Mad Cow Disease
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- * FOURTH TEENAGER IS KILLED BY
CJD
- * TAKE ONE LAST LOOK
- * HARD EVIDENCE LINKING MAD COW
DISEASE WITH HUMAN DEATHS
- * ON AVERAGE, WE'VE EATEN 80 MEALS OF
CONTAMINATED BEEF EACH
The Mad Cow Deceit Night & Day's Campaigning Investigation By
Peter Martin - Special Report [London UK] Mail On Sunday NIGHT &
DAY FEBRUARY 18 1996
FOURTH TEENAGER IS KILLED BY CJD
Creutzfeld-Jacob Disease used to take
decades to kill. Sufferers tended to be over 55. But CJD is changing.
Now it kills the young. Can it be a coincidence that, in the last 10
years, we've eaten 1.5 million BSE-infected animals?
On Friday morning at 11 o'clock,
20-year-old Peter Hall was buried at Chester-le-Street Parish Church
cemetery, near Sunderland, Co Durham. He was killed by Creutzfeldt
Jakob Disease (CJD), the human equivalent of Mad Cow Disease (BSE).
First striking him at 19, just 13 months ago, it made Peter Hall the
fourth British teenager to succumb to the disease to date.
Two others died last year-Stephen
Churchill, at 19, and an un-named 17-year-old girl. The very first
teenage CJD victim, Victoria Rimmer, 16 when she was diagnosed by
live biopsy late in 1994, is still in a coma.
Government scientists argue that the
recent increase in surveillance is the most likely reason why more
cases, including teenage cases, are now being identified. But
Britain's leading CJD specialist, Dr John Collinge, at St. Mary's
Hospital, Paddington, disagrees. 'Given the rarity of CJD in
teenagers,' he says, 'It is unlikely that such cases would have been
previously missed.' In other words, we're faced with something new.
The Government still insists that there is no evidence to link BSE
and CJD. Most recently, Health Secretary Stephen Dorrell said that
'there was no conceivable risk' in eating beef. But the facts tell a
different story.
Before BSE, there was no recorded case in
this country of CJD in a teenager. Usually striking people aged 55
and over, CJD is so rare among young people generally that there have
been only five reported teenage cases-ever-in the rest of the world,
as against four in Britain in the last two years.
The evidence of a link between BSE and
CJD-as exclusively reported in Night & Day last December-is
mounting. For one thing, since the BSE outbreak, the whole pattern of
CJD in Britain has been changing. As well as striking younger people,
it also attacks a different part of the brain-the part which BSE
attacks in cattle. The initial symptoms are different, too. In
old-style CJD, the kind which usually struck those over the age of
55, the first sign of serious trouble was forgetfulness-very much
like Alzheimer's. But today, as in these teenagers, an equally common
major symptom is so-called 'ataxia'-exactly the kind of staggering
and loss of balance seen in BSE-riddled cattle.
Now, too, we are seeing a sprinkling of
CJD among people in their twenties and thirties: Jean Wake, 38,
Michelle Bowen, 29, and Maurice Callaghan, 30, all died last year.
And what of the four farmers who've died of CJD? All had worked on
BSE herds, which hardly seems random. Indeed, given the worldwide
incidence of CJD of one case per million population, and 20,000
British farmers at risk, only one farmer would be expected to succumb
every 50 years-not four in the past three years.
None of this, it must be said, amounts to
concrete proof of a link between BSE and CJD. But the Government's
insistence that there is no evidence of a link is plainly untrue.
That there are four known teenage CJD cases in Britain to date is bad
enough. But given that any parents would be reluctant to go to the
media once their child had been pronounced terminally ill, as were
Derek and Frances Hall, there is a strong likelihood that there could
be more British teenagers out there dying of CJD. The Halls decided
to 'go public' only after the publication of Night & Day's
article last year.
Calculated to protect Britain's beef
trade, and first deployed in 1989, the Government's initial gambit
was to insist that BSE posed only a 'remote risk' to man, when there
was no evidence whatsoever to back the claim.
Stuck with that half-lie thereafter, the
Ministry of Agriculture actually refused to develop a postmortem
abbatoir test which would determine, once and for all, the full
extent of the BSE epidemic. Dr Harash Narang, the government
scientist who'd formulated the test, pushed hard to get it used and
thereafter was officially side-lined, demoted, smeared, and finally
made redundant at the end of 1994.
Working entirely off his own bat, however,
Dr Narang is now perfecting a BSE urine test for cattle. As well as
eradicating the disease, it would restore our beef trade at a stroke.
