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These are vaccinations included in a vaccination program after the performance of a risk-benefit analysis. The use of risk-based vaccinations may vary regionally, from population to population within an area, or between individual horses within a given population. Disease risk may not be readily identified by laypersons; it is important to consult a veterinarian when developing a vaccination program. 


Anthrax 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. (View map of U.S. outbreaks.) Vaccination is indicated only for horses pastured in endemic areas.


The only vaccine currently licensed for use in horses is a live Sterne strain, non-encapsulated spore-form. The vaccine has been shown to be effective; however, vaccination of pregnant mares is not recommended. Adverse reactions to the vaccine have been reported in young, and miniature horses. Local swelling may occur at the injection site, most of which resolves within a few days.

Appropriate caution should be used during storage, handling and administration of this live bacterial product. Consult a physician immediately if human exposure to the vaccine occurs through accidental injection, ingestion, or otherwise through the conjunctiva or broken skin.

Antimicrobial drugs should not be given concurrently, as this may interfere with adequate response to the vaccine.

Vaccination Schedule:

Adult horses previously vaccinated against anthrax: Annual vaccination.

Adult horses previously unvaccinated or of unknown vaccinal history:  Administer a primary series of 2 subcutaneous doses of vaccine with a 2 to 3 week interval between doses. Vaccinate annually thereafter.

Pregnant mares: Not recommended.

Foals: There is no specific information available regarding the vaccination of foals against anthrax.


Botulism has been observed in horses as a result of the action of potent toxins produced by the soil-borne, spore-forming bacterium, Clostridium botulinum:

  • Wound botulism results from vegetation of spores of Cl. botulinum and subsequent production of toxin in contaminated wounds.
  • Shaker Foal Syndrome (toxicoinfectious) 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, including improperly preserved hay or haylage, or animal carcass remnants present in feed.

Botulinum toxin is the most potent biological toxin known and acts by blocking transmission of impulses from nerves to muscles, resulting in muscle weakness progressing to paralysis, inability to swallow, and frequently, death. Of the 8 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 U.S.


A killed vaccine (toxoid) directed against Cl. botulinum type B only is licensed for use in horses in the United States. Vaccination is warranted for all horses, as C. botulinum type B can be found in soil samples from many areas of the country and movement of horses or forage from non-endemic to endemic regions occurs frequently.  Vaccination is recommended for horses at increased risk of developing botulism due to residence in (or travel to) endemic regions, including Kentucky and the Mid-Atlantic states.  Particularly susceptible groups within those regions include adult horses fed high-risk forages and foals born to unvaccinated mares.  The feed sources most commonly linked to “forage poisoning” in adult horses include fermented feeds (haylage or silage) and improperly processed or stored large bales of hay.

Foals born in endemic regions are at risk for toxicoinfectious botulism (Shaker Foal Syndrome) unless protected by colostral transfer of antibodies produced by vaccination of the pregnant mare. Almost all cases of Shaker Foal Syndrome, a significant problem in Kentucky and in the mid-Atlantic seaboard states in foals between 2 weeks and 8 months of age, are caused by Cl. botulinum type B. Limited information suggests that foals vaccinated with the toxoid at 2 weeks, 4 weeks and at 8 weeks of age developed adequate serologic response, even in the presence of passive maternal antibodies.

Currently, no licensed vaccines are available for preventing botulism due to Cl. botulinum types A or C or other subtypes of toxins. Cross-protection between subtypes does not occur.


Vaccination Schedule:

Previously vaccinated pregnant mares:  Vaccinate annually with a single dose 4 to 6 weeks before foaling.

Previously unvaccinated pregnant mares:  Vaccinate during gestation with a primary series of 3 doses administered at 4-week intervals and scheduled so that the last dose will be administered 4 to 6 weeks before foaling to enhance concentrations of immunoglobulin in colostrum (i.e. months 8, 9, 10 of gestation).

Foals of vaccinated mares (in endemic areas):  Administer a primary series of 3 doses, at 4-week intervals, starting at 2 to 3 months of age. As maternal antibody does not interfere with vaccine response, foals at high risk may have the vaccination series initiated as early as 2 weeks of age.

