FINAL REPORT OF A MISSION CARRIED OUT IN THE UNITED KINGDOM
FROM 19 TO 29 JANUARY 2010
IN ORDER TO EVALUATE MEASURES CONCERNING BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)
In response to information provided by the Competent Authority, any factual error noted in the draft report has been corrected; any clarification appears in the form of a footnote.
This report describes the outcome of a Food and Veterinary Office specific audit carried out between 19 to 29 January 2010, which formed part of the general audit 2009 of the United Kingdom conducted under the provisions of Regulation (EC) No 882/2004.
As part of the general audit, the objective of this specific audit was to evaluate that official controls are carried out in conformity with the multi-annual national control plan drawn up in accordance within Article 41 of Regulation (EC) No 882/2004. The specific audit evaluated the implementation of certain protective measures against Bovine Spongiform Encephalopathy (BSE).
Overall, the report concludes that active surveillance was satisfactory and that some progress has been made as regards the quality of samples for BSE testing. Passive surveillance was appropriately carried out and measures related to suspect animals and following confirmation of BSE were implemented in line with Community requirements.
The arrangements in place for collection and handling of specified risk material were mainly satisfactory, although there were some weaknesses in commercial documentation.
In Great Britain, the identification of users of fish meal and feed containing fish meal has significantly progressed but the registration and authorisation process of such users was far from being completed. Some important steps have been taken to improve the risk prioritisation of inspections, but it remains affected by an incomplete knowledge of some key feed operators. In Northern Ireland, the identification of users of feed containing fish meal was still on-going. The priorities set for inspections in the national control programme were not complied with, resulting in very few visits to on-farm mixers and mixed species farms, including those using fish meal or feed containing fish meal; moreover, the prioritisation of feed ban controls did not take account of the significant use of bulk feather meal as organic fertilisers on farms. The large majority of the said farms were therefore not visited despite several incidents concerning cross-contamination of feed with feather meal that occurred in the recent past. In addition, limited enforcement actions and sanctions had been taken following a number of breaches of feed ban rules.
The report makes a number of recommendations addressed to the United Kingdom competent authorities aimed at rectifying the shortcoming identified and further enhancing the implementing and control measures in place.
5.5 FEED BAN
5.5.1 Requirements along the chain
Art. 7 of Regulation (EC) No 999/2001 prohibits the feeding to farmed animals of products derived from animals in accordance with the conditions laid down in its Annex IV, which establishes a number of derogations from the said prohibition and specific conditions for the application of such derogations.
The relevant recommendation of report 8316/2006 concerned the authorisation of establishments using fish meal for the production of feed, the use of feed containing fish meal on mixed species farms and the labelling of feed containing fish meal. In response to this recommendation, the CCA undertook to take all necessary actions in the following National Feed Audit (NFA) programmes. Since the last mission, the procedure in place for authorising and registering users of fish meal or other derogated products derived from animals, which is described in detail in report 8316/2006, has been simplified. In Great Britain, authorisations to produce feed containing derogated products derived from animals have replaced registrations as in both cases the requirements to comply with were deemed very similar. Official permission to store or use complete feed containing derogated products derived from animals on premises with ruminants present is granted following a satisfactory official inspection.
According to DARD and DEFRA, there is no evidence of use of dicalcium or tricalcium phosphate of animal origin in the United Kingdom. Concerning the use of blood and blood products, both the CCAs declared their use is very limited, and one industry assurance scheme in the UK includes a voluntary ban on the feeding of blood products to pigs.
Commission Regulation (EC) No 956/2008 has not yet been transposed into BSE domestic legislation, which therefore does not provide for a derogation in relation to the use of fish meal to unweaned farmed animals of the ruminant species. Consultations are on-going or about to be launched by the different CCA in order to amend the different domestic legislations. A few samples on milk replacers have been taken in Great Britain but were tested negative for the presence of fish meal. According to DEFRA, little interest has been expressed by the feed industry and farmers associations as regards the use of fish meal in milk replacers.
The mission team noted that:
• Lists of authorised users of fish meal were being kept by AH and DARD. However, in Northern Ireland, the activities indicated on the list of users did not always reflect the actual activities carried out by the operators.
