Mad Cow Disease and Your Pets

By Jean Hofve, DVM

In December 23, 2003, the first official U.S. case of “mad cow disease” (Bovine Spongiform Encephalopathy or BSE) was reported in the news; a second followed shortly thereafter. However, astute researchers and even the pet food industry acknowledge that a BSE-like disease has been present in the U.S. for many years. Is this a threat to our pets? Let’s look a little closer at this unusual disease.

Around the end of 1985, the first cases of a bizarre bovine neurological disease, nicknamed “Mad Cow Disease,” were reported in England. British beef was quarantined and hundreds of thousands of cattle destroyed. As early as 1988, some experts thought that this disease might be transmissible to humans. However, a definitive link to a “new variant” of the human degenerative neurological disease, Creutzfeld-Jacob Disease (nvCJD), was not established until 1996. Consumption of infected beef meat was considered to be the cause.

However, more recent research suggests it may not be the meat itself, but whole-body contamination with brain tissue during the slaughter process, which is to blame. The brain and spinal cord of infected animals carries a high concentration of infective particles, called “prions.” Captive bolt stunning, which is the usual way of knocking a cow unconscious just prior to slaughter, splatters brain matter into the bloodstream, where it is rapidly disseminated throughout the animal’s body, literally within a heartbeat. This apparently happens faster than the animal can be hoisted and moved to the next stage of slaughter, where it is bled out, even though this normally occurs in less than 60 seconds. Subsequent removal of the brain and spinal cord may thus be inadequate to prevent infected material from directly contaminating edible tissues.

Cattle presumably acquired BSE from eating food containing rendered material from sheep infected with scrapie, a common ovine disease. This feeding practice was banned in the U.K. about 18 months after the first BSE cases came to light.

One European country after another subsequently discovered BSE within its borders. France, Ireland, Portugal, Switzerland, the Netherlands, Belgium and Denmark all reported cases of BSE in the 1990s. It has also leaped to far-off places as Japan, the Falkland Islands, the Azores, Oman, and Canada. In 2000, BSE was discovered in Germany, much to the consternation of the ministers who had prided themselves on strong regulations intended to keep the fearsome disease at bay. One report stated that Italy and Spain are “likely to have been infected,” and that BSE “cannot be ruled out in four other European countries, as well as Australia, Canada, and the USA.” There have been some 180,000 infected cows identified worldwide since the outbreak began in Britain. More than 100 people have died from nvCJD related to BSE.

In addition to human victims, more than 100 domestic and big cats, as well as several ruminant species in zoos, have been affected.

In 1993 the epidemic reached its peak as the 100,000th BSE case was identified. Wrangling over which beef or sheep products could be used for what, and where and how they could or could not be exported, continued throughout the 1990s and into the new millennium.

Until the end of 2003, the U.S. government kept itself busy congratulating itself on preventing such transmission in this country by virtue of its “active surveillance program.” However, it was never certain that we didn’t have BSE in American livestock. The U.S. banned importation of British-origin beef in 1985 for other reasons, but by then the disease was entrenched in British cattle, and possibly present in imports prior to that time.

About 500 live British cattle were imported into the U.S. between 1981 and 1989, when the USDA banned the importation of live cattle. While most of these cattle were traced and located, 34 could not be found. These were presumed dead, and most of the rest of the other cattle were also known to have died or been slaughtered. Of most interest, perhaps, is the disposition of the carcasses, but this is not known in all cases. It is possible, if not likely, that at least some of these animals were rendered. If any of them were infected, it is also possible that they may have become “downers,” and routed into the human and/or animal food chains.

A similar scenario was blamed for several outbreaks of a BSE-like disease among mink in fur farms. We also have sheep scrapie in both the U.S. and Canada, which was recognized in the 1940s. But not until 1989 did the American rendering industry initiate a “voluntary ban” on accepting potentially infected sheep parts for processing. And even then, a USDA survey three years later found that 6 of 11 inspected plants were still accepting the banned parts. The feeding of sheep and other ruminants back to ruminants was not officially banned in the U.S. until October 1997.

In July 2000, a “foreign” spongiform encephalopathy was found in four imported sheep in Vermont. This prompted the USDA to declare an “extraordinary emergency.” More than 700 animals in three flocks of milking sheep were quarantined as a result. In March 2001, two flocks were seized for testing and destruction. USDA assumed the responsibility for ensuring that, as these sheep are destroyed, they do not enter the human or ruminant food chain; but there is nothing to prevent them being routed into pet food.

In early 2001, USDA announced that inspections of feed mills and rendering facilities found almost 800 lacking required warning labels and/or systems in place to prevent mixing of banned products into ruminant feeds. Thousands of facilities had yet to be inspected. In fact, USDA apparently has only a vague idea of how many such facilities actually exist. Just two weeks after that announcement, 1,200 cattle in Texas were quarantined because they may have been fed banned materials.

Is BSE a threat to our companion animals? One industry analyst suggested early on that potentially infected materials should be excluded from cat foods, since cats were susceptible to the disease in Europe (about 100 domestic and exotic cats died from TSEs). Food-producing animals that die from unknown causes (which may include BSE or similar diseases) are typically routed into pet food and animal feeds. The presumed agent of transmission of BSE is not inactivated by rendering or most other types of processing, including cooking, formaldehyde, dry heat, autoclaving, or even incineration. There are a handful of methods that are known to destroy the prion, but they are highly impractical for most uses.

