Prion disease in zoo animals
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Britain's exports of BSE-infected zoo animals
America's imports of BSE-infected zoo animals
Chimps eaten in Brussels restaurant
Dating unpublished zoo BSE
Narang's nvCJD victim list
What offal ban? -- testimony of AJ Fleetwood
Zoo people: contact information
Earlier articles on zoo animal TSE
British zoos did save primate samples

British zoos did save primate samples

Correspondence UK Veterinary pathologists  1 June 99
It 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.

Britain's exports of infected animals: the license record is available

7 May 1999 webmaster
It 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.

Export Health Certificates for live animals, genetic material and animal products

"Veterinary certification is usually needed when live animals, genetic material and animal products are exported to EU Member States or to other countries. They are issued by MAFF either through local offices or by Animal Health (International Trade) Division at Tolworth [J W Harris Block B Government Buildings Hook Rise South Tolworth KT6 7NF tel 0181 330 8656] depending on the country, species or product involved. For some countries conditions have been agreed and a 'model' certificate exists. Where new certificates have to be drafted, extra time is needed to agree the conditions with the importing country. First point of call should be the local Animal Health Office, listed in the table below. Further advice is also available in the section Help with exporting."

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

Import Licences for live animals, genetic material and animal products.

Live animals, genetic material, meat and animal and meat products imported into the country must meet either UK national or European Community animal health requirements. For further information contact:
MAFF Animal Health (International Trade) Division
Block C
Government Buildings
Hook Rise South
Tel: 0181 330 8194
Fax: 0181 330 6678 

America's imports of zoo animals from Britain and France

12 May 99 webmaster
The 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
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.

New York's zoo animal import center

"What do kudus, bongos, dikdiks, and black back duikers all have in common? Besides being African mammals, representatives of each species have moved through the ports of New York and New Jersey and have been quarantined at APHIS' New York Animal Import Center at Newburgh, NY. Located at Stewart Airport, the 20-acre site operated by VS has been open since March 1980.

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.

Housing Animals

The New York Animal Import Center consists of 17 buildings. Upon arrival, imported animals and birds are contained within a fenced compound that includes 13 barns. Cattle, horses, birds, waterfowl, and zoo animals are each housed in different barns designed specifically for them. The barns are separated by 100 feet of open space, and each barn is equipped with a ventilation system designed to prevent airborne infection spreading from one lot of animals to another. The largest horse barns hold up to 38 horses; the Center can accommodate 125 horses at one time.


Once animals are admitted to the quarantine building, they remain within a biologically secure unit. In order to ensure the integrity of the biosecurity, all employees and visitors must wear Government-issued clothing. Persons entering and leaving the different quarantine areas must wash their boots in a chemical foot bath. Also, when entering or leaving the facility and when going between some of the barns, visitors must take showers.

Import Permits

To obtain an import permit for the Port of New York as well as to reserve space at the Center, applicants must complete form VS 17-129 and return it with the appropriate reservation fee. The reservation fee is 100 percent of the anticipated quarantine charges. A list of fees as well as the necessary forms are available and may be obtained from the Center. To make arrangements to import animals through the New York Animal Import Center or to receive a list of user fees, contact
                        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.

Harry S Truman Animal Import Center

Imported animals must have an import permit and health certificate when they are brought into the United States. 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, the purpose for which they are being imported, and a description of the animal. All of this information is important because it allows Center employees to identify each animal and track it.

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.

July 31, 1998 Legislative and Regulatory Notes

Harry S Truman Animal Import Center - In the July 13 1998 Federal Register APHIS announced that in anticipation that the Harry S Truman Animal Import Center (HSTAIC) in Fleming Key, FL, may be closed, APHIS is giving notice that APHIS does not plan to hold a lottery in December 1998 for exclusive use of HSTAIC in calendar year 1999.

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.

Chimps sold in Brussels restaurants

Times Newspapers Ltd.May 16 1999 by Annamarie Cumiskey  and Richard Woods
Bushmeat 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."

Dating unpublished zoo BSE

10 May 99 webmaster
It 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:

Sat, 7 Jun 1997 
a HREF="">Dorothy Preslar
Briefing to the TSE conference hosted by the New Zealand MAFF
In 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.

