Vaccinations for Horses
Vaccines have been true godsends the world over. Diseases that once laid waste to large segments of the human population now are held in check by vaccines. One of those killing diseases, smallpox, has been eradicated. Much the same has happened in the equine population, although perhaps in less dramatic terms--that is until just recently. The current drama is being produced by research involving DNA vaccines. Researchers at the University of Wisconsin have developed an effective DNA vaccine for equine influenza, and ongoing research is aimed at making it even more effective. In Australia, scientists believe they are on the threshold of an effective DNA vaccine to control herpes-virus 1 (rhinopneumonitis), the deadly virus that can cause abortion in horses.
In addition, it is hoped that in the near future, a DNA vaccine for rotavirus will be available, as well as one for equine infectious anemia.
All in all, the future is as bright as it has ever been in the field of vaccines. Those that are available now have some drawbacks, and the same might ultimately be found for DNA vaccines. However, at the moment, the potential advantages of DNA vaccines seem to outweigh by far any disadvantages.
The advantages of DNA vaccines were best summed up by Tom Chambers, PhD, of the Maxwell H. Gluck Equine Research Center at the University of Kentucky. In an article outlining DNA vaccination in the January 1999 Equine Disease Quarterly, Chambers presented six distinct advantages for DNA vaccines:
1. They ought to be safe because DNA is not infectious and can be highly purified. Concerns that DNA vaccines might induce autoimmune reactions or anti-DNA antibodies have so far proved unfounded.
2. DNA is stable at room temperature or even tropical temperatures, so vaccine shelf life is enhanced and refrigeration unnecessary--an important consideration for use in Third World countries. By contrast, the "cold chain" of refrigeration from manufacturer to recipient required by conventional vaccines decreases their utility and adds tremendously to their costs.
3. DNA is easy to work with, so new modifications quickly can be developed. This is particularly advantageous for vaccines that need periodic updating, like those for influenza. It also promises to cut down the time needed to develop vaccines against newly emerging diseases.
4. Because DNA vaccination produces foreign proteins in the cells of the recipient similar to an infection, the immune response to DNA vaccines is a better imitation of the response to natural infection as compared to the response of killed vaccines.
5. The kind of immune response the body produces to DNA vaccine can be biased in the direction most favorable for disease protection by adding to the vaccine genes coding for natural immune modulators, called cytokines. A variety of equine cytokines have been discovered, and their effects on the immune system are being unraveled.
6. The ease and versatility of genetic technology promise to cut the cost of vaccine production.
How does a DNA vaccine work? Chambers noted the following:
"A fundamental tenet of biology is that DNA, the molecule of genetic information, codes for the proteins that are the realization of genetic information. There are DNA ‘codes’ or sequences for all the proteins that constitute infectious agents, like bacteria or viruses. If a DNA molecule of the correct sequence is taken up by a cell, the cell makes the protein encoded by the strange DNA, almost as though it were the cell’s own DNA. The immune system won’t be fooled and will respond to the strange protein by making the required T and B cells. The animal will become immune."
A lot of good news lies in the above six points. The only downside at the moment is that these vaccines are not yet on the market in the equine world. We’ll take an in-depth look at research involving the use of DNA vaccines, plus present an updated list of recommendations for the employment of vaccines currently on the market. First, a look into history. We must understand how vaccines came into existence and how they function before we can look to the future.
History Of Vaccines
A study of the history of vaccines reveals that they have been around in one form or another for a long time. The first glimmer of knowledge likely came when it was discovered that if someone contracted a particular disease and recovered from it, that person was almost never so afflicted again.
The Chinese are credited with being among the first to make use of these observations. They are the first to use a form of vaccination in a fight against smallpox. The prevention method was crude by today’s standards.
Their approach was to expose uninfected individuals with some of the matter from the blisters caused by smallpox. One method involved removing pus and fluid from a smallpox lesion and injecting it under the skin of someone who was not infected. Another method involved peeling scabs from lesions and grinding them into a fine powder, with the uninfected person inhaling the powder. Still another method was to inject powder from scabs directly into the vein. These approaches are called variolation.