BSE-like diseases (transmissible spongiform encephalopathies, or TSEs) have been present in the U.S. for decades. Chronic wasting disease of elk and deer is well characterized as a prion disease. Sheep scrapie has been recognized since the 1940s in the US and Canada. Feeding of scrapie-infected sheep was blamed for the presence of a TSE disease among mink farms as early as 1947. However, in at least two instances, affected mink had not been fed sheep. A variant that caused an outbreak on two fur-farms in Wisconsin in 1985, where mink had been fed exclusively downer dairy cows, was shown to cause BSE lesions in experimentally infected cattle. Significantly, the infected steers did not develop symptoms of “madness” like British cattle, but instead became ataxic and went down.

“What if the strain of BSE in American cattle produces more of a ‘downer cow syndrome’ than mad cow syndrome?” speculated the researchers. “This possibility would definitely complicate surveillance programmes for BSE in the United States, a country that has hundreds of thousands of downer cows each year and no means for routinely diagnosing their cause.” And in fact this exact scenario has played out in the U.S.

Downer cows in the U.S. were, until 2004, still slaughtered for human consumption; and to this day they are commonly used in pet food. Moreover, with non-ruminant proteins in high demand for ruminant feeds, ruminant proteins are now more likely to be processed into pet foods.

Interestingly, although many species have been affected, cats seem to be especially susceptible. No canine cases were ever confirmed in the U.K., and it was presumed that dogs were somehow resistant. However, in 1997 a golden retriever who died in Norway had brain lesions consistent with a TSE-like disease, allegedly from dog food it consumed in the 1980s. Furthermore, a disease called “hound ataxia” has affected U.K. hunting dogs since the 1930s. Hunting hounds are commonly fed offal from downer cattle and sheep. Research in the early 1990s showed that microscopically, this disease shares pathological features with scrapie, and at the electron microscopic level, Scrapie Associated Fibrils (SAF) were detected. These facts imply the presence of BSE many years before its official debut in 1986. However, both the initial study and further research to explore this possibility have been ignored or suppressed by the British government.

The U.S. and Canada long believed they were free of bovine spongiform encephelopathy (mad cow disease). However, a significant portion of this confidence was based on the fact that BSE had not been found in any tested animals, including downer cows at slaughterhouses. Of the 37 million cattle slaughtered for meat each year in the U.S., about half a million cattle are downers. Canada tests fewer than 1,000 cattle a year. The U.S. currently tests about 7,500 downers per year (about 0.15%). Switzerland tested 20,000 cattle in a single year — and found five with BSE. Despite the lack of vigilance and appallingly inadequate testing, confirmed BSE cases were finally found in both Canada and the U.S. in 2003. One can only imagine how many cases continue to go unnoticed.

UPDATE: 4/27/05  Whistleblowers claim Mad Cow cover-up by USDA (from Organic Consumers Association). “The USDA has been covering up cases of Mad Cow Disease, according to a USDA veterinarian in charge of monitoring cattle for the fatal disease. On the eve of retirement, Dr. Masua Doi confessed to sketchy testing since 1997. “I don’t want to carry on off to my retirement,” said Doi. “I want to hand it over to someone to continue, to find out. I think it’s very, very important. How many did we miss?” Doi’s concerns are shared by other USDA contracted scientists, like Dr. Karl Langheindrich who runs a test lab in Georgia and says the appropriate animal parts are not sent to him for accurate testing. In addition, two weeks ago, U.S. agriculture inspector Lester Friedlander offered testimony to a Canadian House of Commons committee revealing the U.S. has been covering up Mad Cow cases.”

What can you do to prevent this disease in your home? The main consideration is to not buy commercial beef, particularly ground beef (which is plagued with many other contamination problems as well). However, organically grown beef from long-established herds, who have never been fed animal proteins, are most likely safe for human and feline consumption. Commercial pet foods containing beef (and possibly lamb) may or may not be safe; they are probably best avoided. Pork is still considered safe, primarily because most hogs are slaughtered young; lambs, too, are slaughtered by 1 year of age–before they have time to develop the disease. Because birds’ metabolism is so different from mammals, poultry is still a safe choice, and game meats (except deer and elk, which can harbor a related prion disease), rabbits, and other non-commercially raised mammals are unlikely to harbor BSE.

UPDATE: 10/10/11

New research from the University of Texas suggests at least some cases of “sporadic” Alzheimer’s disease “arise from an infectious process,” likely related to BSE. This may confirm the suspicions of those who believe that many (if not most) cases of Alzheimer’s are in fact a prion disease. Consider this report published in 2004 (Could Mad Cow Disease Already be Killing Thousands of Americans Every Year?):

The most frequent misdiagnosis of CJD among the elderly is Alzheimer’s disease.[55] Neither CJD nor Alzheimer’s can be conclusively diagnosed without a brain biopsy,[56] and the symptoms and pathology of both diseases overlap. There can be spongy changes in Alzheimer’s, for example, and senile Alzheimer’s plaques in CJD. Stanley Prusiner, the scientist who won the Nobel Prize for his discovery of prions, speculates that Alzheimer’s may even turn out to be a prion disease as well. In younger victims, CJD is more often misdiagnosed as multiple sclerosis or as a severe viral infection…Nobel Laureate  [D. Carleton]Gajdusek, for example, estimates that 1% of people showing up in Alzheimer clinics actually have CJD. At Yale, out of a series of 46 patients clinically diagnosed with Alzheimer’s, six were proven to have CJD at autopsy.


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