• In Great Britain, important progress has been made in the identification, authorisation and permitting process of users of fish meal and feed containing fish meal. AH achieved such progress by requesting feed mills to provide the lists of purchasers of fish meal and feed containing fish meal. As a result of this exercise, around 10,000 purchasers were identified. The central operations delivery team of AH, which has taken over the authorisation and permissions database, had already contacted around 5,200 of these premises and 393 had been sent to AHROs and AHDOs for inspections, resulting in 329 of them being authorised or permitted. However, the identification process is still incomplete as one half of the purchasers identified (around 5,000) has still to be contacted.
• The tracing exercise carried out centrally by AH focused on farms purchasing fish meal and feed containing fish meal. According to AH, intermediaries or feed stores present on the lists obtained and possibly supplying such feed to other farms or feed operators have not yet been contacted. In some of the AHOs and AHDOs visited, AH staff requested updates of lists of purchasers of feed containing fish meal from local feed business operators. In some cases, such lists (which contained significant proportions of new purchasers) have been sent to AH central operations delivery team (further delaying their authorisation or permission) while in other cases they have been dealt with at local level.
• AH staff inspecting ABP plants, in particular those handling fish meal, have been requested to forward to the NFA lead veterinary officer any relevant information allowing the identification of users. However, importers, brokers or storage plants have not yet been requested to provide list of purchasers of fish meal and it could be confirmed that a limited feed back has been received from AH staff performing ABP inspections; for instance, not all plants involved in bulk storage of fish meal were known by the NFA lead veterinary officer.
• In Northern Ireland, DARD had recently obtained lists of purchasers of feed containing fish meal from feed mills. Around 70 farms keeping ruminants and non-ruminants and buying such feed have been identified and are in the process of being registered.
• All authorised users of fish meal visited were also producing ruminant feed. Adequate arrangements, including physical separation and dedication of equipments or means of transports, were in place to avoid cross-contamination of ruminant feed except in one onfarm mixer visited, where there was an incomplete physical separation between the storage of bulk feed material used for ruminant feed and the area where feed containing fish meal was manufactured.
• Labelling requirements for fish meal and feed containing fish meal were complied with and in most cases a warning sentence was printed on the bags. In one on-farm mixer visited, bags of fish meal were not properly labelled but this had been identified by AH which had taken immediate corrective actions.
• On a number of consignments of imported fish meal checked during the mission, it was verified that microscopy testing had been carried before they were released for free circulation.
Legal and administrative arrangements are in place in order to ensure that the use of products derived from animals is subject to the requirements of Art. 7 of Regulation (EC) No 999/2001 and there is a good level of compliance amongst the feed operators using derogated products derived from animals. However, even if the authorisation and permission process of such users has made important progress since the last FVO mission, it is still far from being completed. As a consequence, it can not be yet ensured that the use of derogated products derived from animals is always carried out in accordance with the conditions established in Annex IV to Regulation (EC) No 999/2001.
6 OVERALL CONCLUSIONS
Active surveillance was satisfactory and that some progress has been made as regards the quality of samples for BSE testing. Passive surveillance was appropriately carried out and measures related to suspect animals and following confirmation of BSE were implemented in line with Community requirements.
The arrangements in place for collection and handling of specified risk material were mainly satisfactory, although there were some weaknesses in commercial documentation.
In Great Britain, the identification of users of fish meal and feed containing fish meal has significantly progressed but the registration and authorisation process of such users was far from being completed. Some important steps have been taken to improve the risk prioritisation of inspections, but it remains affected by an incomplete knowledge of some key feed operators.
In Northern Ireland, the identification of users of feed containing fish meal was still on-going. The priorities set for inspections in the national control programme were not complied with, resulting in very few visits to on-farm mixers and mixed species farms, including those using fish meal or feed containing fish meal; moreover, the prioritisation of feed ban controls did not take account of the significant use of bulk feather meal as organic fertilisers on farms. The large majority of the said farms were therefore not visited despite several incidents concerning cross-contamination of feed with feather meal that occurred in the recent past. In addition, limited enforcement actions and sanctions had been taken following a number of breaches of feed ban rules.
5.1 BSE SITUATION
The number of BSE positive cases in Great Britain and Northern Ireland is shown in the table below (data as of 31 December 2009; information provided by the DEFRA).
