The spectre of bovine spongiform encephalopathy has changed the British beef industry forever.
And as new cases of BSE are reported almost daily in continental Europe, the British are hoping their food regulatory system will protect them from a recurrence of this public health crisis.
A second serious outbreak of BSE in the United Kingdom would demolish the fragile confidence British consumers have regained for domestic beef. It would also undermine their faith in scientists who insist the problem is under control.
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Disease, a fatal brain illness in humans, is linked to eating beef from BSE-infected
cattle. They suspect the cattle were infected by eating contaminated feed. But so far, these theories are unproven.
“Does that mean there is something else that causes BSE that we don’t know about?” asked Richard Lowe, manager of the Meat and Livestock Commission, a producer-funded group responsible for beef, lamb and pork promotion in the U.K.
In response to public outcry, the U.K. has created a multi-layered regulatory system intended to protect the entire food industry “from farm to fork.”
“As the scientists had more of a grasp on the facts, so the legislation evolved,” said John Cross, chair of the commission.
“It couldn’t evolve any faster than science would let it.”
BSE in Britain
BSE was listed as a reportable disease in 1988, but British regulations were tightened in 1996 when the disease was officially linked to new variant CJD. Regulations
consist of three main BSE controls.
- All cattle over the age of 30 months are prohibited from entering the food chain. Breeding stock may be retained but eventually, all animals over 30 months of age are slaughtered and incinerated. Bones, blood, intestines and offal are removed from the food chain and incinerated.
- No mammalian meat and bone meal may be fed to farm livestock.
- All bovines must carry eartags and have passports that record their movements.
The British government also formed the Food Standards Agency on April 1, 2000 to protect the consumer from food hazards.
Getting to that point was an arduous journey as government and scientists were confounded by the disease that seemed to have come out of nowhere in 1985.
BSE, dubbed “mad cow disease” by the British press, is a progressive, fatal disease of the nervous system. It is known as a transmissible spongiform encephalopathy, or TSE. Other TSEs include scrapie in sheep, chronic wasting disease in deer and elk, and Creutzfeld-Jakob Disease in humans.
In Great Britain, the disease affected mostly dairy cattle that were fed protein supplements derived from rendered beef carcasses.
As BSE took hold in the late 1980s, the government formed the spongiform encephalopathy advisory committee to monitor research and advise government.
In 1990, the committee wrote a letter to government, saying the disease appeared similar to scrapie, a condition that had been recognized in sheep for centuries.
The letter said there was no risk to human health because there is no evidence that scrapie is hazardous to people. The committee also assured government that cooking meat would probably destroy the abnormal protein particles associated with the disease.
Committee members were proven wrong when research discovered one gram or less of infected material could cause death if ingested by cattle.
The infected material was so potent that accidental cross-contamination of cattle feed with pig or poultry feed containing meat and bone meal was a significant factor in spreading BSE after the ban on meat and bone meal in cattle feed was implemented.
By this time, thousands of British animals had been diagnosed with the disease. The public was demanding that the government fund more research and develop tougher regulations.
According to the government-commissioned BSE inquiry written by Lord Nicholas Philips, “BSE did not emerge at a propitious time so far as research was concerned.”
A mood of deregulation
Cost-cutting measures and a mood of deregulation had prevailed in Great Britain since 1983 under Conservative prime minister Margaret Thatcher.
In 1985, government ministers accepted a recommendation that funding for research into animal diseases was disproportionate and should be reduced by 20 percent. Implementation of this policy resulted in staff cuts at many research institutions.
The BSE inquiry conducted years later said deregulation did not have any significant impact on the government’s approach to BSE or on the nature or timing of the measures it took to control the disease.
“However, it colored perceptions of how such measures ought to be enforced.”
The issue of deregulation arose in 1993 in connection with the proposed national Meat Hygiene Service. Government members questioned whether such an agency was cost effective or could enforce new regulations.
They believed spot inspections in slaughterhouses should catch inconsistencies in hygiene regulations. But it was learned later that new procedures were not taken seriously enough and researchers believe bovine offals still got into animal feed after the rules went into effect.
The Meat Hygiene Service took over enforcement of regulations in 1995.
Since then, almost no violations in slaughterhouses have been reported.
Renewed Focus
By the mid-1990s, government and the spongiform encephalopathy advisory committee were beginning to realize the extent and seriousness of BSE. An extensive research program developed tests for TSEs.
Since then, the British government has spent more than £140 million, or $315 million (Cdn) on research into BSE and other transmissible spongiform encephalopathies.
The British ministry of agriculture releases regular updates on what is known about the disease and what is theorized.
Although the exact cause of bovine spongiform encephalopathy is unknown, it is believed to be caused by a disease agent known as a prion, a proteinaceous particle smaller than a virus. There is no treatment or vaccine for the disease.
There are numerous theories about the cause of BSE. One theory postulates that a mutation occurred in the brain cells of a cow. The cow died and her carcass was probably converted into protein pellets and fed back to the next generation of dairy cattle in southern England where the disease first took hold.
If this disease was a mutation, no one knows what triggered it. Speculation ranges from mineral deficiencies in bovine diets to an asteroid carrying a virus crashing on English soil. Besides searching for a cause, researchers are concentrating their efforts on live animal testing.
“If the Brits had had a test 15 years ago, they wouldn’t have had the problem they had,” said Claude Levin of the Canadian Food Inspection Agency.
“They would have been able to test the national herd and eliminate the animals that carry the disease and free themselves.”
British researchers know the average incubation period for BSE is five years. The earliest the disease appeared was in an animal 32 months of age.
There is very little testing of brain tissue
of cattle slaughtered between 18 and 24 months of age because no infection would be detectable.
Another question is which tissue should be tested. Most immunological tests that can detect the abnormal prion work best on brain tissue obtained post-mortem. In some species, such as sheep, it may be possible to use lymph nodes, tonsils or the spleen.
In Canada, researchers are working on a test that checks the third eyelid of sheep. However, the test is expensive and impractical in the field.
The only way to make a live diagnosis is to observe clinical symptoms. However, about 20 percent of the cattle suspected of being positive turn out to be negative after post mortem examinations.
One test that shows promise for live animals comes from the United States Department of Agriculture.
Capillary immuno-electrophoresis detects scrapie-infected sheep by testing blood samples. It also appears to work on chronic wasting disease in elk.
British scientists hope this test might be modified as a test for BSE. However, the agent causing BSE in cattle appears to be quite different from that of scrapie.
Alternative diagnostic tests look at urine because changes have been detected in the constituents of urine of Creutzfeld-Jakob Disease patients, sheep with scrapie and cattle with BSE.
Protein diagnostic studies are also under way. Certain proteins present in normal animals are released in larger quantities in spinal fluid as a result of damage to central nervous tissue in CJD and in BSE. These changes may be disease specific and their detection could be useful in making a diagnosis.
