A first-person chronicle of the development and mishandling of the BSE crisis.
The first event in Britain that led to the development of bovine spongiform encephalopathy (BSE) in British cattle began around 1980. That’s when the British government forced the heat-digestion processors of offal to discontinue the use of trichloroethylene as a fat solvent in the rendering process. The source of this offal was slaughtering plants and animals that had died of various causes – including sheep with scrapie.
The reason for the discontinuance was that trichlorethylene irritated the eyes and upper respiratory tract of the workers in the plants. Little effort was made to find another solvent, however, because the value of fat had dropped drastically due to a drop in demand by the soap industry.
Trichloroethylene had been used for many years in Britain to extract the fat from animal residues, which includes meat meal, meat scraps, tankage and bone meal. During this time, there hadn’t been any problems with cattle developing the central nervous system changes characteristic of BSE.
In retrospect, it appears it was trichloroethylene that was destroying the prions, the acronym for the proteinaceious infectious particles of sheep scrapie. These prions were in the offal of slaughtered sheep and sheep that had died of scrapie.
(Incidentally, trichloroethylene was used to extract the oil from soybeans in the U.S. in the early 1950s. It was discontinued, however, because the residue that adhered to the meal destroyed the blood forming cells of the bone marrow in ruminants.
If sufficient heat were used to vaporize the remaining trichloroethylene, the result was the destruction of the soybean protein. With animal residues, sufficient heat was used in the processing to vaporize the remaining trichloroethylene.)
When trichloroethylene was removed, uneasy British regulatory officials suspected the compound could be destroying the scrapie prions since Britain had a relatively high number of sheep flocks with scrapie. They knew scrapie had been transmitted to mink being fed sheep offal infected with scrapie and that scrapie had been transmitted to other sheep by injections of infected brains.
They also knew that infected brains and spinal cords subjected to autoclaving, which is 250?F for 15 minutes at 15 lbs. of pressure, remained infectious when injected into sheep and had produced the clinical signs and lesions of scrapie.
To compensate for the possible prion destruction by trichloroethylene and the heat resistance of the prions, the British regulatory officials decided to increase the temperature to which the animal residues were subjected in the processing plants. What happened was that the additional heat made the animal residues containing the prions of sheep scrapie more infectious. It probably did this by freeing the prions from the sheep tissues in the heat-digesting process and providing more available prions to the cattle.
After the first few cattle developed the clinical signs and lesions of scrapie in Britain in the late 1980s, but before the British or the continental European public was told of the seriousness, word was leaked to the processors of animal residue that the use of their product for cattle and sheep would be discontinued. To minimize economic loss, the processors immediately shipped and sold most the product they had on hand to continental Europe, namely France, Belgium, Netherlands and Germany, British veterinarians told me.
I was told by British veterinarians after this occurred that within 15 years these countries also would have BSE. It’s a prophecy that has come true.
The British Problem Erupts
When the first cattle in Britain developed BSE, the regulatory officials knew they had a gigantic problem. Their policy was to keep it quiet, hoping it would go away.
Several veterinarians told me the ban on the sale of meat and bone meal derived from ruminant offal imposed in 1988 was only minimally enforced until 1996. This, they said, was due to the prevailing anti-regulatory philosophy of Margaret Thatcher, the Prime Minister at that time.
In 1990, British veterinarians were in the U.S. hoping to find the disease. They had no luck. The only other country where they found the disease was in Saudi Arabia in several cows purchased previously from Britain.
The toll on the British livestock industry has been disastrous. Britain has some of the best beef cattle in the world, and many countries depended upon it as a source of breeding stock.
With the development of the human variant disease of Creutzfeldt-Jakob Disease (CJD) in the mid-1990s, supposedly from the eating of meat from BSE-infected cattle, a new wall of secrecy has been established, various news organizations report.
The effects of BSE now extend to other countries. BSE has increased the concerns of Europeans and Asians toward genetically modified crops, and toward U.S. beef from cattle given hormones of plant origin to increase their rate of gain. It’s also undermined the trust among EU member nations.
Scrapie Is Endemic
Scrapie has been around for centuries. It’s endemic in the sheep of many countries, including Britain and the U.S.
The first case of scrapie on Earth probably was the result of a mutation. It appeared in high numbers in the U.S. after World War II when numerous sheep of the Suffolk breed were imported from Britain.
I remember in the 1950s while in veterinary school at the University of Minnesota when all of the pens on one side of the veterinary clinic were full of sheep with this disorder. They spent all of their time rubbing against the sides of the pen and bunting each other.
The name, scrapie comes from scraping their skin because it itches. At the time, most of the faculty thought that the cause was a genetic disorder. Then in the early 1960s, I saw at Purdue University that it could be transmitted to other sheep with infective brains. Also, that it could be transmitted with injections of infective brain subjected to autoclaving.