Official policy, instead of protecting the beef trade, appears to be
having the opposite effect. Just this week, fed up with the
Government's ducking and diving, five German states banned all
British beef imports.
Again, all on his own, Dr Narang has
already perfected a urine test for CJD. It was immediately after
learning of this test in Night & Day that the Halls invited Dr
Narang to test their son. Twice they'd asked Peter's neurologist if
he could be suffering from CJD, twice he insisted it was highly
improbable in one so young. In January, Dr Narang's test confirmed
the contrary.
That the Government still refuses to
recognise and utilise Dr Narang's test isn't merely a political
outrage. Without fast and accurate diagnosis of CJD, of which Dr
Narang alone appears currently capable, there remains no possibility
of any ameliorating treatment for this hideous disease, let alone a
cure.
In the last five months of his life, Peter
Hall was offered no treatment whatsoever. And, except for a weekly
visit from his neurologist, nor was his illness closely monitored.
Eloquent with anger, Derek Hall says: 'If Peter's condition was
unique and devastating, as we'd been told it was, why is it that no
one bothered to study what he was suffering from?'
Coming up to Christmas of 1994, Peter Hall
was right as ninepence. Never ill, and with 100 per cent school
attendance certificates at the back of his wardrobe to prove it, he
was doing the first year of an environmental studies degree at
Sunderland University and gigging in his spare time in a heavy metal
rock group. (He called the group Tantalum which, as students of
metallurgy will know, is a very heavy metal indeed.) Peter had long,
Seventies hair but was very Nineties about it, washing it every day,
and was meticulous about his appearance.
'That was the first thing we noticed,'
recalls Derek Hall. 'An unusual self-neglect setting in around
January 1995. Peter was looking scruffy, not eating, losing weight,
becoming withdrawn and dark, and we thought, as did our GP, that it
was classic student depression. But three kinds of anti depressant
tablets proved of no use whatsoever. Finally, the psychologist ruled
out depression and Peter underwent a whole battery of tests-a CT
scan, ECG, bone marrow, lumbar puncture, chest X-rays, an endoscopy,
and pints and pints in blood tests. All showed nothing.'
By May 1995, Peter's short-term memory was
shot and, by early July, his loss of balance-'Like he was drunk all
the time,' said his father-confined him to a wheelchair. 'By early
July,' Frances Hall explained, 'he was completely apathetic-not
talking except in a whisper, and even when the television was on,
just sitting in his wheelchair staring at the wall.'
In August-now incapable of feeding
himself, incontinent, sometimes hallucinatory-Peter was admitted to
the respite ward of the local Earl's House hospital, where his mother
nursed him daily. Derek Hall, who's a bricklayer, drew up plans to
build an extension so they could bring Peter home. Desperate, and
with no other treatment forthcoming, the Halls arranged for him to
have acupuncture and herbal infusions. Amazingly, through October and
November he 'plateau-ed out', according to his neurologist. Then he
relapsed. In January, after Dr Narang's test confirmed that Peter had
CJD, Derek Hall in formed the neurologist. 'He said, "We must keep an
open mind." But when we pressed him further, all he'd say was, "Hand
on heart, I can't honestly say it isn't CJD."
Before Stephen Churchill died last May,
his neurologist had had exactly the same reaction: he couldn't
believe that CJD could strike someone so young. But why the
disbelief? Can there be a doctor left in the country who is unaware
of the increased incidence of CJD among younger people?
At one point during his illness, Peter
Hall was shown to a panel of 50 medical people and his symptoms
described. Pronouncing his condition merely 'baffling', no one
suggested CJD. The results of the postmortem will not be known for a
few days yet, but the death certificate, issued last Tuesday, reads:
'A) Disease or condition directly leading to death: bronchial
pneumonia.' And underneath, 'B) Other disease or condition, if any,
leadingto A): Chronic neurological illness.' And then, next to the
word 'cause', the issuing doctor wrote '?'.
Could it be that the medical profession is
running scared of CJD?
Given the Government's 'no evidence' hard
line, the fact that a good number of hospital doctors are on
short-term contracts these days, and the collapseof Dr Narang's
career after he stuck his neck out, it might not be too surprising.
The CJD orthodoxy, however, is already swinging Dr Narang's way. His
unique discovery of the DNA-based nemavirus-as the one true tell-tale
sign of spongiform brain disease - has been confirmed by NobelPrize
winner Dr. Carleton Gajdusek.
And take the recently-changed position of
Dr. Stanley Prusiner, regarded by british government scientists as
the oracle on CJD. Dr. American Orthodoxy himself, Prusiner had
argued for 15 years that the spongiform disease agent is a non-DNA
type-until last November, that is, when he conceded in a scientific
paper that a DNA-based agent is implicated after all.
