The American Association of Equine Practitioners (AAEP) defines risk-based vaccines as those that are included in a vaccination program after the performance of a risk-benefit analysis by a veterinarian.
The use of risk-based vaccinations can vary geographically, from population to population within an area, or between individual horses within a given population. Disease risk might not be readily identified by lay persons; it is important that veterinarians are involved when vaccination programs are developed. Risk-based vaccines include those for anthrax, botulism, equine herpesvirus (EHV), equine influenza, equine arteritis virus, leptospirosis, Potomac horse fever, rotavirus, snakebite and strangles.1
Veterinarians are uniquely positioned to understand the risks posed to individual horses by considering the region in which they live, the lifestyles they lead, and the diseases that are currently active in a practice area. Reviewing the facts about equine diseases that can be prevented or minimized through vaccination is important for good decision-making as well as client education.
In the case of diseases that have been in the forefront in recent years (e.g. EVA, EHV), knowledge about the pathogens is often advancing through research.
Here is refresher information for you and your staff, and tidbits you can share with your clients to help educate them and encourage them to comply with your recommendations.
The Pathogens and Their Epidemiology
Anthrax is caused by infection with Bacillus anthracis. It is a serious and rapidly fatal septicemic disease caused by proliferation and spread of the vegetative form of Bacillus anthracis in the body. Infection is acquired though ingestion, inhalation or contamination of wounds by soil-borne spores of the organism.
Anthrax is encountered only in limited geographic areas where alkaline soil conditions favor survival of the organism. Anthrax outbreaks are most commonly found in regions such as the Great Plains states (North Dakota going south to Texas) and the Intermountain Basin states (Nevada and Utah) in the United States. This bacterium forms spores, making it extremely resistant to environmental conditions such as heating, freezing, chemical disinfection or dehydration.
Anthrax is a zoonotic, reportable disease that primarily affects herbivores such as cattle, sheep, goats, antelope and deer, but horses can also be affected. Horses can consume the spores while grazing in areas where anthrax has been concentrated. Flies and other insects can also spread the disease from infected animals to other animals.
After exposure, the typical incubation period is from three to seven days. Once the bacteria infect an animal, they produce a potent and lethal toxin that causes cell death and breakdown of the infected tissues. The resulting inflammation and organ damage leads to organ failure.
Signs occur rapidly in a previously healthy animal; high fever and agitation are quickly followed by chills, severe colic, loss of appetite, depression, disorientation, difficulty breathing or exercise intolerance, muscle weakness and seizures. Bloody diarrhea might be observed. Swelling often occurs around the neck and might be so severe that suffocation is possible. Swelling of the chest, lower abdomen and external genitals can also happen. Death usually occurs within two to three days of disease onset.
Laboratory diagnosis depends on bacterial culture and isolation of B. anthracis; detection of bacterial DNA, antigens or toxins; or detection of a host immune response to B. anthracis. Human cases of anthrax can follow contact with contaminated animals or animal products. It is important to wear gloves, protective clothing, goggles and masks when handling potentially infected animals or their remains.
Vaccination of horses is only indicated for those pastured in endemic areas or areas known to be contaminated. The only vaccine currently licensed for use in horses is a live Sterne strain, non-encapsulated spore-form.
Anthrax is controlled through targeted vaccination, rapid detection and reporting, quarantine, antibiotic treatment of any animals exposed to the bacteria, and the burning or burial of dead animals. Early treatment and vigorous implementation of a preventive program are essential. Uninfected horses should be moved to another pasture away from any possible site of soil contamination. Contaminated stables and equipment must be cleaned and disinfected.2
Botulism occurs in horses when they are affected by potent toxins produced by the soil-borne, spore-forming bacterium Clostridium botulinum. There are several forms of botulism that are seen in horses. Wound botulism results from production of toxin in wounds contaminated by spores of Cl. botulinum. The toxicoinfectious form (“Shaker Foal Syndrome”) results from toxin produced by vegetation of ingested spores in the intestinal tract. Forage poisoning results from ingestion of preformed toxin produced in decaying plant material or present in animal carcass remnants present in feed or bedding.
