Wednesday, January 23, 2019

CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019

Guidance on Specified risk material (SRM)

Although the Safe Food for Canadians Regulations (SFCR) came into force on January 15, 2019, certain requirements are being phased in over the following 12 to 30 months. For more information, refer to the SFCR timelines.

On this page

Part I: Removal of Specified Risk Materials
Part II: Enhanced feed ban controls and SRM management

Definitions

For the purposes of this guidance the following definitions apply:
Cattle
means animals of the species Bos taurus or Bos indicus and any animal that is the result of a cross with a Bos taurusor Bos indicus animal.; but does not include other ruminants such as bison, muskox, yak or water buffalo. All cattle crosses, therefore, will be subject to SRM guidelines and BSE policy. Canadian Food Inspection Agency (CFIA) inspection personnel will perform categorization of crosses by phenotypic (observable physical characteristics) examination. To challenge the inspector's phenotypic categorization for any possible disagreement, industry must provide documented proof of purebred status (e.g. yak or bison registration).
Specified Risk Materials (SRM)
means the skull, brain, trigeminal ganglia, eyes, palatine tonsils, spinal cord and dorsal root ganglia (DRG) of cattle aged 30 months or older, as well as the distal ileum of cattle of all ages.

Note: The brain, trigeminal ganglia, eyes, palatine tonsils, spinal cord, dorsal root ganglia and distal ileum are designated as SRM because, in Bovine Spongiform Encephalopathy (BSE) infected cattle, these tissues contain the BSE agent and may transmit the disease. The OTM skull, excluding the mandible and horns, is designated as SRM as well because of the high probability of it becoming contaminated at the time of stunning and during manipulation of the other tissues if their separate removal was permitted.
UTM
means cattle that are under 30 months of age.
OTM
means cattle that are 30 months of age or older.

Part I: Removal of Specified Risk Materials (SRM)

1.0 Introduction

These controls came into effect on July 24, 2003 and enhanced on July 12, 2007. The 2007 enhancements were introduced to mainly protect health of animals, whereas the 2003 SRM control requirements were introduced strictly to protect public health.
Part I of this document provides guidance on removal of SRM from cattle slaughtered in Canada in order to prevent tissues that may contain BSE infectivity from entering the human food chain. It is also a guidance to ensure that SRM does not enter the animal feed chain. The enhanced feed ban controls described in Part II of this guidance require the removal and effective segregation of all SRM tissues from raw material destined for the production of animal feed, pet food and fertilizers.
The information in this document pertains to requirements under Part I.1 of the Health of Animals Regulations, describing minimum standards beef slaughter and cutting/boning licence holders must meet to ensure that specified risk material neither enters human food nor the animal feed chain. These Health of Animal requirements will also meet the outcome of section 125 (1) (e) of the SFCR, meaning that the edible product does not contain any specified risk material (SRM). These practices have been historically considered as acceptable by international trading partners and fundamentally allow Canada to demonstrate its BSE surveillance and SRM controls.
Therefore, a license holder wishing to use alternate procedures to those described within must have them evaluated and approved by CFIA prior to their implementation.

1.1 Regulatory basis

Pursuant to Safe Food for Canadian Regulations (SFCR), specified risk material has the same meaning as in section 6.1 of the Health of Animals Regulations. (matériel à risque spécifié).
Under SFCR section 125 (1) (e), a licence holder may identify a meat product as edible only if the meat product is edible and is not contaminated, including that it does not contain any specified risk material.
Under SFCR section 155 (3), the licence holder must keep a meat product that is a specified risk material, contains a specified risk material or is derived from a specified risk material in a separate area of the inedible products area and must handle and destroy it in accordance with Part I.1 of the Health of Animals Regulations.
In addition, the licence holder must meet all the applicable provisions of the Health of Animals Regulations and Food and Drug Regulations.
The guidance is designed to meet the following objectives:
  1. to ensure removal of all specified risk materials (SRM); and
  2. to prevent cross contamination of edible meat products by SRM during slaughter and cutting/boning operations
  3. to ensure removal of all SRM from the animal feed chain

1.2 Preventive Control Plans

SRM is a food safety hazard and must be addressed in licence holders Preventive Control Plan (PCP) under the SFCR. When implementing PCP, licence holders are required to clearly identify Critical Control Points (CCPs) for animal aging (either by dentition examination or birth date documentation) and SRM removal. The licence holder is responsible for the development, implementation, and maintenance of control programs that address all components of this SRM removal guidance. These control programs are to be submitted to the CFIA for examination prior to their implementation and their implementation must demonstrate ongoing and effective control, including but not limited to, control over animal identification and aging, OTM carcass identification and marking, SRM removal and OTM carcass segregation. This is to make sure CFIA approved methods of preventing SRM cross contamination of product destined for the production of animal feed, pet food and fertilizer are consistent with the Health of Animal regulation components.

2.0 Cattle identification, age determination, marking and segregation of carcasses upon arrival and during slaughter/dressing, chilling, cutting and boning procedures

Licence holders slaughtering or cutting/deboning UTM and OTM cattle must develop and implement procedures for identifying and separating these two types of cattle from their arrival at the establishment throughout the slaughter process, and during chilling, and/or cutting/deboning operations.
At the slaughter establishment the identity of the cattle carcass and all its parts must be maintained until their final disposition is known. To achieve this, the Canadian Cattle Identification Agency (CCIA) and Agri-Traçabilité Québec(ATQ) ear tag will be attached, after its insertion into a plastic bag, to the fore shank of the carcass following hide removal.