SE Diagnoses In Exotic Species

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

BSE in Great Britain: A Progress Report

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

Narang's nvCJD victim list

 BSE Inquiry statement from Harash Narang
Comment (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.

victimS.U.deathageduration (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 1

* Victim 1 died in 1984 after an illness of 3 months. [Age is not stated.] Her first symptoms were that she became somewhat forgetful and then began to stumble and have trouble walking. Initially diagnosed by her GP as having had a nervous breakdown, she was later referred to hospital as her condition worsened. There she was finally diagnosed as suffering from CJD. Her clinical symptoms were consistent with new strain CJD. Victim 1¼s family recalls that before her death a man came from a hospital and took a full history of Victim 1. He was very interested in the fact that Victim 1 had at one time lived on a farm in Canada. After that he wanted to know if she had ever been to Papua New Guinea and explained that his question related to the disease Kuru. He was also interested in the fact that she had lived on a farm and wanted to know whether she had been in contact with sheep. Her favourite meal was calves brains on toast.

Victim 2

* Victim 2 died in 1989. The first sign of trouble was when Victim 2 complained about problems with his eyes. He became frightened and the fear grew so intense that he could not put one foot in front of the other. He forgot who his relatives were. Victim 2 was in his 50's when he died. There was no post mortem but when Victim 2 was in hospital a brain biopsy was done. Using my touch technique I confirmed that he had CJD. His clinical symptoms were consistent with new strain CJD.

Victim 3

* Victim 3 died in her 30's from CJD in 1993, four months after the initial symptoms of the disease appeared. Her symptoms started with depression, balancing problems and shaking, similar to those seen in BSE in cattle. Her clinical symptoms were consistent with new strain CJD.

Victim 4

* Victim 4 died in his 60's in 1993 after being diagnosed as suffering from CJD. His symptoms started with balancing problems and shaking similar to those seen in BSE cattle. His clinical symptoms were consistent with new strain CJD. In 1991 his family were told by a neurological centre that Victim 4 had "the human equivalent of mad cow disease". They were not told that he had CJD (Victim 16 also died of CJD while a student, near to where Victim 4 lived).

Victim 5

* Victim 5 died in her 60's from CJD in 1993. The first symptoms were tiredness followed by balancing difficulties and falling over similar to those symptoms seen in BSE cattle. Her clinical symptoms were consistent with new strain CJD. Subsequently she became forgetful, she would scream and become fidgety. Doctors initially said that she was neurotic. She was given a number of tests in hospital and "someone from Edinburgh" [home of Surveillance Unit] was sent to us. He asked Victim 5's family to complete a questionnaire with questions such as "did we live near farms, did she eat sausages". The only time this person spoke to the family he informed them that Victim 5 had CJD.

Victim 6

* Victim 6 was in her 60's when she died from CJD in 1994. Her partner who cared and looked after her during her 6 months illness told me about the frustrations he had to suffer while she was being investigated. Her clinical symptoms were consistent with new strain CJD (depression, falling over and difficulty walking). Her partner was told in hospital by the doctor that she had CJD. The doctor explained to him that the disease was "similar to mad cow disease". The family was interviewed by Dr De Silva from Edinburgh and the family completed a lengthy questionnaire. Dr De Silva told the family that Victim 6 had CJD and asked the family to "keep it quiet". He said that if they said anything about it the press would get hold of it and "make a hell of a meal of it".

Victim 7

* Victim 7 aged in her 50's, died from CJD in 1994. Her family who cared and looked after her during her 6 months illness told me about their frustrations during the course of the investigation of her illness. Victim 7 herself wrote in her diary "they are going to test me for mad cow disease". Her clinical symptoms were consistent with new strain CJD.

Victim 8

* Victim 8 died suffering from CJD in 1994 in her 40's. She started experiencing "funny feelings" and while walking would bump into people. She had balancing problems and developed jerky movements in her legs. Her clinical symptoms were consistent with new strain CJD.