Cl. botulinum toxin is the most potent biological toxin known and acts by preventing the release of acetylcholine at neuromuscular junctions. Acetylcholine normally transmits a nerve impulse to a muscle, signaling the muscle to contract. By blocking the action of this neurotransmitter, botulinum toxin causes flaccid paresis progressing to paralysis, and often death. The signs of botulism include cranial nerve deficits (disturbed vision, difficulty in chewing and swallowing), generalized progressive paresis and progressive motor paralysis. Death is usually due to respiratory or cardiac paralysis.
Definitive diagnosis can be difficult, as no characteristic gross and histologic lesions develop, and pathologic changes might be ascribed to the general paralytic action of toxin, particularly in the muscles of the respiratory system, rather than to the specific effect of toxin on any particular organ.3
The National Botulism Reference Laboratory at New Bolton Center provides diagnostic services for both suspected individual cases of botulism as well as possible outbreaks. The laboratory provides testing for samples from multiple animal species, including equine, bovine, avian and canine, as well as suspected feedstuffs and forages. The best samples to submit for botulism testing are stomach or GI contents, feces, spoiled forages, parts of dead animals found in suspect feed, and soil from underneath affected areas.4 Of the eight distinct toxins produced by sub-types of Cl. botulinum, types A, B and C are associated with most outbreaks of botulism in horses; however, type A is rarely seen east of the Mississippi River in the United States.
Treatment of botulism can be successful if early administration of specific or polyvalent antitoxin occurs before recumbency. Supportive care is essential; prognosis is poor in recumbent animals.
A killed vaccine for Cl. botulinum (type B only) is available for use in U.S. horses. Vaccination is recommended for horses in endemic regions, including Kentucky and the Mid-Atlantic states.
Equine herpesvirus type 1 (EHV-1) and equine herpesvirus type 4 (EHV-4) both can cause subclinical to severe respiratory disease. EHV-1 can also cause major outbreaks of abortion; the birth of weak, nonviable foals; or neurologic disease (equine herpesvirus myeloencephalopathy or EHM). Recently, the D752 and N752 strains of EHV-1 (defined by a single point mutation) were revealed to be commonly associated with neurologic disease (EHM). Molecular diagnostic techniques can identify these strains. While both of these strains cause neurological disease, infection with D752 can result in a higher clinical attack rate and a higher case fatality rate. It is estimated that 80-90% of neurological disease is caused by D752 isolates and 10-20% by N752 isolates.
The finding of D752 or N752 variants of the virus can have implications for the management of EHV-1 outbreaks or individual horses actively infected with these strains. There is some evidence that 5-10% of healthy horses normally carry the D752, which complicates management. However, in the face of an active outbreak of EHV-1 disease, identification of a D752 isolate creates increased concern about the risk of development of neurological disease.
Both EHV-1 and EHV-4 are endemic in most equine populations. Infection with EHV-1 and EHV-4 typically first occurs in foals in the first weeks or months of life, but recurrent clinical infections are seen in weanlings, yearlings and young horses entering training, especially when horses from different sources are commingled. Both viruses spread primarily by contact with nasal secretions. Contact with an aborted fetus, placental and fetal fluids, or a placenta also spreads EHV-1. Similar to the actions of herpesviruses in other species, most horses become asymptomatic carriers after infection.
When stressed, horses can experience reactivation of either virus, resulting in short-term shedding of the virus. Reactivation can also occur in pregnant mares, causing abortion. Existence of latent infections seriously compromises efforts to control these diseases and explains why outbreaks of EHV-1 or EHV-4 can occur in closed populations of horses.
Even after infection, horses might not be protected against the abortigenic or neurologic forms of the disease, and mature or aged horses are more commonly affected by the neurologic form of the disease than juvenile animals.
The incubation period of EHV-1 infection is highly variable and depends on the stress level of the host, the virulence of the virus and environmental factors. The average incubation period is four to seven days, with the majority of cases being three to eight days, but with some taking up to 14 days. When neurological disease occurs, it is typically eight to 12 days after the initial infection. Fortunately, most horses exposed to EHV-1 will develop a fever and possibly nasal discharge, then go on to recover.5
The initial clinical signs of EHV infection might be nonspecific and include fever of 102°F or higher. Fever might be the only abnormality observed. Other signs can include lethargy, anorexia, nasal discharge, cough and mandibular lymphadenopathy. Some horses develop injected mucous membranes.