Today’s standards involve utilizing sterilized needles and refrigerated, safe vaccines. Nevertheless, there were success stories with those crude methods. True, some of the uninfected individuals treated in one or another of the above manners became ill, and others died. However, the fact remained that the incidents of smallpox in populations using variolation were substantially less than in areas where it was not used.
The process soon moved to England, and that was historically fortuitous. Edward Jenner, a country doctor in England, had experienced variolation as a young boy. During his rounds as a rural doctor, Jenner observed a relationship between an equine disease called "grease" and the bovine disease known as "cowpox." Farmers who had horses which needed treatment for "grease" often wound up also being farmers who had "cowpox" in their milking herd. Cowpox, on the surface, seemed similar to smallpox. There was one critical difference. Cowpox was relatively benign, while smallpox was deadly. All that remained in the wake of cowpox were small scars at the site of blisters.
Jenner noticed something else that would ultimately make a profound difference. He observed that people who milked cows regularly rarely were afflicted with smallpox, even though they might be exposed repeatedly. Could it be that they were being exposed to cowpox and that it was causing them to become immune to smallpox?
Jenner had to know, so he conducted an experiment that would not be tolerated in today’s society. The year was 1796.
He started the experiment by infecting a young boy with cowpox. The boy developed cowpox, but recovered fully. Once recovery was ascertained, Jenner did the unthinkable. He infected the boy with smallpox.
The boy did not get smallpox.
Jenner was jubilant, but the scientific community of the day did not share his enthusiasm. Undeterred, Jenner collected case histories of people who had contracted cowpox and had been exposed to smallpox, but hadn’t been afflicted.
Determined that this knowledge should be disseminated, Jenner wrote a book on his observations. The word began to spread, and soon many people in England were intentionally contracting cowpox in the hope that it would prevent them from coming down with the dreaded smallpox. In a great many cases it worked.
Jenner’s process of infecting people with cowpox became known as vaccination, partly because of the cow. In Latin, the word for cow is "vacca." Thus, the words vaccine and vaccinate.
When Diseases Invade
Before we can understand the role vaccines play in fighting disease, we must understand what happens when disease-causing organisms invade the body.
W. David Wilson, BVMS, MS, MRCVS, Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California-Davis, provided a succinct explanation of the process:
"Viruses, bacteria, and other infectious agents cause disease by entering the body, usually by inhalation, ingestion, or injection, after which they gain entry into vital organs, such as the lung, intestine, blood, liver, and kidney. The body has a number of non-specific barriers--such as the skin, the acid conditions of the stomach, and the mucous layer lining the lungs--to help prevent invasion by the millions of microbes we come into contact with each day. In addition, the surface of our bodies, the lining of our respiratory and gastrointestinal tracts, and our internal organs are patrolled by scavenger cells called macrophages and neutrophils that devour and neutralize infectious agents.
"In addition, these scavenger cells present ingested microbes to specific immune cells named lymphocytes, which are responsible for generation of a specific immune response and ‘immunologic memory.’ The specific immune response involves gearing up the machinery of lymphocytes to produce neutralizing antibodies and programming other lymphocytes to become ‘killer’ cells, the assassins of the immune system.
"Production of specific antibodies and programming of killer cells lead to neutralization of the invading microbes and recovery from the infection. This process may take several weeks, and antibody levels may not peak until one month or more after infection occurred. However, the memory cells programmed during the previous infection with a microbe are rapidly recruited when the same microbe is encountered again, resulting in rapid elimination of the infectious agent without development of signs of disease."
This means the animal has gained immunity. But, there is an important fact to remember--the immunity is for that disease only. Wilson used the analogy of a lock and a key.
The surface of each infectious agent or vaccine antigen, he points out, has a unique three-dimensional structure, similar to that of a key. The immune cells of the body recognize this structure as being an invader that must be eliminated.
