health
Inspection Service [Docket No. APHIS-2013-0044] Environmental Impact Statement;
Animal Carcass Management Agency Animal and Plant Health Inspection Service,
USDA.
Action Notice of intent to prepare an environmental impact statement and
proposed scope of study.
Summary We are announcing to the public that the Animal and Plant Health
Inspection Service intends to prepare an environmental impact statement (EIS) to
examine the potential environmental effects of animal carcass management options
used throughout the United States. This notice identifies potential alternatives
and environmental effects that will be examined in the EIS and requests that the
public comment on these proposed alternatives and environmental effects and
identify other issues that could be examined in the EIS.
Dates We will consider all comments that we receive on or before November
25, 2013.
Addresses You may submit comments by either of the following methods:
Federal eRulemaking Portal: Go to http://www.regulations.gov/#!documentDetail;D=APHIS-2013-0044-;0001.
Postal Mail/Commercial Delivery: Send your comment to Docket No.
APHIS-2013-0044, Regulatory Analysis and Development, PPD, APHIS, Station
3A-03.8, 4700 River Road Unit 118, Riverdale, MD 20737-1238. Supporting
documents and any comments we receive on this docket may be viewed at http://www.regulations.gov/#!docketDetail;D=APHIS-2013-0044
or in our reading room, which is located in room 1141 of the USDA South
Building, 14th Street and Independence Avenue SW., Washington, DC. Normal
reading room hours are 8 a.m. to 4:30 p.m., Monday through Friday, except
holidays. To be sure someone is there to help you, please call (202) 799-7039
before coming.
For Further Information Contact For questions related to the carcass
management program, contact Ms. Lori P. Miller, PE, Senior Staff Officer,
National Center for Animal Health Emergency Management, VS, APHIS, 4700 River
Road Unit 41, Riverdale, MD 20737; (301) 851-3512. For questions related to the
EIS, contact Ms. Samantha Floyd, Environmental Protection Specialist,
Environmental and Risk Analysis Services, PPD, APHIS, 4700 River Road Unit 149,
Riverdale, MD 20737; (301) 851-3053.
Supplementary Information Background The Animal Health Protection Act (7
U.S.C. 8301 et seq.) authorizes the Secretary of Agriculture to order the
destruction or removal of animals to prevent the introduction and spread of
livestock pests or diseases. Large numbers of animals and carcasses may need to
be disposed of or otherwise managed during or after an animal health emergency.
Examples of an animal health emergency include, but are not limited to, an
outbreak of a foreign animal disease, a natural disaster, or the introduction of
a chemical or radiological agent. As carcasses begin to degrade, bodily fluids,
chemical and biological leachate components, and hazardous gases such as methane
are released into the environment, potentially impacting the health and safety
of surrounding humans, livestock, and wildlife. Therefore, the management of
large numbers of carcasses during an animal health emergency must be timely,
safe, biosecure, aesthetically acceptable, and environmentally
responsible.
Current Animal and Plant Health Inspection Service (APHIS) regulations
regarding carcass management, including those found in 9 CFR 53.4, are based on
World Organization for Animal Health (OIE) recommendations and sound science.
APHIS regulations specify that animals infected by or exposed to foot-and mouth
disease, pleuropneumonia, rinderpest, and certain other communicable diseases of
livestock or poultry are required to be disposed of by burial or burning,
unlessotherwise specified by the APHIS Administrator. Traditionally, burial has
involved placement of carcasses in unlined pits or trenches, and burning has
involved open pyres (i.e., combustible heaps). APHIS may work in conjunction
with States to manage animal carcasses during or after an animal health
emergency. However, State regulations concerning carcass management vary, and
Federal and State regulations are not always based on the most current
scientific information with regard to impacts of such activities on the
environment and public health.
Environmental Impact Statement To examine the potential environmental
effects of animal carcass management options used throughout the United States,
APHIS is preparing an environmental impact statement (EIS). The EIS will analyze
and compare all major and readily available mass carcass management options that
may be utilized during an animal health emergency. APHIS is considering
classifying mass carcass management as management of 50 tons or more of biomass
per premises. In the EIS, we intend to compare unlined burial and open-air
burning disposal methods with other available carcass management options. These
may include composting (on- or off-site), rendering, landfills compliant with
the Resource Conservation and Recovery Act (RCRA), and other fixed facility
options, such as incinerators compliant with the Clean Air Act, that could
accommodate a large volume of carcasses over a short period of time.
The findings of the EIS will be used for planning and decision making and
to inform the public about the potential environmental effects of currently
available carcass management options. Additionally, when mass carcass management
options are utilized, site-specific environmental documents may be required. If
such documents are needed, APHIS may use information presented and analyzed in
the EIS, which will help APHIS to promptly fulfill its environmental compliance
obligations when an emergency situation arises requiring immediate action.
We are requesting public comment to help us identify or confirm potential
alternatives and environmental effects, as well as any other issues, that could
and should be examined in the EIS. The EIS will be prepared in accordance with:
(1) The National Environmental Policy Act of 1969 (NEPA), as amended (42 U.S.C.
4321 et seq.), (2) regulations of the Council on Environmental Quality for
implementing the procedural provisions of NEPA (40 CFR parts 1500-1508), (3)
USDA regulations implementing NEPA (7 CFR part 1b), and (4) APHIS' NEPA
Implementing Procedures (7 CFR part 372).
Alternatives We have identified the following alternatives for further
examination in the EIS:
Take no action. Under the no action alternative, existing APHIS regulations
that recommend unlined burial and open-air burning will be used as the baseline
against which alternative carcass management methods may be compared. This
action does not involve changes to the current situation.
Alternative action. Under the alternative action, APHIS is considering
alternatives in addition to unlined burial and open-air burning as carcass
management options. Alternative actions may include one or some combination of
the following: Composting (on- or off-site), rendering, RCRA-compliant
landfills, and other fixed facility options, such as incinerators compliant with
the Clean Air Act.
Environmental Effects for Consideration We have identified the following
potential environmental effects for examination in the EIS. We are requesting
that the public comment on them during the scoping period:
Effects on soil, air, and water quality. Effects on humans: Health and
safety. Agricultural lands. Industries and the economy. Public perception.
Cultural and historic resources. Effects on wildlife populations, including
effects on federally listed threatened and endangered species. Effects on plant
populations, including effects on federally listed threatened and endangered
species. Comments that identify other issues or alternatives that could be
considered for examination in the EIS would be especially helpful. All comments
received during the scoping period will be carefully considered in developing
the final scope of the EIS. Upon completion of the draft EIS, a notice
announcing its availability and an opportunity to comment on it will be
published in theFederal Register.
Authority 7 U.S.C. 8301-8317; 7 CFR 2.22, 2.80, and 371.4.
Done in Washington, DC, this 21st day of October 2013. Kevin Shea,
Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2013-25158
Filed 10-24-13; 8:45 am] BILLING CODE 3410-34-P
Environmental Impact Statements; Availability, etc.: Animal Carcass
Management [Docket No. APHIS-2013-0044]. COMMENT SUBMISSION TERRY S. SINGELTARY
SR.
Greetings APHIS et al, and thank you kindly for allowing me to comment on
Environmental Impact Statements; Availability, etc.: Animal Carcass Management
[Docket No. APHIS-2013-0044].
I don’t believe I saw the BSE TSE prion aka mad cow type listed in this,
but I thought I should list my concerns there from anyway, with relations to
this Environmental Impact Statements; Availability, etc.: Animal Carcass
Management [Docket No. APHIS-2013-0044]. With the USDA/APHIS et al now letting
the mad cow disease freely trade between countries, I was surprised to see this
concern for animal disease and pyres there from, even though it seems anymore,
the USDA/APHIS et al can’t even say the word anymore. I well remember what was
said long ago ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
with the recent mass bovine deaths from the floods, the drought, the recent
snow storm, and the known fact that mad cow disease of the c-BSE, atypical
h,g-BSE, atypical h-BSE, and the atypical l-type BASE BSE, two strains of CWD in
cervids, and the deaths there from in the cervid populations from cwd, and ehd,
all this proves the USA is, and has been, far from being prepared for any type
of major animal disease outbreak, foreign or domestic. also, with all the mass
cattle deaths of late, it would have been a perfect time to test for mad cow
type disease, if anyone would have attempted such a task, but we know how mad
cow TSE testing goes by the USDA et al, that would have just made too much sense
to test a mass cattle death for mad cow disease, and of course difficult,
with such short time available when turning in and testing samples for a TSE
prion disease, but still, a perfect opportunity gone by and missed.
I have long been concerned with the Transmissible Spongiform Encephalopathy
TSE prion disease, and all it’s strains in the many different species in North
America, and the ramifications there from when considering carcass disposal, and
I recent put together the following, about soil contamination from the TSE
prion, along with other recent science on the potential update of prions to
plants.
Chronic Wasting Disease CWD, and other TSE prion disease, these TSE prions
aka mad cow type disease know no borders.
these TSE prions know no age restrictions.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
I wish to submit the following recent and old TSE prion science, some from
PRION2013, PRION2012, PRION 2011, data on mass livestock mortality death
disposal methods such as Alkaline hydrolysis, composting, burial, rendering,
incineration, and some data from the BSE Inquiry submissions going back to 1989,
some of which I hope you may find useful. the BSE Inquiry submissions will be at
the bottom of my submission here. First, the latest science on the TSE prion
disease and reports there from, then what do other countries think of the USA
and it’s capability of carcass disposal, and types of methods to dispose of
large animal mortality events, and last, the old science from the BSE INQUIRY
and what they thought on carcass disposal and the TSE PRION.
‘’There are many disposal options for dead livestock currently in use
throughout the world; however, the knowledge that TSEs and some pathogens may
not be completely destroyed may limit their utility in the wake of changing
legislation (e.g. the amended EU Animal By-Products Regulation (1069/2009) which
comes into effect in March 2011). On-farm disposal methods are favoured by the
farming community due to the perceived environmental, practical, economical and
biosecurity benefits, therefore processes such as composting and anaerobic
digestion have found favour in countries such as the USA and Canada. Under the
ABPR in the EU, these options are not deemed safe’’
I lost my Mom to the hvCJD back in December 14, 1997, and have been
disturbed and fascinated at the same time of the science of the TSE prion aka
mad cow type disease.
I find even more disturbing at some of the regulations, and or lack of, for
the TSE prion disease, and how it seems that the OIE, and the USDA et al, have
dumbed down the science for the TSE prion disease, and then regulations there
from. by now allowing all countries trade in the TSE prion disease, the relaxing
of the BSE TSE testing, the relaxing of the feed bans, the relaxing of BSE
surveillance now, is a very bad decision, and was not based on sound science to
date, all of which I have listed why, below in references as follows ;
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
Wednesday, July 10, 2013
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
BMC Veterinary Research 2013, 9:134 doi:10.1186/1746-6148-9-134
AD.81: Detection of prion protein associated with cervid chronic wasting
disease in environmental samples
Chad J. Johnson, Christen B. Smith, Michael D. Samuel and Joel A. Pedersen
University of Wisconsin; Madison. WI USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
(TSE) or prion disease affecting North American members of the deer family
(cervids). The disease agent may enter the environment through decomposition of
carcasses and shedding in feces, saliva, and urine. Once in the environment
disease associated prion protein (PrPTSE) can bind to soil components and remain
bioavailable for extended time periods. Assessment of the environmental load of
the disease agent is difficult because relevant levels are below the detection
limits of immunochemical methods and bioassay is prohibitively expensive to use
as a surveillance technique. Here, we report that a combination of detergent
extraction and protein misfolding cyclic amplification with beads (PMCAb)
substantially improves the sensitivity of PrPTSE detection in environmental
samples. Using this technique we are able to achieve detection limits
substantially lower than animal bioassay. Working with amended soils we are able
to extract and amplify PrPTSE to detectable levels. We have investigated factors
contributing to PMCAb inhibition and methods to circumvent those inhibitions.
This technique holds promise for helping to clarify the relative importance of
direct and indirect transmission of CWD, assess the effectiveness of
environmental remediation, and determine environmental loads of infectious
agent.
=====
AD.80: Kinetics of chronic wasting disease prion shedding in cervid saliva
and urine
Nicholas J. Haley, Davin Henderson, Glenn C. Telling and Edward A. Hoover
Colorado State University; Fort Collins. CO USA
Efficient horizontal transmission is a unique hallmark of chronic wasting
disease (CWD) of deer, elk, and moose. Saliva trans- fer, for example via
grazing or mutual grooming, is thought to be the primary mechanism of horizontal
transmission, although urine and feces are also thought ro play an important
role. It is not known how shortly after exposure an animal may begin shedding
PrPCWD, though it has been reported that both clinical and pre-clinical animals
may successfully transmit CWD to naive deer. We hypothesized that transmission
would occur primarily in end-stage disease, though the purpose of this study was
to identify earlier time points during the course of CWD infection in which
saliva and urine may carry infectivity. Using both transgenic mouse bioassay and
real-rime quaking-induced conversion (RT-QuIC), we evaluated saliva and urine
from two experimentally infected white tail deer for which samples were
available from multiple time points post-inoculation (p.i.) (e.g., 3, 6 and 12
mo p.i., as well as immediately prior to euthanasia at 24-27 mos). We found that
while saliva collected during clinical disease was infectious in mouse bioassay,
saliva collected 12 mo p.i., prior to the onset of clinical signs was also
variably infectious. Saliva from time points earlier than 12 mo p.i. failed to
transmit infection, while urine collected from clinically affected deer had very
low potential to transmit infection, as has been reported previously. These
findings extend our understanding of CWD shedding in the natural host, and may
improve control of CWD transmission in captive and free-ranging settings.