Horses with neurological disease (EHM) caused by EHV-1 infection develop signs including toe-dragging, weakness and incoordination of the hind end, and they might have trouble standing. The cranial nerves are not often affected. Other neuro-logical deficits that might occur include a weak, floppy tail, inability to defecate and urinary incontinence due to effects on caudal innervation. Signs of brain dysfunction, including extreme lethargy and a coma-like state, might also occur.
Diagnosis of EHV includes nasal swab (Dacron tip with plastic shaft) collection for detection of virus by polymerase chain reaction (PCR) assay and/or virus isolation, and whole blood (EDTA) collection to detect the virus by PCR assay or by virus isolation.6
According to the AAEP Vaccination Guidelines, EHV vaccines are indicated to prevent EHV-1 abortion and to reduce the severity of respiratory disease in foals, weanlings, yearlings, and young performance and show horses that are at high risk for exposure.
Repeated vaccination appears to reduce the frequency and severity of respiratory disease and limits the occurrence of abortion storms. However, biosecurity is the most important factor in control of abortion caused by EHV-1 as well as outbreaks of EHM neurologic disease. None of the available vaccines has a label claim to prevent the neurologic form of EHV-1 infection. It has been suggested that vaccines might assist in limiting the spread of outbreaks of EHM by limiting nasal shedding of EHV-1. The vaccines with the greatest ability to limit nasal shedding and viremia of the neuro virulent strain include the vaccines Pneumabort-K, Prodigy, Rhinomune and Calvenza.7
The newly issued USEF GR845 Equine Vaccination Rule states: “At Federation licensed competitions, horses entering the grounds must be accompanied by documentation of Equine Influenza Virus and Equine Herpes Virus (Rhinopneumonitis) vaccinations within six months prior to entering the stables.”
Equine influenza (EIV) is one of the most common infectious respiratory diseases of horses, and many different strains have emerged and will continue to develop. Influenza is endemic in the U.S. equine population and throughout much of the world. Sporadic outbreaks of EIV result from the introduction of an infected horse into a susceptible population.
Avoid infection by quarantining newly arriving horses for at least 14 days and by appropriate vaccination. EIV does not typically circulate asymptomatically in horse groups, but those that are partially immune can become subclinically infected and shed virus.
Immunity following vaccination with inactivated influenza vaccines can be short-lived, allowing recently vaccinated horses to become infected and shed virus. For these reasons, EIV continues to circulate within equine populations.
Immunity to EIV can be overwhelmed in horses frequently exposed at shows or similar athletic events or when the current strains of EIV circulating within a given horse population become antigenically distinct from the vaccine. Frequent contact with large numbers of horses from diverse origins increases the chance of disease.
Equine influenza is highly contagious and the virus spreads rapidly through groups of horses in aerosolized droplets dispersed by coughing. The severity of clinical signs depends on the degree of existing immunity. The clinical signs include fever, depression, harsh dry cough, loss of appetite, nasal discharge, muscle pain and/or weakness. Secondary bacterial pneumonia is not uncommon.
Diagnosis of EIV is made by PCR of nasal swabs or tracheal wash samples, serology performed on blood samples and/ or virus isolation from blood, nasal swabs or tracheal wash samples.
Although in the past, EIV vaccines have been administered at intervals as short as three months to horses considered at high risk of infection, all currently marketed (both modified live and inactivated) equine influenza vaccines are likely to provide protection of at least six months’ duration. However, maintaining this level of protection will depend on vaccine manufacturers continuously improving vaccines through the inclusion of new antigenically distinct equine influenza viruses that appear in the horse population in the future.
Antigenic drift of EIV allows the virus to evade vaccinal immunity, contributing to the regular outbreaks of influenza among equine populations. Vaccines confer protection primarily by generating antibodies targeting the surface glycoproteins of EIV. The AAEP Vaccination Guidelines recommend that equine vaccines contain killed viral antigens from clinically relevant isolates obtained within recent years. Available vaccines include inactivated, modified live and canary pox vector vaccines.