"These immune cells," Wilson explained, "then gear up to produce special protein antibodies, which, like a lock, have a surface configuration reciprocal (opposite) to that of the antigens (keys) that induce them. This reciprocal lock and key arrangement allows the antibodies to bind to and neutralize the inducing antigens on the surface of the virus or bacteria, rendering the microbe harmless and speeding its elimination from the body."
With that knowledge as a base, researchers through the years have sought to develop vaccines that would mimic the specific immune response of a microbe without allowing it to cause disease.
One approach involves simply killing the organism. This means it could not possibly multiply in the body and cause the disease, but still could stimulate an immune response. Although killed, the vaccine still would contain the proteins that would stimulate the body to mount an immune response.
An example is the vaccine used to prevent equine influenza.
Another approach involves using a live microorganism in a weakened state. Thus, it would stimulate the immune response, but wouldn’t be powerful enough to cause the disease itself. This was the approach taken in the development of the smallpox vaccine.
There are strong positives and equally strong negatives to this approach. The positive is that the live microorganism has a powerful stimulatory effect on the immune system in the production of antibodies. The downside is that there always is the danger that the vaccine can cause the disease it is seeking to prevent.
Then there is the approach that involves using only the antigenic part of the disease causing organism. This is called the acellular approach. These vaccines are similar to "killed" vaccines in exciting the immune response.
There are also "conjugated" vaccines. These are vaccines that are used in conjunction with each other. Some vaccines are made from toxins. These vaccines are treated to overcome the harmful effects of toxin. The finished product is called a toxoid. Vaccines for tetanus and diphtheria are examples of toxoids.
The problem with the toxoid vaccines is that they excite only a light immune response and as a result are administered with an adjuvant, an agent that increases the immune response. In humans, the tetanus and diphtheria vaccines often are mixed with a vaccine to prevent whooping cough. The combination of these vaccines serves to arouse the immune system quickly.
All of these approaches have been effective in their own ways. Killer diseases, in many cases, have been defeated and lifespans have expanded in the human world. The same is true in the horse world, but some of the vaccines used for certain diseases aren’t totally effective.
A prime example is equine influenza. The vaccines available help in some cases, but do little or no good in others, when considering that the goal with vaccination is to elicit the same type of immune response as if the body had been invaded by the live disease-causing organism. The effectiveness of the vaccine also is short-lived. For this reason, it generally is recommended that the equine influenza vaccine be administered every three months.
Researchers at the University of Wisconsin made a point concerning the effectiveness of conventional equine influenza vaccines with an experiment a couple of years ago. Listed as the lead researcher was K. M. Nelson, a graduate student under the tutelage of Paul Lunn, BVSc, MS, PhD, MRCVS, Diplomate ACVIM, the man who heads up the University’s research on DNA vaccines. Lunn authored a paper on the study.
Involved in the study were eight unvaccinated ponies from a herd that had no serological evidence of having been exposed to equine influenza virus. The ponies ranged in age from one to seven years and were of both sexes.
The eight were split into two groups of four each. The group to be vaccinated received two intramuscular injections of a conventional commercial vaccine. The second shot was administered three weeks after the first injection.
The other four ponies were inoculated with a strain of equine influenza virus. All four of these ponies developed clinical signs of disease within three to five days. All four developed a cough and nasal discharge, and three of the four had an elevated temperature--101.5° to 103.5° F. All eventually recovered.
One hundred days later, ponies from both groups were inoculated with the influenza virus. The goal was to learn whether the vaccinated ponies would have established the same type of immunity as the group that had been afflicted and recovered.
When the ponies which had sustained the disease were challenged with the same strain of influenza 100 days later, they were found to be immune. They did not exhibit a single clinical sign of the disease.