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP
from soil by tomato plants although it should be noted that this study had not
been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
Tuesday, October 29, 2013
***Risk of Prion Disease Transmission through Bovine-Derived Bone
Substitutes: A Systematic Review
Saturday, November 2, 2013
***APHIS Finalizes Bovine Import Regulations in Line with International
Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type
disease around the Globe
Saturday, November 2, 2013
***Exploring the risks of a putative transmission of BSE to new
species
Wednesday, October 30, 2013
***SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE
70-13 10/30/13
Monday, August 26, 2013
***The Presence of Disease-Associated Prion Protein in Skeletal Muscle of
Cattle Infected with Classical Bovine Spongiform Encephalopathy
Saturday, November 2, 2013
*** Recommendation of the Swiss Expert Committee for Biosafety on the
classification of activities using prion genes and prion protein January 2013
***
Tuesday, October 29, 2013
*** VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
PO-031: Aerosol transmission of chronic wasting disease to white-tailed
deer
Nathaniel Denkers,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Sally Dahmes,2
David Osborn,3 Karl Miller,3 Robert Warren,3 Candace Mathiason,1 Edward Hoover1
1Colorado State University; Fort Collins, CO USA; 2WASCO Inc.; Monroe, GA USA;
3Warnell School of Forestry and Natural Resources, University of Georgia;
Athens, GA USA
Purpose. A signature feature of chronic wasting disease (CWD) is its
efficient lateral transmission in nature, almost surely by mucosal exposure. Our
previous studies employing Tg(cerPrP) mice determined that CWD can be
transmitted to a susceptible host by aerosol exposure, a route with relatively
little investigation. The present study was designed to determine whether CWD is
transmissible by aerosol to a native cervid host, white-tailed deer.
Materials and Methods. Nine white-tailed deer were exposed to two (2)
aerosol doses of a 5% w/v CWD+ (n = 6) or CWD- (n = 3) brain homogenate,
delivered via the nasal passages using a customized aerosol apparatus. At
3-month intervals post inoculation (mpi), tonsil and recto-anal
mucosa-associated lymphoid tissue (RAMALT) biopsies were collected and assayed
for CWD infection by protein misfolding cyclic amplification (PMCA), western
blotting (WB), and immunohistochemistry (IHC).
Results. At 3 mpi and 6 mpi, tonsil and RAMALT biopsies were collected from
5 of the 6 CWD + aerosol-exposed deer. Three of the 5 (60%) tested positive for
CWD by PMCA but not IHC or western blot analysis at 3 mpi. By 6 mpi, 5 of 5
(100%) were tonsil and/or RAMALT biopsy positive by at least two of the three
assays. Biopsies were collected from all CWD+ aerosol-exposed deer at 9 mpi,
with 6 of 6 (100%) tonsil and/ or RAMALT positive by western blot or IHC. At 10
mpi 3 of the 6 prion-exposed deer have developed early clinical signs of CWD
infection (hyperphagia, polydypsia, wide leg stance and head/neck
dorsi-flexion). All sham-inoculated deer are showing no clinical signs and have
remained CWD negative as assessed by all three assays. Interestingly, the prion
dose delivered to the deer by aerosol-exposure is estimated to be 20-fold lower
than the historical oral dose that has resulted in detectable CWD infection at 6
or 12 mpi.
Conclusions. This study documents the first aerosol transmission of CWD in
deer. These results further infer that aerosolized prions facilitate CWD
transmission with greater efficiency than does oral exposure to a larger prion
dose. Thus exposure via the respiratory mucosa may be significant in the facile
spread of CWD in deer and perhaps in prion transmission overall.
PO-073: Multiple routes of prion transepithelial transport in the nasal
cavity following inhalation
Anthony Kincaid, Shawn Feilmann, Melissa Clouse, Albert Lorenzo, Jason
Bartz Creighton University; Omaha, NE USA
Introduction. Inhalation of either prion-infected brain homogenate or
aerosolized prions has been shown to cause disease, and in the case of
inhalation of infected brain homogenate, the nasal route of infection has been
shown to be 10–100 times more efficient than the oral route. The cell types
involved in the in vivo transport of prions across the nasal cavity epithelium
have not been determined. M cells in the follicular associated epithelium have
been shown to mediate transcellular transport of prions in vitro and in the gut
of experimentally infected mice. We tested the hypothesis that M-cell mediated
transport was responsible for prion entry across nasal cavity epithelium
following inhalation.
Materials and Methods. Hamsters were inoculated extranasally with 50 or
100ul of infected (n = 31) or mock-infected (n = 13) brain homogenate. Control
animals were inoculated with buffer (n = 4) or were untreated (n = 5). Following
survival periods ranging from 15 to 180 min, animals were perfused, skulls were
decalcified and nasal cavities were embedded in paraffin. Tissue sections were
cut and processed immunohistochemically for glial fibrillary acidic protein to
identify brain homogenate, or for the disease-associated form of the prion
protein. Tissue sections not further than 112 um apart through the entire extent
of the nasal cavity were analyzed using light microscopy; photomicrographs were
obtained wherever inoculum was observed on the surface of, within, or deep to
the nasal mucosa for each animal.
Results. Infected or uninfected brain homogenate was identified within the
nasal cavities of animals at all time points and was seen crossing the nasal
cavity epithelium within minutes of inoculation; the transepithelial transport
of brain homogenate continued for up to 3 h after inoculation. Infected or
uninfected brain homogenate was seen adhering to, or located within, M cells at
all time points. However, larger volumes of infected or uninfected brain
homogenate were identified crossing between cells of the olfactory and
respiratory epithelia in multiple locations. In addition, infected or uninfected
brain homogenate was identified within the lumen of lymphatic vessels in the
lamina propria beneath the nasal mucosa at all time points.
Conclusion. Transepithelial transport of prions across nasal cavity mucosa
begins within minutes of inhalation and can continue for up to 3 h. While M
cells appear to transport prions across the follicular associated epithelium,
larger amounts of prions are transported between the cells of the respiratory
and olfactory epithelia, where they immediately enter the lymphatic vessels in
the lamina propria. Thus, inhaled prions can be spread via lymph draining the
nasal cavity and have access to somatic and autonomic nerves in the lamina
propria of the nasal cavity. The increased efficiency of the nasal cavity route
of infection compared with the oral route may be due to the rapid and prolonged
transport of prions between cells of the respiratory and olfactory
epithelia.
PO-033: Replication efficiency of soil-bound prions varies with soil type
Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie
Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA;
2Creighton University; Omaha, NE USA
Prion sorption to soil is thought to play an important role in the
transmission of scrapie and chronic wasting disease (CWD) via the environment.
Sorption of PrP to soil and soil minerals is influenced by the strain and
species of PrPSc and by soil characteristics. However, the ability of soil-bound
prions to convert PrPc to PrPSc under these wide-ranging conditions remains
poorly understood. We developed a semiquantitative protein misfolding cyclic
amplification (PMCA) protocol to evaluate replication efficiency of soil-bound
prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy
(TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log
decrease in PMCA replication efficiency with a corresponding 1.3-log reduction
in titer. The increased binding of PrPSc to soil over time corresponded with a
decrease in PMCA replication efficiency. The PMCA efficiency of bound prions
varied with soil type, where prions bound to clay and organic surfaces exhibited
significantly lower replication efficiencies while prions bound to sand
exhibited no apparent difference in replication efficiency compared to unbound
controls. PMCA results from hamster and CWD agent-infected elk prions yielded
similar findings. Given that PrPSc adsorption affinity varies with soil type,
the overall balance between prion adsorption affinity and replication efficiency
for the dominant soil types of an area may be a significant determinant in the
environmental transmission of prion diseases.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep
with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the
intracranial route had evidence of PrPSc accumulation. PrPSc was detected in
lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer
that was necropsied at 15.6 months had widespread distribution of PrPSc
highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues
prior to the onset of clinical signs. IC inoculated deer necropsied after 20
months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread
distribution of PrPSc in neural and lymphoid tissues.
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD. ... snip...see more here
;
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
Monday, July 16, 2012
Persistence of the bovine spongiform encephalopathy infectious agent in
sewage
Thursday, August 08, 2013
Characterization of the first case of naturally occurring chronic wasting
disease in a captive red deer (Cervus elaphus) in North America
Friday, December 14, 2012
*** DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being
introduced into Great Britain?
A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011. Overall,
therefore, it is considered there is a __greater than negligible risk___ that
(nonruminant) animal feed and pet food containing deer and/or elk protein is
imported into GB. There is uncertainty associated with this estimate given the
lack of data on the amount of deer and/or elk protein possibly being imported in
these products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
SNIP...SEE ;
Friday, December 14, 2012
*** DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being
introduced into Great Britain? A Qualitative Risk Assessment October 2012
Sunday, September 01, 2013
*** hunting over gut piles and CWD TSE prion disease ***
CWD TO CATTLE OR BSE TO CERVIDS, potential risk factors ??? LET’S see what
the science says to date ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby -- David Colby, PhD
Assistant Professor Department of Chemical Engineering University of
Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
never say never with the potential transmission of one of the strains of
CWD transmitting to cattle OR humans, OR ANY OTHER SPECIES. ...TSS
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the
wild...
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging
and captive cervid species in North America, and there is evidence suggesting
the existence of multiple CWD strains. The susceptibility of human CNS and
peripheral organs to the various CWD prion strains remains largely unclear.
Current literature suggests that the classical CWD strain is unlikely to infect
human brain, but the potential for peripheral infection by CWD in humans is
unknown. We detected protease-resistant PrpSc in the spleens of a few humanized
transgenic mice that were intracerebrally inoculated with natural CWD isolates,
but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our
ongoing bioassays in humanized Tg mice indicate that intracerebral challenge
with such PrpSc-positive humanized mouse spleen already led to prion disease in
most animals. These results indicate that the CWD prion may have the potential
to infect human peripheral lymphoid tissues.
=====
HD.12: Comparative study of the distribution of the prion protein in the
squirrel monkey (Saimiri sciureus) following experimental challenge with variant
and sporadic CJD
Diane L. Ritchie,1 Paul Brown,2 Susan Gibson,3 Thomas R. Kreil,4 Christian
Abee3 and James W. Ironside1
1National CJD Surveillance Unit; Edinburgh, UK; 2Bethesda; Bethesda, MD
USA; 3Deparment of Comparative Medicine; University of South Alabama; Mobile, AL
USA; 4Baxter Bioscience; Vienna, Austria
Introduction, Reports suggest that the number of tissues and organs showing
the presence of the abnormal prion protein (PrPTSE) in variant CJD (vCJD)
patients may be greater than previously thought. A limited peripheral
involvement in some cases of sporadic CJD (sCJD) has also been reported. This
accumulation of PrPTSE outside the brain has raised concerns about the possible
iatrogenic transmission risk of vCJD. The squirrel monkey (Saimiri sciureus) has
been shown to be highly susceptible to experimental challenge with human prion
disease. Neuropathological and biochemical analyses of CNS tissue have shown
that sCJD and vCJD can be distinguished in the squirrel monkey and that many of
the strain characteristics that define these agents are conserved after
transmission. Following on from these initial studies, immunohistochemistry and
western blot analysis were performed on a wide range of peripheral tissues
including, lymphoreticular tissues and peripheral neural tissue to establish the
full-body distribution of PrPTSE in this primate animal model.
Materials and Methods. Brain homogenates from sCJD or vCJD patients were
inoculated into the frontal cortex of squirrel monkeys. Animals were kept under
constant clinical surveillance. At post-mortem, formalin fixed CNS tissue and a
wide range of peripheral tissues were taken for immunohistochemical analysis
together with frozen tissues taken for the biochemical detection of PrPTSE.
Results. Immunohistochemical analysis showed no evidence of PrPTSE
deposition in peripheral tissues in either variant or sporadic CJD-infected
animals. However, western blot assays detected PrPTSE in the spleen of a
proportion of the vCJD- infected animals. The PrPTSE isotype resembled that
detected in CNS tissue from the vCJD- infected animals and from human vCJD
cases. ***In addition, western blot analysis detected PrPTSE in the spleen of a
single animal following challenge with sporadic CJD. The PrPTSE type in this
animal resembled that found in CNS tissue from the same animal, with a PrPTSE
type similar to that found in human sCJD type 1 cases.
Conclusion. This study confirms the accumulation of PrPTSE in the CNS and
spleen of a proportion of squirrel monkeys infected intra-cerebrally with human
vCJD. Furthermore, this study extends the evidence that there may be a
peripheral involvement in some cases of sCJD. PrPTSE typing confirms the
conservation of PrPTSE type on transmission to the squirrel monkey and suggests
that there are no tissue-specific adaptations in the biochemical phenotype of
the agent strain following primate-to-primate transmission.
=====
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE,
classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease
isolates are as efficient as C-type BSE and vCJD in converting human prion
protein in this in vitro assay. However, they also show that there is no
absolute barrier ro conversion of human prion protein in the case of chronic
wasting disease.
=====
Invited.16: Studies of chronic wasting disease transmission in cervid and
non-cervid species
Edward A, Hoover,1 Candace K. Mathiason,1 Davin M. Henderson,1 Nicholas J.
