15: Political Persuasion
Kenya clarified my thinking and in 1993 I decided to leave my job. The next question was whether to continue with the important areas which I felt the Vegetarian Society had abandoned - actively campaigning on farm animal abuse and trying to influence the next generation. I really had no choice and Viva! came into being.
The first, low-key announcement of its existence was made at the World Vegetarian Congress in Holland in August 1994, where I was a speaker. Then, on 26 October 1994, Viva! was launched. All the battles, disappointments, doubts or concerns which had preceded this day evaporated as I looked at the packed room in the Union Club in London’s Gerrard Street, in Soho. We had drastically underestimated the numbers who would attend and the anticipated 50 had swelled to nearer 100.
Alongside me as speakers were Michael Mansfield, QC, a Viva! trustee, a friend and a brilliant and principled defence barrister; David Gee, ex-Director of Friends of the Earth; David Ryde, the wonderful vegan GP who served on the medical sub-committee of the British Olympic Association; Jon Wynne-Tyson, the eminent author of works on humane thought and animal rights; Guardian writer, author and cookery devotee Colin Spencer; Darling Buds of May actress and devoted vegetarian Pam Ferris; and the dreadlocked, kind and gentle poet Benjamin Zephaniah, who read some of his poems to end the launch on exactly the right note of humour and hope.
One person who I would have liked to be there unfortunately couldn’t attend. I don’t have many heroes or heroines, but one of them is Professor Richard Lacey, the person most responsible for bringing the dangers of bovine spongiform encephalopathy (BSE, commonly known as ‘mad cow disease’) to the public’s attention. He is one of the few academics who does not weigh his career prospects against his beliefs and is brave, fearless and totally principled in an age when all three qualities are in very short supply.
Just for the record, Richard Lacey is a professor of clinical microbiology at a Leeds hospital and also a medical doctor. He has had over 200 papers published and was a Government adviser as a member of MAFF’s Veterinary Products Committee until his resignation in 1989. Subsequently, both his professional standing and his sanity have been challenged by Conservative MPs in an obvious attempt to undermine his standing.
Professor Lacey has written that the Government has jeopardized public safety in order to save the livestock industry from ruin and this policy has considerably increased the chances of humans catching the disease. If he is right - and he puts the odds at about 60 per cent - then Britain faces a most frightening epidemic of a fatal and incurable disease - Creutzfeldt Jakob disease (CJD), which is the human version of BSE. CJD has been known about for some years but hit the news in 1986 when cattle were diagnosed with a similar disease which attacks the nervous system and turns the brain into a sponge-like substance, honeycombed with holes. By 1995 it had spread to at least 150,000 cows.
The most baffling aspect of the story is the agent which causes BSE and possibly also the CJD infection - it has never been identified. It is neither a virus nor a bacterium and has broken all the most basic rules of biology. It appears to be able to alter its form, one minute being inanimate and capable of withstanding enormously high temperatures, while another minute being active and highly infectious. It is so infectious that some doctors have refused to perform autopsies on those who have died from CJD and some hospitals have declined to admit people believed to be infected with it. Any prospective cure lies at the very limits of current science.
With extraordinary short-sightedness, in August 1988 the Government offered farmers only half the market value for cows diagnosed with BSE. Not surprisingly, the number of reported cases remained comparatively low, but when the compensation was increased to the full value of the animal in February 1990, the number shot up. You don’t have to be Einstein to work out the reason why.
The youngest cow so far to develop BSE was 18 months old and the oldest 18 years. The incubation period in humans can be as long as 30 years, so any apparent failings in Government policy are unlikely to show up for an election or two. The link between cows and humans has yet to be proved but the Communicable Disease Surveillance Centre reported that people who regularly eat veal or beef products are 13 times more likely to die of CJD than those who don’t. Professor Lacey is convinced that CJD and BSE are one and the same disease.
In May 1988, the Government set up the Southwood committee, charged with the task of investigating BSE. The committee contained no experts on the subject and didn’t consult any. Despite this, it eventually instructed that all infected cattle should be slaughtered. But the action came too late - meat from over 600 obviously diseased cows had already found its way into the shops.
This figure was eventually made to look like chicken feed by a Granada TVs World in Action documentary programme, ‘The Hidden Epidemic’, transmitted in October 1995. It revealed that secret Government papers admitted that for every cow diagnosed with BSE at least another two infected cattle were entering the food chain. Microbiologist Dr Stephen Dealler estimates that by the year 2001, 1.8 million infected cattle will have been eaten, ensuring that the majority of the British population will have eaten beef or beef products from BSE infected cattle.