2.1 Age determination, identification and marking of carcasses

Licence holders will reassess their Preventive Control Plan (PCP) and to develop a Critical Control Point (CCP) for age determination procedures (for example: by date of birth documentation review and/or dentition examination).
The age of cattle can be established by using reliable documentation that indicates the birth date of the animal or by examining the teeth. The birth date document, rather than dentition, provides the best means for determining the age of cattle. When documentation is available it should be used as the primary means of determining the age of animals.
Licence holders must maintain records of the age and identity of slaughtered cattle. The records are to include:
  • information regarding the procedures used to determine the age of animals
  • if age is determined by documentation, the document is to be maintained with the records for a period of two years from the date of slaughter
Determining age by birth date documentation
Submission of accurate birth date information by producers is strongly supported by the CFIA. Birth date information in the Canadian Cattle Identification Agency (CCIA) database, or the Agri-Traçabilité Québec (ATQ) database in the case of Quebec, is a CFIA recognized to dentition for domestic meat inspection purposes, and live animal or meat exports. The availability of acceptable birth date information on a timely basis will mean that dentition assessment should not be necessary.
The CFIA also recognizes the original copies of official birth date documents issued by registered breed associations.
Agriculture and Agri-Food Canada (AAFC) has a web page that offers more details on the Animal Pedigree Act as well as a full list of Incorporated Breed Associations.
Acceptable methods for determining the age of an animal in the CCIA or the ATQ database include either the actual date on which a calf is born or the first day of the calving period in which a group of calves was born. In cases where "estimated" birth dates are provided based on other methods, the date of birth is not to be accepted, and dentition will be used for aging.
CFIA will examine birth date documentation used by the licence holder for determining the age of cattle. If any deviations are observed at head inspection, CFIA will follow up on any discrepancy between birth date documentation and physical appearance of the head.
Loss of identification or no identification will result in the animal being aged by its dentition.
Determining age by dentition examination when no birth date documentation is provided
For the purposes of this guidance, cattle are considered to be aged 30 months or older (OTM) when they have more than two permanent incisor teeth erupted (that is, the first pair of permanent incisors and at least one tooth from the second pair of permanent incisors).
Note
For the purpose of this guidance, a permanent tooth is considered erupted when any part of the tooth is protruding through the gum. This will include teeth that have erupted behind or in front of the existing deciduous incisor. Cattle will be considered as less than 30 months of age (UTM) as long as the erupting third permanent incisor is not above the surface of the gum, whether it is at the back, on the top or at the front of the mandible. See Appendix Aof this guidance for illustration and pictures of bovine incisor teeth and the corresponding age.
Visual examination of the incisor teeth of each carcass occurs at or before the head inspection station.
The licence holder will examine the incisor teeth of each carcass, and will determine if the carcass is derived from an OTM animal. The designated trained employee examining the teeth must be able to recognize permanent incisor teeth and be knowledgeable of this guidance. Alternatively the licence holder may decide to treat all slaughtered animals as being derived from OTM animals. In such a case, examination of the incisor teeth would not be required.
Identification and marking of carcasses
The licence holder will apply following measures:
  • the identification and marking of both sides of the carcasses of OTM animals must be done as soon as possible after the carcass has been aged. The licence holder will apply one of the marks described in Appendix D by means of a stamp (for example, using blue edible ink) to each side of the OTM carcass.
  • the mark must be visible to the employee responsible for splitting carcasses in order to ensure the use of appropriate splitting saw. When a single saw is used for splitting all carcasses, it shall be cleaned and sanitized after splitting an OTM carcass if it is to be subsequently used to split a UTM carcass.
  • control and identity of the carcass, head and parts must be maintained. The head is identified as OTM by means acceptable to the Veterinarian with supervisory authority.
  • the licence holder must apply edible blue ink to exposed surfaces of the vertebral column of each OTM carcass side following removal of the spinal cord and before chilling. For proper identification the licence holder will apply edible blue ink to the vertebral canal and may include the vertebral body, however, the spinous (dorsal) processes should not be stained with ink as it compromises grading. All vertebrae including the sacrum will be stained with blue edible ink in order to achieve a readily visible mark at the time of cutting/boning.
  • application of the blue ink to the vertebrae shortly after the carcass has exited the carcass wash, occurs when the licence holder has a written program in place that can demonstrate ongoing effective controls, including a carcass identification and marking system that will ensure all OTM carcasses are properly identified and marked. The written program must be submitted to the Veterinarian with supervisory authority for examination prior to its implementation.
Licence holders of slaughter establishments may be able to employ other procedures providing the same outcome is achieved. For example, a licence holder may decide to treat all slaughtered cattle, or cattle slaughtered from a particular lot, as being derived from OTM animals. In such a case, SRM would be removed from all carcasses regardless of their age and there would be no need to examine incisor teeth for the purpose of age determination. However there would still be a requirement to apply one of the marks described in Appendix D by means of a stamp to each carcass side if the licence holder also slaughters UTM. Every vertebral column of OTM carcasses must be marked and stained as per the above procedures.

2.2 Control and segregation of carcasses during dressing, chilling, cutting and boning procedures

Slaughter establishments
Licence holders that slaughter UTM and OTM cattle will ensure that OTM animals are slaughtered as a definable group. The CFIA strongly recommends that the slaughter of the OTM group(s) proceed at the end of the production day, in order to facilitate operational control and verification of SRM removal. If a licence holder chooses to slaughter and segregate OTM cattle using alternative methodology, a written control program, that is able to achieve the same outcome, must be prepared and be submitted to the CFIA for examination. This must be reviewed and found acceptable to the Veterinarian with supervisory authority prior to implementation. The licence holder is responsible to ensure that the proposed segregation method meets all the eligible exporting requirements.
However, licence holders of all federal slaughter establishments will visibly group the carcasses of OTM cattle in the cooler and schedule the cutting/deboning of such carcasses at the end of the production day. Alternatively, a licence holder of a federal establishment could ship the carcasses to another federal establishment for cutting/deboning.
Licence holders of slaughter establishments will track the number of OTM cattle slaughtered in the establishment. The number of OTM cattle will be recorded after CFIA examination of the head is complete and before the carcasses have left the kill floor. The total number of OTM carcasses identified on the kill floor must reconcile with the number of carcasses found in the carcass cooler and the number of carcasses entering the cutting/deboning room or shipped from the establishment.
Cutting/deboning establishments
Licence holders of cutting/deboning establishments that receive sides and/or quarters of OTM cattle must develop and implement a control program to maintain the identity of these products until the vertebral column is removed and disposed as SRM. The procedures include:
  1. recording of the number of OTM carcasses/sides/quarters received and reconciliation of this number with the number of OTM carcasses deboned and cut-up;
    and
  2. cutting/deboning of such carcasses/sides/quarters at the end of the production day.
For domestic purposes it is not required to segregate meat by age category when boning of the vertebral column has been completed.