That wasn’t the case with the ponies which had been vaccinated. All four developed one or more signs of the disease within four days of being inoculated with the virus. One pony became anorexic for 48 hours. Two of the four ponies developed a cough. Three of the four developed a fever with temperatures ranging from 101.6° to 102.6° F. Three of the ponies had nasal discharge that persisted up to nine days following infection.
In testing for the antibodies produced by vaccination and natural infection, it was found that the natural infection stimulated production of the antibodies needed to ward off future attacks while the conventional vaccine did not. The researchers identified the antibodies produced as the result of natural infection as immunoglobulin A (IgA), immunoglobulin Ga (IgGa), and Immunoglobulin Gb (IgGb).
"These antibody responses," Lunn wrote in his report, "were associated with protection from challenge infection 100 days later. Conventional vaccination induced an IgG(T)--immunoglobulin G(T)--response only, and vaccinated ponies showed no resistance to challenge infection with influenza virus."
So, the question surfaces, how does one improve equine influenza vaccine so that it provides an immunological response that will mimic that which occurs when the disease itself strikes?
Lunn and his colleagues believe they know the answer: DNA vaccine.
Vaccines Of Tomorrow
"DNA vaccination offers a radical alternative to conventional vaccines, with the potential to generate the same protective immune responses seen following viral infection," Lunn wrote in an article for Vaccine magazine. "Current vaccination strategies can be divided broadly into administration of ‘live’ and ‘dead’ vaccines. Live vaccines, while often successful in generating immunity, carry significant safety risks. Dead vaccines might be safer to use, but frequently fail to induce appropriate immune responses. In contrast, DNA vaccination results in the in vivo synthesis of antigenic proteins generating both potent CTL (cytotoxic T lymphocytes) and antibody responses. Overall, DNA vaccines can deliver the immunogenic advantages of live vaccines, but at a low cost and with minimal safety concerns."
Assisted with grants from the Grayson-Jockey Club Research Foundation, the Wisconsin researchers already have developed a DNA vaccine for equine influenza that they feel is superior to any of the conventional vaccines available. They now are at work on the approach described by Chambers in point number 5--making use of the genes’ coding for natural immune modulators, called cytokines.
First, a word about an experiment to prove their point--that DNA vaccine for equine influenza is effective. This experiment involving horses followed in the wake of murine (pertaining to rats and mice) research. Using the rodents as models, the researchers had discovered that a DNA vaccine was effective in preventing equine influenza.
Then, it was time to move the research to equine models. Once again, ponies were used in the study.
The administration of the DNA vaccines sounds a little like something out of science fiction--a loud gene gun firing microscopic pellets of gold, coated with DNA vaccine, was used.
First, the researchers had to decide on the sites of inoculation. One group of ponies was to receive the vaccine both at skin level and in the mucosa; the other group at a skin site only. The decision was that the thin skin in the inguinal (groin) and perineal (the area between the thighs, bounded in the male by the scrotum and anus and in the female by the vulva and anus) regions should serve as sites for the skin inoculation. The sites for mucosal administration were the bottom of the tongue and the conjunctiva and third eyelid.
Pressurized helium gas in the gene gun was used to propel the microscopic pellets.
Three experimental pony groups were established with four ponies in each group. Two groups would be vaccinated as described above. The third group was the control group of unvaccinated ponies.
In the skin vaccination group, gene gun vaccination was applied at 13 non-overlapping locations on inguinal skin and 10 on the perineum.
In the skin and mucosal vaccination group, additional mucosal vaccinations were applied at 10 locations on the bottom of the tongue and a total of four sites on the conjunctiva and third eyelid of each pony.
The DNA vaccine was administered on Day 0, 63, and 138 of the experiment.
Thirty days after the third vaccination, all of the ponies in the study groups were infected with equine influenza virus and studied for an additional 30 days.
The results were significant.
After receiving the challenge infection, three of the four unvaccinated ponies showed clinical signs of influenza for three to five days, Lunn reported. The ponies had nasal discharge, coughing, and two of them developed a fever.
