Correspondence UK Veterinary pathologists 1 June 99It turns out that major zoos in the UK, such as the Zoological Society of London, do in fact routinely save brain samples from a wide variety of species, regardless of the post mortem findings or of the animals' potential prior exposure to TSE. In fact the London Zoo has has a much larger archived sample of both fixed and frozen primate brains than was available to French researcher Noelle Bons. Since valuable and rare zoo animals can hardly be sacrificed for routine disease surveys, these stored brain specimens represent a very important resource.
A small number of animals had histology performed on ileum and Peyer's patch apparently with negative results, apparently on animals already testing positive neurologically or asymptomatic animals. Tonsils from zoo animals have not been as yet been examined for TSE in the UK. Too often negative findings never surface as publications; more information may be available shortly. It is not clear whether the UK maintains a country-wide list of species that have died, with date of death and clinical symptoms, like the US does.
Discussion are reportedly underway with the MAFF about conducting a parallel study to that of Bons which would involve much larger number of individuals and species. A similar study was rejected by both MAFF and MRC in 1995. Funding is not really an issue because collaborators abroad with grants could easily be brought in.
7 May 1999 webmasterIt is quite easy for Britain to determine which zoo animals have been exported to which zoos abroad and to notify recipients that they may be housing an animal infected with BSE. Recipient zoos may wish not to have these animals rendered into feed upon their death and to avoid "in-feeding" (use of fallen zoo animals to feed the carnivores, to save money).
To export a zoo animal (infected with BSE or not) takes an export license. Similarly, to import (say, a French primate to a British zoo or an Asiatic lion from the wild to a contaminated enclosure in Edinburgh) takes an import license. Naturally any good British bureaucracy retains copies of these licenses back to Roman times. And MAFF provides the proper contact information. Reciprocally, the US import side is available through a Freedom of Information request; USDA may be the agency handling import licences.
Live animals
Miss J Johnson Animal Health (International Trade) Division Room 49, Block C Government Buildings Toby Jug Site Hook Rise South Tolworth KT6 7NF Tel: 0181 330 8165 Fax: 0181 330 6678
MAFF Animal Health (International Trade) Division Block C Government Buildings Hook Rise South KT6 7NF Tel: 0181 330 8194 Fax: 0181 330 6678
12 May 99 webmasterThe only British zoo animal ever found to be negative for BSE was a 1991 kudu. This raises the question of who falsifies the export health certificates on British zoo animals sent to other countries. Ironically, APHIS, the USDA agency responsible for determining whether BSE is present in US cattle, requires these health certificates for zoo animals imported into the US.
The highly publicized HIS program on imported BSE cows never mentions the many thousands of suspect zoo animals that have slipped in from Britain and France apparently with zero surveillance or follow-up. These imports are supposedly online at the APHIS site providing data on who exported which zoo animal when and to whom or call for an explantation of special rules that apply to imported zoo animals.; for information on these imports, phone (301) 734-8170.
However, an anonymous account in the July 1993 USDA APHIS VS CEAH document: "BSE: Implications for the United States," pg 18, states:
"Veterinary pathologists at the major zoos in the US routinely examine the brains of cases exhibiting neurologic signs. In addition, all animals that die at major zoos usually undergo necropsy in compliance with guidelines ot he American Association of Zoological Parks and Aquariums. A records search conducted by two major zoos showed that no fatal diseaseas with unexplained clincial signs or presenting signs suggestive of spongiform encephalopathy had occurred since the onset of computerized record keeping in 1964 and 1975, repectively, (W. Heuschele, San Diego Zoologoical Gardens and R. Montali, National Zoological Park, personal communication). "
[Dr. Heuschele died in this winter. Dick Montali is currently out of the country at meetings in Europe, returning the first week of June. He suggests contacting veterinary authorities at CDC in Atlanta to find out about imports as well as Dr. John Strandberg at NIH, who oversees the Regional primate centers.]
