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“Doc – What can you tell me about this West Nile Virus, Mad Cow Disease and Food & Mouth Disease?”
© A.J. Neumann, D.V.M.
published in The Draft Horse Journal, Summer 2001

That is a big order to fill when attempting to answer a question such as this. However, these three diseases are on the minds of a good many people, especially horsemen, livestock producers and government regulatory officials, as well as those individuals and organizations that are involved with research dealing with these conditions.

So, to begin to answer the question, let’s first deal with the West Nile Virus.

WEST NILE VIRUS ENCEPHALITIS

According to the literature I have read, the West Nile Virus (WNV) was first isolated in 1937 in Uganda from cases of human and equine encephalitis. At the same time it was also recovered from some species of birds which had died from the virus infection. Since that time the virus has been endemic in Europe, Africa and some areas of Asia.

The Japanese B virus is related to WNV. The first outbreak of Japanese B encephalitis was reported from Japan in 1871, but it attracted very little attention until 1924, when another epidemic occurred in Japan involving more than 6,000 persons, of which 3,797 died. In 1940, scientists discovered that certain species of mosquitoes were the vectors of this virus.

In late July, 1999, WNV made its appearance in New York City and Long Island, primarily in Suffolk County, New York. Its appearance was heralded by a rash of deaths involving crows, blue jays, sea gulls and some red-tailed hawks. There were reported cases of human and equine encephalitis. Blood and tissue samples of affected birds, horses and humans were analyzed and tested at state and federal laboratories. WNV was established as being the causative agent.

How did the virus get here? We know the virus is transmitted by mosquitoes and was probably brought here on a migrating bird or carried on a human being. Once established, the infection is spread by migrating birds, which become infected by the carrier mosquitoes.

Four states were involved in the WNV outbreak in 1999. They were New York (largely in New York City and Long Island), New Jersey, Maryland and Connecticut.

In this outbreak there were 62 human cases, of which there were seven fatalities. Twenty-five horses were diagnosed on Long Island with WNV encephalitis, with a 32% fatality rate.

The virus successfully overwintered in the mosquito population and spread in the year 2000, so it is now found in 12 eastern states and the District of Columbia. It was diagnosed in cases occurring as far south as northern North Carolina, north in Vermont and New Hampshire and as far west as Erie, Pennsylvania.

There were 59 equine cases of WNV documented in the year 2000 in seven states. Of these, 39% were put down or died. In addition, it is known that bats, a rabbit, chipmunk and skunk were also infected.

WNV accounted for over 100,000 bird deaths, of which some 16,000 were tested after death for evidence of the virus. Crows are especially susceptible. In fact, 96 to 98% of infected birds will die in four to five days following exposure to the virus. The presence of dead crows is often indicative of the presence of WNV. The infected crow will shed a lot of the virus in its feces, and finding an average of 1.5 to 2 dead crows per square mile is indicative of the presence of WNV in the crow population and, therefore, in the mosquito population.

So what is in store for the year 2001 as far as WNV is concerned? The virus could spread west, north, and south of its present boundaries. Dr. Peter Timoney, director of the Gluck Equine Research Center at the University of Kentucky, states “It is a virus that can survive and adapt to a wide spectrum of species of birds and mammals. There is no room for complacency about this virus. You don’t want to panic people but you do need to educate them.”

So what should you look for in an affected horse? You could be suspicious of WNV if the animal shows a staggering, wobbly gait, or if it is unable to stand or has a paralysis of one or more of its legs. In addition, any horse that shows listlessness, depression, paralysis of the lower lip and inability to eat should be a suspect. Any sudden or acute death of a horse should be also viewed as possible WNV disease.

If the virus continues to journey southward along the eastern coastal states, it will soon reach areas where mosquitoes are active year round. The incidence of this disease could then take on a whole new aspect.

Enter into the picture the Asian Tiger mosquito. It entered the U.S. at Houston, Texas, from Asia in a shipment of old tires, and it very quickly became at home. It is a known resident in 21 of the 50 states. I have been told we cannot get rid of our own old tires, so why did we have to import some and bring this rascal along with ‘em?

Anyway, the Asian Tiger mosquito is a dry weather breeder. It breeds and survives nicely in drought conditions. At present it is not known to harbor the WNV; however, it is known to be a host to many other viruses. If it should become a carrier of WNV, the whole southern area of the U.S., including many hot and dry places, could become at risk to this form of encephalitis.

Another mosquito which has recently been introduced to northeastern America is Iedes japonicus, which comes to us from the Far East. This mosquito has experimentally been infected with WNV and therefore has the potential to become naturally infected, which would make it another vector in the spread of the disease.