Haley,1 Davis M. Seelig,1 Nathaniel D. Denkers,1 Amy V. Nalls,1 Mark D. Zabe,1
Glenn C. Telling,1 Fernando Goni2 and Thomas Wisniewski,2
1Prion Research Center; Colorado State University; Fort Collins, CO USA;
2New York University School of Medicine; New York, NY USA
How and why some misfolded proteins become horizontally transmitted agents
and occasionally cross species barriers are issues fundamental to understanding
prion disease. Chronic wasting disease (CWD) of cervids is perhaps a prototype
of horizontal prion transmission, encompassing efficient mucosal uptake,
lymphoid amplification, neuroinvasion, peripheralization, and dissemination via
mucosal excretion. Efficient mucosal transmission of CWD in deer has been
demonstrated by oral, nasal, aerosol, and indirect contact exposure. In
addition, other studies (Mathiason CK, et al.) reported at the symposium support
a significant role for pre- and/or postnatal transmission of CWD from doe to
offspring. Accumulating, yet still incomplete, evidence also suggests that the
period of relatively covert CWD infection may be longer than originally thought.
Given the above, minimally invasive sensitive assays based on body fluids from
live animals would aid substantially in understanding the biology of CWD. We
have been applying seeded realtirne quaking-induced amplification of recombinant
PrP substrates (i.e., RT-QuIC methodology) to: (1) investigate antemortem CWD
detection, and (2) model PrP-based species barriers and trans-species
adaptation-topics we previously explored using sPMCA and in vivo bioassays. At
this symposium, we report sensitive and specific detection CWD prions in saliva,
urine, blood (Mathiason lab), and rectal and pharyngeal lymph node samples
(Haley NJ, et al.) from pre-symptomatic and symptomatic experimentally and
naturally exposed deer. Other ongoing studies are employing RT-QuIC methodology
to model amplification barriers among CWD, FSE, BSE, and CJD prions using
cervine, feline, bovine, human, and promiscuous rPrP substrates and the above
species prion seeds, cellular co-factors, and transgenic mice. Finally, in
collaboration with the Wisniewski laboratory, we are conducting of experimental
CWD vaccination studies in deer employing oral administration of an attenuated
Salmonella vector expressing cervid PrP epitopes.
=====
AD.06: Detecting prions in the brain and blood of TSE-infected deer and
hamsters
Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2
Richard Bessen,1 Jason Bartz3 and Candace Mathiason1
1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain
Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA
While large quantities of protease resistant prion protein (PrPres) can be
demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain
tissues harvested from prion-infected animals, these conventional assays are
less reliable as means to detect the small quantities of prions thought to be
present in bodily fluids or associated with early and asymptomatic phases of TSE
disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of
detecting prions at concentrations below the level of sensitivity of
conventional assays and provides a real-time fluorescent readout negating the
use of proteases. We have made modifications to the RT-QuIC assay to utilize it
for the detection of PrPres in brain and blood harvested from various species
infected with prions. In this study, we analyzed CWD-infected deer and
CWD/TME-infected hamster whole blood to determine the effect of:
(1) various anticoagulants,
(2) freezing and
(3) NaPTA precipitation.
Brain tissue and blood collected from naive deer and hamsters served as
negative controls.
We were able to demonstrate amplifiable prions in
(1) brain and blood samples harvested from CWD/TME-infected animals,
(2) heparinized blood,
(3) frozen vs. fresh blood and
(4) NaPTA treated samples.
The RT-QuIC assay is able to detect PrPres in various species of animals
and shows promise as an antemortem diagnostic tool for blood-borne TSEs.
=====
Oral.08: Mother to offspring transmission of chronic wasting disease in
Reeve's Muntjac deer
Amy Nalls,1 Erin McNulty,1 Jenny Powers,2 Davis Seelig,1 Clare Hoover,1
Nicholas Haley,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Paula Stewart,3 Wilfred
Goldmann,3 Edward A. Hoover1 and Candace K. Mathiason1
1Colorado State University; Fort Collins, CO USA; 2National Park Service;
Fort Collins, CO USA; 3The Roslin Institute and Royal School of Veterinary
Studies; Edinburgh, UK
To investigate the role mother to offspring transmission plays in chronic
wasting disease (CWD), we have developed a cervid model employing the Reeve's
muntjac deer (Muntiacus reevesi). Eight muntjac doe were orally inoculated with
CWD and tested PrPCWD lymphoid positive by 4 mo post infection. Fourteen fawns
were born to these eight CWD-infected doe-3 were born viable, 6 were born
non-viable and 5 were harvested as fetuses from early or end-stage CWD-infected
doe. All three viable fawns have demonstrated CWD IHC lymphoid biopsy positivity
between 43 d post birth and 11 mo post birth. Two of these three CWD positive
viable offspring have developed clinical signs consistent with TSE disease
(28-33 mo post birth). Moreover, CWD prions have been detected by sPMCA in 11 of
16 tissues harvested from 6 full-term non-viable fawns and in 7 of 11 fetal
tissues harvested in utero from the second and third trimester fetuses.
Additional tissues and pregnancy related fluids from doe and offspring are being
analyzed for CWD prions. In summary, using the muntjac deer model we have
demonstrated CWD clinical disease in offspring born to CWD-infected doe, and in
utero transmission of CWD from mother to offspring. These studies provide basis
to further investigate the mechanisms of maternal transfer of prions.
=====
AD.63: Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1
1Colorado State University; Fort Collins, CO USA; 2University of Minnesota;
Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD. These results demonstrate that
CWD can be transmitted and adapted to the domestic cat, thus raising the issue
of potential cervid-to- feline transmission in nature.
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
*** PRION2013 ***
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, ***humans, domestic
cats, blood, and mother to offspring transmission
Prion2013
Friday, August 09, 2013
***CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
Uptake of Prions into Plants
Wednesday, September 04, 2013
*** cwd - cervid captive livestock escapes, loose and on the run in the
wild...
Thursday, August 08, 2013
*** Characterization of the first case of naturally occurring chronic
wasting disease in a captive red deer (Cervus elaphus) in North America
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
Saturday, July 6, 2013
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
Saturday, November 02, 2013
OREGON DETECTS SCRAPIE
Sheep disease pops up in Douglas County; 300 animals euthanized
Friday, July 26, 2013
Voluntary Scrapie Program USA UPDATE July 26, 2013 increase in FY 2013 is
not statistically meaningful due to the sample size
Wednesday, October 09, 2013
*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY,
£41,078,281 in compensation REVISED ***
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb ***
Monday, October 14, 2013
*** Researchers estimate one in 2,000 people in the UK carry variant CJD
proteins ***
Friday, August 16, 2013
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and
Contaminated blood products induce a highly atypical prion disease devoid of
PrPres in primates
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010
Sunday, October 13, 2013
CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Sunday, September 08, 2013
Iatrogenic Creutzfeldt-Jakob disease via surgical instruments and
decontamination possibilities for the TSE prion
Thursday, September 26, 2013
Minimise transmission risk of CJD and vCJD in healthcare settings Guidance
Sunday, June 9, 2013
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory
Committee Meeting Webcast
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a
methodological outline for evidence-based guidance
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 ***
Tuesday, March 05, 2013
A closer look at prion strains Characterization and important implications
Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Number 41 January 2009
*** Ruminant Carcass Disposal Options for Routine and Catastrophic
Mortality ***
An optimal disposal method should mitigate the disease agent or other cause
of mortality. For complete effectiveness, certain disease agents or other causes
of mortality may require specific disposal methods or technologies (e.g.,
high-temperature incineration or alkaline hydrolysis for transmissible
spongiform encephalopathy (TSE)-infected material).
snip...
The disposal of carcasses associated with confirmed mortalities from
chronic wasting disease (CWD) in landfill sites is not recommended in the United
States at the present time. The behavior of the infectious agent associated with
TSEs, the prion, in a landfill presently is not clearly understood. (See
Appendix 1, page 14, for more information about disposal of TSE-infected
carcasses.) If a catastrophic situation arose in which thousands of diseased
carcasses needed to be disposed of in a landfill, the liability likely would
have to be accepted and indemnified by the federal government.
snip...
Fungi and protozoans do not remain active in an anaerobic environment.
Discussions about prions in landfills have taken place only recently. In the
early stages of the bovine spongiform encephalopathy (BSE) epidemic in the U.K.,
some BSE-infected carcasses were disposed of in landfill sites before routine
incineration was introduced. Most of these sites were unlined municipal solid
waste disposal landfills. Nevertheless, a risk assessment carried out for the
Environment Agency concluded that the potential risks to people through
contaminated drinking water were extremely small. But the fate of prions in
landfills and leachate presently is unknown, and no clear method of study or
testing exists. There are current studies to address these questions, but the
results will not be known for some time. Presently, the majority of landfill
owners in the United States are not accepting prion-infected ruminant carcasses
for disposal because of (1) the inability to monitor for the long-term viability
of prions and (2) potential liability issues. (See Appendix 1 for further
information on the disposal of TSE-infected carcasses.)
snip...
Composting also is attractive because it can be performed on-site,
eliminating the need to transport infected or potentially infected material
during a disease outbreak. It is advisable, however, to consult local and state
authorities regarding regulations governing composting of ruminant carcasses;
there may be issues with composting carcasses infected with certain biological
agents or TSEs. The regulations may describe what can be done with the composted
material or may prevent composting altogether.
Research assessing the environmental impacts and biosecurity issues
associated with composting livestock mortalities during an emergency suggests
that composting can be a relatively biosecure process when performed properly
(Glanville et al. 2006). (See Appendix 1 for a more in-depth discussion of
disposal options for TSE-infected carcasses.)
Table 8. Summary of potential health risks for various methods of handling
animal by-products1, 2
Exposure of Humans to Hazards from Each Option
Disease/Hazardous Agent Rendering Incineration Landfill Pyre Burial
Prions for BSE, scrapie3 Moderate Very small Moderate Moderate High
Rendering, Incineration, Landfill, Pyre, Burial
Moderate, Very small, Moderate, Moderate, High
3Risk of human exposure to TSEs was rated as very small when solid products
of rendering were incinerated
snip...
Comparisons Open-air burning can be relatively inexpensive, but it is not
suitable for destroying prions of TSE-infected carcasses. The method is
dependent on weather and fuel availability, has the potential for environmental
contamination, and may pose a problem for public acceptance. Fixed-facility
incineration is capable of effectively destroying prions of TSE-infected
carcasses and is highly biosecure (Kastner and Phebus 2004; TAHC 2005).
Disadvantages of fixedfacility incineration are limited availability, high cost
of operation, necessity of transporting carcasses to the facility, difficulty of
securing local licensure or allowance, and inability of equipment to burn large
volumes of carcasses. Air-curtain incineration is mobile and relatively
environmentally acceptable. In addition, this method is suitable for combination
with combustible debris removal, such as downed trees from weather-related
damage, if dry. Air-curtain incinerators are fuel intensive and require
experienced personnel operators. Currently, open air-curtain incinerators are
not validated to dispose of TSE-infected carcasses safely.
snip...
Alkaline Hydrolysis
Description of Process
Alkaline hydrolysis is a natural process by which complex molecules are
broken down into the constituent small molecules from which they were
synthesized. The process of alkaline hydrolysis occurs through the action of the
hydroxyl ions (OH¯) on the bonds connecting the small molecules. This process
occurs in nature when animal tissues and carcasses are buried in soil of neutral
or alkaline (high) pH, aided by the digestive processes of soil organisms. In
digestion, alkaline hydrolysis is the primary process whereby the complex
molecules of proteins, fats, and nucleic acids are broken down in the small
intestine into small nutrient molecules that are absorbed by the intestinal
cells. Alkaline hydrolysis for carcass disposal is based on the same chemical
reaction, with strong alkali and heat used to speed the process.
The current process for application of alkaline hydrolysis to the disposal
of animal carcasses and tissues—including infectious and radioactive tissues,
carcasses, and biohazardous and hazardous materials— dates back to 1992. The
method was introduced for the release of radionuclides from experimental animal
carcasses so that this type of low-level radioactive waste could be disposed of
safely and economically (Kaye, Methe, and Weber 1993; Kaye and Weber 1994).
Subsequently, the method was applied to the disposal of other research animals
and infectious human and animal tissues and carcasses. Equipment is commercially
available for disposal of animal carcasses by this process.
In the simplest current application, whole animal carcasses and tissues are
loaded into a stainless steel, steam-heated pressure vessel. Once the vessel is
loaded and the lid is sealed, an appropriate amount of concentrated alkali
solution and water are added. The vessel is heated to 302ºF (150ºC) and
maintained at that temperature for a minimum of 3 hours (depending on the target
pathogen, vessel, and carcass sizes) and up to 6 hours for destruction of
prions. At the end of the process, the hydrolyzate— a solution of amino acids,
small peptides, sugars, soaps, and electrolytes— is cooled and drained, leaving
only “bone shadows” (i.e., the pure calcium phosphate remains of bones and teeth
from which all the collagen has been digested). The hydrolyzate is a resource
that can be used directly as liquid fertilizer, dried or absorbed to make a dry
fertilizer, used as feedstock for anaerobic fermentation biogas generation, or
further treated to precipitate the lipid components for subsequent conversion to
biodiesel, still leaving the nutrient solution for other uses.
Alkaline hydrolysis leads to the random breaking of nearly 40% of all
peptide bonds in proteins, the major solid constituent of animal cells and
tissues. Under the extreme conditions of high temperature and alkali
concentration, the protein coats of viruses are destroyed and the peptide bonds
of prions are broken. Validation testing has demonstrated that all pathogens in
animal tissue (Kaye et al. 1998), including prions, are completely destroyed
under the combined operating conditions of heat, moisture, and pH.
Alkaline hydrolysis has been written into European Union Animal By-Products
legislation as the only alternative technology approved for all categories of
animal by-products, including the most highly infectious and prion-contaminated
material (EC 2005).