Despite their apparent lack of expertise, the Southwood committee produced other recommendations and reassurances. They said that the risk of humans catching the disease through what they ate was remote, seemingly ignoring the fact that it was from feed that cows themselves had first caught it. They thought that the sheep encephalopathy called scrapie had passed to cattle in their feed when sheep offal, including brains, had been rendered down and turned into a high-protein supplement. Professor Lacey, however, is not convinced by this scenario and believes that a similar process of turning cow body parts into feed may have triggered the infection, which he thinks may have always been present in cattle. Certainly it was this which caused the disease to spread so rapidly.
However, the Southwood committee also concluded that there was no risk of mother cows passing the disease on to their calves. Just as important, they were convinced that cows would prove to be ‘dead end hosts’ and would not pass BSE on to other species. Had they been sufficiently inquisitive they would have known that even as they were writing their report, animals other than cows had already been infected with BSE. Their reassurance that cows would not infect their calves was also later to be proved conclusively wrong.
The report concluded: ‘... if our assessment of these likelihoods is incorrect, the implications would be extremely serious.’
The Southwood committee’s final recommendation advocated the formation of another committee to carry out more research. This second committee, the Tyrrell, published its report in early 1990 and recommended that brains of all slaughtered cattle, whether they were showing symptoms or not, should be checked for BSE. It also proposed that all cases of CJD should be monitored for 20 years.
Both these recommendations would seem to be both logical and necessary. Monitoring of all slaughtered cattle would obviously show if the disease were widespread amongst animals not showing symptoms and monitoring human cases would show if there were any increase in CJD. But the Government has failed to act on either recommendation.
As already mentioned, the cause of BSE in cattle was initially thought to be the practice of rendering meat and carcasses to produce high-protein animal feeds. In 1988 this was banned, but there was little effect on the ballooning statistics. The number of new cases rose from 500 in January 1989 to 900 in December 1989. Exactly one year later the figure rose to 1,500 a month. Another of the predictions in the Southwood report had been that the disease would peak at 400 cases a month...
In May 1990, a domestic cat died from BSE but the Government refused to acknowledge the fact. By July, however, 52 cats had been infected and the Government had to admit that pet food containing beef was probably the cause. The question now was how many other species were at risk and whether humans were one of them.
In the following year, 1991, we started to find out. Numerous tests and studies on other animals had been conducted and seven out of eight species of mammals which were fed infected meat developed the disease. This was later to increase to 18 species. They included pigs and monkeys. Reports also came in of a puma and a cheetah dying of BSE. In a pronouncement of sublime complacency, MAFF then announced that the disease would peak that year and would disappear altogether by 1994.
By the end of 1992, the number of reported cases had risen to 25,025 and the disease showed no signs of abating. It was obvious that as the apparent source - infected animal feed - had been banned, some other transmission route was at work. The evidence pointed to vertical transmission - mother cows passing it on to their calves. The Government still refused to admit this until in 1994 the number of cases rose to 7,000, six times greater than Southwood’s worst case scenario.
However, the admission was retracted a year later and MAFF maintained that the reason for the continuing outbreaks of BSE was the illegal use of banned slaughterhouse products - ‘specified offal’ - in vitamin and feed supplements which found their way into fish and other meals. If you were a cynic, you might believe this about-face has something to do with protecting the export of veal calves to Europe. Who would buy and eat veal believed to be infected with BSE? If humans can catch CJD from cattle, Britain has ensured that Europe shares this frightening prospect with us.
Despite having been consistently wrong on almost everything else, the Government continues to insist that the infection is restricted to the nervous system and is not present in the flesh of animals. Removing the brains, spinal column, spleen, thymus gland and tonsils makes beef safe to eat. But cells from all these organs enter the blood and find their way to other organs, including the liver and bones - and bones are the principal source of gelatine, made through a process of concentration. Knowing that the agent can withstand incredibly high temperatures, Professor Lacey’s fear is that gelatine may turn out to be a particularly potent source of infection. Its widespread use in dozens of prepared foods, from confectionery to aspic, jellies to pork pies, makes that possibility extremely disturbing.
These fears were given a chilling boost by an extraordinarily detailed and technical seven-page article in the Mail on Sunday Review of 17 December 1995. Entitled ‘Mad Cow Disease and Human Deaths - A New Link’ and written by Peter Martin, it traced a path of Governmental complacency and apparent deception surrounding the two diseases. The first clue that CJD and BSE might be linked, it seemed, was established by neuro-pathologist Dr Robert Perry and clinical virologist Dr Harash Narang in 1989 after examining two CJD cases. Narang, then a Government scientist with the Public Health Service Laboratory (PHSL), went on to develop a comparatively simple test for diagnosing sub-clinical BSE in cattle which hadn’t yet shown symptoms of the disease but which would end up in the food chain. We now know from the large number of cases which fall into this category, estimated by Dr Stephen Dealler to be 1.5 million by 2001, that the cost of full compensation would be enormous - in the region of £1.4 billion. The Government chose not to use the test.