In the group of ponies which received the skin vaccination only, a slight mucoid nasal discharge developed in two of the four ponies, but it was not nearly as severe as in the unvaccinated ponies. The same two ponies developed coughing and some fever for three to five days.
In the group receiving DNA vaccine from both skin and mucosal sites, there were no clinical signs of equine influenza after the challenge infection.
Thus, the researchers found, the DNA vaccine was indeed effective and that it was most effective when both skin and mucosal sites were used for administration.
While the experiment produced some seemingly conclusive results, it also produced a mystery. It had been found in earlier studies that when the immune system produces antibodies after being challenged with natural infection, there is a strong immunoglobulin A (IgA) response.
Mucosal IgA, reported Lunn, is considered a critical component of protective immune responses to influenza virus "and we have previously demonstrated that protective immunity to equine influenza virus after a primary infection is strongly associated with a mucosal IgA response."
Now for the mystery.
"Nevertheless," Lunn wrote, "the protective immunity resulting from DNA vaccination in this study was not associated with any detectable IgA response. The lack of an IgA response to DNA vaccination in this instance, even when administered at mucosal surfaces, may have resulted from generations of a limited repertoire of immune responses."
More research is needed to clear up the mystery.
The important thing is that the DNA vaccine had elicited a systemic immune response to ward off future attacks of equine influenza that mimicked, as far as effectiveness is concerned, what occurred in the wake of natural infection.
"Our new goals," wrote Lunn in the application for additional Grayson-Jockey Club Research Foundation funds, "are to advance these studies through employment of cytokine-expressing plasmids as adjuvants for DNA vaccination. This approach has the potential to make DNA vaccination the safest and most effective means of generating protective immunity to influenza virus infection, and potentially many other infectious agents.
"In the current Grayson-Jockey Club Research Foundation project, we have demonstrated that DNA vaccination of horses can generate protective immunity, which is mediated by IgGa and IgGb responses. These results represent one of the very first successful applications of DNA vaccination in a large animal species. It is likely that these equine immune responses to DNA vaccination can be manipulated through the use of cytokine-expressing plasmids as adjuvants. This approach may increase the strength and longevity of the resulting immune response and has the potential to induce mucosal IgA responses, a central goal of this project."
Research on DNA vaccines is going on at other institutions as well.
At the equine health conference held in March, 1998, in Dubai, a report was presented by M. Whalley, Macquarie University in Sidney, Australia, that produced hope for an improved vaccine to prevent equine herpesvirus-1 (rhinopneumonitis).
The research is in its infancy. Mice were used as models, Whalley reported at Dubai. The mice were injected with a DNA vaccine against EHV-1. Within two weeks after injection, the mice were showing an antibody response. By four weeks, the antibody levels had risen strongly without any additional immunization. Antibody levels in these mice still were increasing at eight weeks post-injection. Mice given a DNA booster injection at four weeks, Whalley reported, showed an enhanced antibody response compared to the mice receiving a single injection.
One can surmise that we are on the threshold of some exciting breakthroughs in this field, and the ultimate beneficiary will be the horse. Lunn, who is working with the Australian researchers, says there is much to be done before a DNA herpesvirus vaccine is on the market, but research results thus far are promising.
Vaccines Of Today
As mentioned earlier, however, those breakthroughs are not yet to the point where a DNA vaccine is on the market. In the meantime, we must use the weapons available in our battle to prevent disease.
The horseman faces a series of questions, such as: What should I vaccinate against? When should various vaccines to be administered? How old should my foal be before it gets its first shots? Are boosters needed?
The list goes on.
The answers to these and other questions often depend on geography. There are some universal rules of thumb, but some parts of the country are more prone to certain diseases than others. Just as in the case of a deworming program, the horse owner should sit down with his or her veterinarian and design a vaccination strategy for that particular locale and his or her particular horses.
There is another important matter to consider. Vaccinating against disease is only part of a good herd health program. When disease spreads from horse to horse, there are two components required. One is the horse carrying the disease and the other is a horse that is receptive to the disease. Granted, vaccinations can help make that second horse resistant, but there are other things that can be done to reduce disease transmission risks. More about that later.