Types of Systems
Alkaline hydrolysis systems may be fixed or mobile. The capacity of
currently available equipment is up to 10,000 lb/cycle for fixed systems and
4,000 lb/cycle for mobile systems. Designs are available, however, for systems
that combine pulverization and initial steam disinfection with the tissue
destruction and resource conservation capability of mobile systems capable of
processing more than 25,000 lb/hr.
Fixed-base and mobile systems currently are able to handle the routine
disposal of infectious and suspect animal carcasses and tissues brought to state
and federal veterinary diagnostic laboratories. These systems also could serve
for disposal of materials, such as specified risk material, at livestock
processing facilities.
Since 2004, a single 4,000 lb-capacity mobile system has been used to
dispose of more than one million pounds of deer confirmed or suspected of having
CWD, a TSE, in a depopulation program near Madison, Wisconsin.
It is important to distinguish between the issues related to disposal of
routine infectious and TSE-infected or suspect animals and the issues related to
disposal in mass animal epidemics or other catastrophic situations. Fixed-base
systems are able to handle routine and TSE material because the volumes are
relatively small. Also, TSE outbreaks can be managed by isolation and transport
of the affected animals without risk to noninfected animals. In mass animal
epidemics or natural disasters, however, disposal often must take place at the
site of the outbreak and be done quickly to prevent spread of infectious
disease; for these situations, mobile systems can be used. The hydrolyzate from
such a system is only partly hydrolyzed; it exits the system as slurry into a
tanker truck or rail tank car in which hydrolysis continues until the
hydrolyzate is emptied into a fertilizer storage trench, fed into a biogas
generation system, field spread, or otherwise processed for resource
recovery.
Fixed-base systems generally use institutional steam supplies for heating
the vessels and domestic water for filling and cooling. Mobile systems require
“slave trucks” carrying diesel or propane-fired electrical and steam generators,
as well as alkali and water (if needed). In theory, a fleet of large volume
mobile comminution-disinfection- digestion systems, strategically distributed
around the country in a sort of “fire station” pattern, could be gathered on
short notice to deal with mass animal disposals. When not in use in emergency
situations, these units could be kept operable and their operators trained by
using the units for routine depopulations of avian and ruminant livestock and
control of small outbreaks. The fixed-base units would always be in use for
disposal of animal carcasses and tissues after routine necropsy and diagnostic
procedures.
snip...
Appendix 1: Special Considerations for Material Potentially Infected with
TSEs
Introduction to TSEs
Transmissible spongiform encephalopathies
(TSEs) are a group of rare neurodegenerative diseases, sometimes called
prion diseases, that can affect both animals and humans. The discovery of
prion-related cattle diseases in England between 1986 and 2002 changed the
disposal industry’s perception of the risk involved in disposing of even a small
number of ruminant carcasses (Karesh and Cook 2005). The occurrence of bovine
spongiform encephalopathy (BSE) in England changed policies in the United States
as well, even though there have been only two cases of BSE identified in the
United States (OIE 2008) and a relatively small number of TSEs identified in
other susceptible species.
The main characteristics of TSE diseases are
• Progressive debilitating neurological illness that is always fatal
• Spongiform change in grey matter areas of the brain
• Long incubation period of months to several years
• No detectable specific immune response in the host.
These diseases are experimentally transmissible and some (e.g., familial
Creutzfeldt-Jakob Disease [CJD], Gerstmann-Sträussler-Scheinker syndrome (GSS),
and fatal familial insomnia) are genetically inherited.
Types of TSEs
There are several forms of TSEs in different animal species and
humans.
Scrapie is a TSE disease of sheep and goats that has been recognized for
more than 200 years and is endemic in North America and many parts of Europe.
Despite this occurrence, there has never been any proven association between
scrapie in sheep and any human disease. In cattle, BSE first appeared in the
U.K. in 1986. There have been approximately 184,000 cases of BSE in the U.K.,
plus an additional 5,200 cases in 21 other countries. In 1996, the
identification of a new form of Creutzfeldt-Jakob Disease (vCJD) in young people
in the U.K. raised the concern that the causative agent for BSE had transmitted
from cattle to humans. There is strong evidence that this is the case, and it is
now generally accepted that vCJD in humans is caused by exposure to material
from BSE-infected cattle, although many questions remain about the exact nature
of the route of transmission. There are other forms of TSEs in humans; sporadic
CJD is the most common. Other TSEs in animals include CWD, present in wild and
farmed deer and elk populations in some areas of North America, and
transmissible mink encephalopathy that appeared in farmed mink
populations.
TSEs and Prions
The commonly accepted infectious agent for TSEs (generally designated as
PrPSc or PrPTSE 3) is a misfolded isoform of a normal cellular protein (PrPc)
and is called a prion (Prusiner 1998). The term prion was derived from
proteinaceous and infectious and is defined by Prusiner (1998) as a
proteinaceous infectious particle that lacks nucleic acid. The normal isoform is
soluble and primarily monomeric in solution, whereas the infectious form creates
insoluble aggregates. Prions are not deactivated by the normal procedures that
would destroy most disease agents. They are resistant to inactivation by heat,
chemical disinfection, radiation, and proteolytic enzymes (Taylor 2000).
Disposal of prion-infected carcasses requires high heat, is costly, and is not
practical.
snip...
Considerations for Specific Disposal Options
Burial and Landfill
Concerns about worker and public safety, associated with the fate and
transport of prions disposed in landfills, have prompted the U.S. disposal
industry to reassess the long-term risks of this type of disposal.
Analytical methods presently do not exist to quantify the destruction and
retention of prions in the landfill mass. The majority of landfill operators
will not accept even rendered carcasses that are known to be infected with
prions. Discussants and presenters at the National Carcass Disposal Symposium in
December 2006 generally agreed that disposal of carcasses potentially infected
with TSEs may not be a conservative option (Hater, Hoffman, and Pierce 2006; Lin
2006).
There are no data on what might happen to the infective agent in a
landfill, although some studies are now in progress. The original limited data
on the behavior of a TSE agent when buried in the ground is from a single
experiment reported by Brown and Gajdusek (1991); this research has been used to
support the assumption that TSE infectivity will degrade in the ground. Comer
and colleagues (1998) indicated that 98% of TSE infectivity will degrade in the
ground over 3 years (or longer). The results also showed only limited leaching,
with most of the residual infectivity remaining in the originally contaminated
soil. Johnson and colleagues (2006) have studied the interaction of PrPTSE with
common soil minerals and soils. They showed that PrPTSE can bind strongly to
soils and could be difficult to desorb, and they found that the PrPTSE bound to
the soil particles remained infectious. Leita and colleagues (2006) also showed
that PrPTSE was absorbed in all three soil types tested. More recently, Seidel
and colleagues (2007) have shown that the scrapie agent can transmit disease by
the oral route after persistence in soil for up to 29 months. The change in
infectivity over time was not measured, but Western blot analysis clearly showed
a marked decrease in the strength of the target protein after one month and
further decrease over time up to 29 months.
The Institute for Animal Health in Edinburgh currently is conducting a
study of the behavior of infectivity in carcasses buried in the ground. An
initial report was given at Prion 2006 (Fernie et al. 2006), which stated that
TSE infectivity may bind strongly to soil components and has very limited
mobility in soils with controlled rates of water percolation.
These results and the biophysical properties of the prion protein suggest
that any infectivity released from decaying animal material is likely to remain
bound to solid matter in the landfill and, thus, is unlikely to be present in
the leachate. With current knowledge, however, it is not possible to be certain
that TSE infectivity could not be present at some level in leachate.
A number of risk assessment studies have considered the risks from TSE
material deposited in landfill sites or by burial. Not all these studies are in
the public domain, but they have shown that the potential risk to people or
other livestock through contamination of drinking water is extremely small (DNV
1997a, 2001b).
Isolation using macro-encapsulation in the landfill is an option for
TSE-related deaths. Macroencapsulation, however, is an unusual practice in
subtitle D landfills and does add significant costs to landfill disposal.
Current research may determine whether the additional costs are justified.
Rendering
Research has demonstrated that rendering lowers the infectivity of prions,
but no currently available rendering processes totally inactivate the prions
(Taylor, Woodgate, and Atkinson 1995). Cohen and colleagues (2001) reported that
batch rendering systems achieved a 1,000- fold reduction in BSE infectivity,
whereas continuous systems with and without fat recycling reduced infectivity
100-fold and 10-fold, respectively. Because rendering does not totally
inactivate prion infectivity, any product from the disposal of TSEdiseased
carcasses should not be used in animal feeds.
There may be other practical difficulties with rendering as an option for
prion-contaminated materials. As was found during the 2001 FMD outbreak in the
U.K.—when rendering was regarded as the preferred option— rendering facilities
may already have existing functions and requirements, limiting their capacity.
In addition, rendering plants may rely on the sale of meat and bone meal and
tallow as part of their production cycle; use of those end products would almost
certainly cease to be an option if there was risk of TSE-agent contamination in
them.
Composting
Presently, no work has been done to demonstrate TSE-agent inactivation by
composting. There has been some laboratory work related to prion destruction by
specific enzymes, but no field research has been done involving the addition of
such enzymes to composting operations.
Certain challenges exist in using composting for prion disposal, including
(1) the need for some form of enclosed vessel to avoid environmental
contamination and to prevent scavenger access, (2) the need for complete mixing,
(3) potential difficulties in accessing neural tissue encased within bone (skull
and spinal cord), and (4) ensuring the correct conditions are maintained (e.g.,
temperature and levels of microbial degradation).
Incineration
Incineration is one of the most effective techniques for removal of
infectivity from prion-contaminated material. Disadvantages, however, include
the large energy requirement, environmental concerns, location of incinerators,
and the need to ensure a consistent and complete burn.
Incinerators vary from small animal incinerators, used to dispose of small
amounts of material, to large commercial operations, or even to power station
furnaces used to dispose of the products of rendering. Analysis of the ash for
protein content after incineration of BSE-infected carcasses suggests that prion
infectivity is reduced by at least 1 million-fold (DNV 1997b, 2001a). Some
facilities in the U.K. currently use fixed gasification units for processing
carcasses that potentially contain prions. Research continues in the United
States on similar portable gasification equipment that should offer a daily
capacity of more than 25 tons per unit.
Alkaline Hydrolysis
The alkaline hydrolysis process has been through a validation study by the
Institute of Animal Health, and an Opinion has been issued by the Scientific
Steering Committee of the European Commission (EC 2002) on the effectiveness of
the process. There was detectable infectivity from samples held for 3 hours, but
not from samples held for 6 hours. The committee concluded that the by-products
after 3 hours of processing could contain some residual TSE infectivity and that
this risk may decrease with increased duration of processing.
Glossary
snip...see ;
Alkaline Hydrolysis
========================================
There are many disposal options for dead livestock currently in use
throughout the world; however, the knowledge that TSEs and some pathogens may
not be completely destroyed may limit their utility in the wake of changing
legislation (e.g. the amended EU Animal By-Products Regulation (1069/2009) which
comes into effect in March 2011). On-farm disposal methods are favoured by the
farming community due to the perceived environmental, practical, economical and
biosecurity benefits, therefore processes such as composting and anaerobic
digestion have found favour in countries such as the USA and Canada. Under the
ABPR in the EU, these options are not deemed safe;
========================================
Review
The environmental and biosecurity characteristics of livestock carcass
disposal methods: A review
Ceri L. Gwyther a, A. Prysor Williams a,⇑, Peter N. Golyshin b, Gareth
Edwards-Jones a, David L. Jones a a School of Environment, Natural Resources and
Geography, College of Natural Sciences, Bangor University, Gwynedd, LL57 2UW, UK
b School of Biological Sciences, College of Natural Sciences, Bangor University,
Gwynedd, LL57 2UW, UK
a b s t r a c t
Livestock mortalities represent a major waste stream within agriculture.
Many different methods are used throughout the world to dispose of these
mortalities; however within the European Union (EU) disposal options are limited
by stringent legislation. The legal disposal options currently available to EU
farmers (primarily rendering and incineration) are frequently negatively
perceived on both practical and economic grounds. In this review, we assess the
potential environment impacts and biosecurity risks associated with each of the
main options used for disposal of livestock mortalities in the world and
critically evaluate the justification for current EU regulations. Overall, we
conclude that while current legislation intends to minimise the potential for
on-farm pollution and the spread of infectious diseases (e.g. transmissible
spongiform encephalopathies, bacterial pathogens), alternative technologies
(e.g. bioreduction, anaerobic digestion) may provide a more cost-effective,
practical and biosecure mechanism for carcass disposal as well as having a lower
environmental footprint. Further social, environmental and economic research is
therefore warranted to assess the holistic benefits of alternative approaches
for carcass disposal in Europe, with an aim to provide policy-makers with robust
knowledge to make informed decisions on future legislation.
snip...