The last BSE positive case identified by passive surveillance in a herd without previous BSE cases occurred in 2007. In 2009, six BSE positive cases were animals born before 1 August 1996.
Great Britain Northern Ireland
Passive surveillance Active surveillance Passive surveillance Active surveillance
2007 7 46 0 14
2008 2 31 0 4
2009 1 8 0 3
snip...please see full text here ;
16 March 2010
Annex 1 – Comments on DG(SANCO) 2010-8344 – MR DRAFT
Section Reference Page UK Comment Abbreviations III
Amend “Department for Agriculture and Rural Development” to “Department of Agriculture and Rural Development”
With regards to the sentence commencing “Representatives of the Food Standard Agency and of the Meat Hygiene Service”, note that there were no representatives of the Food Standards Agency present at the slaughterhouse in England.
The sentence “Since then , BSE cases were notified either in sub-populations of fallen stock or animals slaughtered for human consumption” is incorrect as there were cases detected as clinical suspects, by passive surveillance in 2008 and 2009.
The sentence commencing “In 2009, the last...” should be amended as follows “In 2009, six BSE positive cases were animals born before 1 August 1996”
5.2.1 (Bullet 1) 4
Amend “Cattle Cohort and Offspring System” to “Offspring and Cohort Cull (OCC) System”.
5.2.2 (Bullet 2) 5
Amend “In one of the slaughterhouse visited...” to “In one of the slaughterhouses visited...”
In sentence commencing “The relevant recommendations of report...” amend “from being slaughter” to “from being slaughtered”.
5.2.3 (First full paragraph on page) 6
Replace paragraph beginning “According to DARD...” with “According to DARD, several changes have been introduced in procedures concerning the extraction and entry of data from and onto APHIS. The Required Method of Operations (RMOPs) in all slaughterhouses were reviewed and amended to require post slaughter identification checks. These are designed to ensure the correct identification of all animals prior to BSE sampling."
5.2.3 (Fourth full paragraph on page) 6
The facility to check the cattle ID database (i.e. CTS) at slaughterhouses does not apply in GB. GB operates the policy of passport seizure. NI does not use passports.
? Amend the sentence commencing “DEFRA continued the policy which had been implemented...” to “The CCAs in Great Britain continued the policy which had been implemented...”
? Amend the sentence commencing “In addition restricted animals received special status in CTS and APHIS, which allows their identification at slaughterhouses...” to “In Northern Ireland, restricted animals received special status
16 March 2010
in APHIS, which allows their identification at slaughterhouses...”
5.2.3 (Bullet 3) 7
Amend the paragraph commencing “According to the OV met in the slaughterhouse...” to “According to the OV met in the slaughterhouse visited in Northern Ireland, animals with clinical signs consistent with BSE would be rejected at ante-mortem inspection, and animals with localized lesions such as distal limb lameness were not recorded as sick at ante-mortem and therefore considered as healthy slaughtered. On the spot checks detected one animal which should have been recorded as sick at ante-mortem but which was recorded as healthy slaughtered. All ante-mortem information was recorded on APHIS and this triggered the BSE testing category on the sample label, however timing of data entry could result in the default printing of the label as healthy slaughtered”.
5.2.3 (Bullet 6) 7
Amend the paragraph commencing “In Northern Ireland, there was...” to “In Northern Ireland, there was one case in 2009 where a bovine animal eligible for testing was slaughtered for human consumption and not tested. According to the CCA, this was due to a human error by the manufacturer of a replacement tag. When this error was identified, the meat from this animal had already been placed on the market. Following that case, an additional document verification procedure was put in place in the lairage for animals of all ages as an obligatory check.” 5.2.3 (Conclusions)
DARD considers that the conclusions reached are overstated based on the evidence identified. Further evidence of subpopulation recording can be provided. For example:
? in 2008 in NI, 426 UA (24-30 month sick at ante-mortem animals) category animals were recorded. 101 of these were identified in the slaughterhouse visited;
? in 2009 in NI, 71 TC (O48 emergency slaughter) category animals were recorded. 18 of these were identified in the slaughterhouse visited; and
? in 2009 in NI, 218 TA (O48 sick at ante-mortem animals) were recorded. Further statistics are available at
5.2.4 (Findings, second paragraph)
The number 54000 in the sentence commencing “According to the CCA...” is incorrect. In the response to the evaluation plan, we advised that as of 30 September 2009, there were around 75000 cattle in GB born before 1 August 1996, of which around 54000 were born before 1 August 1995. As of 1 February 2010, the number of cattle in GB born before 1 August 1996 had reduced to 66834 of which 48275 were born before 1 August 1995.