3.0 Stunning, dressing, boning and SRM removal

3.1 Dedicated SRM tools

The licence holder must use, except as detailed later in the following section of this guidance, dedicated tools (for example, knives), identified by colour-coding or another visual system, for all procedures involving the incision and direct or indirect handling of the tissues designated as SRM.

3.2 Stunning

During routine slaughter, the use of a penetrating percussion device which injects air into the cranial cavity or the use of pithing rods is not permitted. In the case of ante-mortem condemnation and euthanasia in the lairage (that is, non-ambulatory and compromised animals discarded as inedible), the use of such methods may be tolerated provided that the licence holder has in place a control program ensuring that OTM carcasses are entirely handled as SRM. Such a control program may include, for example, a marking procedure additional to the usual denaturation policy and/or letter of guarantee from the rendering/salvaging establishment. The outcome is to demonstrate that the licence holder can clearly segregate any OTM carcasses that have been exposed to such methods from those that have not, as well as ensuring that renderer or salvager receiving such OTM carcasses are fully aware that no material can be harvested as pet food or removed to the prohibited material stream from these carcasses. Once exposed to such methods, all tissues derived from any OTM carcass are considered SRM.
The licence holder must develop, implement and maintain an effective control system to collect brain tissue that has been externalized at the time of stunning prior to bleeding of OTM cattle or from all animals if UTM and OTM cattle are not identified before stunning. This control system must include measures to ensure brain matter does not enter or contaminate meat products, animal food products (for example, hides saved for gelatin or collagen, blood salvaged for edible and/or animal food including blood meal that can be used as feed for calves).
Brain tissue that has fallen on the floor must be discarded as SRM.
When OTM cattle are stunned by penetrative captive bolt, there is a strong likelihood that blood may be contaminated with SRM (neural tissue). The following methods are approved to prevent SRM-contamination of bovine blood that may be used in feeds and food for animals:
  • blood collected by open method from age verified UTM will be considered exempted material if it does not contain blood from a OTM animal (zero tolerance)
  • humane stunning using a non-penetrative method (for example, electrical kill stunning, ritual slaughter without stunning, etc.)
  • closed blood collection method (for example, hollow knife or cannula);
  • or any other method that is approved by the CFIA. The licence holder must develop control measures for the prevention of cross-contamination of the blood during the slaughter process and have a CFIA approved written protocol. For more information on blood collection during slaughter refer to enhanced animal health safeguards at Blood collection during slaughter.
The incidental stunning of OTM cattle poses a potential risk of SRM cross-contamination of UTM cattle skulls and any Meat and Bone Meal (MBM) produced from them. For more information on prevention of cross-contamination from incidental stunning of OTM cattle, refer to enhanced animal health safeguards at Incidental OTM cattle stunning and contamination with specified risk material (SRM) in slaughter of UTM cattle.
Refer to the tables below for disposition of face plates, that is, head hides from bovines. The licence holder must develop and maintain specific control program for this purpose.
1 Face plates from UTM animals
#OptionsOutcome
1AUTM Animals stunned by a penetrating or non-penetrating stunning device.Routine (non-SRM) inedible stream provided no cross-contamination with brain material or any other SRM from OTM animals takes place.
2 Face plates from OTM animals
#OptionsOutcome
2AOTM animals stunned by a non-penetrating stunning device (for example, electrical kill stunning, ritual slaughter without stunning, etc.)Routine (non-SRM) inedible stream unless cross-contamination with brain material or any other SRM from OTM animals takes place.
2BOTM animals stunned by a penetrating stunning device.Routine (non-SRM) inedible stream provided the leakage of brain tissue from the stun hole is prevented with CFIA approved methods such as the application of edible grease, tampons or other equivalent devices, and grossly visible brain material is removed from the face plate by trimming, washing, scraping and/or vacuuming.
2CThat are not processed as per options 2A or 2BSRM
Additional CFIA guidance on prevention of contamination of food, animal feed, pet food and fertilizer with SRM are available at:

3.3 Head separation and removal of skull, brain, trigeminal ganglia, eyes and tonsils

Cattle age should be determined prior to removing the head from the carcass. If this is not possible due to plant design, the head removal process is performed by using a knife not dedicated for SRM to cut most of the muscles and connective tissue attaching the head to the carcass. This results in partial separation of the head at the junction of the occipital condyles and the first cervical vertebrae.
A knife dedicated, uniquely identified (that is, colour coded) for SRM removal is used to sever the spinal cord and is rinsed and sanitized after each animal. A non-dedicated knife is then used to complete the removal of the head. Both knives are adequately rinsed and sanitized after each animal.
The skull including the brain, trigeminal ganglia, eyes, palatine tonsils of OTM cattle must be disposed of as SRM. The removal of the head must be achieved without contamination of the carcass or other meat products with SRM (that is, spinal cord, brain) or other contaminants. The licence holder must take measures to prevent the contamination of edible products (head meat and tongues for example) by SRM.
As soon as the inspection of the head is completed and the tongue and cheek meat have been harvested, the remainder of the head shall be placed without delay into a SRM leak proof container of suitable dimensions to prevent subsequent contact between the SRM head and any other meat products. Boning of the occipital area of the head including the area of the foramen magnum of OTM cattle is not permitted.