So what can be done to halt or impede the spread of this disease? Mosquito control programs are the best solution to date. People should be on the lookout for mosquito breeding areas and when found, they should be eliminated or treated if at all possible. Every effort should be made to eliminate breeding sites of mosquitoes.

Development of a vaccine is being undertaken, but officials believe a vaccine will not be available until the end of the year 2001.

This new virus may very well be here to stay, and it will be a problem that equine breeders and owners will have to face now and in the future, much as they have had to deal with the eastern and western equine encephalitis viruses.

Now, since we’ve discussed a relative newcomer on the stage, let’s go on and check out an old-timer which has staged a reappearance and is causing great financial repercussions for the governments of the United Kingdom and many countries in Europe.

FOOT AND MOUTH DISEASE

Foot and mouth disease (FMD) is an acute infection whereupon blisters or vesicles develop on the mucous membranes of the mouth and on the skin of the udder and teats.

Primarily it is a disease of cattle, hogs, sheep, goats and other cloven-hooved animals. However, other animals and, very, very rarely, man may become infected secondarily.

It is the most highly contagious disease to which cattle and swine can be exposed.

The history of FMD is shrouded in the mists of time. For some past centuries it was known and recorded in Central Europe, but its infectious nature was not recognized until 1764. It took another century to develop its etiological nature. An outbreak recorded in 1911 in Central Europe affected 3,366,369 cattle, 1,602,927 sheep, 2,555,731 hogs, and 53,674 goats, or about one out of every seven animals in that area.

It is interesting to note that since 1850 to 1933, FMD has appeared in the United States on twelve different occasions. In 1870 the disease spread into New England and New York State. It was thought to have come from Scotland, by way of Canada, and was brought under control in a short time. In 1880, FMD was discovered in three lots of imported cattle, and it was controlled before it could spread further. In 1884, a third outbreak was discovered in Portland, Maine, but again was brought under control before spreading. All three of these epidemics were caused by the importation of diseased cattle. Soon after the last outbreak, the U.S. Department of Agriculture was formed, and strict inspection measures on imported cattle have been enforced.

The fourth outbreak of FMD, in 1902, appeared at Chelsea, Massachusetts, and spread through New England. This onset was due to contaminated cowpox virus which was brought in from Japan for the production of smallpox vaccine. Most people do not know this, but the cowpox virus was inoculated by scarification into the skin of calves. This, in turn, was harvested and the product was the smallpox vaccine used on humans to prevent smallpox. 4,712 cattle were slaughtered, as well as several hundred sheep and goats. In November of 1908, the fifth outbreak occurred in Michigan and spread to Maryland, Pennsylvania, and New York. This again was caused by contaminated vaccine brought in from Japan for the production of the smallpox vaccine. The calves were infected, as well as the vaccine which was produced. A second firm purchased some of the contaminated vaccine and in turn infected its calves. These calves were sold on the open market and infected other cattle. One hundred fifty-seven farms were infected, and 3,636 animals were slaughtered, valued at $90,033. The government recalled all of the contaminated vaccine. Since that time, the Federal Government, through the United States Public Health Service, has assumed control of vaccines and health products for humans, while the Bureau of Animal Industry does likewise for the same classes of products bound for veterinary use.

In October 1914, the most extensive and costly outbreak of FMD broke out near Niles, Michigan. This was the sixth recorded, and the virus probably found its way there from South America in or on some merchandise.

The Chicago Stock Yards became infected, and, to make matters worse, the National Dairy Show was being held there at the time. A plant manufacturing hog cholera virus was also infected, and one lot of contaminated hog cholera virus was released for vaccination purposes. From Iowa to Massachusetts, the District of Columbia and twenty–two states were affected with 3,556 herds being slaughtered at a cost of over $6,000,000.

The seventh outbreak occurred around the San Francisco Bay area, caused by garbage on a ship from the Orient which was fed to hogs. This took place in 1924, and from the Bay area, it quickly spread in six months to 16 counties in California. 58,791 head of cattle were destroyed, along with an unknown number of hogs, sheep and goats.

An incident during this outbreak quickly caught the public’s attention. It was called the “border war” between Arizona and California. Arizona prohibited automobiles from coming into the state from California. Cars and tourists were stranded at the border, until at one time 700 people and 200 cars were waiting to get across the border into Arizona. In 1924, that was a lot of people and autos! They were finally allowed to proceed on their way after thorough disinfection of people, autos and baggage.

In September of 1924, the eighth outbreak appeared in Texas. It was not related to the California onset, but was thought to have been brought in by crewmen from several ships that came from infected ports, who were taking on cattle for food. The outbreak was brought under control in 30 days by the complete and immediate slaughter of 148 herds.