This proves that the USDA was well aware of the risk at that time, though in fairness no one knew how dramatically the British had concealed the risk until the Bons PNAS paper of 30 March 99. The database was manifestly inadquate: it failed to catch mule deer at the Denver Zoo, Laramie zoo and Metro Toronto Zoo that died of confirmed CWD in the 1970's and 1980's. Perhaps 1 case in 20 would be noticed with non-targeted histopathology by a non-specialist. There is little value to a clinical screen because the course is so variable.
The bottom line question is how many zoo animals in the US, whether symptomatic or not, imported from France or Britain, have tested negative using modern immunohistochemistry 1989-1999 on a high titre tissue such as the obex. That number appears to be zero. No US zoo animals have ever been tested. No a single UK or Fernch zoo animal has ever tested negative for BSE.
"Imports and Exports: APHIS stakeholders will be able to track APHIS import and export activities through detailed report retrieval. Information will be able to be obtained on such things as animal herds imported from other countries, including the quantity of animals received and final shipping destinations. Similar information will be able to be tracked for plants and exports."
Dr. Gary Colgrove, Chief Staff Veterinarian The National Center for Import and Export USDA, APHIS, VS Unit 38 4700 River Road Riverdale, MD 20737-1232
The agency seems to have done nothing in the years 1980-1999 to inspect or prevent the importation of infected zoo animals from Britain and France. Not a single negative IHC result exists on these high-risk animals.
The quarantine of livestock at Newburgh is an important link in the chain of the import process. This process includes the development of protocol between the exporting and importing counties, monitoring of disease prevalence and occurrence on a global level, the import application, the issuance of a permit, transportation, quarantine, applicable diagnostic tests, and notification to the receiving State that animals are being released from quarantine. A Parade of Animals
Animals, poultry, and other birds must have an import permit and health certificate when they are brought into the country. The permit shows what types of animals are being imported, their country of origin, who is exporting them, who is importing them, their ports of embarkation and arrival, their route, their mode of travel, and the purpose for which they are being imported. All of this information is important because it allows Center employees to identify each animal and track it. Accompanying health certificates show that the animals were inspected before they left their country and have received the proper diagnostic examination and treatment for entry into the United States.
All animals must be imported through the Center if they are susceptible to or are capable of carrying diseases or pests that could seriously endanger U.S. domestic livestock or poultry. From May 15, 1994, through May 15, 1995, more than 5,000 animals and 1,400 birds passed through the Center.
When a shipment of animals arrives either by plane or ship at the ports of New York or New Jersey, an APHIS port veterinarian gives the animals a preliminary examination. The veterinarian also checks the identification of the animals, the health certificates, and permits. The animals then are transferred to a truck that takes them directly to the Center. If any information is lacking such as residence, health statistics, or pre-export history the animals are refused entry and held at the Center until the problem is corrected. If the problem cannot be corrected, the animals are returned to their country of origin.
USDA, APHIS, VS
New York Animal Import Center
200 Drury Lane
Rock Tavern, NY 12575
The Foreign Animal Disease Diagnostic Laboratory at Plum Island Animal Disease Center seems incompetent judging from documents released under FOIA.
The accompanying health certificate shows that the animal was inspected before it left its country and has received the proper treatments for entry into the United States. To improve animal genetics and food and fiber resources, live animals are allowed to enter the United States through the Harry S Truman Animal Import Center. Restrictive quarantine and rigorous diagnostic procedures are carried out in the country of origin and at the Center. These measures are necessary to ensure the livestock industry that the imported animals are free of disease and parasites. After the animals finish their 90-day quarantine, the Center undergoes exhaustive decontamination. The Center's decontamination process is so thorough that only three shipments of animals, each requiring a 90-day quarantine, can enter the Center each year.