4. Conclusions
There are many disposal options for dead livestock currently in use
throughout the world; however, the knowledge that TSEs and some pathogens may
not be completely destroyed may limit their utility in the wake of changing
legislation (e.g. the amended EU Animal By-Products Regulation (1069/2009) which
comes into effect in March 2011). On-farm disposal methods are favoured by the
farming community due to the perceived environmental, practical, economical and
biosecurity benefits, therefore processes such as composting and anaerobic
digestion have found favour in countries such as the USA and Canada. Under the
ABPR in the EU, these options are not deemed safe; however, the legal
alternatives are not favoured by the farming community leading to widespread
non-compliance and potentially greater environmental risk (due to illegal
dumping, etc. (Kirby et al., 2010)). There is therefore a real need for new
methods to be developed and validated and the legislation reconsidered following
submission of new evidence. From this perspective, bioreduction and freezing
seems to be promising on-farm storage methods for livestock mortalities,
limiting the need for offfarm transport thus reducing associated biosecurity
risks. While the implementation of highly precautionary, risk-averse mortality
disposal systems is admirable in many ways, similar risk assessments and
legislation do not apply to other components of the livestock sector which may
pose a similar or even greater risk to human health or environmental
contamination (e.g. spreading of animal waste, animal access to watercourses,
public access to grazing land). It is important therefore that mortality
disposal systems are based on a realistic and proportionate level of acceptable
risk in comparison to other components of the food chain, rather than the
current zero-risk approach. It is clear that more evidence is needed on each
disposal and storage method in order to make substantiated risk assessments,
e.g. the effects of spreading carcass ash on crops or the potential of leachate
from burial to contaminate ground or surface water. This review has initiated
this process by applying a simple five-star award system to each livestock
disposal and storage method (Table 3 and Table 4, respectively) in order to
rudimentarily classify various biosecurity and environmental factors based on
current scientific evidence. Methods in need of greater research have also been
highlighted where there is either limited or no existing published literature.
Further research into the economic impacts of dead livestock disposal is
necessary for legislators to appreciate the cost implications on the livestock
sector, whilst life-cycle assessments are needed to help provide more
environmentally sustainable disposal solutions.
OPINION AND REPORT ON : THE TREATMENT OF ANIMAL WASTE BY MEANS OF HIGH
TEMPERATURE (150°C, 3 HOURS) AND CORRESPONDING HIGH PRESSURE ALKALINE
HYDROLYSIS.
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16 MAY
2002
FINAL OPINION AND REPORT ON : A TREATMENT OF ANIMAL WASTE BY MEANS OF HIGH
TEMPERATURE (150°C, 3 HOURS) AND HIGH PRESSURE ALKALINE HYDROLYSIS.
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 10-11 APRIL
2003
BSE INQUIRY 1989 TO ...
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence)
SECOND STATEMENT TO THE BSE INQUIRY
Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing,
University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London
and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
BSE INQUIRY DATA 1989 through the 1990’s REPORT ON BOVINE CARCASE
INCINERATION, incinerations temps., plume, etc. ...tss
some unofficial info. from a source on the inside looking out;
Confidential!!!!
As early as 1992-3 there had been long studies conducted on small pastures
containing scrapie infected sheep at the sheep research station associated with
the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are
documented...I don't know. But personal recounts both heard and recorded in a
daily journal indicate that leaving the pastures free and replacing the topsoil
completely at least 2 feet of thickness each year for SEVEN years....and then
when very clean (proven scrapie free) sheep were placed on these small
pastures.... the new sheep also broke with scrapie and passed it to offspring. I
am not sure that TSE contaminated ground could ever be free of the agent!! A
very frightening revelation!!!
xxxxxxxxxxx
you can take that with however many grains of salt you wish, and we can
debate these issues all day long, but bottom line, this is not rocket-science,
all one has to do is some experiments and case studies, but for the life of me,
i don't know what they are waiting on?
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
more here;
INCINERATION TEMPS
requirements include;
a. after burning to the range of 800 to 1000*C to eliminate smell;
well heck, this is just typical public relations fear factor control. do
you actually think they would spend the extra costs for fuel, for such extreme
heat, just to eliminate smell, when they spread manure all over your veg's. i
think not. what they really meant were any _TSE agents_.
b. Gas scrubbing to eliminate smoke -- though steam may be omitted;
c. Stacks to be fitted with grit arreaters;
snip...
1.2 Visual Imact
It is considered that the requirement for any carcase incinerator disign
would be to ensure that the operations relating to the reception, storage and
decepitation of diseased carcasses must not be publicly visible and that any
part of a carcase could not be removed or interfered with by animals or birds.
REPORT ON BOVINE CARCASE INCINERATION
IF GOD DEMANDED
full text;
http://web.archive.org/web/20040521230540/http://www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600Ò à °C suggests an inorganic template of
replication
Paul Brown*, [dagger ] , Edward H. Rau [Dagger ] , Bruce K. Johnson*,
Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton GajdusekÒ à §
* Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, and [Dagger ] Environmental Protection
Branch, Division of Safety, Office of Research Services, National Institutes of
Health, Bethesda, MD 20892; and Ò à § Institut Alfred Fessard, Centre National
de la Recherche Scientifique, 91198 Gif sur Yvette, France
Contributed by D. Carleton Gajdusek, December 22, 1999
Abstract Top Abstract Introduction Materials and Methods Results Discussion
References
One-gram samples from a pool of crude brain tissue from hamsters infected
with the 263K strain of hamster-adapted scrapie agent were placed in covered
quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at
temperatures ranging from 150Ò à °C to 1,000Ò à °C. Residual infectivity in
the treated samples was assayed by the intracerebral inoculation of dilution
series into healthy weanling hamsters, which were observed for 10 months;
disease transmissions were verified by Western blot testing for
proteinase-resistant protein in brains from clinically positive hamsters.
Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to
150Ò à °C, titers equaled or exceeded 6 log10LD50/g, and after exposure to
300Ò à °C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600Ò à °C
completely ashed the brain samples, which, when reconstituted with saline to
their original weights, transmitted disease to 5 of 35 inoculated hamsters. No
transmissions occurred after exposure to 1,000Ò à °C. These results suggest
that an inorganic molecular template with a decomposition point near 600Ò à °C
is capable of nucleating the biological replication of the scrapie agent.
transmissible spongiform encephalopathy | scrapie | prion | medical waste |
incineration
Introduction Top Abstract Introduction Materials and Methods Results
Discussion References
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600Ò à °C. It has been assumed, without proof, that incineration totally
inactivates the agents of TSE, whether of human or animal origin. It also has
been assumed that the replication of these agents is a strictly biological
process (1), although the notion of a "virus" nucleant of an inorganic molecular
cast of the infectious [beta ] -pleated peptide also has been advanced (2). In
this paper, we address these issues by means of dry heat inactivation
studies.
snip...
GUTTING DEER/ELK AND THOSE THIN GLOVES;
Distribution of prion protein in the ileal Peyer?s patch of scrapie-free
lambs and lambs naturally and experimentally exposed to the scrapie agent
Ragna HeggebÃ’â¬"à ¸1, Charles McL. Press1, Gjermund Gunnes1, Kai Inge
Lie1, Michael A. Tranulis2, Martha Ulvund3, Martin H. Groschup4 and Thor
Landsverk1
Department of Morphology, Genetics and Aquatic Biology1 and Department of
Biochemistry, Physiology and Nutrition2, Norwegian School of Veterinary Science,
PO Box 8146 Dep., N-0033, Oslo, Norway Department of Sheep and Goat Research,
Norwegian School of Veterinary Science, Kyrkjevegen 332/334, 4300 Sandnes,
Norway3 Federal Research Centre for Virus Diseases of Animals, Paul-Ehrlich-Str.
28, 72076 TÃ’â¬"à ¼bingen, Germany4
Author for correspondence: Charles Press. Fax +47 22964764. e-mail
Charles.Press@veths.no
A sensitive immunohistochemical procedure was used to investigate the
presence of prion protein (PrP) in the ileal Peyer?s patch of PrP-genotyped
lambs, including scrapie-free lambs and lambs naturally and experimentally
exposed to the scrapie agent. The tyramide signal amplification system was used
to enhance the sensitivity of conventional immunohistochemical procedures to
show that PrP was widely distributed in the enteric nervous plexus supplying the
gut wall. In scrapie-free lambs, PrP was also detected in scattered cells in the
lamina propria and in the dome and interfollicular areas of the Peyer?s patch.
In the follicles, staining for PrP was mainly confined to the capsule and cells
associated with vascular structures in the light central zone. In lambs
naturally exposed to the scrapie agent, staining was prominent in the dome and
neck region of the follicles and was also found to be associated with the
follicle-associated epithelium. Similar observations were made in lambs that had
received a single oral dose of scrapie-infected brain material from sheep with a
homologous and heterologous PrP genotype 1 and 5 weeks previously. These studies
show that the ileal Peyer?s patch in young sheep may be an important site of
uptake of the scrapie agent and that the biology of this major gut-associated
lymphoid tissue may influence the susceptibility to oral infection in sheep.
Furthermore, these studies suggest that homology or heterology between PrP
genotypes or the presence of PrP genotypes seldom associated with disease does
not impede uptake of PrP.
======================================================
BSE, KURU, DENTAL AND ___CUT ABRASIONS___ from gutting a deer
perhaps;
snip...
since there was a suggestion that kuru had been transmitted through the
gums and/or gum abrasions...
snip...
http://web.archive.org/web/20040625025306/http://www.bseinquiry.gov.uk/files/yb/1989/04/17005001.pdf
Summary of Conclusions on the Vulnerability of Groundwater to Contamination
by BSE Prions at Thruxted Mill.
[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ... File
Format: PDF/Adobe Acrobat - View as HTML ... his Statement of March 1998 to the
BSE Inquiry ... systems subject to regular or intermittent contamination by
rapid movement of recharge water ... www.bse.org.uk/files/ws/s490.pdf
BSE INQUIRY
Statement of behalf of the Environment Agency Concerning Thruxted Mill By
Mr C. P. Young Principal Hydrogeologist, Soil Waste and Groundwater Group WRc
plc; Medmenham, Bucks
OPINION ON SIX ALTERNATIVE METHODS FOR SAFE DISPOSAL OF ANIMAL BY-PRODUCTS
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 10-11 APRIL 2003
OPINION on the use of small incinerators for BSE risk reduction (Scientific
Steering Committee Meeting of 16-17 January 2003)(158KB)
OPINION on open burning of potentially TSE-infected animal materials
(Adopted by the Scientific Steering Committee at its meeting of 16-17 January
2003)
OPINION n the use of burial for dealing with animal carcasses and other
animal materials that might contain BSE/TSE (Adopted by the Scientific
snip...
4. CONCLUSION In the absence of new evidence the opinion of the SSC
â¬SOpinion on Fallen Stock⬠(SSC 25th June 1999) must be endorsed strongly
that land burial of all animals and material derived from them for which there
is a possibility that they could incorporate BSE/TSEs poses a significant risk.
Only in exceptional circumstances where there could be a considerable delay in
implementing a safe means of disposal should burial of such materials be
considered. Guidelines should be made available to aid on burial site
selection.
snip...
> What about alkaline tissue digestion?
UPDATED OPINION AND REPORT ON : A TREATMENT OF ANIMAL WASTE BY MEANS OF
HIGH TEMPERATURE (150°C, 3 HOURS) AND HIGH PRESSURE ALKALINE HYDROLYSIS.
INITIALLY ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16 MAY
2002 AND REVISED AT ITS MEETING OF 7-8 NOVEMBER 2002
snip...
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2
OPINION BACKGROUND AND MANDATE Commission Services received a submission
and accompanying dossier from a commercial company requesting endorsement of a
process for the safe disposal of animal waste which may be contaminated by TSEs.
This process consists of a treatment of animal waste by means of high
temperature (150°C, 3 Hours) and corresponding high pressure alkaline
hydrolysis. Scientific Steering Committee (SSC) was requested to address the
following questions: 1. Can the treatment of animal waste, as described by the
dossier, be considered safe in relation to TSE risk? Can the liquid residues be
considered safe in relation to TSE risk? 2. Can the by-products resulting from
this treatment (i.e. ash of the bones and teeth of vertebrates ) be considered
safe in relation to TSE risk? It is not in the remit of the SSC to endorse
specific commercial products and processes. This opinion therefore relates only
to the nature of the process in regard to possible human health and
environmental risks arising from possible exposure to BSE / prion proteins. The
opinion does not address practical issues such as economics and potential
throughput of carcasses/tissues. An opinion was initially adopted on 16 May
2002. Subsequently, comments, substantial additional data including analytical
results, a risk assessment as well as a number of proposals for the safe
recycling or disposal of the residues were submitted to the SSC secretariat by
the company in June 2002. These were analysed by the rapporteurs, the TSE/BSE ad
hoc Group (at its meeting of 5 September 2002) and the SSC (at its meeting of
7-8 November 2002). The amended opinion and report follow hereafter.
OPINION 1. Regarding the first question of the mandate the SSC concludes
that the liquid residue after a 3-hour digestion cycle could retain infective
potential. Under controlled laboratory conditions in a single experiment the
treatment of animal waste by means of high temperature (150°C, 3 Hours) and
high pressure alkaline hydrolysis has been shown to reduce the infectivity of
TSE/BSE by a factor of 103.5 ⬠104.5. Due to constraints specific to this
experiment, further studies on the combination of heat, pH and time in clearance
studies are needed before any final assurance could be given regarding the
safety of the process with respect to TSE risks. No infectivity was found after
6 hours. This may indicate that the clearance after 6 hours processing time is
higher than after 3 hours. However, these experiments can only give a measure of
the minimum clearance possible and do not permit the quantification of the
clearance factor after 6 hours. Regarding the second question of the mandate,
the SSC concludes that, on the basis of the data available, by-products of the
3-hour process could carry a risk of BSE/TSE infectivity and that this risk may
decrease with the duration of processing; further data would be needed in order
to make a definitive statement.
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3
The SSC refers to the attached report for some comments on the experimental
conditions, which were considered when drawing the above conclusions.