Amend the sentence commencing “A similar situation was not
16 March 2010 3
(Findings, second paragraph) observed...” to “Although the OCDS ended on 31 December 2008, cattle keepers in NI could still avail of the free collection and disposal service for these older fallen cattle until November 2009”.
5.3 (Findings) 9
In the sentence commencing “Following the confirmation of BSE...” delete the words “all cattle on the affected farm (if necessary)” as we only have powers to kill cohorts and offspring in line with Regulation (EC) No.999/2001 5.4.1 (Findings, Bullet 4) 10
The MHS has clarified that at the time of the visit to the slaughterhouse in England, there were five vehicles on site used to transport animal by-products. Three vehicles were in use and two were empty. One vehicle was in the boning hall disposal bay and contained Category 3 material. It was labelled “Category 3” with a temporary paper label which was not strictly compliant with Regulation (EC) No.1774/2002 in that it did not contain the words “not for human consumption”. Two vehicles were in the back yard, contained SRM and were correctly labelled “Category 1 – for disposal only”. Two vehicles were in the front yard, were empty and unlabelled and were awaiting Category 3 material.
Delete the sentence “However, in one of them (England), means of transport used for the collection of SRM were not identified as required as no category nor any warning sentence were mentioned on most of the trailers used.”
5.4.1 (Findings, first paragraph on page)
11 Fat is combusted in the plant in NI at between 1200°C and 1400°C. The figure of 950°C quoted during the mission was the temperature reached in the secondary chamber where vapours from the plant are oxidised.
With reference to the clarification above (Section 5.4.1 on page 10) regarding identification of vehicles used to transport SRM, amend the sentence commencing “However, the traceability of SRM...” to “However, the traceability of SRM was affected by weaknesses in commercial documentation, which was not in line with the requirement in Art. 7 of Regulation (EC) No 1774/2002”.
5.4.2 (Findings, Bullet 2)
Amend the sentence commencing “In was only after several months...” to “It was only after several months”. 5.4.2 (Final sub-bullet)
In the paragraph commencing “Validation of Category 1 processing plants visited...” the official has clarified that although the plant was validated based on the particle size after the cooker, the official had since insisted on changes to the plant to allow the particle size to be assessed before the cooker. This historic deficiency regarding visual assessment of the particle size had been rectified by the time of the FVO mission visit. 5.5.1 (Findings, third paragraph)
With regards to the sentence commencing “According to DARD and DEFRA, there
To see the Competent Authority comments on the draft report, click here ( (255Kb) -
To see the Competent Authority response to the report recommendations, click here
FISH AND PRIONS
Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata)
In transmissible spongiform encephalopathies (TSEs), a group of fatal neurodegenerative disorders affecting many species, the key event in disease pathogenesis is the accumulation of an abnormal conformational isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). While the precise mechanism of the PrPC to PrPSc conversion is not understood, it is clear that host PrPC expression is a prerequisite for effective infectious prion propagation. Although there have been many studies on TSEs in mammalian species, little is known about TSE pathogenesis in fish. Here we show that while gilthead sea bream (Sparus aurata) orally challenged with brain homogenates prepared either from a BSE infected cow or from scrapie infected sheep developed no clinical prion disease, the brains of TSE-fed fish sampled two years after challenge did show signs of neurodegeneration and accumulation of deposits that reacted positively with antibodies raised against sea bream PrP. The control groups, fed with brains from uninfected animals, showed no such signs. Remarkably, the deposits developed much more rapidly and extensively in fish inoculated with BSE-infected material than in the ones challenged with the scrapie-infected brain homogenate, with numerous deposits being proteinase K-resistant. These plaque-like aggregates exhibited congophilia and birefringence in polarized light, consistent with an amyloid-like component. The neurodegeneration and abnormal deposition in the brains of fish challenged with prion, especially BSE, raises concerns about the potential risk to public health. As fish aquaculture is an economically important industry providing high protein nutrition for humans and other mammalian species, the prospect of farmed fish being contaminated with infectious mammalian PrPSc, or of a prion disease developing in farmed fish is alarming and requires further evaluation.