Equine viral arteritis (EVA) is caused by equine arteritis virus (EAV), an RNA virus. EAV can cause abortion, neonatal death, fever and vasculitis in adult horses, and establish a long-term carrier state in males. While horse breeds appear equally susceptible to EAV, higher rates of infection are seen in Standardbreds and Warmbloods. Out-breaks of EVA are increasing, likely due to increased global movement of horses, breeding activity of carrier stallions and use of shipped EAV-infected semen.
EAV transmission occurs through contact with respiratory secretions or through natural or artificial insemination of fresh, cooled or frozen semen from infected stallions. EVA can be transmitted via embryo transfer where the donor mare is bred with infective semen.
The majority of primary EAV infections are subclinical or asymptomatic. Clinical signs, if they occur, typically develop three to seven days post-infection and might include fever, depression, anorexia, dependent edema (lower limbs, scrotum and prepuce or mammary glands), localized or generalized urticaria, supra or periorbital edema, conjunctivitis, and serous to mucoid nasal and/or lacrimal discharge. Abortion or neonatal death frequently follows infection in the unvaccinated pregnant mare. The carrier state can develop following EAV infection in a colt or stallion. The virus persists in the reproductive tract of stallions and can result in lifelong infection. The carrier stallion serves as a reservoir of EAV.
Diagnosis of EVA is made by virus isolation and/or paired serology. Virus isolation sampling can include whole blood (EDTA or heparin), nasopharyngeal swabs, conjunctival swabs or fetal and placental tissues/ fluids. Paired (acute and convalescent) blood samples are submitted for serology.8
A modified live vaccine for EVA is available in the United States. It is recommended that at-risk stallions be vaccinated for EVA annually, as well as mares being bred with EAV-positive semen. As it is not possible to differentiate vaccine-induced antibody response from that due to natural infection, mares intended for export and all stallions should be screened serologically before primary vaccination to prove non-carrier state. The EVA vaccine has also been used successfully to curtail large outbreaks of the disease.
Vaccinated horses often shed the virus short-term and can transmit disease during this time, so they should be isolated.
Equine leptospirosis is a disease caused by the bacteria Leptospira interrogans. It affects domestic species as well as wildlife, and it has zoonotic potential. There are several different serovars that vary in pathogenesis and their host specificity. In horses, most infections result in a self-limiting pyrexia and anorexia; however, clinical presentations might include recurrent uveitis, late-term abortion and acute renal failure or hepatic disease.
Leptospirosis is seen sporadically, but it can be significant in some regional locations. Infection with Leptospira interrogans can also cause placentitis, stillbirth or perinatal disease, depending on the serovar and the stage of gestation when infected. Approximately 3-4% of equine abortions are caused by Leptospirosis, and most frequently are due to serovar Pomona or, occasionally, Harjo. Abortion is usually late term, at about nine months of gestation. Infection is acquired through exposure to the urine of wildlife hosts or the placenta, fetal fluids and urine of an affected mare in abortion cases.
Diagnosis of equine leptospirosis is primarily through fluorescent antibody testing of aborted fetal tissues or by paired serology samples. Healthy horses can carry titers to multiple Leptospira serovars. In the United States, diseased horses typically are infected with Leptospira interrogans pomona.
Vaccination is indicated for horses or herds where Leptospirosis has been a significant problem. A killed, whole cell bacterin vaccine is now available.
Potomac horse fever (PHF) is known as equine neorickettsiosis. In 1979, the first cases emerged involving horses near the Potomac River in the eastern United States. Now PHF is seen in many other geographic locations in the United States and Canada.
PHF is caused by Neorickettsia risticii (formerly Ehrlichia risticii), a gram-negative bacterium that is harbored in flukes (flatworms) that develop in aquatic snails. During warm weather, infected immature flukes, called cercariae, are released from the snails into wetlands or streams. These immature microscopic flukes can then be swallowed by horses drinking from rivers or streams, but more commonly they are ingested by aquatic insects such as caddisflies, mayflies, damselflies and dragonflies, where they develop into their next life stage, metacercariae. Aquatic insects infected with metacercariae hatch in large swarms, then have the potential to infect horses, which ingest them. These insects might be present in pastures or even inside barns when attracted to lights.