Dr Narang tried to get funding for his test and in 1990 received a rejection from MAFF, despite having proved the test successful at the Central Veterinary Laboratory at Weybridge at the end of 1989. Also in 1990, the House of Commons Agriculture Committee asked for submissions from scientists on the dangers of BSE, including two written requests to Narang. According to the Mail on Sunday, these requests were never passed to Narang by his superiors. Eventually he was contacted by phone. What he told the committee was disturbing.
He stressed the need for urgency and explained that his test would cut the time necessary for the results of infectivity studies from between one and three years to just 20 days. On the question of BSE posing only a remote risk to humans, as claimed by the Government, Narang is reported to have said that, compared to other encephalopathies, BSE was a unique superstrain with an unusually short incubation time - half that of sheep scrapie. He maintained that because 23 different species of animal had died from BSE, this indicated that humans were not totally resistant to it. Again MAFF turned down his test, as did the Ministry of Health.
With the onset of the BSE epidemic, the nature of CJD appeared to change. Before 1985, CJD tended principally to attack the cerebral cortex and sometimes the cerebellum. In 1995, the Mail on Sunday claimed to have discovered six recent cases of CJD, chosen randomly, in which the infection had taken a different course. It had principally attacked the central grey matter of the brain and the cerebellum. This is exactly what happens in the brains of cattle infected by BSE!
Another change in CJD appears to be the young age at which some victims were being diagnosed - three teenagers in Britain and four others world-wide. Again, Dr Narang believes this could be as a result of intravenous infection in children through the sockets of lost milk teeth.
Dr Narang’s trail of discovery became somewhat disrupted in 1991 when the PHSL accused him of failing to register his work under new health and safety regulations. His work obviously fell outside the scope of the new Health and Safety Executive (HSE) regulations which were to safeguard against genetic manipulation which was dangerous to humans. However, in 1992, he was suspended by the PHSL following complaints of alleged professional misconduct in obtaining patients’ notes improperly.
The complaint was still hanging over Dr Narang in 1993 when the PHSL instructed him to leave his specially equipped laboratory in Newcastle and go to work in London. An ex-MAFF employee was put in as his assistant and in his absence, the PHSL destroyed a number of his valuable spongiform samples. The end came in 1994 when Dr Narang was made redundant.
This abridged newspaper report is a remarkable document, not least in its detail. It reveals that possibly the most knowledgeable man in Britain on the subject of BSE, the one person who holds the key to its understanding, its diagnosis and its possible future course is ñ ‘redundant’. Dr Narang was also, of course, one of the few scientists able to challenge the Government’s oft repeated challenge that beef is safe to eat.
At the time of writing, in 1996, the furore surrounding BSE has died down, but there is a sense of waiting to see what will happen next. Four dairy farmers who had infected cattle in their herds are known to have died from CJD. Also, in May 1994, Vicky Rimmer, a 15-year-old girl, was diagnosed as having CJD and diet was thought to have been the cause. Proper tests will not be possible until after her death. One of the most disturbing aspects of this sad case was reported in the Daily Mirror on 25 January, 1994. It claimed that Vicky’s mother maintains that a doctor from the CJD surveillance unit examined her daughter and asked Mrs Rimmer not to make the case public. ‘Think of the economy and the Common Market,’ he is reported to have said. If this report is true, then of all the rallying cries with which people have faced death, this probably ranks as one of the most banal and insulting.
We still know almost nothing about BSE and the Government’s handling of the outbreak indicates that its primary concern throughout has been to protect the beef and dairy industries. To that end it has gambled with human safety.
Don’t dismiss this as an isolated incident. In 1990, the US administration admitted that a new virus had become widespread in the country’s cattle herd. This bovine immunodeficiency-like virus (BIV) is the cattle equivalent of AIDS and a member of the same family of lentiviruses.
It was only a question of time before the infection arrived in Britain and it happened in 1993. The first outbreak was in a herd of Holstein dairy cows just 10 miles from my home. MAFF’s attitude to it was predictable. BIV was, they said, a mild infection which, like all lentiviruses, was extremely slow in producing symptoms. It posed no threat to cattle and there was no need to make it a notifiable disease. Above all, it was species specific and could not infect humans. In other words, business as usual.