The next year, 1925, the same set of circumstances led to the ninth outbreak, again in Texas. In this instance 153 infected herds and 848 exposed herds were slaughtered and the outbreak was completely controlled.

Infected garbage from a ship from South America, which was fed to hogs, caused the tenth outbreak, again in California. It was limited to five herds of hogs. This outbreak lasted from January to March, 1929. Several new methods were employed to control this episode along with the slaughter of infected and exposed herds.

Outbreak number eleven happened in April of 1932, again in Southern California. This one involved 37 herds of hogs, and the source of the virus was, again, infected garbage from ships from the Orient. In three weeks the outbreak was under control.

The last outbreak of FMD happened in 1933. It was a small incident in some hogs in San Diego, California. The source of infection, once more, was contaminated garbage from ships which was fed to the pigs.

FMD is caused by a virus which has a wonderful propensity to survive under many conditions and retain its highly infectious nature. There are at least seven different types and many sub-types of the virus. Immunity to one type does not necessarily provide immunity to any of the other types.

It has been found that the virus may remain alive and lethal for six months if kept in cool, moist surroundings at temperatures from 3.5 to 5.5 degrees Celsius. It has been known to stay alive and be active on an infected premise for 283 days and on another for 345 days. It is very resistant to some disinfectants, but heating at 55 degrees Celsius for 15 minutes will destroy it.

The virus causing foot and mouth disease in cloven-hooved animals is closely related to those which cause vesicular stomatitis in horses and vesicular exanthema in hogs. The three viruses can only be identified by certain pathogenic and immunologic properties.

How is this virus spread? Recently, APHIS has printed a bulletin on foot and mouth disease. They put it very well, and the following is a direct quote from the article:

  • “FMD viruses can be spread by animals, people or materials that bring the virus into physical contact with susceptible animals. An outbreak can occur when:
  • People wearing contaminated clothes or footwear or using contaminated equipment pass the virus to susceptible animals.
  • Animals carrying the virus are introduced into susceptible herds.”(That would include dogs, cats or wildlife, which could physically carry the virus from one point to another.)
  • Contaminated facilities or vehicles are used with susceptible animals.
  • Raw or improperly cooked garbage containing infected meat or animal products is fed to susceptible animals.
  • Susceptible animals are exposed to materials such as hay, feed- stuffs, hides or biologics contaminated with the virus or drink common source contaminated water.
  • A susceptible cow is inseminated by semen from an infected bull.”

To this list, I might add several more methods by which the FMD viruses might find their way to susceptible animals. Wind action is one way. The virus has been known to blow 140 miles on dust particles. Contaminated straw or bedding of any kind. Water is alluded to by APHIS, and it is known the virus can travel up to 18 miles in a running stream of water and infect susceptible animals which drink it.

Humans and other animals who have been closely associated with FMD-stricken livestock can harbor the virus in their lungs, and be a source of infection for up to five days after leaving the infected premises.

Again, look at the roster of the animals susceptible to FMD. They are: cattle, hogs, sheep, goats, American bison, water buffalo, deer, elk, moose, antelope, llama, camel, giraffe, and other cloven-hooved animals. One can readily see that in certain areas of the U.S., wildlife could become infected and could become a factor in the spread of FMD, which would, by its very nature be difficult to control.

Dr. John Carr, an Iowa State University veterinarian who recently was in England, says a single pig can contaminate 125 miles and it will produce 3,000 times more foot and mouth virus than an infected cow, which has the capability of infecting other animals within a one mile radius. This article appeared in the Sioux City (Iowa) Journal on Monday, April 16, 2001.

What would an infected animal exhibit? Since most veterinarians or livestock personnel in this country have never seen a case, we need to quote APHIS again.

The signs are:

  • “Blisters followed by erosins in the mouth or on the feet and the resulting slobbering are the best known signs of the disease. Often, blisters may not be observed because they easily rupture, leading to erosins.
  • Temperatures rise markedly, then usually fall in about 2 to 3 days.
  • Ruptured vesicles discharge either clear or cloudy fluid and leave raw, eroded areas surrounded by ragged fragments of loose tissue.
  • Sticky, foamy, stringy saliva is produced.
  • Consumption of feed is reduced because of painful tongue and mouth lesions.
  • Lameness with reluctance to move is often observed.
  • Abortions often occur.
  • Conception rates may be low.
  • FMD can lead to inflammation of the muscular walls of the heart, and death, especially in newborn animals.
  • Animals do not normally regain lost weight for many months. Recovered cows seldom produce milk at their former rates.”