3.4 Palatine tonsils

Palatine tonsils are removed from the head of all cattle during the preparation of the head for inspection. Palatine tonsils are considered inedible material for cattle of all ages, and SRM for OTM cattle.

3.5 Tongue and cheek meat

The removal of the tongue, cheek meat and other edible portions must be achieved without contamination of the carcass and other edible meat products with SRM (that is, spinal cord, brain) or other contaminants.

3.6 Removal of the distal ileum

The distal ileum of all cattle, regardless of their age, is designated as SRM. Therefore, the distal ileum must be removed and disposed of as SRM in accordance with this guidance. The licence holder complies with this requirement by choosing one of the following two options:
  1. removal and disposal of all cattle small intestines with the ileo-cecal junction as SRM; or
  2. removal of the distal ileum from the small intestine and disposes of the removed distal ileum as SRM. To ensure the complete removal of the distal ileum, the ileo-cecal junction and at least 200 cm of the attached and uncoiled small intestine proximal to the ileo-cecal junction must be removed (see Appendix C of this guidance for a diagram of the cattle gastrointestinal tract). After the removal of the distal ileum, the remainder of the small intestines from cattle of all ages can be harvested as edible meat products, provided the intestines were found free of pathological defects, and are from carcasses approved for human consumption.
Under this option, the licence holder must develop, implement and maintain a control program within their PCP (for example, HACCP system) that ensures that the entire distal ileum is removed according to the specifications stated above. The program includes a description of the landmarks, procedures and equipment used to define and measure the distal ileum to be removed. In place of a measuring device, an alternate piece of equipment that consistently provides the same outcome is acceptable. Prior to its implementation, the control program must be reviewed and found acceptable to the veterinarian with supervisory authority.
The licence holder must also ensure that no piece of the distal ileum is included with any edible meat product or animal food product. If the large intestine is salvaged, there must be a control program in place that identifies the landmarks for the portion being salvaged. See Appendix C of this guidance.

3.7 Carcass splitting

For the carcass splitting saw the licence holder has the option either to use dedicated equipment or to ensure that the equipment used on an OTM cattle carcass is cleaned and sanitized before being used on a UTM cattle carcass or on carcasses and parts of carcasses of other food animal species. The level of cleaning required is equivalent to what is required when the carcass splitting saw becomes contaminated (that is, the organic material must be removed to ensure adequate sanitation). A device (for example, catch tray/ screen) must be installed to capture SRM fragments in areas where potential for SRM cross contamination exists.
The carcass splitting saw should separate the vertebral column in the midline to facilitate removal of the spinal cord. If the saw is equipped with an automatic rinse system, the exhaust water must be ducted away from carcasses and other edible and inedible products. The water-exhaust effluent should be adequately trapped. The trap should be emptied, cleaned and renewed as and when necessary. All residues should be treated as SRM and emptied into a SRMcontainer.
The licence holder shall immediately identify any incorrectly split carcasses and ensure that the spinal cord is properly removed in the evisceration area. Incorrectly split carcasses will not be approved by CFIA until the spinal cord is properly removed. The licence holder must take appropriate corrective measures to prevent the occurrence of incorrectly split carcasses.

3.8 Removal of the spinal cord and its verification

The spinal cord of OTM cattle is SRM. It must be removed in its entirety prior to stamping of the carcass sides with the meat inspection legend and before the carcass leaves the kill floor. Particular attention needs to be paid to the extremities of the vertebral canal, since it is usually in these areas that pieces of spinal cord are found. Lifting the spinal cord out of the vertebral canal can be achieved using a dedicated SRM knife. Other specialized tools can be used, but chain link gloves are not recommended unless covered with intact rubber/latex gloves to minimize the risk of gross cross-contamination.
The spinal cord of UTM cattle is not designated as SRM. It is not required to remove the spinal cord from UTM cattle carcasses. Nevertheless, it is strongly recommended to remove the spinal cord from all split carcasses on the kill floor before the final carcass wash as it is a practice recognized by the trading partners. This is further recommended to prevent incorporation of spinal cord tissue into any meat products, ensuring compliance with established meat product standards and simplifying verification measures.
Hand tools used for spinal cord removal should be uniquely identified (for example, colour coded) and dedicated to this purpose. Specialized spinal cord removal equipment, including vacuums can be used on all age categories of cattle. However, if used before final carcass inspection, specialized spinal cord removal equipment must be sanitized between each carcass. If used after carcasses have been approved, they must be sanitized as required and after each time they are used on an OTM cattle carcass before being subsequently used on UTM cattle carcasses or on carcasses of other food animal species.
Licence holder verification of the complete spinal cord removal is one of the most important control points. The licence holder must make a thorough check of every carcass side to ensure that no remnants of spinal cord are present before the carcass is marked with the meat inspection legend. When any spinal cord remnant is discovered, the carcass must be retained for immediate rework by the licence holder (that is, zero tolerance policy applies).
In the case of carcasses that are split after chilling (veal carcasses), the spinal cord should be removed during boning/cutting operations if the vertebral column is split in a federally inspected establishment.