Victim 9

In his late teens Victim 9 died from new variant CJD in 1995. The Lancet Medical Journal published his case in October 1995 and this immediately rang alarm bells. Sporadic CJD usually strikes people far older and Victim 9 had had no links with known sources of the disease, such as infected growth hormone. Victim 9 had clinical symptoms consistent with new strain CJD. I talked to Victim 9's family before his death. They had great concern about the way their son was being treated and insisted that I should be present at their his post mortem. A day after the post mortem I confirmed to Victim 9¼s parents that his death was due to CJD.

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.

Victim 10

* Victim 10 was in his 50's when he died in 1995 after being ill for three months. Following an unrelated eye accident his partner became aware that his behaviour was changing and within weeks she noticed that he was having difficulty holding a cigarette to his mouth because of a tremble in his hand. His driving became erratic and he was never able to return to work. His clinical symptoms were consistent with new strain CJD but no post mortem was performed. Victim 10 was seen by a doctor from Edinburgh who took a blood sample. He told the family that Victim 10 had CJD. He told the family that this was "the same as mad cow disease".

Victim 11

Victim 11 died of CJD in her 20's in 1995. Her partner told me of the enormous problems he had in obtaining a diagnosis of CJD. Victim 11's clinical symptoms were wholly consistent with new strain CJD. Her partner was told by Dr Zeidler from the CJD unit that Victim 11 had CJD. He told him that there was no connection with beef. He said that CJD had been around for centuries.

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.

Victim 12

* Victim 12 died in 1995 from CJD aged in her 30's. Victim 12 was diagnosed, while still alive, as having CJD after her family asked me to conduct my urine test. She died shortly after I confirmed that she had CJD. One of Victim 12's family wrote a series of letter to Government Ministers, including the Prime Minister John Major and the opposition leader, campaigning for recognition of my urine test for CJD. Her clinical symptoms were consistent with new strain CJD. The surveillance unit identified a PrP mutation [If so, this case should be dropped.]

Victim 13

Victim 13 died aged in his 30's in 1995 from new strain CJD. He had wasted away for 8 months prior to his death. He had been a fit man who rarely needed to see the doctor. He would cycle as well as being a keen basketball player. An inquest found that Victim 13 died of new variant CJD.

Victim 14

* Victim 14 who had also worked in an occupation that involved the handling of meat for a number of years, died from CJD in his 50's in 1996. As a hobby he often brought home beast heads, removed the horns and carved them. Victim 14¼s partner contacted me and asked me to test Victim 14 using the urine test for CJD. The test was performed a month before his death and was found to be positive for CJD. His clinical symptoms were consistent with new strain CJD. The post mortem confirmed CJD.

Victim 15

Victim 15 died in 1996 in her 30's. The cause of her death, established by post mortem, was bronchial pneumonia brought on by new variant CJD. The first signs of a developing illness were first noticed by her family in 1987 although the significance was not realised at the time. These initial signs included a complete change in her personality. Victim 15 was referred to a hospital for tests for diabetes and thyroid deficiencies.

Victim 16

Victim 16 showed the first symptoms of CJD in his late teens. He died, in his early 20's in 1996. Six months later a coroner determined that it was "more likely than not" that his death had been caused by eating contaminated beef before 1990. Victim 16 was a vegetarian from the age of 16 but his favourite food as a youngster had been beef burgers. The consultant neuropathologist of told the inquest "most neurologists would link CJD to the BSE epidemic, but would probably not say so in public".

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.

Victim 17

Victim 17 was in her 40's when she died from CJD in 1996. Her symptoms started with depression, balancing and walking difficulties and clinical symptoms consistent with new strain CJD. Her partner told me that medical staff blamed him for causing depression. After her death she was confirmed as one of the first 10 cases of new strain CJD. Victim 17 was a blood donor. Her partner was told by Dr Martin Zeidler from the CJD surveillance unit that the cause of her illness was a rogue gene. He said that in 99.9% cases there are cases on the other side of the victims¼ family with Alzheimer¼s Disease. Following Mr Stephen Dorrel¼s announcement Dr Zeidler came back to her partner to confirm that Victim 17 was one of the 10 cases referred to in the announcement.

Victim 18 and Victim 19

* Victim 18 and Victim 19 were twins. They both died of CJD. Victim 18 died first in her 50's in 1989. She woke up one morning with her shoulder hurting. Her doctor diagnosed a trapped nerve in her shoulder. Within days she developed weakness in her legs and found it difficult to walk. She was treated for depression. Huntington¼s Chorea was suspected. After an EEG test, her family was told that she had CJD. Her clinical symptoms were consistent with new strain CJD. Victim 18 had been a blood donor from 1981.