2. The possible human BSE exposure and/or environmental contamination risks
under field conditions not only depends on the maintenance of the efficiency of
the equipment during processing, but also on factors such as: the probability
that a TSE-infected animal is processed, the type of material processed (e.g.,
carcasses as compared to byproducts and waste from animals that tested negative
for BSE), the relationship between effectiveness and throughput and workplace
control, dilution of the possible residual infectivity, and environmental
protection measures. The consideration whether or not the inactivation capacity
of a process is effective must take fully into account such factors, but the SSC
nevertheless considers, as a principle, that the release into the environment of
residual TSE infectivity should be avoided.
3. The dossier supporting the request for the endorsement of the process
states that the levels of 68 priority pollutant semi-volatiles was low and that
odour emission was moderate. Detailed analyses provided recently1 by the company
shows that dioxins in the air could not be detected nor chlorophenols and other
polychlorinated hydrocarbons in the residual fluid of the alkaline process, but
high biological oxygen demand (BOD) and chemical oxygen demand (COD) values were
identified in the residual fluid. Most of the volatile organic compounds (VOCs)
were reported to be below the given chemical detection limits. For the compounds
detected most concentrations were below their respective odour thresholds.
Emissions of some reduced sulphur compounds and amines require special attention
in order to avoid potential odour impacts. Appropriate emission-reduction
measures and air ventilation exhaust systems are recommended. The SSC is
nevertheless concerned about the fact that, if formed in a liquid medium, dioxin
is most unlikely to pass into air, instead it will adsorb to solids or to the
sides of the processing chamber. The analyses of air emissions are therefore not
a sufficient method to exclude the possible presence of dioxins in the effluent
(either as â¬Snatural⬠environmental background contamination or as newly
formed substances during the alkaline treatment). As the air emission analysis
is not sufficient to confirm the possible presence of dioxins in the effluent,
additional data/ analyses are needed to verify whether during the alkaline
hydrolysis process described in the attached report, dioxins are formed in
addition to background levels that may already have been present. For that
purpose samples taken both before and after the process would need to be
analyzed using a method of sufficient sensitivity. Such results would also
provide the basis to decide whether or not the levels of possibly newly produced
dioxins and dibenzofurans (if any) would exceed pre-set safety margins. The
solidification of the digestate is reported by the company to be uncommon.
However, from the test experiments that exclusively used materials of sheep
carcass (with a high fat content) it appears that, if hydrolysate is released on
a large scale to a sewer in a warm condition without extensive dilution, it
might solidify under certain circumstances. In the absence of data to the
contrary it must thus be assumed that any 1 On 18 July 2002, following a
recommendation in the initial opinion adopted on 16 May 2002.
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4 residual BSE/TSE material could co-precipitate and hence be accessible to
sewer vermin. On the basis of the above evidence, the SSC considers that for the
time being the direct discharge of the liquid residues to the sewer without
further treatment is not appropriate. The SSC opinion of 24-25 June 1999 on
â¬SFallen Stock⬠2provides some further guidance on the disposal or possible
recycling for certain uses of the residues. As a summary this opinion implies: -
If the risk of TSE infectivity can be excluded, recycling of residues from the
treatment of animal waste by means of high temperature (150°C, 3 Hours) and
high pressure alkaline hydrolysis could be acceptable for various purposes
provided the other risks discussed in the SSC opinion of 24-25 June 1999 are
excluded (e.g., presence of heavy metals, toxic substances, etc.). If analyses
of the various types of residues (air, effluent, sludge) from the field
equipment, carried out as part of a risk analysis prior to its installation,
show that such is the case3, the use of the sludge as fertiliser, as soil
additive or as feed is acceptable provided the standards4 for these uses are
met. - If the presence of residual TSE infectivity cannot be excluded, residues
should be disposed of as described in the SSC opinion of 24-25 June 1999. This
opinion of 1999 did not consider anaerobic digestion as safe because the TSE
clearance level by anaerobic digestion process is unknown. However, should
reliable published data show that the levels of residual TSE infectivity in
biogas are likely to be very low and would be eliminated during the burning of
the gas, the recovery of bio-energy from anaerobically produced biogas could be
acceptable if sufficient precautions (e.g., filters) are taken to exclude
contamination of the gas. As the anaerobic process for the production of biogas
may result in sludge containing infectious activity, burning, incineration or
controlled landfill should be the methods of disposal for the residual sludge,
filter contents, etc.
Note: The formation of chlorophenols, dioxins and polychlorinated
hydrocarbons in a combustion process can use any form of chlorine including
chloride ions. Combustion of the effluent could thus give rise to dioxin
formation. However, the SSC considers that this risk is minimized/excluded if
the standards set for that purpose are respected, i.e., a rapid combustion at
900°C or above followed by rapid chilling (quenching) and with appropriate
filtration by adding charcoal to the emissions or other air pollution devices.
4. Like for all waste disposal and recycling processes, a site-specific risk
assessment of the process as a whole (from animal collection to final disposal
of the residues) is required when considering the installation of the equipment
in a particular situation, so as to minimise workers exposure, environmental
impacts, etc. 2 Scientific Opinion on The risks of non conventional
transmissible agents, conventional infectious agents or other hazards such as
toxic substances entering the human food or animal feed chains via raw material
from fallen stock and dead animals (including also: ruminants, pigs, poultry,
fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish)
or via condemned materials. Adopted By the Scientific Steering Committee at its
meeting of 24-25 June 1999 and re-edited at its meeting of 22-23 July 1999. 3
The dossier and the additional effluent analysis data submitted for this
opinion, and taking into account the scientific report attached to its opinion
of 24-25 June 1999, indicate that these other risks are probably minimal or
excluded. But this would need to be confirmed for each installation and for each
type and source of waste to be processed. 4 For example: Na or K concentrations
and pH of the fertiliser.
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5 UPDATED REPORT ON : A TREATMENT OF ANIMAL WASTE BY MEANS OF HIGH
TEMPERATURE (150°C, 3 HOURS) AND HIGH PRESSURE ALKALINE HYDROLYSIS
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6 I.
MANDATE AND BACKGROUND According to the EU regulation in force on 1 January
2001, animals, animal waste or products derived thereof (e.g., animal meat and
bone meal), potentially contaminated with TSE agent by-products, shall be
disposed of by incineration or co-incineration. Alternative ways may be allowed
following a positive scientific opinion. The Scientific Steering Committee (SSC)
has previously provided opinions on the use of rendering and incineration to
reduce the risk from TSEs in animal tissues and products derived from these. It
has also provided a framework for evaluating the risks involved in the storage,
transport and handling of animal materials which may contain TSEs. The
Commission has now received a submission from a commercial company requesting
endorsement of a process for the safe disposal of animal waste which may be
contaminated by TSEs. This process consists of a treatment of animal waste by
means of high temperature (150°C, 3 Hours) and high pressure alkaline
hydrolysis5. The Commission Services therefore submitted the following questions
for opinion to the Scientific Steering Committee (SSC):
1. Can the treatment of animal waste, as described by the dossier, be
considered safe in relation to TSE risk? Can the liquid residues be considered
safe in relation to TSE risk?
2. Can the by-products resulting from this treatment (i.e. ash of the bones
and teeth of vertebrates ) be considered safe in relation to TSE risk?
A report was initially prepared for the SSC, who discussed it at its
meeting of 16 May 2002. Subsequently, comments, substantial additional data
including analytical results, a risk assessment as well as a number of proposals
for the safe recycling or disposal of the residues were submitted to the SSC
secretariat by the company at various dates between June and November 2002 (see
list of references at the end of the report). At the request of the SSC, the
secretariat also organised additional external expertise. All this information
was analysed by the rapporteurs Prof.Dr.J.Bridges and Prof.Dr.Em.M.Vanbelle, the
TSE/BSE ad hoc Group (at its meeting of 5 September 2002) and the SSC (at its
meeting of 7-8 November 2002). The amended opinion and report follow hereafter.
III BASIS FOR THE OPINION III.1. NATURE OF THE PROCESS
A whole carcass or parts of a carcass is placed in a steel alloy container.
A measured amount of alkali is added either in solid form or as a solution of
NaOH or KOH, (starting concentration: 1 molar), the vessel is sealed and the
contents heated at 150° for 3 to 6 hours and at a high pressure (approximately
5 Bars). (In practice, the volume of alkali solution is and the duration of the
process may be adjusted according to the load and composition of the material).
In respect to basicity at ~ 1 N base 5 This process is currently applied in the
USA on high volumes of several carcasses of deer and elk carcasses with CWD.
concentration, almost no difference exists between NaOH and KOH. At the
beginning of the process, entire animal carcasses can be used. Six parts of
aqueous alkaline solution are used to 4 parts of tissue material. The physical
energy generated by a constant pumping action continually circulates the liquid
material present in the vessel thereby aiding the digestion process. Under these
conditions the tissues are dissolved and bones and teeth softened. The solid
residue is a small fraction of the original weight. The use of alkaline
conditions minimises gaseous emissions of gases such as CO2, NO2, SO2.
III.2. HUMAN HEALTH AND ENVIRONMENTAL CONSIDERATIONS
In evaluating the process in respect of the questions posed by the
Commission Services, three issues need to be addressed:
i) Does the process destroy/inactivate TSEs (including BSE) and if so how
effective is the destruction/inactivation?
ii) Are there pathogens and/or chemicals whose potency is not reduced
significantly or inactivated by the process?
iii) Are any of the end products of the process of concern from a human
health risk or an environmental risk viewpoint?
In considering the evidence available to deal with these issues it is
important to consider whether the data has been generated under very controlled
laboratory conditions or under practical large scale working conditions. In this
context it should be noted that it is often the case that data derived under
laboratory conditions demonstrates higher efficiency in destruction/inactivation
and lower levels of contamination than will occur in regular use at the
industrial scale.
snip...
EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions C1 - Follow-up and dissemination of
scientific opinions
OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES AND OTHER
ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE ADOPTED BY THE SCIENTIFIC STEERING
COMMITTEE MEETING OF 16-17 JANUARY 2003 1 OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which safe
burial of potentially TSE-infected (animal) materials can be achieved. The
details of the SSC's evaluation are provided in the attached report. The SSC
concludes as follows:
(1) The term "burial" includes a diversity of disposal conditions. Although
burial is widely used for disposal of waste the degradation process essential
for BSE/TSE infectivity reduction is very difficult to control. The extent to
which such an infectivity reduction can occur as a consequence of burial is
poorly characterised. It would appear to be a slow process in various
circumstances.
(2) A number of concerns have been identified including potential for
groundwater contamination, dispersal/transmission by birds/animals/insects,
accidental uncovering by man.
(3) In the absence of any new data the SSC confirms its previous opinion
that animal material which could possibly be contaminated with BSE/TSEs, burial
poses a risk except under highly controlled conditions (e.g., controlled
landfill).
The SSC reiterates the consideration made in its opinion of 24-25 June 1999
on "Fallen Stock"1. The limited capacity for destruction of animal wastes in
certain countries or regions in the first place justifies the installation of
the required facilities; it should not be used as a justification for unsafe
disposal practices such as burial.
However, the SSC recognises that for certain situations or places or for
certain diseases (including animals killed and recycled or disposed of as a
measure to control notifiable diseases), the available rendering or incinerator
or disposal capacity within a region or country could be a limiting factor in
the control of a disease. Thus if hundreds or even millions of animals need to
be rendered after killing or if the transport of a material to a rendering or
disposal plant proved to be impractical, an appropriate case by case risk
assessment2 should be carried out before deciding upon the most appropriate way
of disposal. In principle, the risk is expected to be the lower for small
incinerators3 as compared to burial. As such decisions in practice may have to
be taken at very short notice, risk management scenarios according to various
possible risks should be prepared in advance to allow for a rapid decision when
the need arises.
1 Scientific Opinion on The risks of non conventional transmissible agents,
conventional infectious agents or other hazards such as toxic substances
entering the human food or animal feed chains via raw material from fallen stock
and dead animals (including also: ruminants, pigs, poultry, fish,
wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via
condemned materials. Adopted By the Scientific Steering Committee at its meeting
of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999. 3 See SSC opinion of
16-17 January 2003 on the use of small incinerators for BSE risk reduction. 2
THE USE OF BURIAL FOR DEALING WITH CARCASSES AND OTHER MATERIALS THAT MIGHT
CONTAIN BSE/TSE REPORT
1. MANDATE On 17 May 2002, the Scientific Steering Committee (SSC) was
invited by Commission Services to advice on the examples of conditions under
which safe burial of potentially TSE-infected animal materials can be achieved.
The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and
amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the
SSC at its meeting of 16-17 January 2003.
2. GENERAL CONSIDERATIONS "Burial" covers a range of disposal situations
ranging from the practice of burying animals on farms and other premises in a
relatively shallow trench (with or without treatment such as lining) to deep
disposal to a lined and professionally managed landfill site (SSC 2001). Buried
organic material is normally decomposed by microbial and chemical processes.
However this is not a process amenable to control measures. As noted by the SSC
"Opinion on Fallen Stock" (SSC 25th June 1999) there is little reliable
information on the extent and rate of infectivity reduction of BSE/TSEs
following burial. An old paper by Brown and Gajdusek 1991 assumed a reduction of
98% over 3 years. However it is noted that the rate of degradation of materials
following burial can vary very considerably between sites. This is not
surprising because the degradation process is strongly influenced by factors
such as water content of the site, temperature inside the site, nature of
adsorptive "material" present etc. The previous SSC opinion noted that BSE/TSEs
appear to be resistant to degradation when stored at room temperature over
several years. It also raised concerns that mites could serve as a vector and/or
reservoir for the infected scrapie material. Burial sites may have a thriving
animal population. Uncovering of risk material that is not deeply buried is
therefore possible. The SSC in its opinion of 28th-29th June 2001 set out a
framework for assessing the risk from different waste disposal processes. These
criteria may be applied to burial as follows:
(1) Characterisation of the risk materials involved. Unlike many other
waste disposal options there are no technical or economic factors that would
limit the nature of the material that can be disposed of by burial. Moreover in
many cases the location of burial sites is uncertain. The potential for
transmission of BSE/TSEs for SRM that is buried near the surface is also poorly
characterised.3
(2) Risk reduction. The extent to which the infectivity is reduced is
likely to vary substantially according to the nature of the site depth of burial
whether pre-treatment by burning or through the addition of lime is used etc.