Do humans contract this disease? The answer is yes, but the incidence is extremely rare. A researcher in this field, Trautwein, in 1932, could find only three human cases where symptoms of the disease in man were verified by animal inoculation. This was reported in Arch.Ohren–USW.Heilk. 1932, 130–249. So, for all practical experience, man does not have to worry about contracting this ailment.

Today it is estimated that a third of England’s farms will lose livestock to the disease and slaughter as the country tries to control and contain FMD. The loss in dollars is simply staggering and it will be felt by the nation and its people for years to come.

The same can be said for the countries of Western Europe where outbreaks of FMD have been discovered and efforts are underway by their respective governments to contain and eradicate the disease.

To prevent the introduction of FMD into the United States, the USDA has imposed severe restrictions on the importation of any livestock, livestock products, or even pets from countries affected with FMD. Travelers coming from these areas must submit themselves and their baggage to certain procedures upon arriving in the U.S.A.

To have FMD get a foothold in our livestock industry would produce devastating social and economic problems. Look at what is happening in England and Western Europe today.

BOVINE SPONGIFORM ENCEPHALOPATHY OR BSE FOR SHORT

Recently two very good papers written about BSE were published in The Veterinary Practice News. One in the March 2001 issue written by John B. Herrick, D.V.M. and the second written by Mr. Ron Bast, was published in the April 2001 issue. Both articles are excellent in their discussion of BSE and it is from the material presented in these issues that I will try to give you an accurate insight into the disease or condition. This is so you might understand it and not be carried away by media-induced panic on the subject.

I personally, as well as the authors of these papers, do not believe the term coined by the media as “mad cow disease” is at all accurate or, indeed, appropriate. During my years of large animal practice I have seen many “mad” cows. I’ll describe them for you. They are up on their feet, their heads are held high, ears are pointed forward, eyes are wide open and focused right on you. Their nostrils are dilated and the nose is thrust somewhat forward, which gives you the impression that they are “looking down their nose at you.” And they are! These cows are very angry and at this stage of the game could be called a “mad cow.” If you give them half a chance they will “clean your plow.”

According to both of these authors and other descriptions I have read about how an afflicted cow behaves, a different picture begins to emerge. The affected cow will often show incoordination, difficulty in rising. She will struggle to get onto her feet and show anxiety and depression. Affected animals will exhibit loss of body condition and may display changes in temperament, such as nervousness or aggression. Many of these animals will continue to eat, as their appetites do not seem to be impaired.

BSE first appeared in Great Britain in 1986. It is a fatal degenerative disease of the central nervous system. In November, 2000 new cases were reported in Germany, Spain and France. Ninety-two cases were reported in 2000 by the French government. According to Mr. Bast, BSE has claimed 178,000 cattle worldwide since 1986 and 95% of all cases to date have been from the United Kingdom.

BSE is classified as a spongiform disease. Two other similar diseases are scrapie in sheep and Creutzfeldt-Jakob disease (nv CJD) in humans.

In 1982 researchers in California described the cause of scrapie in sheep to be a protein substance which they called a prion. These prions are small protein-like particles which contain no nucleic acid, no DNA or RNA. They are very resistant to destruction or inactivation by most procedures that change nucleic acid, and the theory is they may be a new kind of contagious disease producer. These prions can withstand autoclaving and the one causing BSE can withstand rendering, doses of radiation and ultraviolet light.

Let’s put this all on a level plane for you to understand. Our bodies have a protein called PrP which is used in nerve cells. If untold numbers of these PrP particles gather together, they form plaque in the brain. According to Dr. Herrick, some scientists believe that the prion attaches itself to the healthy PrP and turns it into another prion.

This process, it is believed, repeats itself until a large mass of the protein material is formed in the brain, thus causing the lesions which are found there. This also will account for the “spongy” feeling of the tissue and will cause the symptoms as seen in transmissible BSE.

Great Britain’s BSE epidemic apparently was caused by feeding cattle contaminated meat and bone meal. Remember, the prions are not destroyed by rendering. An oral dose of one-half to one gram of infected brain tissue appears to be sufficient to infect the susceptible cow.

Apparently humans can develop (v CJD) by eating the contaminated meat from these infected cattle. No cases of (v CJD), the human form of BSE, have been reported among veterinarians or other people who have worked and been in contact with BSE cattle in Great Britain.

To date, 85 human deaths have been attributed to the disease in Great Britain. This number may go higher, as it is known the disease or condition may be harbored in the body for as long as ten years before symptoms of the condition appear. It appears BSE, thus, has been curtailed but at a tremendous price. Beef consumption in the U.K. has dropped over 50%.