So, how much longer do the Ministries of
Health and Agriculture think they can afford to ignore what Dr Narang
has to offer? Last month, a pharmaceutical company estimated that his
cattle urine test would be worth 15 million on the open market. To
date, in destroyed animals and lost beef sales, the BSE epidemic has
already cost an estimated 2 billion. Aside from the swing in American
scientific orthodoxy,in Britain
there is also a groundswell-of farmers
anxious to assist Narang to perfect his cattle test and many more
desperate to use it, and of the surviving relatives of CJD victims
who, acutely aware of the absence of treatment, of confident medical
support and official candour, are offering whatever help and advice
they can to other families now entering CJD's dark tunnel. A chief
priority of the newly formed Northern CJD Support Group, of which the
Halls and Jean Wake's family are members, is to dispel fear. 'No one
explained to us,' said Derek Hall, 'that CJD is transmissible -you
getit by eating something infected- but that it's not actually
infectious.When tending to someone, precautions are sensible, but
it's important toknow that you can't actually catch CJD like a
cold.'
[Thus: CDJ is transmissible; infection
requires intimate contact with affected material, usually through
eating. The disease is not communicable. The "cold" is not a
disease!- J.C]
At present, there seems to be no standard
procedure for the burial of CJD victims. On advice from Newcastle
General Hospital, no viewing of Peter's body was allowed and the
coffin was kept closed. In January, however, when Maurice Callaghan
was buried in Belfast, special precautions included a closed coffin,
a specially limed grave dug to a depth of nine feet, not the usual
six, and the gravediggers issued with protective clothing and
surgical gloves. The Callaghan family have no idea who ordered the
precautions. Since then, the Callaghans have achieved something
unprecedented-the grant of an inquest on the grounds, as his brother
Gerry explains, 'that Maurice's death from CJD, given he was only 30,
may not have been by natural causes. We discovered, too, that in law,
an inquest must be granted if there's- and I quote-"a continuance of
circumstances which comprise a threat to public safety". Which, to
us, certainly seemed to apply to the possible dangers which BSE poses
to humans.' The inquest is scheduled for September.
The Northern CJD Support Group is also
determined to bring CJD out into the open, not least by lobbying to
have it classified a notifiable disease, which would ensure that
every suspected case of CJD was centrally reported and collated. They
also want the Government to publish not just the annual numbers of
CJD deaths but also a breakdown of all victims by age, the major
symptoms, and the specifc area of brain attacked. 'Then we'll have a
clearer idea of whats happening to us' said Derek Hall.
The Northern CJD Support Group tel 0191
281 5311
The Mad Cow Deceit Exclusive Investigation
by Peter Martin [London UK] Mail On Sunday 17 December 1995
TAKE ONE LAST LOOK
It's ten years since the first colossal
outbreak of Mad Cow Disease.
We were told then that Creutzfeldt-Jakob
Disease, the nearest human equivalent, could take 30 years to
incubate. We were also told-a stupendous lie, this-that beef was
safe. Yet a rare, scarcely researched form of CJD is now striking
teenagers. You will be shocked (but not surprised) to learn that the
Government is still not investigating their deaths. As for the Sunday
roast, you'd be forgiven for never wanting to see it again...
HARD EVIDENCE LINKING MAD COW DISEASE
WITH HUMAN DEATHS
Contrary to the Government's insistence,
there is strong evidence that Mad Cow Disease (BSE) does cause
Creutzfeldt-Jakob Dementia (CJD) in humans. The first, key piece of
evidence-two cases of CJD which closely resemble BSE-was discovered
in 1989 by neuropathologist Dr Robert Perry, and Dr Harash Narang, a
government scientist.
That same year, Narang, a clinical
virologist for the Public Health Service Laboratories (PHSL), devised
a random slaughterhouse test for diagnosing sub-clinical BSE in
cattle that hadn't yet shown symptoms of the disease but which were
going-as they still do-straight into the national diet. As a first
step to eradicating BSE, the test would have proved how widespread
the disease really was. John MacGregor, then Minister of Agriculture,
refused to use it. But Narang wouldn't be put off. He kept pushing
the test, and working to formulate still better ones. This made him a
political liability: beef was already safe, the Government insisted.
Since then, Narang's once brilliant career, based on much original
work on spongiform disease over 25 years, has been all but
destroyed.
This disgraceful saga may yet have the
best possible ending. For it appears that Narang now has the very
means to rid Britain of BSE, which has afflicted 52 per cent of dairy
herds so far. [Remember: milk from contaminated and uncontaminated
cattle is mixed- J.C] Having already formulated a simple urine test
for diagnosing CJD, he is just now perfecting a similar test for BSE.