Unfortunately, the facts didn’t fit the theory. The farmers who had the outbreak, Tim and Linda Blything, had bought some new cows from Holland and within days of arriving on the farm they had all gone down with a whole range of diseases. Days later the rest of their herd followed. By pure luck, their local vet had just returned from the US and suspected BIV. He informed MAFF.
Suddenly confusion and contradiction engulfed the Blythings. Samples were taken, visitors arrived and departed, tests were done and undone. There was a whole series of admissions and denials, followed by counter denials and counter admissions, but no diagnosis.
Meanwhile, almost every pregnant heifer aborted as she approached full term and most calves which were born lasted only a day or two. One minute they were suckling, the next they looked ill and by the following day they were dead. Within a few months, over half the herd had either died or had been destroyed to save suffering. Still MAFF refused to diagnose BIV and continued to insist that BIV was, in any case, a benign infection.
The moment the words ‘cow AIDS’started to be attached to the Blythings’ herd, they were virtually finished in the locality. Deliverers didn’t want to deliver, neighbours didn’t want to be neighbourly and no one wanted to touch their cattle. Although they could have officially sold their stock, no one locally would buy them and the Blythings felt it would be irresponsible to take them elsewhere and sell them secretly.
After a few months the symptoms largely subsided in the remaining herd, but when the cows approached full-term pregnancy again, the same distressing deaths started to happen once more.
When I visited the farm towards the end of 1994, some cattle lay almost motionless, exhibiting almost total lethargy. Calves were equally depressed, with discharges from the eyes. Most of the cattle had lost huge amounts of body tissue and looked like skeletons, particularly around the hind quarters. And as one cow was herded into the milking parlour she showed similar symptoms to those associated with BSE - she was extremely nervous and jumpy and on the point of panic. As MAFF still refused to accept that BIV was the cause, I decided to carry out my own research.
The virus was first discovered in a cow in Louisiana in 1969 when it was looked at with only mild interest, frozen and forgotten. It was labelled R29, the number of the cow from which it was taken. With the outbreak of human HIV and AIDS, suddenly interest perked up and the virus was defrosted and cloned hundreds of times over in the belief that it might provide an understanding of the human disease.
Few scientific papers had been published on BIV, but two early ones showed success in infecting human cells. Early work also indicated that the effect on cattle was not quite so benign as MAFF has maintained. All subsequent laboratory experiments, however, showed it wasn’t virulent and wouldn’t infect human cells. Something didn’t add up!
All experimental work, I discovered, had been carried out on the one and only R29 sample which had been cloned so many times that it had become extremely weak, indicating that the later tests were probably valueless. What was disturbing was a discovery which showed that BIV, too, could jump species - to rabbits, sheep and goats - both in vivo and in vitro. The man who had originally identified BIV in the US was Professor Gene Luther of the University of Louisiana. He flew to Britain in July 1994 to inspect the Blythings’ herd and study the post-mortems on the dead cattle. He disagreed with much that he read and was in no doubt as to what afflicted the cattle - BIV. He also disagreed with MAFF’s insistence that BIV was a benign infection, citing the US experience.
In the private report he prepared for the Blythings, he set out his own experiences. He wrote that herds in Oklahoma and Texas had accidentally been infected with BIV in 1991 by a contaminated commercial vaccine. It resulted in abortions, infertility in both heifers and bulls, chronic wasting, diarrhoea, pneumonia, lameness, mastitis and unexplained deaths - an almost exact catalogue of the Blythings’ problems. Professor Luther had kept track of one of these herds and by 1994 it had been reduced to two animals, the remainder having died or been destroyed - an outcome which was far from benign.
At his own university in Louisiana, the 139-strong herd were all descendants of the original poor old R29 and in 1989 80 per cent were BIV positive. Three years later only 12 of them were still alive. Death of the calves born to this herd was almost total.
The professor also followed a US beef herd for three years when it was kept on open pastures with little or no stress. All the cattle appeared to prosper and flourish, apart from occasional bouts of depression and nervousness. But after they had been slaughtered he discovered that every single animal had brain lesions, swelling of the brain, meningitis and enlarged lymph nodes. They were very sickly cattle.
A copy of Professor Luther’s report was presented to MAFF towards the end of 1994. As a consequence MAFF sent a delegation out to Louisiana to interview him. During this visit, Professor Luther stressed to the delegation that the outbreak of BIV at the Blythings’ farm presented a unique opportunity. He advised that the farm should be turned into one enormous laboratory in which it would be possible to study BIV, in particular this newly mutated and seemingly virulent version of the virus. He was left with the impression that this was what would happen. It didn’t!