Because of the restricted amount of space and large number of requests to import animals, the Center holds a lottery each year for applicants who meet qualifications. Applicants provide a $32,000 deposit to enter the lottery. Lottery winners then enter into a cooperative service trust fund agreement with APHIS and pay estimated importation costs before the work begins. The deposit is applied to the estimated costs. The importer is responsible for quarantine costs. These include the expenses for APHIS personnel, laboratory tests, inspection of the embarkation quarantine facility (EQF) in the country of origin, a 60-day quarantine at the EQF in the country of origin, and the 90-day quarantine at the Harry S Truman Animal Import Center. An importer's costs for using the facility often exceed $800,000.
In 1995, the Center quarantined 1,523 animals, including goats and sheep from South Africa and alpacas and llamas from Peru and Bolivia. Since its inception, the Center has processed cattle, swine, goats, sheep, alpacas, water buffalo, and llamas.
In addition, the agency does not intend to enter into any more cooperative-service agreements with prospective importers for exclusive use of the facility unless it is certain the animals can enter HSTAIC on or before December 31, 1998. Ensuring that no animals enter HSTAIC after this date would allow the agency to close HSTAIC before the end of fiscal year l999 if a decision is made to close the facility. This ruling became effective July 13, 1998.
Times Newspapers Ltd.May 16 1999 by Annamarie Cumiskey and Richard WoodsBushmeat chops are a favourite in some backstreet cafes; chimps on the menu in Brussels restaurants
CHIMPANZEES and monkeys are being served up as delicacies at restaurants in the heart of Europe, an investigation has revealed. Some of Man's closest relatives are being cooked for dining tables in Brussels even though two years ago the European Union declared that it would crack down on the illegal trade in what is known as "bushmeat".
Great apes, some of which differ from humans in only 2% of their genetic make-up, are also on the menu in Antwerp and other large cities, according to sources in the restaurant trade.
Earlier this month at the CitÈ Mont-Fleury restaurant, which serves Congolese cuisine in the Etaings Noir district of Brussels, the waitress did not hesitate when an undercover reporter asked whether monkey meat was available. "Yes, we have it," she said.
Forty-five minutes later the dish arrived, an array of skinless pieces of meat in a greeny-brown ragout of African vegetables with rice. The meat smelt strongly of being smoked. A customer passing the table recognised the dish as monkey and the restaurant listed the meal as makaku - monkey - on the bill.
The stew was not eaten but sent for analysis last week at the veterinary department at Ghent University. Tests confirmed that it came from a primate and that it contained bones from the elbow and forearm. Hunters had shot the animal: four lead pellets were lodged in the muscle and bone.
The waitress later said the meat had been brought to Belgium by her cousin from the Congo and that the restaurant received supplies every few months. "Customers telephone to know when we will have it next," she said. "In Africa people eat monkeys, so why can they not eat them here?"
At another restaurant in the backstreets, a waiter showed the menu to a reporter and his companion and said: "We also have other dishes: the chimpanzee is very tasty, if you like that type of thing."
In such restaurants four or five matchbox-sized chunks of meat, served with a sauce and fou fou (a floury African staple), cost anything up to £40.
Eating chimpanzee or monkey is a sign of status among the black community and reminds expatriates of home. One Nigerian man said: "Some people from eastern Africa would not live here if they could not get the meat." Favoured recipes include cooking monkey in white wine or with peanut sauce.
"It is horrific that the trade in bushmeat has turned up in Europe," said Steve Brend, the British representative of the International Primate Protection League. "It is undoubtedly the greatest threat to the great apes."
One man who claimed to know Belgian traders importing the illegal meat said that some had been sold to other European countries including Britain.
After steep declines in their numbers, all apes are protected by the Convention on International Trade in Endangered Species (Cites), and any trade in higher primates, such as chimpanzees, is banned. The chimp population in Africa has collapsed by more than 90% this century and is now estimated to be less than 130,000.
But chimpanzees are not safe from the trade in bushmeat. Last month, after a tipoff, armed police and health officials raided 12 African food shops in the MatongÈ area of Brussels. They were checking hygiene standards and tax evasion but found far worse: in one shop two dead chimpanzees were hanging from the ceiling in a store room. They had been skinned, gutted, dried and salted.