It was not until the mid-1990s, almost 10 years after the first case of BSE appeared in Britain, that a scrapie eradication program was begun in the U.S. One cannot get a state veterinarian to talk about the program because the policy is no publicity, but eradication is occurring. This is evidenced by the lawsuits filed by sheep breeders over the condemnation of their herds and what they consider insufficient indemnity payments.
The U.S. has never had a case of BSE and probably never will unless there is a spontaneous mutation in a single bovine with the formation of prions or a quirk with the transmission of sheep scrapie to cattle.
One favorable factor is that the U.S. has not had to rely on animal-derived supplements due to inexpensive sources of plant proteins. In Britain and Northern Europe, however, it’s too cool to grow cotton and soybeans, and flax seed oil cannot complete with other plant oils in today’s market. Thus, they have to import expensive soybean meal.
How is scrapie related to CJD, a spongiform encephalopathy in humans? The most significant statement I’ve heard about CJD was from C.J. Gibbs, a retired physician at the National Institute of Health in Washington, D.C., who has studied this disease extensively. He said on National Public Radio a few years ago that he has never seen a case in the U.S. that did not involve a person who raised roses.
Why? Because all rose growers use a lot of bone meal, which is high in phosphorus and calcium. Roses require phosphorus as a nutrient and calcium for neutralizing the acid in the soil. In addition, the prions of scrapie in sheep are not only located in the brains and spinal cord, but also in the viscera, lymph nodes and bone marrow.
I postulate that the rose growers he is talking about got CJD by inhaling the crappie prions in the dust of bone meal when it was applied to the soil because:
- The bones and bone marrow of U.S. sheep with scrapie are mixed with the bones of other animals in the processing,
- Bone meal is subjected to high temperatures in the heat-digestion process, thus making the prions in the marrow highly available, and
- Bone meal is very dusty because it is finely ground.
Scrapie-infected ewes have been shown to transmit the disease to their lambs. Whether it is prenatally, through the ewe’s milk or via licking is unknown. The same avenues of transmission are also suspected with BSE.
Trying to detect and identify scrapie or BSE prions in the laboratory is far more complicated than isolating or identifying infective viruses or bacteria. As a result, most studies have been in animals.
Iceland is the only country to eradicate scrapie. Yet, it was reported at a 1998 symposium held in Reykjavik, Iceland, that scrapie-free sheep introduced on pastures previously grazed by scrapie-affected sheep, but idle for several years, developed scrapie.
With the suspicion that the prions of scrapie are discharged by the mouth and the fact that they are extremely hardy, it’s possible that elk or deer, which initially developed chronic wasting disease – another spongiform encephalopathy in the U.S., could have become infected with scrapie prions by grazing pastures simultaneously grazed by scrapie-infected sheep or by eating out of feed bunks or licking salt blocks simultaneously available to scrapie-infected sheep. This proposed transmission route is also possible for our cattle.
Stanley Prusiner, discoverer of the prion, once said that the incubation period for Kuru, a spongiform encephalopathy of humans in New Guinea and similar to scrapie, was up to 40 years. With the remote possibility of sheep scrapie being transmissible to our cattle, and with its long incubation period, why do we in the U.S. allow the many flocks of Suffolk and Suffolk-Southdown sheep with endemic scrapie to survive in a society where the longevity of life is ever increasing? Having prions in the environment, let alone in the food chain, poses a serious health problem.
Prions are an abnormally modified structural form of a normal protein in the neurons of the brain. They’re located as fibrils or fine fibers in and around the neurons that result in the development of large vacuoles in the neuron and is diagnostic of scrapie and the other spongiform encephalopathies. When the neurons die, the result is the microscope holes in the brain.
Spongiform encephalopathy is a microscopic description of the many holes that develop in the brain as a result of the death of nerve cells; there are no gross or visible lesions.
Even though prions don’t contain DNA or RNA, they apparently propagate themselves by contacting their normal metabolic counterparts in the neuron and reshape the conformation of the normal protein into what is a prion. This cycle continues, ever-increasing the number of prions, until the neuron dies.
In summary, the events in Britain which led to the development of BSE in cattle and its spread to continental Europe were:
- The discontinuance of the use of trichloroethylene as a fat solvent in the rendering process,
- Increasing the heat in the digestion of the animal residues after the withdrawal of trichloroethylene, and
- The clandestine shipment and sale of BSE-infected animal residues to other countries of Europe.
LeRoy D. Olson is a professor emeritus in the University of Missouri’s Department of Veterinary Pathobiology in Columbia. His interest in the various spongiform encephalopathies dates to his veterinary education in the mid-1950s. Since that time, he has closely followed the BSE situation and over the past 12 years has discussed the BSE problem extensively with British veterinarians and researchers.