Once the foal is born, the issue to be decided is the time to initiate the vaccination series. The difficulty in determining correct timing involves the question of when the antibodies received from the mare--known as passive immunity--no longer provide adequate protection and vaccination is needed to stimulate the immune system.
If the vaccinations occur too soon, the agents administered can conflict with antibodies already present from the colostrum in passive immunization. If administered too late, it could mean that the foal will go through an unprotected period.
We turn again to Wilson:
"In order to maximize passive protection of the foal," he said, "broodmares should be maintained on a regular vaccination program and should be given booster doses of vaccine four to six weeks before foaling. These booster doses increase the level of specific antibodies in the mare’s blood and allow the mare to concentrate the antibodies in the colostrum to a much higher concentration than she has in her blood.
"During the first 24 hours of life, the intestine of the foal is lined by special cells which absorb the antibodies directly into circulation without being digested. These ingenious mechanisms that allow the mare to concentrate antibodies in colostrum and then permit the foal to absorb the antibodies without being digested result in a level of antibodies in foal blood very similar to the level present in the blood of the mother. It is, therefore, extremely important that foals receive colostrum within the first few hours of birth."
So far, so good. The foal ingests colostrum and gains immunity. What happens next is less certain.
Wilson explained, "The antibodies the foal absorbs from the colostrum are made of protein and are gradually used up by the body. Concentrations of passively acquired antibodies in the circulation of the foal decline with a half-life of about 30 days, meaning that the concentration diminishes by 50% every month. Depending on the level of antibodies absorbed and characteristics of the specific infectious agent, passively derived colostral antibodies may protect the foal from specific infectious diseases for a period ranging from a few weeks to several months."
The way nature has programmed the procedure, the foal, which is constantly in contact with infectious agents of one sort or another, is developing its own immune system. If everything were ideal, the foal’s immune system would peak at the same time that the power of the passive antibodies had all but disappeared. Because all does not work out perfectly in nature, we often must provide assistance to that foal with vaccines to help protect against infectious diseases.
The mystery area involves knowing just when the passive antibodies are no longer effective, and when the administration of vaccine will be effective.
"In order to be effective," Wilson said, "the modified infectious agents present in vaccines must have a surface configuration closely resembling that of the specific infectious agent that causes the disease we are trying to prevent. Thus, it is not surprising that passively derived antibodies can also bind the modified antigens present in vaccines, resulting in a reduction or elimination of their ability to induce a protective immune response. This effect is termed maternal antibody interference."
As a result of this knowledge, there has been a significant revision in the approach to foal vaccination schedules.
Wilson offered more:
"The issue becomes even more complicated within a herd situation because the level of antibody acquired by each foal varies and therefore the duration of passive protection and maternal antibody interference with vaccination varies. Thus, if all foals were to be first vaccinated at a certain age, for instance three months, those foals that no longer have maternal antibodies would be expected to respond to the vaccine whereas those foals with persistent antibodies would not. The horse owner would be left with the false sense of security that all foals were protected when some were not. The uniformity of passive transfer can be maximized by booster vaccinating the mares with the same vaccines at a consistent time--four to six weeks before foaling--but even this approach will not ensure that all foals respond to the same extent."
So, where does the horse owner begin? For starters, a consultation with a veterinarian who knows the diseases prevalent in the area is a must. Wilson offered general help with the following vaccination recommendations:
Tetanus--Tetanus is caused by a spore-forming, toxin-producing bacterium that is present in the intestinal tract and feces of humans, horses, and other animals. It also is present, often abundantly so, on all horse facilities.