"It was horrible. They were immediately recognisable as chimpanzees," said Sagairadji Chevremont, an officer who took part in the operation. Other primate meat, two antelopes and tortoises, which are also regarded as choice morsels, were recovered.
The Congolese woman who ran the shop was unabashed. "We had antelopes, porcupines and snakeskins and monkey meat," she said. Two chimps were on the premises, she admitted, but were not for sale. "It is something we want to eat with our family for special occasions."
Demand by European residents and the activities of Western companies in Africa is expanding the illegal trade, according to environmental groups.
The Ape Alliance, an umbrella group of conservation organisations, says logging of Africa forests by European and Asian companies has opened up remote areas to poachers. Animals once hunted by locals for subsistence have become profitable to smugglers.
The scandal presents deadly risks to the health of humans as well as our evolutionary cousins. Two years ago the eating of chimpanzee meat in Gabon was blamed for an outbreak of ebola, the highly infectious fever. More than 20 people died. Chimpanzees may also be the source of the virus that leads to Aids.
Despite the evidence on its own doorstep of an illegal trade and possible danger to public health, the European Union appears ineffectual. Ten days ago Tony Cunningham, a British MEP who had questioned what was being done to protect great apes after the earlier European resolution, was told that the EU was aware of the grave threats to great apes and "action has been taken to remedy this". No details were given.
Ann DeGrees, director of Global Action, an animal rights group in Brussels, said: "It is completely unacceptable that this meat is on sale. The state has not done enough to stop the smuggling."
10 May 99 webmasterIt is possible to date the deaths of unpublished zoo BSE by looking a time series of press releases.
The table Narang cited in his Inquiry statement was Table 6 of a MAFF document, entitled "BSE Statistics as at 1 May 1996.' Basically it provides a snapshot of the zoo animals dead from BSE at that time that can be compared to the 1 May 99 snapshot at the Maff site and to the last papers of Kirkwood and Cunningham, who threw in the towel in 1995 after Maff and MRC denied funding to look at tonsils and GI tract of zoo animals. (This was never looked at subsequently other than in the 30 Mar 99 PNAS paper by the French and the late 1998 Collinge Lancet paper.) Comparing this to the 1 May 99 totals, we see that 36+ months have elapsed without any published details on 1 eland, 2 pumas, 1 tiger, 2 ocelots, and 2 ankole cows:
eland 2 (1 known to Kirkwood in June 96) puma 2 (2 known to Kirkwood in June 96) tiger 1 (1 known to Kirkwood in June 96) ocelot 2 (2 known to Kirkwood in June 96) ankole 2 (0 known to Kirkwood in June 96) bison 1 (0 known to Kirkwood in June 96)The bison case occurred between June 96 and June 97; 3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).
Keep in mind that only 1 negative asymptomatic animal has ever been reported by the British. That was a kudu in 1991. The best measure of surveillance is the comparison of positive to negative results using the most sensitive possible diagnostic method: if every case tested is positive, that suggests (since the symptoms are so unpredictable) that a large number of untested animals would also have tested positive.
Basically it is forbidden to this day to use prion immunohistochemistry on zoo animals that died for unknown reasons. This is a nationwide ban that applies to all veterinarians and scientists public and private. Zoo animals must be incinerated immediately without saving of brain samples; samples may not be sent to qualified investigators abroad. Unless they are doing secret tests at the CVO, the British are completely in the dark themselves. (Which is how they like it.)
This policy does not exactly instill confidence in the accuracy of taxonomic distribution of zoo animal BSE nor in our knowledge of disease penetrance. By far the best data is that of Bons et al. in France: the observed penetrance in a randomly chosen species of primate was 100% (18/18 of the asymptomatic animals).