3.9 Removal of the dorsal root ganglia

It is the licence holder's responsibility to ensure SRM is not incorporated into any edible meat products. The dorsal root ganglia (DRG) from OTM carcasses must be removed and disposed of as SRM. The vertebral column removal will most likely be done in the cutting and boning room after carcass chilling. In order to ensure complete removal of DRG, the vertebral column of OTM cattle (excluding the vertebrae of the tail, the dorsal and transverse processes of the thoracic and lumbar vertebrae and the wings of the sacrum) must be removed and disposed of as SRM. Cutting and boning procedures used to remove the OTM vertebral column shall not cause the removal of DRG with the edible muscle tissue. As a best practice, the cut separating the edible muscle from the vertebral column should be made approximately 2.5 cm (1 inch) from the vertebral arch to ensure no DRG is inadvertently included with the edible meat.
OTM carcass sides or quarters with the vertebral column attached (that is, DRG not removed) can be shipped under CFIA permit from a federal slaughter establishment to another federal establishment if the following controls are in place.
Shipping OTM carcass sides or quarters with the vertebral column attached to non-federally inspected facilities is not permitted if there is intent to trade to another province or to export.
Slaughter/shipping establishments
Slaughter establishments that do not remove DRG from vertebral columns on-site will have to implement identification and shipping control system satisfactory to the CFIA. The controls should include written confirmation that the receiving plant has a verifiable control system in place and an agreement and notification system regarding the number of carcasses sides or quarters to be expected exist between both establishments.
Receiving establishments
The receiving establishment must have a CFIA permit to receive carcasses containing SRM. The receiving establishment must have a verifiable control system in place which will demonstrate to the satisfaction of the CFIA that the sections of the vertebral column containing DRG are removed and appropriately disposed of as SRM. The receiving establishment must also advise the slaughter establishment of the number of OTM carcasses that they have received.
Note
The vertebral column of OTM cattle must not be used as raw material in the preparation of mechanically separated meat or finely textured meat.

3.10 Verification by the licence holder of SRM removal and rework

The licence holder must verify the complete removal of all SRM. Any carcass or part that is found to be harbouring fragments of SRM (for example, spinal cord) must be retained by the licence holder for immediate rework and subsequent presentation for further examination by the licence holder. The licence holder should have a system which allows retention and rework of carcasses harbouring residual SRM to occur successfully and without gross SRM cross contamination to meat products. The licence holder must demonstrate control of the system at all times.

4.0 SRM handling and disposition

This section describes effective separation of SRM from the carcass, provisions for storage of SRM and hygienic standards associated with floor waste and inedible containers. Because of structural differences between establishments, procedures for separating and isolating the various SRM may vary. Generally, separation of SRMshould occur as soon as possible and care must be taken to avoid contamination of edible and inedible products and the establishment environment by SRM.

4.1 Handling of SRM within the establishment

SRM should be separated from carcasses at the earliest opportunity during the dressing process. SRM should be placed in dedicated containers without delay and regularly moved to a designated area in the inedible products section for SRM staining. This must include all SRM separated from the carcass, SRM from the floor and all others debris collected in the SRM areas. Basic principles of hygiene must be observed at all times.

4.2 Floor waste

Areas where SRM is removed or handled must be regularly attended to by plant employees assigned this function. Systems for containing gross debris and operational cleaning of these areas are important. Carcass material and debris shovelled or squeegeed from the floor in areas where SRM is removed or handled and any debris collected from the channels and drain covers/traps derived from these areas must be disposed of as SRM and deposited in dedicated SRM containers. Collection of SRM from drain covers and traps must occur daily.
Where there are effective controls to prevent floor from contact with SRM, floor waste and debris collected from the corresponding drain covers and traps do not need to be disposed of as SRM. An acceptable method of containing SRMin areas where SRM is removed or handled to prevent extensive floor contamination with SRM is through the implementation of strategic physical barriers such as troughs, trays, raised floor curbings or barriers of equivalent effects. The licence holder should have a written program in place, to the satisfaction of the CFIA, to prevent the cross-contamination of floor from SRM tissues in these specific areas (see Floor waste and Wastewater materials).

4.3 SRM containers

It is important that all SRM and debris are contained within dedicated leak proof containers clearly and indelibly marked on the outside with the words "Specified Risk Material / Matériel à risque spécifié" or "SRM / MRS" in both official languages.

4.4 Cleaning of SRM containers

The licence holder ensures that:
  • all equipment and containers used in the handling of SRM are cleaned and sanitized after being emptied and prior to reuse
  • dedicated inedible and SRM containers are visibly clean at all times. If containers are being returned by a rendering company in an unclean state they are not be used until they are cleaned and sanitized
  • cleaning of SRM containers does not occur in area where potential contamination of the meat products and non-SRM inedible may occur. The cleaning and sanitizing of SRM containers is an integral part of the cleaning schedule of the premises, and verified during the pre-operational inspection
  • dedicated inedible containers and equipment, such as chutes, augers etc, are cleaned and sanitized using a non-food chemical that is suitable for use following accidental contamination with SRM and prior to reuse
  • blood and non-ruminant dedicated containers and equipment, if accidentally cross-contaminated with SRM are cleaned, and disinfected prior to reuse using a suitable priocidal chemical

5.0 SRM controls

The licence holder is responsible for the development, implementation, and maintenance of documented control programs that address all the components of this SRM guidance including ante mortem inspection, age determination, carcass identification and SRM removal. The control programs must ensure compliance with the relevant provisions of the Safe food for Canadian Regulations and the Health of Animals Regulations with respect to the control and disposition of bovine SRM and inedible material, including animals that are found dead on arrival or die of the causes other than the slaughter in the establishment. Licence holders are required to reassess, and if required modify, their PCP so that the food safety hazards of BSE are clearly stated and controlled.
The licence holder and all staff directly involved should have demonstrable knowledge of the establishment's SRMcontrol programs and be able to demonstrate with accurate records that the SRM controls they have put in place have been implemented in practice, resulting in full compliance with the regulations and guidance. The licence holder's SRMcontrol programs must be auditable and verifiable.

Part II: Enhanced feed ban controls and SRM management

6.0 Introduction

The Canadian government implemented a ruminant to ruminant feed ban in 1997 to limit the spread of BSE. That feed ban prohibited the feeding of most mammalian proteins to ruminant animals, such as cattle, sheep and goats. Control measures related to the enhanced feed ban control regulations that came into effect on July 12, 2007 prevent accidental exposure of susceptible animals to BSE and accelerate the time for the eradication of BSE from the national cattle herd. The enhanced feed ban controls require the removal and redirection of all SRM tissues from animal feed, pet food and fertilizers, as are removed from human food (Part I of this guidance). To effectively implement these controls, all SRM be segregated from other edible and inedible materials, identified by staining; and handled appropriately until disposal.
In every establishment where SRM is handled, the licence holder will implement the practices described in Part II of this guidance, as required.