"Just test their urine, you see," he says, "and you could clean every
herd of those animals harbouring the disease." His crucial test might
well have been in use already had he not, a year ago, been made
redundant by the PHSL, and denied essential laboratory facilities
ever since.
But first, the evidence. When Ministers
and officials insist, as they do daily at the moment, that there is
'no evidence' linking BSE with CJD, they're wrong on two counts. What
they mean is that there's no concrete proof-and that's true. As every
one knows by now, since BSE was discovered in 1985, CJD has been on
the increase -27 cases in 1985 rising to 55 cases in the last
recorded year, 1994. There are three basic types of CJD and before
the BSE outbreak the vast majority of cases were of Types One and
Two. But since 1985, there has been an increase in the third, very
rare type of CJD-the so-called ataxic or Kuru type. In its major
characteristics, it closely resembles BSE. If BSE had nothing to do
with CJD, all the newer cases would have been far more likely to be
of Types One and Two. Another indicator of a link is that, since the
BSE outbreak, the pattern of CJD has been changing in four key ways:
the age it strikes people, the major symptoms, its tell-tale
pathology-that is, the area of the brain it attacks-and its shortened
incubation time. * Age spread: before BSE, the vast majority of CJD
cases were confined to people aged 55 and over. Back then, there was
not one recorded British case of CJD among teenagers, and only three
cases in the rest of the world. Now, there are three British teenage
cases as against just four others world-wide.
The Government's 'no evidence' orthodoxy
argues that the recent increase in surveillance is the most likely
reason why more cases, including teenage cases, are now being
identified. But Dr John Collinge, who is the leading orthodox
voice-he heads up the Prion (spongiform disease) Group at St Mary's
Hospital, Paddington-holds the contrary view: "Given the rarity of
CJD in teenagers," he says, "it's unlikely that such cases would have
been previously missed."
Today, too, there's more of a broad
sprinkling of CJD cases down through the under-55s. Just last month,
in a Manchester hospital, a 29-year-old woman in the terminal stage
of CJD had her baby born by Caesarean section three weeks before she
died. The child appears well, but only Narang has the practical means
to test whether or not vertical transmission of CJD, mother to child,
has occurred.
* Symptoms: the second big change in CJD
is in its clinical symptoms. Before the BSE outbreak, typical
symptoms resembled those of Alzheimer's disease-most notably
forgetfulness and impaired, out-of character behaviour. Today,
according to specialists who have worked on post-1985 CJD cases, an
increasingly common symptom is ataxia-the kind of shuddering, loss of
balance and drunken gait you see in BSE stricken cattle.
Ataxic shuddering and unsteadiness are
also the major symptoms of Kuru, a type of CJD once common in a New
Guinea tribe, the Fore, who ritually ate their dead. (In dialect,
kuru means 'shaking disease'. Since the Fore stopped their
cannibalistic practices in the late Fifties the disease has died
out.) Another characteristic of Kuru, in common with post-1985 ataxic
CJD, is that it would strike all age-groups. In children, Kuru's
incubation period could be as short as four years.
The orthodox wisdom on this factor is that
the children probably got infected via cuts or
scratches-intravenously, that is, rather than by eating diseased
flesh. But Narang long ago spotted another intravenous route:
"Children's open gums when they lose their milk teeth". By way of
testing his theory: "I fed infective material to mice, grinding away
at the teeth of some of them first. They all became ill far more
quickly." [Mice traumatised in this way would likely succumb to any
infection more rapidly, this is unlike natural childhood open gums.-
J.C]
* Pathology: thirdly, marked changes have
also been observed in CJD pathology. Before the outbreak, old-style
Alzheimer's-like CJD would attack the brain chiefly in the cerebral
cortex and sometimes the cerebellum. With the rare strain of CJD,
just as with BSE, the disease attacks the central grey matter and the
cerebellum. To date, Night & Day has learned of six such atypical
cases in adults. Since our discovery was random-almost accidental-
there are bound to be more. Stephen Churchill, 19 when he died last
May, might well be another such case. As described in The Lancet of
October 28, his symptoms were actually a mixture of Alzheimer's-like
and ataxic ones. But as post-mortem analysis revealed, the disease
was of the ataxic/Kuru type which had chiefly attacked the central
grey matter and cerebellum. * Incubation time: given the recent
increase in CJD cases, incubation time also fits a new pattern. It's
been 10 years since the BSE outbreak, and Kuru's mean incubation time
is between 10 and 15 years in adults, less in children. BSE's
incubation time is also characteristically short: laboratory animals
inoculated with BSE take roughly half the time to die as those
inoculated with scrapie (spongiform disease in sheep). All evidence,
yes, but by no means conclusive evidence that, for example, BSE
caused Stephen Churchill's death. Before 1990, spongiform disease was
unknown in cats but, last year, Dr Moira Bruce, of the
Neuropathogenesis Unit in Edinburgh, solved that mystery. To do so,
however, she first had to inoculate series of mice with infective cat
brain material, and then wait to discover what strain of disease they
would die of. It was BSE. The series took three years to complete. A
similar process will have to be carried out to determine if BSE
killed Stephen Churchill. Currently, brain material from two farmers
who died of CJD is being tested by Dr Bruce in this manner. But the
same work in relation to Stephen Churchill has yet to begin. In great
part because the families concerned want straight answers, Narang has
been given brain samples from three recent CJD victims, one of them
Stephen Churchill.