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Acknowledgments Author Contributions References Evgenia Salta1#, Cynthia Panagiotidis2#, Konstantinos Teliousis3, Spyros Petrakis1,4, Eleftherios Eleftheriadis5, Fotis Arapoglou5, Nikolaos Grigoriadis6, Anna Nicolaou7, Eleni Kaldrymidou3, Grigorios Krey5, Theodoros Sklaviadis2*
1 Department of Pharmacology, Aristotle University of Thessaloniki, Thessaloniki, Greece, 2 Centre for Research and Technology-Hellas, Institute of Agrobiotechnology, Thessaloniki, Greece, 3 Laboratory of Pathology, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece, 4 Max Delbruck Center for Molecular Medicine, Department of Neuroproteomics, Berlin-Buch, Germany, 5 National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece, 6 B' Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece, 7 Department of Business Administration, University of Macedonia, Thessaloniki, Greece
WONDER where all this fish feed that is not supposed to be fed to ruminants is going ?
PRODUCT a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6; Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6 CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT a) CO-OP 32% Sinking Catfish, Recall # V-100-6; Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE Product manufactured from 02/01/2005 until 06/06/2006 RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
CJD WATCH MESSAGE BOARD TSS MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 220.127.116.11
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II ______________________________ PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall # V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing. REASON Possible contamination of animal feeds with ruminent derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
Confucius is confused yet again. how can you be a consultant of something that has not happened yet ???
is this a typo, or what ??? what is R Bradley speaking of in 1983 ??? what is this BSE CONSULTANT in 1983??? i am confused, i thought the first cow documented was 1985, first discovered in 1984, and the diagnosis was rabies or something else besides BSE at first, then later discovered to be BSE, a new strain of TSE in the bovine. ...
APPROVAL OF MATERIAL FOR PUBLICATION
All material for publication including written works to be published in scientific journals, books, proceedings of scientific meetings, abstracts of verbally delivered papers and the like should be scrutinized for risk to the Ministry before dispatch to the publisher. ...
R Bradly Pathology 12 October 1983
1981 nervous disease in a Hereford calf (calves aged 7-14 days shoring progressive nervous signs of the hind limb weakness progressing to paraplegia. ...
Pathologist: Carol Richardson
DIAGNOSIS: 1. Moderat spongiform encephalopathy- acute. 2. Mild renal nephrosis - peracute
REMARKS: These acute changes suggest a toxicity of some description. The non-suppurative reactions are far more chronic, mild and non-specific.
Owner of animal, Mr. Stent
Attempts at virus isolation have proved negative.
Cases reviewed and discussed, ...No conclusion drawn....
Subject: Carol Richardson $ BSE
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 1 Nov 2000 09:51:39 -0800 Content-Type: text/plain Parts/Attachments: text/plain (345 lines)
######### Bovine Spongiform Encephalopathy
dont know if this will help calm nerves a bit, but you might find what you want here, in one of those reference YB numbers. her hand-written notes on the case would be; YB85/9.10/3.1-3.2
It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
The Stent farm cases
12. On 10th September, 1985 specimens (brain, kidney and spinal cord) from a cow owned by a Mr Stent of Pitsham Farm was referred to the CVL by the Winchester VI Centre (Mr J. Watkin-Jones, Veterinary Officer (VO)) for histopathological examination. Referrals from the VI Centres were dealt with on a rota system by the Consultative Pathology Unit (see paragraph 9 above). The veterinary pathologist on duty when the case came in to the Pathology Department was Ms Carol Richardson. At the time both Carol Richardson and I held the position of Senior Research Officer Grade II (SROII), both of us reporting directly to Ray Bradley. Carol Richardson worked in a section of the Department called Ruminant Reproductive Pathology and I believe that she had been working mainly on reproductive disorders in cattle and sheep, with a particular interest in research into infections producing foetal damage. She would, however, have dealt with scrapie cases through some of her previous work with Dr Stanley Terlecki, a former pathologist in the Department.