The diagnosis of the disease in the live animal or human is extremely difficult. No test procedures exist at this time to diagnose the disease before the victim dies. This may change, however, since British scientists have announced in February that they have identified a possible BSE marker in immature blood cells. Boehringer-Ingeheim has recently petitioned the European Union for a global patent for a blood test that detects the disease in living cattle. According to a Reuters report, the test could be in use by late summer 2001.

So what are the U.S. government agencies doing to prevent us from getting BSE established in our cattle?

In 1997 the FDA issued an order banning the feeding of animal protein to ruminants. This includes meat meal, bone meal and blood meal. By-products from poultry, such as feather meal and poultry-by-product meal, can still be used.

In 1989, the USDA placed import bans on live ruminants and ruminant products from BSE infected nations. U.S. herds are constantly monitored for signs of the disease. APHIS has tested the brains of 12,000 slaughtered cattle nationwide. This is more than five times the numbers recommended by the international BSE surveillance standards. None of the tests showed any sign of BSE.

No cases of BSE have ever been reported in the U.S. At the moment our cattle are free of the disease, and our beef is perfectly safe to eat from the consumer’s standpoint. With vigilance and cooperation by all who are concerned with the cattle industry, the health of our beef business should be assured.

Recently, as most of you readers may know, the USDA seized two flocks of Belgian sheep from their owners in Vermont. Tests had shown that four of these animals were infected with scrapie, the sheep spongiform disease.

They were sent to the Federal Lab at Ames, Iowa, to be slaughtered, their brains tested for evidence of the disease and their remains destroyed by being immersed in vats containing boiling lye.

Remember, the prions which cause this type of disease can withstand ordinary cooking and rendering procedures.

Results of the tests may not be known for a period of time, maybe as long as two to three years, since the brain material from the sheep is inoculated into mice for study.

IN SUMMARY

Now, after reading these articles about three very important diseases of livestock, I want you to take a moment and give them some thought.

You, as horsemen and women will be directly concerned with the West Nile Virus as it fans out from its foothold in twelve states along the eastern seacoast. It has the potential to become a major health problem for humans, the horse industry and wildlife. Do what you can to suppress the mosquito populations by removing their breeding areas. Keep informed and abreast of this disease as it continues on its course.

At the present time we do not have either Foot and Mouth Disease or so-called “Mad Cow Disease”in the United States, Canada or Mexico. Be informed of the facts concerning these maladies. I have tried to do this for you. Do not be swayed by any media information which may tend to sensationalize or over-dramatize these conditions in order to create news.

Many of you readers may travel in the near future to countries which are engaged in a struggle against one or both of these diseases. Be careful and please do not make light of rules and regulations that you must observe when returning to this country. Government importation rules, regulations and requirements for importation of livestock, livestock products and even your re-entry into the U.S. are all designed to protect the livelihood, health and welfare of all of us. They protect our very way of life, as we are a livestock producing nation, and its partial or complete loss would be absolutely devastating to our economy and our way of life.

Not all people agree with this philosophy. I leave you with this excerpt from an editor’s editorial which appeared in the April 15, 2001, issue of the Sioux City Journal:

“When we read a Reuters News Service article quoting the president of the People for the Ethical Treatment of Animals (PETA) as saying that she hoped the dreaded foot and mouth disease, currently devastating the livestock industry and economy in Europe, would strike here, we were left with a strong feeling of dismay and fear.

We were dismayed that any individual would wish such a curse on any animal, let alone the livestock economy. Fear manifested itself when we realized that an act of animal terrorism, something PETA is known to support, could bring the disease here.

‘If that hideousness came here, it wouldn’t be any more hideous for the animals—they are all bound for a ghastly death anyway. But it would wake up consumers,’ said PETA co-founder and president Ingrid Newkirk. ‘I openly hope that it comes here. It will bring economic harm only for those who profit from giving people heart attacks and giving animals a concentration camp-like existence. It would be good for animals, good for human health and good for the environment.’

Those words go beyond the scope of human dignity. Any environmentalist or animal rights enthusiast should condemn those comments.”

(Editor’s Note: Doc tells us that his chronicle of outbreaks of Foot and Mouth in the United States was drawn from Diseases Transmitted from Animals to Man, by Thomas G. Hall, 3rd edition, 1947. As many of you might have noted in recent weeks, there have been several stories in our daily papers that list 1929 as the “most recent” oubreak. That obviously isn’t correct. There were a couple of incidents after that one. This 1929 thing, once printed, apparently became the “gospel” for feature writers. Most feature writers and wire service editors are not veterinarians with a penchant for “checking out the facts.”)

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