6.1 Objectives

The enhanced feed ban regulations came into effect on July 12, 2007. The guidance is designed to ensure removal of all SRM from the animal food chain in a manner that minimizes risks associated with:
  1. potential adulteration or cross-contamination of ruminant animal feed with prohibited proteins of ruminant origin; and
  2. potential on-farm misuse of feed containing prohibited protein of ruminant origin.

6.2 Control programs

The licence holder is responsible for the development, implementation, and maintenance of control programs that address all components of this enhanced feed ban control guidance. These control programs are to be reviewed and approved by the Veterinarian with supervisory authority (or IIC as is appropriate) and their implementation must demonstrate ongoing and effective controls over SRM segregation, staining, shipping/ transportation, record keeping and compliance with the CFIA permitting process.

7.0 Collection, segregation and staining of SRM

7.1 Specified Risk Materials (SRM)

Licence holders involved in the slaughter of cattle and/or the cutting/boning of bovine carcasses/quarters shall collect and dispose of the following materials as SRM.
SRM removed from cattle carcasses
This includes SRM tissues removed from cattle carcasses during slaughter, dressing or cutting/ deboning operations (Part I of this guidance).
Animals condemned at ante mortem, post mortem, deadstock and bovine fetuses
The licence holder ensures the following controls are in place:
  • animals condemned at ante mortem and cattle that die from causes other than slaughter are handled as SRM, unless the SRM has been removed from these carcasses.
  • immediate and direct conveyance of the dead stock to a designated area in the inedible product section for staining and disposal in accordance with the Health of Animals Regulations (see section 7.3).
  • carcasses of condemned or dead animals from which the SRM has not been removed are denatured by staining with a wide stripe from head to tail (contrasting with the animal's coat colour) before shipping to another location under CFIA permit (see section 7.3).
  • deadstock collected by companies solely dedicated to SRM (all trucks, all equipment, entire premises) may mark a lesser amount of the deadstock carcasses (for example, just the head). Denaturation of such carcasses by injecting a suitable agent is optional
  • the bovine carcasses condemned at post mortem inspection must be treated as SRM unless they have had all the SRM removed. Once SRM has been removed, the rest of the carcass can be disposed of according to Section 155 of the SFCR
  • an unborn fetus/calf recovered from the uterus of a cow slaughtered in a federal establishment is non-SRM. Any term-fetus with body hair or newborn calf that is found on the ground in side the establishment is SRM, unless the distal ileum has been removed from such animals.
Floor waste
The licence holder ensures that the following controls are in place for management of floor waste:
  • in beef slaughter establishments, the floor waste from areas where SRM is removed or handled will be considered SRM. When there are no effective controls to contain the floor waste generated from areas where SRM is removed or handled, carcass material and debris shovelled or scraped from the floor and debris collected from the channels and drain covers associated with these areas must be disposed of as SRM
  • where there are effective controls to prevent floor from contact with SRM, floor waste and debris collected from the corresponding drain covers and traps do not need to be disposed of as SRM. An acceptable method of containing SRM in areas where SRM is removed or handled to prevent extensive floor contamination with SRM is through the implementation of strategic physical barriers such as troughs, trays, raised floor curbings or barriers of equivalent effects. The licence holders should have a written program in place, to the satisfaction of the Veterinarian with supervisory authority, to prevent the cross-contamination of floor from SRM tissues in these specific areas
  • the floor waste generated in other areas, without any contact with SRM tissues, will not be considered SRM. This is also applicable in areas where the distal ileum (slaughter establishments) and the OTM vertebral columns (cutting and boning rooms) are removed because the SRM is effectively contained within these tissues. However, the licence holders should have a written program in place, to the satisfaction of the Veterinarian with supervisory authority, to limit the cross-contamination of floor from SRM tissues in these areas
Wastewater materials
The licence holder ensures that the following controls are in place for management of wastewater materials:
  • in beef slaughter establishments, the animal material and debris recovered from wastewater must be disposed of as SRM if there are no controls in place to protect the floor from SRM contamination in areas where SRM is handled or removed. To retrieve this material, a screening system consisting of screens with apertures or a mesh size of no more than 4 mm diameter is in place as a step in the treatment of wastewater
  • all animal materials and debris retained in this screening system is collected and disposed of as SRM
  • no grinding or maceration shall take place which could facilitate the passage of animal material through the pre-treatment process. The wastewater beyond this screening system will not be subjected to CFIA's SRM controls but shall be treated in accordance with relevant provincial, municipal or environment legislations.
  • animal material and debris recovered from wastewater screening systems and/or any downstream treatment system, will not need to be treated as SRM if, there are effective controls in place to prevent the wastewater and floor debris from becoming contaminated in areas where SRM is handled or removed
  • the licence holder must be able to demonstrate that materials and debris recovered originated from a non-SRM or SRM controlled area and/or that SRM effluent originating from an SRM area has been treated by passing through a screening system consisting of screens with apertures or mesh size of no more than 4 mm diameter
  • licence holders who wish to exempt the materials and debris recovered from the wastewater derived from the slaughter floor as SRM must have written program in place to the satisfaction of the veterinarian with supervisory authority.

7.2 SRM containers

SRM must be collected and placed in dedicated leak proof SRM containers without delay and regularly moved to a designated area in the inedible products section for staining. The SRM containers must be clearly and indelibly marked on the outside with the words "Specified Risk Material / Matériel à risque spécifié" or "SRM / MRS" in both the official languages.
Contaminants, such as hydraulic fluids, heavy metals and other chemicals, must not be discarded into SRM containers since tallow extracted from rendered SRM is used in animal feeds, cosmetics, soap, etc. The inclusion of such contaminants may pose animal and public health risks.