13. When such diagnostic cases came into CVL from a VI Centre the technician on duty at the time completed a VL99 card summarising the clinical history of the cow and the herd it originated from (based on information provided in the referral letter from the relevant VI Centre). The duty veterinary pathologist prepared the necessary pathological material for histological processing. Sections were then produced from the animal tissues for subsequent examination. The VL99 card for this particular case from Mr Stent's farm is found at YB85/9.10/3.1-3.2. This card and the prepared sections would then have been passed back to the duty veterinary pathologist for examination, which in this instance was Carol Richardson.
14. Carol Richardson conducted the histopathological examination and reported her findings on 19th September, 1985 (YB85/9.10/3.1-3.2). Her hand-written notes on the examination are on the VL99 card (see YB85/9.10/3.1-3.2). The final pathology report prepared by Carol Richardson, which was sent to Mr Watkin-Jones at Winchester VI Centre, is found at YB85/9.19/3.2. It should be noted that the purpose of the pathology reports prepared by the veterinary pathologists for such referrals from VI Centres is to make morphological diagnoses based on an examination of specimens provided. As far as is possible the pathologist then tries to place the diagnosis in the context of the clinical history of the particular animal and its herd or flock to reach conclusions or speculations on an aetiological diagnosis (the cause of the observed changes). This is the purpose of the "Remarks" section of the pathology report. Carol Richardson's examination reported "moderate spongiform encephalopathy" and "mild renal nephrosis" (the morphological diagnoses) and she attributed these observed changes to "a toxicity of some description" (the possible aetiological diagnosis). This was what was reported to the VI Centre. It is notable that nowhere in her report does she mention scrapie or indicate that her observations lead her to suspect any "scrapie-like" disease. The fact that the report mentions "moderate spongiform encephalopathy" is not conclusive in that respect. As highlighted by my short paper on vacuolation previously referred to in paragraph 8, spongiform conditions of the brain can arise from several different causes, including as a reaction to the ingestion of toxic substances, so this observation was consistent with her suggested aetiological diagnosis.
15. At the time this case came in from Mr Stent's farm, I was attending a meeting of the Charles Davis DVM Foundation for Veterinary Pathology in Cheshire. As is often the practice between pathologists in the event of encountering unusual or unexplained findings, Carol Richardson left the specimens and her pathology report for me to examine immediately on my return. A copy of Carol Richardson's report of 19th September, 1985 as annotated in manuscript by myself, is found at YB85/9.19/3.1. When sections are left for colleagues to examine it is not expected that any particular action would be taken by the colleague on his or her own initiative in respect of those sections. The purpose would be simply to offer a view on the material and then return the sections and report to the original examining pathologist, as was the case in this instance. Carol Richardson was absent from the Department on sick leave from 29th December, 1986, and this subsequently became maternity leave on 31st May, 1987. She returned to the Department on 29th December, 1987. Had Carol Richardson felt strongly thatabout the observations she had originally made were those of scrapie in cattle, and my subsequent opinion on her report, I would have expected that she would have come back to me to discuss the matter subsequently or take the matter further herself. in the period between seeing my annotations on her original report on the Stent case in September 1985 and her absence at the end of December 1985.
16. My re-examination of the sections "reinforcedwas consistent with" her original diagnosis in so far as I agreed with her overall observations and that such observations were not artefactual i.e. caused as a result of post-mortem changes or in the preparation of sections. My conclusion was that the brain lesions observed in this case could not in my experience be attributed to a specific disease, but a speculative comment was made that they could possibly be the result of chronic bacteraemia or an endotoxaemia (the production of poisons in the blood due to infection). Whilst the clinical history as described by the referring VI Centre (see YB85/9.10/3.1) describes that seven out of 130 cows were "nervous", this does not equate necessarily to the occurrence of a specific neurological disorder. The history indicated the occurrence of complex metabolic problems within the Stent herd (see paragraph 17 below).