The bison BSE case time window can be narrowed to the period June 96 to June 97; note one cheetah must have died between May 96 and June 97 and another by 1 August of that same year:
TSE - UK: EXOTIC ANIMALS Sat, 7 Jun 1997 a HREF="dpreslar@fas.org">Dorothy Preslar Briefing to the TSE conference hosted by the New Zealand MAFFIn a written reply to the House of Commons, Agriculture Minister of State Jeff Rooker has provided details of Transmissible Spongiform Encephalopathy in animals other than livestock. His report includes confirmed cases of TSE in
2 ankole cows,
1 bison,
3 cheetah,
6 eland,
1 gemsbok,
6 kudu,
1 nyala,
2 ocelot,
1 Arabian oryx,
1 scimitar horned oryx,
3 pumas and
1 tiger,
77 domestic cats.
UK MAFF site as it appeared in August 1997
kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cat (domestic) 78 cheetah 4 + 1 Australia + 1 France + 1 Ireland puma 3 tiger 1 ocelot 2 bison (bison bison) 1 ankole 2
published twice yearly dated May 1996.
kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cat 70 cheetah 2 UK + 1 AU + 1 ROI puma 3 tiger 1 ocelot 2 ankole cow 2
BSE Inquiry statement from Harash NarangComment (webmaster): While it is difficult to correlate these cases with those relleased the the nvCJD Surveillance Unit, and while the diagnostic status of the new cases here is not fully resolved, Narang is certainly presenting some new information that needs to be carefully evaluated. Putting these together with cases in living individuals confirmed by Collinge's tonsil testing program, the net effect would be that the nvCJD epidemic has been seriously understated. Narang has identified with an asterisk* those victims who he believes are not included in official figures of nvCJD. The oldest case of nvCJD admitted to by the official Surveillance Unit is 52 years at death. The actual age distribution is a secret. The table shows unacknowledged victims in order of increasing age (and decreasing liklihood):
If nvCJD is defined so that florid plaques and young age are required, this becomes circular reasoning, which is partly Narang's point. It would have been helpful had the age of onset and age at death been given more consistently -- there is a sharp difference between incidence of sporadic CJD at 39 vs incidence at 30 so giving the ages as "in her 30's" etc. is unfortunate. Case 1 (favorite food: calf brain on toast) has no age range given at all and is of interest because of the 1984 date of death.
| victim | S.U. | death | age | duration (mo) | comment |
|---|---|---|---|---|---|
| 24 | - | 1997 | (20+) | 54 | likely nvCJD |
| 1 | - | 1984 | - | 3 | ate calf brain |
| 22 | - | 1996 | 18+ | 10 | likely nvCJD |
| 3 | - | 1993 | 30+ | 4 | possible nvCJD |
| 8 | - | 1994 | 40+ | - | possible nvCJD |
| 20 | - | 1996 | 40+ | 11 | possible nvCJD |
| 23 | - | 1996 | 40+ | - | possible nvCJD |
| 2 | - | 1989 | 50+ | - | possible nvCJD |
| 7 | - | 1994 | 50+ | - | possible nvCJD |
| 10 | - | 1995 | 50+ | 3 | possible nvCJD |
| 14 | - | 1996 | 50+ | - | meat industry |
| 4 | - | 1993 | 60+ | 24+ | possible nvCJD |
| 5 | - | 1993 | 60+ | - | possible nvCJD |
| 6 | - | 1994 | 60+ | 6 | possible nvCJD |
| 12 | - | 1995 | 30+ | - | confirmed familial CJD |
| 18 | - | 1989 | 50+ | - | twins: familial CJD |
| 19 | - | 1996 | 50+ | 18 | twins: familial CJD |
| 9 | + | 1995 | 18+ | - | official nvCJD |
| 11 | + | 1995 | 20+ | - | official nvCJD |
| 16 | + | 1996 | 20+ | 48+ | official nvCJD |
| 13 | + | 1995 | 30+ | 8 | official nvCJD |
| 15 | + | 1996 | 30+ | 100+ | official nvCJD |
| 21 | + | 1996 | 30+ | 11 | official nvCJD |
| 17 | + | 1996 | 40+ | official nvCJD |
Victim 9 had originally been seen by psychotherapists and psychiatrists and was originally diagnosed as suffering from clinical depression. They were then told by a neurologist that Victim 9 was suffering from a progressive degenerative disease of the brain. He was then subjected to multiple tests at a special unit in London. Eventually his parents were told that he might have CJD. They were asked if Victim 9 had had any blood transfusions or growth hormone treatment.