The disease generally occurs between late spring and early fall, when hatches of aquatic insects occur. Clinical signs are variable, but might include fever, depression, decreased abdominal sounds, endotoxemia, mild to severe diarrhea, severe laminitis and colic. Pregnant mares infected with N. risticii can abort. If Potomac horse fever has been confirmed on a farm or in a particular geographic area, it is likely that additional cases will occur in future years.
Diagnosis of PHF can be confirmed by identification of the DNA of the organism in a blood or manure sample using polymerase chain reaction (PCR) tests, or by paired serology.
Vaccination for PHF has questionable benefit, as protection following vaccination can be incomplete and short-lived. This is thought to be due to lack of strong seroconversion following vaccination and the presence of multiple field strains of Neorickettsia risticii, whereas only one strain is present in the available vaccine.
Rotavirus is a major infectious cause of foal diarrhea and might cause 50% or more of foal diarrhea cases in some regions. As in most species, equine rotavirus is transmitted via the fecal-oral route and destroys the enterocytes on the tip of the villi in the small intestine, resulting in cellular destruction, maldigestion, malabsorption and diarrhea. Strict biosecurity and disinfection is essential in minimizing the spread of foal diarrhea caused by rotavirus.
Diarrhea caused by rotavirus is characterized by depression, anorexia, and profuse, watery, malodorous feces. Rotavirus diarrhea can affect more than 50% of susceptible foals in a herd, but with veterinary intervention, mortality is typically low (<1%). It is usually seen in foals greater than two months old; younger foals typically have more severe clinical signs. The diarrhea usually lasts four to seven days, although it can persist for weeks.
Diagnosis is made by identification of virus by electron microscopy in the feces, or through commercial immunoassay kits designed for detection of human rotavirus. Collecting feces early in the course of disease and sampling several foals improve the chances of virus detection.
The rotavirus vaccine contains inactivated rotavirus, and when administered to pregnant mares, it enhances colostral antibodies against equine rotavirus (Group A). After ingesting colostrum from vaccinated mares, foals will have a significant increase in rotavirus antibody titers, and decreases in incidence and severity of foal diarrhea are observed.
Strangles is caused by infection with Streptococcus equi subspecies equi (S. equi var. equi) . The highly contagious disease commonly affects young horses (weanlings and yearlings), but horses of any age can be infected, especially when commingled in groups or traveling to competitions. Following natural infection, a carrier state of variable duration can develop, and intermittent shedding might occur.
The organism is transmitted by direct contact with nasal or infected lymph node secretions of infected horses or sub-clinical shedders. Contact with objects such as water tubs, feed tubs, stalls, trailers, tack, grooming equipment, attendants’ hands and clothing, or insects contaminated with nasal discharge or pus draining from lymph nodes of infected horses, can also transmit the bacterium. S. equi survives in the environment in moist areas or water sources when protected from exposure to direct sunlight and disinfectants.
Older horses infected with S. equi often exhibit a mild form of the disease characterized by nasal discharge, small abscesses and rapid resolution of disease, whereas younger horses are more likely to develop severe lymph node abscessation that subsequently opens and drains.
Clinical signs might include fever (102-106° F); dysphagia or anorexia; stridor; internal or external lymphadenopathy (+/- abscessation); and copious mucopurulent nasal discharge. Nasal shedding of S. equi usually begins two to three days after onset of fever and persists for two to three weeks in most animals. Although some horses never shed, in others, shedding can persist chronically when infection persists in the guttural pouch. Approximately 75% of horses develop a solid, enduring immunity to strangles after recovery from the disease.
Following natural or vaccine exposure to streptococcal antigens, some horses may unpredictably develop purpura hemorrhagica, an acute, non-contagious syndrome caused by immune-mediated, generalized vasculitis. Clinical signs develop within two to four weeks following exposure to streptococcal antigens and can include urticaria with pitting edema of the limbs, ventral abdomen and head; subcutaneous and petechial hemorrhage; and sloughing of involved tissues. Severe edema of the head might compromise breathing.
Diagnosis of strangles to detect shedding of S. equi currently includes bacterial isolation by aerobic culture and subsequent biochemical identification, and bacterial DNA detection by the polymerase chain reaction (PCR) test. Culture of nasal swabs, nasal washes or pus aspirated from abscesses remains the ‘‘gold standard’’ for detection of S. equi.