There appears to be no scientific basis at present for the prediction of the
rate of loss of infectivity. In the absence of such data, as a worst case, it
has to be assumed that over a three-five year period the loss of infectivity may
be slight. In principle on a well-managed fully contained landfill the risks
from infective material can approach zero. However this requires rigorous
management over many years. This is difficult to guarantee.
(3) Degree to Which the Risks can be Contained The principal concerns are:
* Prevention of access to the SRM by animals that could result in the
transmission (directly or indirectly) of the BSE/TSE.
* Penetration of prions into the leachate/groundwater. It is noted that on
some landfill sites leachate is sprayed into the air to facilitate oxidation of
some organic components. Such a practice could in principle lead to dispersal of
BSE/TSEs. It is also noted that it is not uncommon for landfill sites to be
re-engineered to increase their stability, gas and leachate flow and/or total
capacity. If this re-engineering involved an area where previous burial of
BSE/TSE contaminated material had taken place and additional risk could accrue.
The possibility of contaminated material being dug up in shallow and unmarked
burial sites on farms etc constitutes a considerably greater risk.
3. FURTHER INVESTIGATIONS Research is needed on specific aspects of the
behaviour of prion like molecules in controlled landfills i.e.:
* Potential for adsorption to other material present in the waste that
might limit their mobility.
* Principal factors influencing rates of degradation.
* Effectiveness of encasement in cement in controlling/reducing the risk.
4. CONCLUSION In the absence of new evidence the opinion of the SSC
"Opinion on Fallen Stock" (SSC 25th June 1999) must be endorsed strongly that
land burial of all animals and material derived from them for which there is a
possibility that they could incorporate BSE/TSEs poses a significant risk.
Only in exceptional circumstances where there could be a considerable delay
in implementing a safe means of disposal should burial of such materials be
considered. Guidelines should be made available to aid on burial site selection.
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EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions C1 - Follow-up and dissemination of
scientific opinions
OPINION ON OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16-17 JANUARY
2003
2 OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which safe
burning of potentially TSE-infected (animal) materials can be achieved. The
details of the SSC's evaluation are provided in the attached report. The SSC
concludes as follows:
(1) "Burning" covers a wide variety of combustion conditions. This opinion
is concerned with the process of open burning e.g. bonfires.
(2) There are serious concerns regarding the use of open burning for the
destruction of pathogen contaminated animal waste, particularly for waste which
may be contaminated with relatively heat stable pathogens. Issues include: the
potentially very high variability of the pathogen inactivation, the nature of
the gaseous and particulate emissions, and the risks from the residual ash.
(3) The SSC recommends that open burning is only considered for pathogen
destruction under exceptional circumstances following a specific risk
assessment.
In the case of animal waste possibly contaminated with BSE/TSE in view of
the uncertainty of the risk open burning should be considered a risk.
Suitable monitoring methods for TSE contamination of both air and ash are
needed.
Protocols for safe burning in emergency situations need to be established.
The SSC reiterates the consideration made in its opinion of 24-25 June 1999
on "Fallen Stock"1.
The limited capacity for destruction of animal wastes in certain countries
or regions in the first place justifies the installation of the required
facilities; it should not be used as a justification for unsafe disposal
practices such as burial.
However, the SSC recognises that for certain situations or places or for
certain diseases (including animals killed and recycled or disposed of as a
measure to control notifiable diseases), the available rendering or incinerator
or disposal capacity within a region or country could be a limiting factor in
the control of a disease.
Thus if hundreds or even millions of animals need to be rendered after
killing or if the transport of a material to a rendering or disposal plant
proved to be impractical, an appropriate case by case risk assessment2 should be
carried out before deciding upon the most appropriate way of disposal.
In principle, the risk is expected to be the lower for small incinerators3
as compared to open burning. As such decisions in practice may have to be taken
at very short notice, risk management scenarios according to various possible
risks should be prepared in advance to allow for a rapid decision when the need
arises.
1 Scientific Opinion on The risks of non conventional transmissible agents,
conventional infectious agents or other hazards such as toxic substances
entering the human food or animal feed chains via raw material from fallen stock
and dead animals (including also: ruminants, pigs, poultry, fish,
wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via
condemned materials. Adopted By the Scientific Steering Committee at its meeting
of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999. 3 See SSC opinion of
16-17 January 2003 on the use of small incinerators for BSE risk reduction.
3 OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS REPORT 1.
MANDATE On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which safe
burning of potentially TSE-infected animal materials can be achieved. The SSC
appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by
the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its
meeting of 16-17 January 2003. 2. GENERAL CONSIDERATIONS Burning is a combustion
process to which a range of control measures may be applied to contain emissions
and to ensure the completeness of the degradation process for organic matter.
Depending on the source (waste) material the burning process may or may not
require addition of other energy sources. Incineration/pyrolysis are contained
combustion processes are contained combustion processes and therefore have the
potential for a high level of control. (However see opinion on small
incinerators). At the other end of the control spectrum is open burning; such as
bonfires. Typically combustion of animal waste requires the addition of a high
calorific fuel in order to initiate (and for some materials to sustain) the
process. It is recognised that open burning of animal waste is a very cheap and
convenient method of disposal. However uncontained burning has a number of
problems in terms of the potential risks involved:
(1) In the open burning situation a range of temperatures will be
encountered. It is difficult therefore to ensure complete combustion of the
animal waste. If the waste is contaminated with pathogens there will remain
considerable uncertainty as to the degree of their inactivation.
(2) Gaseous and particulate emissions to the atmosphere will occur and
consequently worker and public exposure is likely. There is very little data to
indicate whether or not some pathogens could be dispersed to air as a
consequence of open burning.
(3) The supporting/secondary fuel may be a source of contamination itself.
For example in the recent foot and mouth disease outbreak in the UK timbers were
used at some sites that were heavily contaminated with pentachlorophenol.
(4) The residual ash must be considered to be a risk source. Its safe
disposal needs to be assured (see opinion on small incinerators) to prevent
human and animal contact and protect from groundwater contamination. While
careful selection of burning sites can reduce the risks open burning should only
be considered in emergency situations. For each such emergency situation a
specific risk assessment should be conducted which must include the risk 4 from
the pathogen of immediate concern but also other pathogens that might be
present.
3. RISK ASSESSMENT OF OPEN BURNING FOR BSE The SSC, at its meeting of
28th-29th June 2001, recommended "a framework for the assessment of the risk
from different options for the safe disposal or use of meat and bone meal (MBM)
and other products which might be contaminated with TSEs and other materials.
Applying the framework to the practice of open burning, the following
conclusions can be drawn:
3.1. Nature of the materials handled Potentially a wide variety of
materials can be used provided suitable secondary fuel is available. The burning
process is very simple in principle and difficult in practice to regulate
effectively.
3.2. Risk reduction due to open burning There is no reliable data to
indicate the extent of risk reduction that could be achieved by open burning. It
is reasonable however to assume that overall it will be rather less effective in
reducing the infectivity of BSE/TSE than wellconducted incineration. Moreover
the reproducibility of the risk reduction is likely to be very variable even at
a single location.
3.3. Airborne emissions and residue ash The composition of airborne
emissions and residue ash is rarely monitored. From a risk assessment viewpoint
particular attention needs to be given to the potential for the airborne
dispersal of relatively heat stable pathogens as a consequence of open burning.
In the absence of reliable data both airborne emissions and residual ash must be
considered to constitute a significant risk if animal waste that might be
contaminated with TSEs is being burnt.
4. FURTHER INVESTIGATION Research is needed particularly on:
* The potential for airborne dispersal of relatively heat stable pathogens.
* Methodologies to improve the efficacy of the combustion process to ensure
the inactivation of pathogen contaminated animal waste.
5. CONCLUSION Open burning potentially represents a significant risk where
the animal waste has the possibility of being contaminated with BSEs/TSEs.
Suitable monitoring methods for TSE contamination of both air and ash are
needed. Protocols for safe burning in emergency situations need to be
established.
C:\WINNT\Profiles\bredagi.000\Desktop\Incinerator_OPINION_0301_FINAL.doc
EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions C1 - Follow-up and dissemination of
scientific opinions OPINION ON THE USE OF SMALL INCINERATORS FOR BSE RISK
REDUCTION SCIENTIFIC STEERING COMMITTEE MEETING OF 16-17 JANUARY 2003 2 OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to
(i) evaluate a risk assessment1 prepared for the UK's Spongiform
Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the
use of small incinerators to dispose of specified risk materials and
(ii) to advise on the safety with regard to TSE risks of the use of such
small incinerators.
The details of the SSC's evaluation are provided in the attached report.
The SSC concludes as follows:
(i) The SSC, at its meeting of 28th -29th June 2001, recommended "a
framework for the assessment of the risk from different options for the safe
disposal or use of meat and bone meal (MBM) and other products which might be
contaminated with TSEs and other materials." This framework comprised five
components:
(1) Identification and characterisation of the risk materials involved, the
possible means for their transmission and potential at risk groups.
(2) The risk reduction achieved by the particular process.
(3) The degree to which the risks can be contained under both normal and
emergency operating conditions. This inevitably includes consideration of the
effectiveness of control measures.
(4) Identification of interdependent processes for example transport,
storage, loading of any TSE related risk materials.
(5) The intended end-use of the products for example disposal, recycling
etc.
The risk assessment prepared for SEAC focuses on the risks involved steps 1
and 2 in respect of BSE/TSEs only and is based on a visit to 10 incinerators out
of a total of 263 in the UK of which 60% had after burners. The risk assessment
is also using a number of assumptions and data that may be valid for certain
incinerator types under certain conditions, but are not necessarily applicable
either for all types of materials to be disposed of, or to the whole range of
types of small incinerators in use the EU and the UK.
(ii) Small incinerators are widely used to meet the needs of local
communities. These incinerators vary greatly in their design, nature of use and
performance characteristics and the quality of their management. As a
consequence of this variability there are many uncertainties in identifying
risks posed by small incinerators that are used to treat SRM materials and each
type should eventually receive its own assessment. Also, general operating and
control criteria should be established for 1 DNV Consulting (Det Norske
Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK
Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report,
February 2001. 24 pages. 3 Potential risk sources arising from the incineration
process include: gaseous emissions and residual ash. Research is currently
ongoing mimicking incineration of TSE-infected brain tissue to assess the
infectivity clearance level under various scenarios2. However, there are no
final reported measurements that enable the risk to be assessed from either the
emissions or the ash from small incinerators. It has been argued that the
protein content of the ash is a reasonable surrogate measure of the degree of
risk deduction caused by the incineration process. This assumption is
questionable in view of the resistance to heat of prions as compared to other
proteins. Protein measurements in ash are however probably a useful general
measure of the overall efficiency and reproducibility of the incineration
process. Results in the aforementioned report1 indicate a large degree of
variability in performance among the small incinerators in the UK that have been
evaluated. It is anticipated that small incinerators, used by other Member
States will also show a considerable variation in performance. In evaluating the
risk of small incinerators, consideration should be given to the risk of
potential contamination of the ash and of the gaseous emissions. In the absence
of generally accepted and enforced performance standards for small incinerators
handling SRMs each such facility therefore needs to be the subject of a specific
risk assessment. The SSC considers that the standards set up by the new Waste
Incinerator Directive (2000/76/EC) and in its opinion of June 1999 on waste
disposal should serve as guidance. In the absence of reliable data on the
possible residual infectivity of the ash, it should be disposed of, i.e., in
controlled landfills as described in the SSC opinion of June 1999 on safe
disposal of waste. The SSC finally wishes to emphasise the need for suitable
monitoring methods in order that risks can be assessed readily for individual
types of small incinerators. 2 P.Brown, pers.comm., December 2002. Publication
in progress.4
THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION REPORT
1. MANDATE
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to
(i) evaluate a risk assessment3 prepared for the UK's Spongiform
Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the
use of small incinerators to dispose of specified risk materials and
(ii) to advise on the safety with regard to TSE risks of the use of such
small incinerators.
The SSC appointed Prof. J. Bridges as rapporteur. His report was discussed
and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by
the SSC at its meeting of 16-17 January 2003.
2. CURRENT LEGISLATIVE FRAMEWORK
Until 2000, small incinerators were exempt from the emission limits set by
the EC for MSW and hazardous waste incinerators with throughputs greater than 50
kg/hour. An "incineration plant" is defined by the new Incineration of Waste
Directive (2000/76/EC) as "any stationary or mobile technical equipment
dedicated to the thermal treatment of waste with or without recovery of the
combustion heat generated". This definition would appear to exclude open burning
of waste. The new Directive, which must be transposed into the legislation of
each Member State by December 2002, replaces a range of previous directives on
incineration. It applies to all new incinerator installations from December 28th
2002 and all existing installations from December 28th 2005. The principal aim
of the Directive is to prevent and/or limit negative environmental effects due
to emissions into air, soil, surface and ground water and the resulting risks to
human health from the incineration and co-incineration of waste. It covers many
aspects from a requirement for afterburners to airborne emission limits and
criteria for the composition of residual ash. Previous EC legislation has
exempted small incinerators (i.e. those operating at less than 50 kg per hour).