Her partner complained to me that Victim 11 was included in the 10 cases of new strain CJD referred to in the announcement in the House of Commons in March 1996. He told me that Martin Zeidler telephoned at 8.30pm on that day and he was very upset that Mr Zeidler had not told him previously that Victim 11 was suffering from the new strain CJD. He put to Zeidler that Zeidler "must have known that Victim 11 was one of the 10" and Zeidler answered that he did. He feels that he was grossly misled.
After repeatedly being told by doctors that Victim 16 was too young to be suffering CJD his parents asked me to perform a urine test. In January 1996 I confirmed that Victim 16 had CJD before he died. This confirmation prompted a full post mortem.
The acknowledgment following the post mortem that Victim 16 died of the new strain of CJD sparked a new urgency in official investigations into the link. If I had not tested Victim 16 the authorities might not had admitted the existence of the new atypical strain of CJD. With Victim 16's case the Government began to accept for the first time that BSE was the likely source of infection. In doing so, they were confirming the validity of what I had been publicly claiming for several years in the face of continuing and regular official opposition and discouragement.
In 1996 Victim 19 died after an 18 month illness aged in her 50's. Around 1991 she had had a blood transfusion following an ulcerated gullet. Starting with a slight tremor in her hands the early symptoms of Parkinson¼s Disease gradually progressed until Victim 19 was staggering and losing her balance. She started falling over just as Victim 18 had done, reminding the family once again of the same symptoms. I was asked to carry out a urine test. This was done and Victim 19 was found positive for CJD. The family discussed the importance of a post mortem with me and asked me to witness the post mortem and carry out other independent tests on her brain. Examination of Victim 19's brain revealed extensive vacuolation of the cerebellum and numerous PrP positive plaques demonstrating that new strain CJD does not only affect the young under 40. [These cases should be discarded unless the prion gene is found normal because familial CJD is indicated.]
The surveillance unit¼s findings on post mortem were that "examination of the fixed brain confirms the clinical diagnosis of Creutzfeldt-Jacob Disease in this patient. The histological and immunocytochemical features in this case are distinct from the new variant of CJD identified earlier this year. The appearances in this case are a characteristic of a subset of sporadic CJD cases in which plaque formation occurs, being most evident on PrP immunocytochemistry and spongiform change is most pronounced in the cerebellum and sub-cortical white matter". However my examination of the brain revealed no significant pathological differences between this brain and those brains identified by the surveillance unit as affected by nvCJD. The surveillance unit clarifies this brain as a "subset" of classic CJD.
Her mother told me of the feeling that she was left unsupported and on her own without anybody to help or counsel the family with the difficulties they faced. The family felt angry and frustrated. Although Victim 22 was clinically diagnosed as suffering from CJD, no advice was given on the importance of a post mortem and therefore none was performed. Victim 22¼s death is therefore not included in the CJD surveillance statistics as a definite nvCJD victim. [This case is highly probable nvCJD because of the young age.]
However Victim 24 then survived for a number of years. Whilst she was alive I wished to carry out a test on her urine, but no arrangements were ever made to allow me to carry out the test. A CSF (cerebral spinal fluid) test was carried out at the end of October 1996. Victim 24¼s family were told that this test had a success rate of 83/84. The test was negative for CJD and the conclusion was therefore drawn that Victim 24 did not have CJD in light of the CSF test and the length of her period of survival.