7.3 Segregation and staining of SRM

The licence holder is responsible for the segregation and staining of SRM after its removal during slaughter or cutting/ deboning. All SRM must be transferred to a dedicated leak proof container/ trailer in a designated area in the inedible products section for staining. It must be conspicuously stained with an indelible marking dye approved by the CFIA (for example, denaturing agent). Carcasses containing SRM (that is, vertebral columns of OTM carcasses containing DRG) must also be conspicuously stained with an indelible marking dye approved by the CFIA (that is, blue meat marking ink).
The stain should be applied to each layer of SRM so that the stain is visible on all surfaces that is, every time the SRMis transferred to a common SRM staining container or trailer, it has to be stained by spraying. A list of denaturing agents and dyes that have been historically considered suitable for use can be obtained from the Health Canada's reference Listing of Accepted Construction Materials, Packaging Materials and Non-Food Chemical Products Database.
The licence holder develops, implements and maintains control programs with the following measures:
  1. segregating and staining of SRM in dedicated SRM containers following its removal from cattle carcasses.
    Notes:
    1. if the licence holder chooses not to segregate SRM from other inedible tissues, all inedible material mixed with the SRM will be considered to be SRM and will have to be stained.
    2. staining requirements would not apply if all the inedible parts of cattle carcasses do not leave the premises (on-site disposal).
  2. marking carcasses of condemned or dead animals from which the SRM has not been removed with a wide stripe down the back of the head and length of the spine using a dye (contrasting with the animal's coat colour) that is conspicuous, indelible and safe for consumption by animals before shipping to another location under CFIApermit. Deadstock being collected by companies solely dedicated to SRM (all trucks, all equipment, entire premises) may mark a lesser amount of the deadstock carcasses (for example, just the head). This would not apply if the carcasses do not leave the premises (on-site disposal).

8.0 Shipping of SRM from the establishment

8.1 Shipping of SRM from the inedible are of the establishment

The Health of Animal Regulations require that no person shall transport SRM to another premise unless it is stained in accordance with the provisions of the Acts and Regulations and it is in a container marked on the outside with the words "Specified Risk Material / Matériel à risque spécifié" or "SRM / MRS" in both official languages.
Licence holders of cattle slaughter and/or cutting/deboning establishments must collect SRM in dedicated leak proof containers (see section 7.0). Only properly identified and stained SRM can be shipped from federal establishments. The licence holder and SRM transporter must maintain records for SRM shipped from the establishment in accordance with section 9 of this guidance.
All SRM, if moving from the premises of origin to another location, in any form with the sole exception being laboratory submissions (level 2 or higher laboratory), must be transported under a CFIA permit. The licence holder of the shipping establishment must develop, implement and maintain a control program that ensures only transport vehicles with a valid CFIA permit are used to remove SRM from the establishment. The responsible CFIA Inspector will verify the licence holders control program.

8.2 Shipping of OTM carcasses containing DRG

Slaughter/shipping establishments
Slaughter establishments that do not remove vertebral columns containing DRG from OTM carcasses on-site have to implement identification, segregation and shipping controls satisfactory to the CFIA (see part 2.2 and part 3.9 of this guidance). The licence holder of a slaughter/ shipping establishment must keep daily records that contain the information stated in section 9 of this guidance.
OTM carcass transporters
All SRM, if moving from the premises of origin to another location, in any form with the sole exception being laboratory submissions (level 2 or higher laboratory), must be transported under a CFIA permit. Licence holders and owners of companies or vehicles who wish to transport OTM carcasses should contact the Veterinarian with supervisory responsibilities/Inspector In-Charge of the establishment or the local CFIA Animal Health District Office for permit application information. Transportation of the SRM must be done in accordance with the conditions of the permit. The transporter will keep records in accordance with the issuance of the permit, the Health of Animals Regulations and section 9 of this guidance. The vehicle/trailer transporting OTM carcasses must be cleaned prior to reloading in accordance with the licence holders written program.
Receiving establishments
The receiving establishment must have a CFIA permit to receive carcasses containing SRM. Licence holders who wish to receive SRM must submit a permit application to the Veterinarian with supervisory responsibilities/Inspector In-Charge of the establishment or local CFIA Animal Health District Office. The application includes written procedures documenting design and operating parameters for the site/facility. The receiving establishment must have a verifiable control system in place (see section 2.2 and section 3.9). The receiving establishments must keep records that contain the information stated in section 9 of this guidance.

8.3 On-site disposal

Inquiries regarding the acceptability of an on-site disposal method should be directed to local CFIA Animal Health District Office. When SRM is treated, confined, or destroyed on-site, the licence holder will keep daily records that include the name and address, date of slaughter and SRM removal, the combined weight of SRM or the number of carcasses (if applicable), the number of the approved tags (CCIA, ATQ etc.) and the date on which and the manner in which the SRM or the carcasses were treated, confined or destroyed (refer to section 9 of this guidance).

9.0 Record keeping

SRM records required by the Health of Animals Regulations

Section 6.23(1-2) of the Health of Animals Regulations requires that SRM records be maintained for at least 10 years by every person who:
  1. is required to remove or stain SRM;
  2. collects the carcasses of cattle containing SRM that died or were condemned at the ante mortem; or
  3. receives SRM or carcasses containing SRM from another person.
In addition to the requirements of this section, the licence holders will maintain additional SRM records as indicated earlier in this guidance.
The licence holder of an establishment that removes (at pre-slaughter, slaughter or OTM deboning), stains, ships, transfers or receives SRM (including meat products containing SRM) shall keep a record for each day on which the SRM is removed, stained or received or the carcasses containing SRM are collected or received. The licence holder must maintain records for 10 years that contain the following information where applicable:
  1. the name of the licence holder and address of the establishment;
  2. the date of SRM removal, staining, shipping, transporting or receiving;
  3. the weight of the SRM, as well as the number of carcasses if applicable, that is shipped; transported or received;
  4. the number of deadstock and animals condemned at ante mortem;
  5. the name of the dye used to identify the SRM or carcasses;
  6. from deadstock containing SRM, the approved ear tag number (CCIA or ATQ) as defined in section 172 of the Health of Animals Regulations; or the information referred to in the paragraph 187(2)(a);
  7. the name and address of the person, company or establishment that transports the SRM or carcasses containing SRM from the establishments or to the establishment; and
  8. the name and address of the person or company that received or will receive the SRM (renderers, deadstock collectors, OTM receiving establishments, etc.).