17. Samples from three other cows in the Stent herd which had died or were killed on the farm had been referred to CVL for examination earlier in March, April and May of 1985 (CVL references VLO11453/85/0286, VLO11453/85/0640 and VLO12473/85/0831 respectively). Following, as far as I can recall, a telephone call from Mr J. Watkin-Jones, on 26th September, 1985 I reviewed the history of the submissions from the Stent herd and discussed them with him. This again, was standard practice where the VIS were investigating a persistent herd problem. A copy of my note of this event, together with the VI Centre referral letters and pathology reports for each case from the Stent farm (with manuscript comments made by myself at the time of this review) are found at YB85/9.26/1.1; YB85/9.10/3.1; YB85/9.19/3.1; YB85/4.31/1.1; YB85/5.9/1.1; YB85/4.6/1.1; YB85/4.16/1.1; YB85/2.13/1.1 and YB85/3.1/1.1 respectively. None of the samples for the three earlier cases included brain tissue and the main post-mortem finding in these cases was internal bleeding. Taken in isolation and in the light of these factors, the case in September 1985 did not at that time suggest that a new disease had been identified. Vacuolar changes in the brain of that particular animal were not severe and there was previous, and current, evidence of other disease problems. The herd from which these animals came had clearly experienced a lot of other health problems including haemorrhagic disorder (internal bleeding), hypocalcaemia (lack of calcium), septic arthritis (pus in joints), renal damage, bovine viral diarrhoea and peritonitis (inflammation of the abdominal cavity) associated with foetal death. This was a complex pattern in a dairy herd indicating that a variety of different diseases might be occurring. It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.
18. Further samples of nervous system tissues and other organs were received at CVL from a cow in the Stent herd on 10th September, 1986 (YB86/9.22/1.1-1.2). These were examined by Dr S. Done, a veterinary pathologist who joined the Pathology Department in 1983. A copy of the VL99 card for this case is found at YB86/9.22/1.1-1.2. Histopathogical examination of the central nervous system (CNS) tissues submitted from this case showed mild spongiform change in the medulla (hind brain). Other brain regions are described as having either no visible lesions or mild focal haemorrhage. See paragraph 31 for further discussion of this case.
4.The single case of BSE that I examined in September 1985 was the one and only case that I have seen.
5.The first officially reported case of BSE
Memory recalls a sequence of events the importance of which can only be made by informed judgement. The following account of an interesting and exciting event is taken largely from my memory. I have used copies of the original letter,case card, diagnostic report, accession books and my 1985 organiser diary to make this account as accurate as possible.
6.I had returned from annual leave and was on rota as duty pathologist. The senior technician of the diagnostic unit asked me to examine an adult bovine brain; the vet wanted a diagnosis a.s.a.p.
7.The history was of 7/130 cows showing nervous symptoms over the previous 5 months; most had gone for casualty slaughter and no gross abnormality had been seen in the viscera. (YB85/9.10/1.1).The Pathology Department had examined pieces of liver, kidney, heart and lung from three previous cases from this farm (YB85/2.15/1.1; YB85/4.9/1.1; YB85/5.3/1.1) (2 adults and 1 calf)and had found chronic mild hepatitis(1),acute hepatic necrosis (1) moderate pulmonary oedema (1) and chronic mild interstitial nephritis (2).
8.The history of these earlier cases was one of internal haemorrhage and samples had been sent for organic mercurial poisoning assay. There had been metabolic problems in this herd and active BVD infection in the calves. The case card numbers of these three cases can be seen in the cross-reference column on the case card of the September specimen- MS1509/85 (YB85/9.10/2.1). In addition to the nervous signs seen in this cow, abscessation of the stifle was also present. On gross examination, the brain was well fixed and relatively undamaged; pieces of spinal cord and a piece of kidney were included and were grossly unremarkable. The meninges appeared thickened but this was probably normal for an adult cow.
9.In the absence of gross abnormality, I made multiple incisions and took standard blocks (13) for histological processing and the production of H&E (see procedures) sections. Blocks of spinal cord and kidney were also sent for processing (11/9/85).
10.I have a set sequence for examining brain sections; when these sections were returned to me (13/9/85) I examined the frontal cerebrum first and progressed caudally scanning each section from dorsal to ventral surface. In this case there seemed to be a mild vacuolation of the cerebral neuropil. At this time Gerald Wells had been investigating the possibility that prolonged exposure of nervous tissue to 70% alcohol could produce neuropil vacuolation. Such prolonged exposure would occur over the week-end but I checked with the technician to ensure that such exposure had not occurred in this case before resuming my examination. I noted finding a mild multifocal non-suppurative peri-vascular infiltration with some eosinophils and in the caudal cerebrum mild focal gliosis. No abnormality was found in the thalamus (cranial midbrain) but mild neuropil vacuolation of the reticular formation in the colliculi. The medulla (a pathogonomic site for Scrapie in sheep) showed moderate neuronal and neuropil vacuolation. I found no abnormality in the cerebellum but the section of lumbar spinal cord showed mild neuropil vacuolation of the dorsal horns. There were two types of lesion in the section of kidney;a chronic mild /moderate non-suppurative interstitial reaction with tubular regeneration and fibrosis; a peracute reaction of a mild multifocal tubular necrosis with hydropic change (protein reabsorption).