Victim 24 died at the end of 1997. Her next of kin agreed that I should be present at the post mortem as an independent observer and agreed that I should be provided with specimens for independent researches. My tests on her brain tissue have revealed that Victim 24 died suffering from CJD. There were gross spongiform changes in her brain including the cerebellum, which is only seen in cases of nvCJD. She also had PrP positive plaques although the plaques were not typical of nvCJD plaques.
However, such variations will be seen in different individuals with different genetic make up. As I understand matters this is now accepted as a possibility by the National CJD Surveillance Unit. This acceptance clearly demonstrates that cases which have not been classified as nvCJD because of their atypical distribution of PrP plaques may well have been, as I have always maintained, nvCJD, the explanation for the plaque distribution differences being variations in the host prion protein. Subsequently the CJD Surveillance Unit confirmed that Victim 24 did indeed have CJD.
15 Sept 98 Inquiry statement and 7 May 99 webmaster commentaryAndrew Fleetwood gave a statement to the BSE Inquiry on 15 Sept 98. He published a paper on the first eland with BSE, at the Port Lympne Zoo. It is clear from this testimony how British monkey chow and other zoo animal feed would be thoroughly contaminated up to 1996 or later.
Fleetwood graduated from the Royal Veterinary College, London in 1983 and worked in large animal veterinary practice in Kent from 1983-1985 and in West Sussex from 1985-1987, joining the State Veterinary Service as a Veterinary Investigation Officer in Wye, Kent, being promoted to Senior Veterinary Officer, Animal Health (Zoonoses) Division, Tolworth.
"Another aspect of my work as a general practitioner was to attend abattoirs, meat cutting plants and meat processing plants as an OVS. At that time OVSs were required to attend slaughterhouses processing animals or meat for export. OVSs were employed by local authorities and were often vets in general practice. I spent about one day in each week in slaughterhouses and other premises in this capacity. In this capacity I learnt a great deal about slaughterhouse practices and conditions in slaughterhouses. ""In December 1989, I investigated the appearance of neurological signs in an eland resident at a local zoo. A diagnosis of spongiform encephalophy was made, and the case reported in the Veterinary Record (J/VR/126/408). I used the general test for scrapie on the basis that the disease was uncertain and a broader spectrum of test was suitable (rather than the specific, although quicker, test for BSE). "
"The Animal Health (Zoonoses) Division at Tolworth was created in 1991.... The Assistant Secretary at the head of the Division was Dr. Richard Cawthorne who had previously acted as Head of the Veterinary Investigation Service. ..I reported directly to Dr Cawthorne and was supported by an Administrative Officer and Administrative Assistant. However, on frequent occasions in relation to BSE, I worked on the direct orders of or reported directly to others in MAFF, most notably the Chief Veterinary Officer (Mr Keith Meldrum), the Assistant Chief Veterinary Officer (Mr Kevin Taylor), the Assistant Secretary Animal Health (Disease Control) Division (Mr Tom Eddy) and the Under Secretary (Animal Health and Welfare) (Mr Martin Haddon). Divisional Veterinary Officers made reports to me in relation to specific tasks I assigned for them to undertake in their Divisions."
"Feed mills and rendering plants are complex plants handling material in multiple tonne quantities. They use automated equipment (such as screw conveyors and blow lines). It is very difficult, if not impossible, to remove all traces of previous material conveyed through the plant....The result of my telephone survey was a substantial shortfall in the estimated SBO which renderers were receiving compared with estimated SBO which ought to have been received by them. Although these were very much estimates, with many variables, they gave a strong indication that the SBO controls were not working...."
"On 28 April 1995 I received a telephone call from the manager of a large rendering plant which processed approximately 60-70% of national SBO. He told me that almost all of the SBO received by his plant for processing was arriving in an unstained state. [Patent Blue V stain]...I also spoke to Mr. Philip Corrigan, Head of Operations at the newly formed Meat Hygiene Service. He advised me that he had received a letter from a large slaughterhouse suggesting they were not complying with the regulations requiring staining. Finally, I asked Mr. Lackenby to find out from the manufacturers of Patent Blue V [a dye to stain offal that actually worked] about orders for the stain. The manufacturers confirmed that they had stocks available for immediate delivery. But, despite several inquiries, few orders had been placed ...."