Professor Luther is convinced that BIV acts in a similar way to HIV. By depressing the cow’s immune system, a whole range of unrelated diseases is allowed to flourish. One of the key factors which leads to the cow showing symptoms appears to be stress - milking, pregnancies, crowded living conditions, calving and transportation. When the cows are left to their own grazing on open pasture, the symptoms subside but the disease remains.
The main difference between the US and British experience was the speed with which the disease had developed in Cheshire. It was no longer a lenti (slow) virus but an amazingly quick one. What had happened to the infection in its passage across the Atlantic? It seemed that a new, more virulent form of the virus was at work.
I unearthed some recent US research which did, in fact, show that the BIV virus has developed substantial genetic variation, that is to say, it has changed its form dramatically. But even more worrying was an indication that it is considerably more complex than other lentiviruses, providing it with an almost endless ability to mutate. There was also the suggestion that different diseases are combining together, enabling each to prosper. One of these is the cow leukaemia virus - BLV.
Following this path, I went to Belgium in August 1994 to see Professor Arsen Burney at Jambloux, an agricultural university. He is a specialist in BLV. He was forthright in his opinions and spoke openly to me:
Governments are against research into animal diseases. They don’t want to pay compensation and so - they ignore them until it’s impossible not to. There is a general attitude surrounding BIV and that is that it’s be better not to ask questions. The truth is that we can’t ignore it any longer.
There is a great danger that nature is beginning to strike back. Cramming millions of birds into one shed, imprisoning 3,000 pigs in one building, pushing cattle to the brink of their ability to cope is simply not sustainable. We are creating huge problems which are likely to be in- soluble. We are creating perfect breeding grounds, we are abusing antibiotics and the result is already a disaster for the animals and it is likely to be a disaster for humans also.
In this instance, if BIV does result in a weakened immune system, and the evidence points to the fact that it does, then we can never say that it cannot pass from cows to humans. I am not convinced that BIV will not infect humans. It is possible for any virus to jump to humans, it just depends upon the circumstances.
Professor Burney’s expression ‘we are abusing antibiotics’ started me down another path. The Blythings believe the cattle they bought from Holland were, in fact, falsely ear tagged and originated from Eastern Europe. It is coming to light that the conditions in which animals are kept there are much worse even than in Britain and very high stocking densities lead to an even greater use of antibiotics. It is known with human HIV that a history of antibiotic use increases the risk of infection and makes the disease progress faster. A similar effect could be happening in cattle.
It is impossible to tell yet whether BIV is a direct threat to humans or not. Most of those working in the field think not but with such a rapidly mutating virus, however, all future bets must off.
But there is another, real and immediate threat which Professor Arsen Burney can see quite clearly:
Because of the weakened immune system in cattle with BIV, the other diseases they suffer from will prosper and many of these will pass to humans.
Professor Richard Lacey was in total agreement when I asked him to comment on this:
About half the infections which affect cattle also affect humans. If a cow’s immune system is weakened, and that’s precisely what appears to be happening, then it is inevitable that it will produce something harmful to us. People don’t die of AIDS, they die of a whole range of illnesses and infections brought on by the reduced immune system. And that is what will happen with BIV. What we are particularly at risk from are salmonella 0517, tuberculosis, listeria, staphylococcus, cryptosporidium and numerous viral complaints and abscesses.
Perhaps it’s no accident that the diseases which look like prospering are the very infections which are increasingly failing to respond to antibiotics.
One thing is certain - if BIV does pose a threat, either directly or indirectly, MAFF has guaranteed that it is now endemic in the UK herd.
When the story first broke, Tim Blything received several phone calls from farmers who believed their stock had also contracted BIV. None of them cared to leave a telephone number. I managed to track down two of them.
The cattle of both farmers had symptoms identical to the Cheshire herd, but because of MAFF’s refusal to regard the disease as anything out of the normal, to make it notifiable and pay compensation, both sold their stock on the open market and they are now distributed amongst other herds.
MAFF has stuck to its position throughout, but not so Milk Marque, the privatized version of the Milk Marketing Board, which refused to accept milk from the Cheshire herd because they were not satisfied that BIV is destroyed by pasteurization.
The main point is that another potentially devastating disease has appeared in cattle and again our leaders have placed commercial concerns above those of either human or animal health.
On March 20, 1996, the day this chapter was to go to press, the British Government was forced into a humiliating U-turn. It confirmed that there is a new form of CJD which is caught from eating beef. The public sense of betrayal was huge.
So, Narash Narang was right all along. Prof. Richard Lacey was also vindicated when a government expert, Prof. John Pattison, confirmed that his prediction of a possible 500,000 human deaths each year may be correct. It is a grim commentary on modern society and a frightening validation of this book.