Both killed and modified live vaccines for strangles are available. Vaccination is recommended on the premises where strangles is a persistent endemic problem or for horses that are expected to be at a high risk of exposure. The influence of vaccination on intermittent shedding of S. equi from chronically infected horses has not been adequately studied.
The Business of Risk-Based Vaccines
While the goal for core vaccines is reaching every horse through education and strong relationships with clients, with the risk-based vaccines, veterinarians have a unique opportunity to serve their clients by making individual recommendations. Each horse’s specific health status, living situation, geographic location and travel schedule will dictate which of the risk-based vaccines are appropriate.
Veterinarians are perfectly positioned to have up-to-date knowledge of outbreaks, unusual presentations or severity of cases, and efficacy of vaccinations in their practice regions.
The Equine Disease Communication Center, found at equinediseasecc.org, supported by the AAEP Foundation and powered by the USEF, aims to provide the most up-to-date information about emerging disease outbreaks.
Clients depend on their veterinarians to guide them during the stressful events of a disease outbreak. The more you assume the role as the trusted informed resource, the more dividends this relationship will pay.
The 2012 AAEP Horse Owners and Trainers Survey revealed that listening carefully to clients’ opinions and respecting their unique perspectives are important to client satisfaction. Having conversations about each patient’s unique needs takes time, but when coupled with an annual exam, will provide a high value to the client. The attention to detail for each horse should include recommendations for risk-based vaccines.
With the education you provide, the client can make the final choice based on his or her risk tolerance. Don’t be afraid to make appropriate recommendations. Although not all horse owners will choose to follow them, they will recognize your caring and concern for their animals.
Clients appreciate having an accurate history kept of their horses’ vaccinations, including brand, serial number and administration site. By archiving this information in a medical record, you can easily find affected patients in the event of a vaccine recall or adverse event. Most clients struggle to organize this information for themselves and appreciate the veterinarian’s role in recordkeeping. Various industry partners offer platforms that allow owners to access patient health and vaccination records through your practice’s unique portal. You can take further advantage of these new channels by posting information about risk-based vaccines to educate clients while providing them with 24/7/365 access to their horses’ medical records.
Having a continuously up-to-date understanding of USEF and FEI requirements is essential for practitioners who serve sport horses. Keeping a finger on the pulse of emerging changes in racehorse management and state regulations for travel is also important. But remember, if you deliberately build the expectation that you are the expert with regard to what vaccinations are needed or required, you must be sure to meet those expectations. By staying abreast of changes in the industry, your practice is providing a needed service to busy competitors who crave convenience and one-stop shopping.
In this busy world, the most successful businesses provide solutions to consumers’ needs while maximizing efficiency and convenience. We see this in the companion animal sector, where many small animal veterinary hospitals have retail outlets as well as grooming and boarding services; and pet supply stores have branched into offering basic veterinary services.
For equine practitioners, creating value for clients in the arena of risk-based vaccinations lies in providing individual attention, seamless and convenient delivery of service and expert advice.
1. Risk Based Vaccines. Accessed 11/2/2015. http://www.aaep.org/-i-166.html
2. Anthrax in Horses. Accessed 11/2/2015. http://www.merckvetmanual.com/pethealth/ horse_disorders_and_diseases/ disorders_affecting_multiple_body_systems_ of_horses/anthrax_in_horses.html
3. Botulism. Accessed 11/2/2015. http:// www.merckvetmanual.com/mvm/generalized_ conditions/clostridial_diseases/ botulism.html
4. National Botulism Reference Laboratory. Accessed 11/4/2015. http://www. vet.upenn.edu/veterinary-hospitals/ NBC-hospital/diagnostic-laboratories/ national-botulism-reference-laboratory
5. Neurologic Equine Herpes Virus. Accessed 11/5/2015. http://web.extension.illinois.edu/ smallfarm/downloads/59508.pdf
6. EHV Testing. Accessed 11/5/2015. http://www.freshfromflorida.com/ content/download/40971/876907/EHV_ PCR_SampleCollectionInstructions.pdf
7. Risk Based Vaccines. Accessed 11/2/2015. http://www.aaep.org/-i-166.html
8. Equine Viral Arteritis. Accessed 11/5/2015. http://www.aaep.org/custdocs/ Equine%20Viral%20Arteritis.pdf