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.]

Victim 20

* Victim 20 died in his 40's in 1996 after an illness of 11 months. His partner told me about his initial symptoms as having difficulty in walking and balancing. He developed shakes similar to those seen in BSE cattle. His symptoms were attributed to muscular pains in his neck. His mental confusion appeared only later. He had diagnosed himself as suffering from mad cow disease. His partner was told by doctors that he could not have BSE because he was too old.

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.

Victim 21

Victim 21 was healthy until CJD struck. She died in her 30's, in 1996 after being ill for 11 months. For most of her illness doctors and psychiatrists treated her for depression. She would fall while walking and had great difficulty balancing herself. Her clinical symptoms were consistent with new strain CJD. Her family suspected that she was suffering from mad cow disease and doubted medical diagnosis. They demanded that Victim 21 be tested for CJD. Results sent from America the day after she died confirmed that she was suffering from CJD. [Presumbably a 14-3-3 test on spinal fluid done at NIH or Cleveland.]

Victim 22

* After being ill for about 10 months Victim 22 died in her late teens. Her clinical symptoms had been those of new strain CJD; depression, balancing difficulties and shaking. She was treated in the same hospital as Victim 16. After a number of tests she was first suspected as suffering from ME and later from a brain tumour. Eventually Victim 22 was diagnosed as suffering from CJD. She had no links with any known source of the disease such as infected growth hormone and there was no history of the disease in her family.

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.]

Victim 23

* Victim 23 became ill in his 40's and in 1996 he changed dramatically from being sociable. As his illness developed he staggered increasingly and had difficulty in walking necessitating the transfer of his bed to the ground floor when he could no longer climb the stairs. His clinical symptoms were consistent with new strain CJD, depression, staggering, falling over, having difficulty in walking. Initially he was sensitive to his tendency to stagger and when out used a walking stick to let other people know that he was not drunk. He had been a regular blood donor and the final occasion on which he had donated blood was only some 6 months before the appearance of his symptoms.

Victim 24

Victim 24 died of CJD but has not been classified as a nvCJD victim. [* was omitted] She is a nvCJD victim. Victim 24 became ill in May 1993. Her immediate clinical symptoms included loss of weight, loss of memory, balancing problems, poor eye sight, depression and tiredness and were consistent with nvCJD. She was admitted to hospital on 6th August 1993 where a brain biopsy was carried out. She and her family were told by the Registrar that she had spongiform encephalopathy. The Registrar was asked to write this down so that the family could remember the words. He wrote "spongieform (sic) encephalopathy".

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.

What offal ban? -- testimony of AJ Fleetwood

15 Sept 98 Inquiry statement and 7 May 99 webmaster commentary
Andrew 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) 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.

Zoo people: contact information

7 May 99 webmaster. Note separate collection for people with CWD involvement
Arthur, Charles, TSE reporter at The Independent who sometimes writes on TSE in zoo animals and pets.

Bons, Noelle, Ecole Pratique des Hautes Etudes Neuromorphologie Fonctionnelle, UniversitÈ Montpellier, France Tel : (33) Fax; (33) 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.

Earlier articles on zoo animal TSE

6 May 99 webmaster: index to 74 earlier wild animal articles
Chronic Wasting Disease (CWD):
06 May 99 -- Mad deer, mad elk: CWD summary, links
19 Mar 98 --14 facilities where CWD has been found

Leaky feed bans:
11 Mar 98 -- Vet's reference to scrapie was cut from speech
14 Jul 96 -- Details of EU cover-up memo
09 Feb 98 -- MAFF lied all along
10 Dec 97 -- Black market in T-bone steaks and oxtail to flourish
05 Jan 98 -- Farmers to defy ban with a feast of oxtail
23 Jul 96 -- Sheep, goat, deer offal finally banned
28 Jul 96 -- Massive beef storage fraud exposed
08 Jul 96 -- Horror at birth of BSE
08 Jan 98 -- US ranchers ignore mad cow rules
01 Aug 97 -- Origins of BSE: rendered meat from Africa?
21 Oct 96 -- Out of Africa: new theory for BSE origins