So here we have it-not only a strain of
CJD which closely resembles BSE. What's turned up in humans could
well be BSE. For it's now accepted that BSE existed at a low level in
cattle well before the 1985 outbreak. It therefore follows that those
rare cases- past and present-could all be BSE. But only a three-year
test series using mice could tell us for sure.
ON AVERAGE, WE'VE EATEN 80 MEALS OF
CONTAMINATED BEEF EACH
As disturbing as the new evidence appears,
it is not very likely that the beef and beef products we are eating
today are putting us at grave risk. What is certain is that we were
all exposed to BSE tainted foodstuffs between the outbreak of BSE in
1985 and the belated 'offal ban' of November 1989.
According to microbiologist Dr Stephen
Dealler, who has recently crunched the numbers, we in Britain have
consumed 1.5 million BSE-tainted animals -around 80 meals each. If
BSE caused some of the recent CJD cases, the infections are most
likely to have occurred during that period of maximum BSE exposure.
Since 1989, of course, the bovine organs known and suspected to
contain infectivity-brain, spinal cord, intestines, spleen, thymus
and tonsils-have been removed at slaughter. That doesn't mean that
beef is utterly safe, nor could it be until BSE is eradicated from
the cattle population.
In this uncertain meantime, however, are
those crucial front-line pattern changes in CJD being looked for? Set
up in 1990 and headed by Dr Robert Will, the Government's CJD
Surveillance Unit in Edinburgh has a 20-year brief to monitor CJD
cases and to investigate the possible link between BSE and CJD. But
the unit's four annual reports to date have concerned themselves
solely with epidemiology-investigating dietary habits and the risk of
occupational exposure for the likes of farmers, slaughtermen, vets
and so forth. No mention of the unit investigating clinical or
pathological changes in the pattern of CJD. Eighteen days ago - at
his request and on the promise that he would respond-Night & Day
faxed a list of questions to Dr Will. Several questions concerned the
unit's monitoring of pathological and clinical changes. Since then,
at our every phone call, Dr Will has not been available for comment.
Just last week, two leading neuropathologists confirmed they'd never
been asked to monitor or report such changes. One remarked, 'Oh, does
Edinburgh want us to provide them with this sort of detail
now?'
As Night & Day demonstrated with
chapter and verse back in March 1994, government policy on BSE has
been a go-slow tactic of wait and see. The core motive remains
economic. First, to manipulate public perception of the possible
dangers so as to afford Britain's 4 billion beef industry the maximum
protection. Second, to save money: in compensation to farmers, each
BSE-stricken animal-including the vast numbers of the sub-clinically
affected which Narang's test could detect-would cost the Government
between 800-1,000. To date, the Ministry of Agriculture, Fisheries
and Food (MAFF) has still done no random testing at abattoirs, and
still has no in-the-field urine test of its own.
But what will it cost the beef industry if
the whole nation follows the example of the current and increasing
school bans on beef? As it happens, just last week, Douglas Hogg,
Minister of Agriculture, indicated that the Government might well
want Narang's tests after all. And they can have them, too, free,'
insists Narang's good hearted backer, Newcastle businessman Ken Bell,
whose brother died of a dementing brain disease. On Monday last,
Narang wrote to Hogg offering his two cattle tests - a post mortem
abattoir test and the live urine test. Separately, Narang has also
developed a quick post-mortem test for CJD. Not the least of its uses
would be to test donors before transplants. As has happened before
with brain repair grafts, a recipient can contract CJD as a
consequence of spare parts taken from donors not known to have been
incubating the disease at time of death. A year before Stephen
Churchill died of CJD, he survived a bad car accident. He was
carrying a donor card.
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