Wilson recommended that a two-dose primary vaccination series for foals should begin at three to six months of age, with the intramuscular injections being one month apart. A third dose administered two to three months after the second might be necessary for optimal response. This should be followed by a yearly booster. The annual booster for pregnant mares should be timed four to six weeks before foaling in order to protect them if they sustain injuries during foaling and to provide protection to the foal via colostrum. Available tetanus toxoid vaccines are relatively inexpensive, safe, and induce solid, long-lasting immunity, said Wilson.
Equine Encephalomyelitis or Sleeping Sickness--In the United States, the concern is with two forms of encephalomyelitis--Western (WEE) and Eastern (EEE). Outbreaks of WEE have been recorded throughout the United States, but EEE is restricted to the eastern and southeastern states. (Venezuelan encephalomyelitis, VEE, normally occurs in South and Central America.) The vaccines available to combat EEE and WEE are effective, Wilson stated. Primary immunization of unvaccinated horses involves intramuscular administration of two doses of WEE and EEE three to four weeks apart. This should be followed by an annual booster shot. Booster vaccination of pregnant mares four to six weeks before foaling provides passive colostral protection for their foals lasting up to six to seven months of age.
Wilson recommended that, in the western United States, foal vaccination be started at six to nine months of age with three or more doses. In the eastern states, vaccination of early foals should begin at three to four months of age. Booster shots should be administered once a year thereafter. Some veterinarians in high-risk states, such as those on the Eastern Seaboard with high mosquito populations year-round, Wilson said, prefer to vaccinate horses twice annually.
Influenza--Wilson recommended that on breeding farms, all mature horses should be revaccinated at intervals of four to six months, with boosters for pregnant mares administered four to six weeks before foaling. Wilson recommended that one start a foal vaccination schedule at six to nine months of age--three or more doses. A booster should be given at three to four-month intervals through two years of age.
Equine Herpesvirus or Rhinopneumonitis--Rhinopneumonitis is an insidious disease that is caused by two types of virus, EHV-1 and EHV-4. Both infect the respiratory tract causing signs of mild fever and nasal discharge. In some cases, there also can be high fever, loss of appetite, lethargy, and coughing. The more vicious of the two viruses is EHV-1 because it can cause abortion in pregnant mares, the birth of weak foals, and a paralytic neurological disease. The diseases, Wilson explained, are spread in droplets from infected coughing horses and, in the case of EHV-1, by infected aborted fetuses. The virus often attacks weanlings and yearlings, with older horses gaining immunity through repeated exposure. However, he adds, it is important to note that there is no immunity engendered against abortion and neurological disease.
Here are Wilson’s recommendations for a vaccination program to prevent EHV-1 and EHV-4:
- Vaccinate dam four to six weeks before foaling.
- Start foal vaccination at four to six months of age.
- Administer at least three doses in the primary series.
- Booster shots at three- to four-month intervals.
Mares, Wilson said, should be vaccinated for EHV-1 during the fifth, seventh, and ninth month of every pregnancy with inactivated vaccine.
Strangles--Strangles is a highly contagious disease caused by the bacterium Streptococcus equi. The disease, said Wilson, is most often a problem on breeding farms, generally afflicting young horses--weanlings and yearlings. Affected horses often run a fever, are depressed, have a sore throat, exhibit a cloudy nasal discharge, and have enlarged lymph nodes that ultimately abscess and drain white, creamy pus on the skin surface. The organism causing strangles can survive in the environment for one year if not exposed to sunlight or disinfectant.
Several vaccines are available to fight strangles, Wilson said, but none is totally effective. Many veterinarians, he said, do not recommend vaccination unless the problem exists on a particular farm. In that case, Wilson recommended use of the new intranasal strangles vaccine (Pinnacle I.N. from Fort Dodge). Two doses are administered three weeks apart, followed by boosters at two-month intervals.
The appropriate age to start foal vaccination with the intranasal vaccines has not been established, but four months is the earliest Wilson would recommend. If one of the inactivated or M-protein injectable vaccines is used, Wilson suggested a three-dose primary series of vaccinations, beginning when the foal is four to six months of age, with boosters at six-month intervals. He also recommended, if strangles is a problem on a particular farm, that the mares be vaccinated four to six weeks before foaling.
