History and Symptoms of Mad Cow Disease
The history of mad cow disease – bovine spongiform encephalopathy (BSE) – is very similar to the incubation and propagation of other infectious diseases, though this particular neurodegenerative disease has caused more fear than most of the others combined. Most of this fear is rooted in the fact that scientists still don’t understand mad cow disease, and cannot explain why it is prevalent in other animals as different strains of the same disease.
Mad cow disease was first recognized as an infectious disease in 1986, after it began to appear in cattle in Great Britain in 1985. As with the current Avian Flu paranoia, the public did not become educated about or interested in the disease until several months afterward. It was made clear that the animals became infected because of eating pieces of cow and sheep in their bone meal (animal food), and the British government outlawed the feeding of bone meal in order to halt the spread of mad cow disease.
However, because of similar infectious diseases throughout history, such as scrapie in sheep, public officials did not think that mad cow disease could spread to humans. Scrapie and other animal diseases caused similar deterioration of the brain, but were not applicable to human beings. They also originally thought that mad cow disease was a virus, when it is in fact not virulent at all.
Scrapie was first discovered in sheep in the early 1700’s, and the most common symptoms were severe itchiness, which caused the ewes to rub themselves against fence posts, trees and other available “Scratching posts” to relieve the itchy skin. Sheep contracting the disease usually died within six months. Much later, in the 1920’s, two doctors by the names of Creutzfeldt and Jakob discovered a relatively rare disease in humans that caused the forming of holes in the human brain. Various strains of that disease have been discovered all over the world, including a small tribe in New Guinea that contracted it through the ritual ingestion of deceased ancestors.
The scariest thing about mad cow disease is that the strains mutate almost constantly, making in nearly impossible to control the infectious mechanism. Although other bovine diseases, such as rinderpest, have killed cattle on a much more epic scale, mad cow disease can translate to a human host, resulting in massive deteriorating of the brain.
Mad cow disease is a form of protein that can pass between individual animals and begin destroying brain tissue, which inevitably leads to severe dementia. It is called something different in every animal that it infects, and in humans it is called Creutzfeldt – Jakob disease (CJD). In most cases, mad cow disease is spread when one animal consumes the tainted remains of another, such as when a cow feeds on the remnants of another, or when a human being eats beef.
It has been confirmed now, however, that the spread of the disease is not confined to simply ingesting infected meat. In can be spread through any bovine product, which can include skin lotions, soaps and milk. The disease can survive any temperature and any chemical agent ever devised by humans, which makes it a formidable enemy. It is not a virus, and cannot be killed by any of the known viral inoculations.
By the year 1990, there were more than 14,000 confirmed cases of mad cow disease compared to a cattle population of more than 10,000,000. Five years later, the mad cow count was up over 150,000, and growing by the thousands each week. Other countries, such as Switzerland and Ireland, were beginning to report nominal instances of mad cow, and public hysteria began to grow.
Finally, in March of 1996, the British government issued a “Mad Cow Warning” that served to warn the public about eating meet and about purchasing cattle that had not been tested. At that point, the public was also made aware of a human strain of the virus – CJD – that caused equally devastating brain deterioration in people. That was the start of the crippling of Britain’s beef export business, and it caused hundreds of restaurants and grocers to begin banning beef from their establishments.
Symptoms that cows infected with mad cow disease displayed abrupt changes in temperament, altered motor skills and significant aggression. Originally, it was thought to be a bovine form of the scrapie disease that affected sheep, but was not transferable to humans.
The history of mad cow disease is filled with the frantic assurances of public officials and the terrified struggles of bovine farmers. It was apparent by 1997 that mad cow disease was not something that could be effectively contained, and that the spread of the disease was inevitable. Further compounding the problem, mad cow disease has a very long incubation period, particularly in humans. Most cattle that contract the disease show symptoms within 30-60 months, while humans can contract the disease and not show symptoms for an estimated forty years.
Mad cow disease in humans is called variant CJD, and had been located in 140 humans in Great Britain by the year 2004, though that number is probably conservative. It is next to impossible to pinpoint the exact number of human cases because the disease can mutate and be transferred without showing up as variant CJD. Essentially, mad cow disease is unlike any other infectious disease known to man.
Mad cow disease is caused by a misshapen protein called a prion, which is concentrated most heavily in the brain and spinal cord of infected animals and humans. It is said that muscle tissues do not contain prion, but it is really unknown where the prions can manifest. It is universally thought that the outbreak of mad cow disease was so large in Britain because British beef contains remnants of brain and spinal cord, though that has not been proven. As it stands now, beef companies are not allowed to include pieces of brain or spinal tissue in their products.
Unfortunately, however, two studies compiled in 2004 concluded that out of 200 variant CJD patients, 32 of them had prions in their muscle tissue. Although mad cow disease prions might not be found in bovine muscle tissue, it has been proven that it can exist in human muscle tissue.
One of the most critical issues facing human consumers today is that mad cow disease cannot be contained, and that it can be spread unknowingly from unwitting farmers of cattle. Since the incubation in cattle is at least thirty months, cows that are slaughtered before they reach that age – as are most of them – will enter the market undetected.
Prions – the misshapen proteins that cause mad cow disease – are decay-resistant and for the most part unable to be killed. Once the host – either human or animal – begins to show symptoms, decline is swift, which gives scientists and doctors even less chance of gaining further understanding of the disease. The prions cause small holes in the brain and can adhere to tissues in the brain and spinal cord, causing numerous problems. The physical symptoms of mad cow disease are similar to that of Alzheimer’s.
Several years ago, a fourth generation cattle rancher named Harold Lyman published the infamous book Mad Cowboy and was subsequently sued by the beef industry. The book has sold more than one million copies and is written much like Upton Sinclair’s The Jungle as an expose about mad cow disease and the cattle industry. He explains in all-to-explicit detail about the use of growth hormones, insecticides and antibiotics in cattle, all of which can be dangerous to human health, and about the shockingly true factors of mad cow disease that makes it a serious threat to the human population.
It is thought by many that more than half of the cases of Alzheimer’s in the world are actually strains of mad cow disease. In Mad Cowboy, Lyman asserts that at least four times as many people have been infected by mad cow disease than is told to the public, and that the threat is growing more serious rather than less.
It is also thought that all of the TSE’s (transmissible spongiform encephalopathy), which are the family of infectious diseases caused by misshapen proteins that attack the brain, will eventually mutate to an extent that they are unstoppable. In cattle, humans, deer, elk, sheep, and a host of other animals, the TSE’s cause inimitable brain deterioration and then death after a frighteningly long incubation period. Thus far, despite some quite tentative advances in treatment, the only hope of preventing TSE’s in general is to find a way to prevent them, which will require expensive and perhaps futile adjustments in the way cattle are raised and slaughtered.