Zoo, captive, and wild animals:
15 Dec 97 -- Bad news on BSE fed to primates
26 Jun 96 -- French prove BSE llnk to primates
15 Jul 95 -- Prion protein gene variation among primates
12 Nov 96 -- Ape colony needed for study on BSE effects
29 Nov 97 -- More cheetahs dead in France
02 July 96 -- Felid update
07 Jul 96 -- Cow to primate situation worsens
26 Oct 98 -- Taiwanese eat raw brain from living endangered macaques
01 Sep 97 -- Zoo animal victims so far
02 Jul 96 -- BSE transmitted to other animals
04 Apr 98 -- Thousands of animals to be infected in BSE experiment
30 Sep 97 -- Neurological disorder, unknown, ibex and chamois
30 Oct 97 -- Scrapie outbreak in bighorn sheep rumored; scabies instead
18 Aug 98 -- Repeat region deletions in other species
01 Dec 96 -- R.F.Marsh: collected TME papers
09 Jun 97 -- Wisconsin researcher helped corral mad cow disease

Scrapie and BSE transmission issues:
17 Jun 96 -- Is Scrapie transmittable to humans?
14 Mar 97 -- Scrapie in sheep embryos
10 Jul 97 -- BSE horizontal transmission likely
28 Mar 98 -- French vache folle of 1883: more work needed
01 Mar 98 -- Reported scrapie in US: 1,117 cases (1947-1992)

Cats and dogs:
01 Oct 98 -- Man and his cat in CJD mystery
02 Oct 98 -- Same strain of CJD kills man and his pet cat
03 Oct 98 -- CJD in a man and pet cat
23 Sept 97 -- Cat prion sequences in conflict: alignment
17 July 97 -- So where is the 1991 dog study or the cat prion sequence?
19 Oct 96 -- 72 house cats down from BSE
01 Jul 96 -- Spongiform encephalopathies of cattle, sheep and cats in Hungary

30 Nov 98 -- MAFF Goes to the Dogs ... a Play in Three Acts
30 Nov 98 -- BSE fibrils found in 19 hunting dogs
07 Aug 98 -- North Carolina dogs end up in dog food
29 Apr 97 -- Report on BSE in dogs suppressed
26 Apr 97 -- Tests on labrador could prove BSE has spread to dogs
13 Nov 96 -- Has transmission to dogs ever been tested?
27 Nov 98 -- Dog prion anomaly confirmed
23 Sep 97 -- Lots of UK dogs with TSE?

18 Oct 96 -- Cat food fears
04 Dec 97 -- Doubts about pet food
23 Oct 97 -- Housecats rendered to pet food may recycle BSE
16 Oct 96 -- BSE fear for millions of British pets
17 Oct 96 -- Owners of pets seek BSE answers

Pigs and chickens:
06 Apr 96 -- NIH expert: pigs and chickens risky
20 Jan 98 -- Pig-to-human transplant ban urged
13 Nov 98 -- Pig feed rules may ban use of animal remains
17 Dec 97 - Pig, chicken feedback loop closed
08 Jun 97 -- This mad pig went to market
11 Sep 97 -- Government urged to allow pig transplants
30 Oct 97 -- World needs cross-species transplants?
17 Jul 97 -- Dutch slaughter 5 million diseased pigs
08 Jun 97 -- Trade-offs on pig brain transplants to humans
06 May 97 -- FDA: OK to still sell TSE-positive material
24 Mar 97 -- The case for mad pigs in the US; USDA response 1, 2
08 Jun 97 -- BSE may have spread to chickens
05 Oct 97 -- Physicians want chicken manure out of cattle feed

30 Aug 97 -- Squirrel brains and CJD in Kentucky
15 Aug 97 -- Squirrels: a natural reservoir for TSEs?
05 Aug 97 -- Baby squirrels dying from tremors
19 Aug 96 -- Squirrel brains and CJD

01 Mar 97 -- Mad migrating salmon?
06 Dec 96 -- Germans shift panic on British food to salmon
29 Nov 96 -- Fish-meal is banned from cattle feed

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