There are some diseases that are more prone to occur in specific geographic areas. Included are rotavirus, botulism, Potomac Horse fever, and equine viral arteritis. Following are Wilson’s vaccination recommendations:
Rotavirus--On farms with a history of rotavirus infection, he recommended vaccinating the dam during the eighth, ninth, and tenth months of gestation, with the procedure being repeated with each pregnancy.
Botulism--On individual farms or in geographic areas with a history of botulism, Wilson recommended that the dam be vaccinated during the eighth, ninth, and tenth months of pregnancy. The dam should be vaccinated four to six weeks before foaling in successive pregnancies. If the risk of infection continues, Wilson said, the weanling should be vaccinated at three months of age or older.
Potomac Horse Fever--Vaccination for this disease, Wilson feels, is only indicated for horses in endemic areas. The dam should be vaccinated four to six weeks before foaling. The foal should be started at six months of age or older with three doses of vaccine and booster shots at six-month intervals thereafter. Wilson added this postscript: "Strong evidence of the effectiveness of injectable Potomac Horse Fever vaccines is lacking."
Equine Viral Arteritis (EVA)--Equine viral arteritis is another insidious disease that can cause abortion. A vaccination program, said Wilson, is recommended only for horses on breeding farms with a high risk of infection and for mares being bred naturally or by artificial insemination to carrier stallions. Vaccination of weanling colts, he added, is effective in preventing establishment of carrier state later in life. Foals should be started on the vaccination schedule at six to 10 months of age and given boosters annually thereafter. Mares should be vaccinated with a modified live vaccine prior to breeding. (See The Horse of February 1999, article #286, for complete guidelines.)
Rabies--The dam should be vaccinated before breeding. A vaccination program for the foal should start at six months of age or older--two doses. A booster shot should be given when the youngster becomes a yearling and annually thereafter.
Other Weapons In The Arsenal
Earlier we pointed out that vaccination is only one of the weapons that must be employed in the battle against infectious disease. It must be remembered that immunity induced by a particular vaccine can be overridden by a massive disease challenge. This is especially true if the horse in question has been on an inadequate diet. The horse which is well cared for normally is much more capable of resisting disease than one which is not. Wilson offered these management comments and suggestions:
"The incidence of infectious disease in the horse population tends to increase as the number and concentration of horses increase, and is also influenced by other management and environmental factors. The conditions on breeding farms, in show horse barns, and at racetracks are ideal for the introduction and transmission of infectious diseases, particularly respiratory tract infections. On breeding farms, the introduction of horses from different sources, the mix of horses of different ages, and the high proportion of young, susceptible animals and pregnant mares pose special problems."
The risk of acquiring infection can be reduced by maintaining distinct groups by age and function. Resident mares and foals should be kept separate from weanlings, yearlings, horses in training, and visiting mares.
New arrivals and visiting mares should be Coggins tested negative for equine infectious anemia, vaccinated, and dewormed prior to arrival. If possible, they should be received and maintained in barns and paddocks separate from the farm population. Foaling mares being sent to another farm for breeding should be shipped six to eight weeks before foaling to allow them time to mount an immune response against infectious agents on the farm and to concentrate antibodies in the colostrum, thereby improving passive protection of the foal. On any farm, a horse which becomes ill with a potentially contagious disease should be isolated promptly from the remainder of the herd for at least 10 days beyond complete recovery.
"A good management program also involves cleanliness in the stable and paddock areas to eliminate sites where disease-causing organisms can proliferate."
If these suggestions are followed and a well-planned vaccination program initiated, the number of infectious diseases that attack your horses will be kept at a minimum. In the meantime, we will wait with keen anticipation the unraveling of even more information involving DNA vaccines. The day might not be far off when we can protect our horses from equine influenza, for example, by simply spraying vaccine into the horse’s nose.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
POLL: Rehabbing the Injured Horse