11.These sections were reviewed by Gerald Wells in 1987 with essentially similar findings but more refined. (See case card at YB85/9.10/2.1).
12.Although I had never seen this type of lesion before in a cow I had frequently seen the combination of neuronal and neuropil vacuolation with this distribution in Scrapie. To me,this was Scrapie in a cow.
13.Before writing the report I sought a second opinion; I needed the opinion of a ruminant neuropathologist and therefore placed the sections, my findings and a request for re-examination on Martin Jeffrey’s bench. I was eager to hear his opinion and immediately after lunch went to collect the slides. Martin had left a note on which was written "Bovine scrapie". As I left his room I met him in the doorway. Apparently this was the first case he had seen but he informed me that Gerald had examined two cases and was expecting another two cases.
14.Interestingly, we apparently had more than one case here from different farms but obviously Gerald was dealing with it. In all my experience, there has not been a case of a novel disease in cattle affecting more than one farm initially: this should have caused alarm bells to ring. If there are several cases at different farms, it is important to cross-reference for the purposes of disease surveillance. A site visit to the Pitsham farm would have resulted in further well-preserved specimens, and more background information.
15.On the 17th-18th Sept. I drafted a batch of diagnostic reports including my report to Winchester VIC (YB85/9.19/1.1).
16.The report is a reiteration of my findings except that the histo-anatomical term `reticular formation’ should have been typed in the sentence above and not under the findings in the medulla. When it came to stating a diagnosis I decided that since the pathological term used for the clinical disease Scrapie of sheep is ovine spongiform encephalopathy then this "new" entity must also be classified as a "spongiform encephalopathy". I called it mild because again projecting onto the sheep situation with only a few sites affected the inclusion of mild as a descriptive term seemed correct. Although there was a chronic interstitial nephritis , I decided to highlight the peracute nephrosis which was probably related to a bacterial toxaemia associated with the stifle abcess.
17.From the history of the case on the Stent farm, it seemed as if the clinical course of the disease was fairly rapid in that metabolic disorders of short duration and heavy metal toxicities were being considered on the farm. Therefore, it seemed likely that the cause(s) of the spongiform changes were a result of an acute clinical disease (rather than a chronic illness) and in the absence of a more likely aetiology, toxicity seemed to be the most appropriate catagory that fitted both symptoms and findings.
18.I dismissed the possibility that a bacterial toxaemia had caused the spongiform change; in my limited experience of ruminant neuropathology, toxaemia was likely to produce frank neuronal necrosis rather than degenerative vacuolation (cf. Clostridial toxaemia).
19.The report was sent for typing; returned and despatched on the 19th September. The second copy and the original letter was filed on VlO 12467, the diagnostic file for cattle diseases. I asked the technician, Dorothy Wells (no relation to Gerald) to cross-reference with similar cases. I always asked the technician to do this, to enter the case numbers of similar cases on the pathology card. In this case I asked Dorothy to cross-reference for the two cases that Gerald had appaerntly already seen.
20.I heard nothing further about my 1985 case.
21.I left the CVL at Christmas 1986, on maternity leave.
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
see full discussion here ;
even the late great Dr. Gibbs once told me personally that even if the Chicken did not contract a TSE, IF the chicken had been fed the TSE tainted feed and then slaughtered, the agent survives the digestinal tract to pass on to other species through feed. The same would hold true with marine fish feed. ..tss
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
Monday, April 5, 2010
Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
Sunday, April 4, 2010
USDA AND OIE OUT OF TOUCH WITH RISK FACTOR ON ATYPICAL TSE
position: Post Doctoral Fellow Atypical BSE in Cattle
Closing date: December 24, 2009
Anticipated start date: January/February 2010
Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
2008 - 2010
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
my comments to PLosone here ;
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518