The Waste Incinerator Directive (WID) (2000) allows such small incinerators to
be exempt from licensing at the national level however they will still be
subjected to the same onerous requirements of the WID as larger incinerators. In
the UK it is proposed that in future incinerators dealing with non-hazardous
waste but with a throughput of less than 1 tonne per hour will be regulated by
local authorities whereas those with a larger throughput will be regulated by
the national authority. It is possible that different regulatory mechanisms may
result in differences in the rigour with which the new standards are enforced.
The position on the disposal of animal waste is complicated. Animal carcass
incineration use not covered by the WID and therefore the existing regulatory
framework (90/66/EEC which covers animal and public health requirements to
ensure destruction of pathogens) will continue to be applied. A new Animal
By-Products Regulation 3 DNV Consulting (Det Norske Veritas), 2001. Risk
assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture,
Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages. 5
(ABPR) will apply in Member States during the first part of 2003. The
relationship to WID has been included in the ABPR. It is important that it does
not result in less strict standards being applied for animal carcass
incineration. In contrast to whole carcasses WID will apply to the burning of
meat and bone meal, tallow or other material (even if they burn animal carcasses
too). Additional specific directives will continue to apply to waste that could
be contaminated with BSE/TSEs. (96/449/EC)
3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE
Small incinerators are used for a variety of purposes and in a range of
locations among Member States. Many are located alongside small abattoirs,
knackers, hunt kennels, or laboratories. Thus they meet the needs of relatively
small communities. Across Member States these small incinerators include a
variety of designs and operating conditions (as indicated above in principle
they will probably be required to meet specific standards for emissions and for
the composition of the residual ash by December 28th 2005). In the UK there are
indications (see DNV Report 2001) that a considerable quantity of SRM which
would have previously been sent for rendering is now being incinerated directly
in small incinerators. Thus evaluation of the risks from such incinerators is of
increasing importance.
4. RISK ASSESSMENT FOR SMALL INCINERATORS
The SSC, at its meeting of 28th -29th June 2001, recommended "a framework
for the assessment of the risk from different options for the safe disposal or
use of meat and bone meal (MBM) and other products which might be contaminated
with TSEs and other materials. This framework comprised five components: (1)
Identification and characterisation of the risk materials involved, the possible
means for their transmission and potential at risk groups. (2) The risk
reduction achieved by the particular process. (3) The degree to which the risks
can be contained under both normal and emergency operating conditions. This
inevitably includes consideration of the effectiveness of control measures. (4)
Identification of interdependent processes for example transport, storage,
loading of any TSE related risk materials.
(5) The intended end-use of the products for example disposal, recycling
etc.
Recently a report has been prepared by DNV consulting (2001) for the UK
Ministry of Agriculture, Fisheries and Food (now known as DEFRA) that assesses
the risks from small incinerators in the UK that receive SRMs. This report
focuses on the risks involved steps 1 and 2 in respect of BSE/TSEs only. 10
incinerators out of a total of 263 in the UK were visited of which 60% had after
burners.
(1) Nature of the materials handled.
The DNV report 2001 starts with the assumption that "the materials
incinerated at small abattoirs will be mainly SRM and bones from animals that
are fit for human consumption. It may also include material from animals failed
by meat inspectors. The likelihood of there being an animal 6 with significant
BSE infectivity is very small and certainly much less than for the fallen stock
handled by hunt kennels and knackers4. For this reason the study has
concentrated on the latter type of operation". The Report notes that "the
material handled by both knacker and hunt kennels is highly variable and
difficult to characterise". In terms of input the key factors to consider are:
* The number of adult bovines processed and the proportion of these
carcasses that are likely to be infected.
* The extent of infectivity (in terms of human oral Infectious Units) that
may occur (average and worst case).
In the DNV (2001) risk assessment only the BSE risk from processing bovine
SRMs was considered. For quantitative risk assessment purposes the mean value of
the oral ID50 for cattle was taken as 0.1 gram. A range of values was taken to
cover uncertainty in the inter-species barrier from 104 to 1 (as recommended by
the SSC 2000). In order to assess the likelihood that a particular carcass could
be infected, UK and Swiss monitoring data was used. An incidence rate based on
Prionics test findings of between 0.013 and 0.0025 was calculated. The DNV
Report notes that prevalence rates are progressively reducing from these 1998/99
figures. Finally the report concludes that the SRM from an infected bovine could
contribute 700 Infectious Units.
(2) Risk reduction due to incineration
Once a carcass/SRM has been introduced into a small incinerator there are
two main sources for the potential release of BSE infectivity
(a) Airborne emissions
(b) Residual ash There is no direct data on the TSE levels that may occur
in those two media.
The SSC however is aware of currently ongoing heat studies mimicking
various incineration conditions and scenarios and aiming at assessing the TSE
clearance efficacy of these processes (P.Brown, pers.comm., 16.01.03) on both
the residual ash and the trapped emission gases. In the absence of final data
from such experiments for individual (small) incinerator types, the DNV Report
(2001) assumes that measurement of the total protein content of ash is a
relevant surrogate for BSE/TSE material. Protein content is a useful indicator
of the general performance of an incinerator. However it is much more
problematic whether it is also a valid marker for possible BSE/TSE contamination
as it known that BSE/TSE are relatively heat resistant as compared to other
proteins. Failure to detect certain amino acids present in prions is encouraging
but the sensitivity limits for amino acids are relatively poor for reassurance
purposes. Equally important, the data provided in the DNV report shows moderate
split sample 4 It may be mentioned that this assumption may be valid for the UK
as a whole, but note necessarily for all other Member States. 7 variation but
often substantial inter sampling variation (up to 600 fold). This indicates a
wide span of performance standards among the small SRM incinerators in the UK
and most likely across the whole of the EU. Typically performance was
substantially poorer than is the case for larger incinerators. Unburned material
is not uncommonly noted in the ash from small incinerators. If the reduction in
protein content due to incineration is accepted as a valid indicator, typical
infectivity reduction can be calculated to be of the order of 1600 (DNV Report
2001). Incinerators are known to emit particulate matter from their stacks.
Larger incinerators have much higher stacks to facilitate disposal of emissions,
they also have gas cleaning equipment to minimise the emission of particulate
matter, metals and acidic gases. Small incinerators generally do not have any
gas cleaning equipment. It can be speculated (as in the DNV Report 2001) that
unburned materials (and therefore potentially infections is much less likely to
be emitted in the form of particulate matter than burnt material. Nonetheless
there is no data to support this assumption.
(3) Other considerations.
(a) Disposal of ash. In the case of small incinerators ash is often
dispersed of locally to a trench, which is typically neither lined, nor is the
residue buried deeply. In contrast for larger incinerators in the UK ash is
normally disposed of to a contained landfill. The risk from disposal to a trench
is difficult to gauge in the absence of reliable data on the possible
infectivity of the ash.
(b) Management factors. Almost inevitably the level of expertise available
for the management of small incinerators is highly variable because few such
facilities can afford to employ specialists in incineration. This is also likely
to be often the case for the inspectors as well. While such considerations
cannot formally be taken into account in a risk assessment, they are not the
less relevant factors that need to be considered in assessing the risk from a
particular plant.
(c) Benchmarking. The DNV 2001 risk assessment relies greatly on the
assumption that BSE/TSE contaminated material is very unlikely to be processed.
The Report seeks to compare the risks from a small incinerator with that from
large SRM incinerators which the author had assessed previously (DNV, 1997). It
identifies that the risk is four-five -fold less from a typical small
incinerator because the scale of activities is much lower. However it is noted
that the amount of experimental data to back this conclusion is extremely
limited and does not take into account either risks from the residual ash or any
consequences of a substantially lower stack height limiting the dilution of the
emitted particulate and gaseous matter. 8
5. FURTHER INVESTIGATIONS
In view of the uncertainty regarding the risks due to BSE/TSE contamination
of the fly and bottom ash and airborne emissions it is recommended that further
research is conducted to identify the residual risks (along with attendant
uncertainties) from the burial of ash (without further treatment,) in
uncontained sites. It is essential that suitable monitoring methods are
developed.
6. LITERATURE EC (European Commission), 1999.
Opinion on The risks of non conventional transmissible agents, conventional
infectious agents or other hazards such as toxic substances entering the human
food or animal feed chains via raw material from fallen stock and dead animals
(including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur
animals, cats, laboratory animals and fish) or via condemned materials. Adopted
By the Scientific Steering Committee at its meeting of 24-25 June 1999 and
re-edited at its meeting of 22-23 July 1999. DNV Consulting (Det Norske
Veritas), 1997. Risks from disposing of BSE infected cattle in animal carcass
incinerators. Report prepared for the UK Environment Agency. DNV Consulting (Det
Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK
Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report,
February 2001. 24 pages. SEAC (Spongiform Encephalopathy Advisory Committee,
UK), 2001. Public summary of the SEAC meeting of 25 April 2001.
Revised TSE Guidance Part 4 Part 4 Infection control of CJD and related
disorders in the healthcare setting Summary of revised advice published: 2 June
2003
snip...
Use of laser for tonsillectomy : smoke plumes 4.45 Some ENT surgeons may
use laser techniques as an alternative to conventional surgery for
tonsillectomy. There is no evidence of the transmission of TSEs by the
respiratory route. Any risk to surgeons from smoke plumes is thought to be very
low, but there are no data on vCJD. General guidance on the safe use of lasers,
Guidance on the safe use of lasers in medical and dental practice, Medical
Devices Agency (MDA) (1995) is available from MDA Business Services on tel: 0207
972 8360.
snip...
some other data on incineration and plume, filters, etc;
what about those healthy looking deer/elk everyone wants to bury?
> The DOW Web site advises hunters "not to shoot, handle or consume any
animal
> that appears sick" and to avoid consuming the "brain, spinal cord,
eyes, spleen, tonsils
> and lymph nodes of harvested animals."
THOSE HEALTHY LOOKING DEER/ELK ''SUB-CLINICAL'' INFECTION
DEAD DEER WALKING
Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION
INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the National
Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form
of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the 'species barrier'
- the main protective factor which limits the ability of prions2 to jump from
one species to infect another. They found the mice had a 'sub-clinical' form of
disease where they carried high levels of infectivity but did not develop the
clinical disease during their normal lifespan. The idea that individuals can
carry a disease and show no clinical symptoms is not new. It is commonly seen in
conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease. However, on
closer inspection they found that the mice had high levels of mouse prions in
their brains. This was surprising because it has always been assumed that
hamster prions could not cause the disease in mice, even when injected directly
into the brain.
In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of prions. While
some barriers are quite small (for instance BSE easily infects mice), other
combinations of strain and species show a seemingly impenetrable barrier.
Traditionally, the particular barrier studied here was assumed to be
robust.
Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure species
barriers in the laboratory, and that we should not assume that just because one
species appears resistant to a strain of prions they have been exposed to, that
they do not silently carry the infection. This research raises the possibility,
which has been mentioned before, that apparently healthy cattle could harbour,
but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected material
getting into the food chain and for those considering how best to safeguard
health and reduce the risk that theoretically, prion disease could be contracted
through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET
BY THE JOURNAL.
Aguzzi warns of CWD danger
The TSE family of diseases also includes chronic wasting disease (CWD) in
deer, a condition that has spread in the US in recent years (Nature 416, 569;
2002). Speaking at the Days of Molecular Medicine conference in La Jolla in
March, prion expert Adriano Aguzzi issued a strong warning against
underestimating this form of TSE.
"For more than a decade, the US has by-and-large considered mad cows to be
an exquisitely European problem. The perceived need to protect US citizens from
this alien threat has even prompted the deferral of blood donors from Europe,"
he said. "Yet the threat-from-within posed by CWD needs careful consideration,
since the evidence that CWD is less dangerous to humans than BSE is
less-than-complete. Aguzzi went on to point out that CWD is arguably the most
mysterious of all prion diseases.
"Its horizontal spread among the wild population is exceedingly efficient,
and appears to have reached a prevalence unprecedented even by BSE in the UK at
its peak. The pathogenesis of CWD, therefore, deserves a vigorous research
effort. Europeans also need to think about this problem, and it would be timely
and appropriate to increase CWD surveillance in Europe too." Aguzzi has secured
funding from the National Institutes of Health to investigate CWD, and the
effort will be lead by Christina Sigurdson in his department at the University
of Zurich. KAREN BIRMINGHAM, LONDON
This quote from Dr. Gambetti is especially significant since he is the
rather cautious TSE researcher under contract with the Centers for Disease
Control to examine the brains of individuals who have died of CJD.
-----------------
Pierluigi Gambetti, director of the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland, said all
deer should be tested for chronic wasting disease before any processing is
done.
"There is no way around it," he said. "Nobody should touch that meat unless
it has been tested."
--------------------------------------
Greetings again,
extreme caution should be used, plume should be taken very seriously, with
the best filters available being used, but by far, incineration is the only way
to go, with present knowledge of agent...
do not bury this material in any land fill!
TSS
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
END...NOV...2013
LAYPERSON
MOM DOD 12/14/97 HEIDENHAIN VARIANT OF CREUTZFELDT JAKOB DISEASE a rare
sub-type of the infamous sporadic CJDs, just one of many strains of the sporadic
CJDs. ...UNKNOWN ROUTE AND SOURCE. ...TSS
Terry S. Singeltary Sr.
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Friday, October 09, 2015
ReplyDeleteTexas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
http://chronic-wasting-disease.blogspot.com/2015/10/texas-twa-chronic-wasting-disease-tse.html