10.0 Compliance and verification

Licence holders responsibilities

The licence holder will develop, implement, and maintain documented control programs that address all components of regulations and associated guidance including SRM collection, segregation and staining, shipping/ transportation, record keeping and compliance with CFIA permitting process.
The control programs must ensure compliance with the relevant provisions of the Safe food for Canadian regulations and the Health of Animals Regulations with respect to the control and disposition of bovine SRM and inedible material, including animals that are found dead on arrival or die of the causes other than the slaughter in the establishment. The licence holders SRM control programs must be auditable and verifiable to the satisfaction of the CFIA officials.


PRION 2018 CONFERENCE

P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge 

Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. 

reading up on this study from Prion 2018 Conference, very important findings ;

***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. 

***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.

PRION 2018 CONFERENCE ABSTRACT


WEDNESDAY, OCTOBER 24, 2018 

Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy



MONDAY, JANUARY 09, 2017 

Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle 

CDC Volume 23, Number 2—February 2017 

*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.

*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.


TUESDAY, AUGUST 28, 2018 

USDA finds BSE infection in Florida cow 08/28/18 6:43 PM


WEDNESDAY, AUGUST 29, 2018 

USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT


WEDNESDAY, AUGUST 29, 2018 

Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018


***> P.108: Successful oral challenge of adult cattle with classical BSE

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. 

We are further examining explanations for the unusual disease presentation in the third challenged animal.


***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama

National Institute of Animal Health; Tsukuba, Japan

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.


P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion

***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion

Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada

Keywords: Atypical BSE, oral transmission, RT-QuIC

The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.

The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.

Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.





Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy 

Ivett Ackermann1 , Anne Balkema‑Buschmann1 , Reiner Ulrich2 , Kerstin Tauscher2 , James C. Shawulu1 , Markus Keller1 , Olanrewaju I. Fatola1 , Paul Brown3 and Martin H. Groschup1* 

Abstract 

In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earli‑ est time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplifcation (PMCA) assays. For the frst time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indi‑ cate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.

In summary, our study demonstrates for the frst time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confrm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Terefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.


A study comparing preclinical cattle infected naturally with BSE to clinically affected cattle either naturally or experimentally infected with BSE by the oral route found the most abundant PrPSc in the brainstem area (39), which is consistent with ascension to the brain from the gut by sympathetic and parasympathetic projections (40). In our experiment, abundant prions were observed in the brainstem of cattle with clinical signs of BSE, which is similar to the amount in their thalamus or midbrain regions. Interestingly, prions in the brainstem of cattle with clinical evidence of BSE seeded the RT-QuIC reactions faster than any other brain region despite the brainstem area having lower EIA OD values (Table 2) in comparison to other brain regions. This suggests that higher concentrations of prions do not necessarily seed the reaction faster. Perhaps prions of the brainstem exist in a preferred conformation for better conversion despite being present in lower concentrations.

snip... 


The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

see ;


CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."

OR, what the Honorable Phyllis Fong of the OIG found ;

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain


IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe. I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved... 

Monday, May 05, 2014

Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing


Friday, December 5, 2014

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide


IN A NUT SHELL ; (Adopted by the International Committee of the OIE on 23 May 2006) 11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,


MONDAY, JANUARY 21, 2019 

Bovine Spongiform Encephalopathy BSE TSE Prion Surveillance FDA USDA APHIS FSIS UPDATE 2019


Prion Conference 2018

O5 Prion Disease in Dromedary Camels 

Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria. 

Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions. 

Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues. 

Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie. 

PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected. 

The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel. 

Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure. 


CDC

New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES

Mad Camel Disease

Volume 24, Number 6—June 2018 Research 

Prion Disease in Dromedary Camels, Algeria
Abstract

Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.

SNIP...

The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries.
Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.
In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***


USA MAD COW CASE 2018 FLORIDA

WEDNESDAY, SEPTEMBER 26, 2018 

JAVMA In Short Update USDA announces detection of atypical BSE


ZOONOSIS OF SCRAPIE TSE PRION

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). 

Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 


***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
***> why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. 

***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. 

***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY



Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 


***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***

Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.



Saturday, December 15, 2018 

***> ADRD Summit RFI Singeltary COMMENT SUBMISSION BSE, SCRAPIE, CWD, AND HUMAN TSE PRION DISEASE December 14, 2018


SATURDAY, JANUARY 5, 2019 

Low levels of classical BSE infectivity in rendered fat tissue 


***> FRIDAY, DECEMBER 14, 2018 MAD COW USA FLASHBACK Texas Style

FRIDAY DECEMBER 14, 2018 


THURSDAY, JANUARY 3, 2019 

MAD COW USDA DISEASE BSE TSE Prion 


THURSDAY, OCTOBER 22, 2015 

Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened

HOW TO COVER UP MAD COW DISEASE IN TEXAS




WEDNESDAY, AUGUST 29, 2018 

OIE Bovine spongiform encephalopathy, United States of America Information received on 29/08/2018 from Dr John Clifford, Official Delegate, Chief Trade Advisor, APHIS USDA

''The event is resolved. No more reports will be submitted.''

well, so much for those herd mates exposed to this atypical BSE cow, and all those trace in and trace outs.

The OIE, USDA, and the BSE MRR policy is a joke, a sad, very sad joke...


Saturday, July 23, 2016

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016


Tuesday, July 26, 2016

Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016


Monday, June 20, 2016

Specified Risk Materials SRMs BSE TSE Prion Program


Terry S. Singeltary Sr.





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