"My suspicion was that staff from the SVS inspecting slaughterhouses were often quite junior and easily browbeaten by the slaughterhouse managers. I also had doubts about the extent to which visits were truly unannounced (as they were supposed to be)....in a letter of 12 June 1995 to Mr. Meldrum from Mr. Peter Carrigan, representing a firm of consultants to the meat industry. Mr. Carrigan suggested that unscrupulous abattoirs had cheated and would continue to cheat the SBO legislation and that SBO was little better than a joke in certain quarters of the industry.... In a minute of 1 December 1995 from a veterinary officer at Leicester (YB 95/12.1/2.1-2.2) I was advised of the results of a visit to an oleochemical plant where unstained heads, including brains, were found in incoming raw material."
In 1996, an exacerbated Fleetwood quit his job at MAFF on 28 February 1996 to take up a research and development position in the pharmaceutical industry. No contact information is available.
Arthur, Charles, TSE reporter at The Independent who sometimes writes on TSE in zoo animals and pets.7 May 99 webmaster. Note separate collection for people with CWD involvement
Bons, Noelle, Ecole Pratique des Hautes Etudes Neuromorphologie Fonctionnelle, UniversitÈ Montpellier, France Tel : (33) 04.67.52.40.08 Fax; (33) 04.67.63.33.27. Major 1999 PNAS article on BSE transmission to primates in French zoos.
Brinch, Torsten, Danish expert on epidemics, webmaster of major BSE resource, knowledgable about zoos and zoo animals
Cunningham, Andrew...Institute of Zoology, London Zoo. Colleague of Kirkwood who investigated early cases of zoo BSE.
Dealler, Stephen... Knowledgeable on many aspects of TSE, webmaster. Web
Edwards, Dennis J , maintains Vet. Record website, back issues not yet available.
Gibbs, CJ, veteran TSE researcher at NIH 301-496-6321, 301-496-9964, or (30l) 496-4821
Hosegood, Martin reported on eland cases 2-4 while a regional MAFF veterinarian, now at The Scott Veterinary Clinic, 405 Goldington Road, Bedford, Bedfordshire MK41 0DS, UK.
IUCN, International Union of Nature Conservation headquarters.
Kelly, Don F. Author of original white tiger SE paper, now dept chair, Univ. of Liverpool veterinary pathology.
Kirkwood, James, former London Zoo vet who tracks TSE in zoo animals, now at UFAW after MAFF refused to fund further in 1995. With Benbow and Cunningham, first called attention to endangered species implications of TSE. tel: 01582-831818, fax: 01582-831414
MAFF webmaster, help desk, declines to answer technical questions on exotic animals at MAFF web site.
Pincbeck, Matthew involved in BSE lion case on behalf of Edinburgh Zoo.
Quantum Conservation, German group that maintains a zoo, EEP, and director list with contact information.
Richardson, Douglas, Asiatic lion endangered species program coordinator, concerned about situation at Edinburgh Zoo.
Reid, Gordon M , Director, Chester Zoo (North of England Zoological Society), Chester, UK. Tel +44 1244 650201; Fax +44 1244 371273. Refers questions to Chris West who refers questions to a senior Veterinary Technician.
Spratt, David Zoo Check Manager, Born Free Foundation, West Sussex, UK. Tel : 01403 240170, Fax : 01403 327838
Stronach, Dr., Director of Fota Wildlife Park in Ireland, does not respond to cheetah questions.
Wells, Gerald AH, veteran pathologist at the Central Veterinary Laboratory.
6 May 99 webmaster: index to 74 earlier wild animal articlesChronic Wasting Disease (CWD):