Foals of unvaccinated mares (born in, or moving to, endemic areas):  Administer a primary series of 3 doses, at 4-week intervals, beginning at 1 to 3 months of age. Foals at high risk may have the vaccination series initiated as early as 2 weeks of age.  Foals of unvaccinated mares may benefit from transfusion of plasma from a vaccinated horse or from administration of Cl. botulinum type B antitoxin. The efficacy of these practices needs further study.

All other horses (where indicated):  Administer a primary series of 3 doses of vaccine given at 4-week intervals and followed by annual revaccination.

Horses that are naturally intoxicated or exposed: Duration of immunity following natural intoxication is highly variable; clinical experience suggests that in many cases natural intoxication does not stimulate a protective immune response.  A primary 3-dose series (given at 4-week intervals between doses) should be initiated as soon as clinical disease is recognized, as serum antibody does not interfere with response to vaccination.  In outbreak situations involving unvaccinated animals, an accelerated vaccination schedule is frequently recommended, with the 3-dose series administered at 2-week intervals.

Equine Herpesvirus (Rhinopneumonitis)

Equine herpesvirus type 1 (EHV-1) and equine herpesvirus type 4 (EHV-4) infect the respiratory tract, the clinical outcome of which can vary in severity from sub-clinical to severe respiratory disease. Clinical infection is characterized by fever, lethargy, anorexia, nasal discharge, cough, and mandibular lymphadenopathy. Infection of the respiratory tract 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. Equine herpesvirus type 1 can cause major outbreaks of abortion in naïve mares, the birth of weak nonviable foals, or a sporadic neurologic disease (equine herpesvirus myeloencephalopathy-EHM) secondary to lytic infection of endothelial cells resulting in the development of thombi in the small blood vessels supplying the spinal cord and brain.

Both EHV-1 and EHV-4 spread primarily by the respiratory route, by direct and indirect (fomite) contact with nasal secretions, and, in the case of EHV-1 and infrequently EHV-4, by contact with aborted fetuses, placental and fetal fluids, and placentae. Like herpesviruses of other species, these viruses establish latent infection in the majority of horses, which become asymptomatic carriers of one or both viruses.  Such horses may experience reactivation of either virus, resulting in replication in certain white cell elements in the blood and short term shedding of the virus when stressed. Some pregnant mares in which reactivation of virus occurs, may abort.  Existence of a carrier state seriously compromises efforts to control these diseases and explains why outbreaks of EHV-1 or EHV-4 can occur in closed populations of horses.

Because both viruses are endemic in many equine populations, most mature horses have developed some immunity through repeated natural infection; thus, most mature horses do not develop serious respiratory disease when they become reinfected but may be a source of infection for other susceptible horses. In contrast, horses may not be protected against the abortigenic or neurologic forms of the disease, even after repeated infection, and mature or aged horses are in fact more commonly affected by the neurologic form of the disease than juvenile animals.

Recently, a genetic variant of EHV-1 has been described (defined by a single point mutation in the viral DNA polymerase [DNApol] gene) that is more commonly associated with neurologic disease (EHM). This mutation results in the presence of either aspartic acid (D) or an asparagine (N) residue at position 752.  Molecular diagnostic techniques can identify EHV-1 strains carrying these genetic markers. The finding of a neuropathogenic variant of the virus can have implications for the management of EHV-1 outbreaks, or individual horses actively infected with these strains. It is important to understand that both virus genotypes can and do cause neurological disease. However, infection with D752 strains 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.  It is possible that 5-10% of all horses normally carry the D752 form (this estimate is based on limited studies at this time). In the face of an active outbreak of EHV-1 disease, identification of a D752 isolate may be grounds for increased concern about the risk of development of neurological disease.

Primary indications for use of equine herpesvirus vaccines include prevention of EHV-1-induced abortion, and reduction of severity and duration of signs of respiratory tract disease (rhinopneumonitis) in foals, weanlings, yearlings, young performance and show horses that are at high risk for exposure. Many horses produce post-vaccinal antibodies against EHV, but the presence of those antibodies is not indicative of protective immunity. Repeated vaccination appears to reduce the frequency and severity of disease and limits the occurrence of abortion storms.  As with all forms of equine herpes viral disease, biosecurity management is of primary importance for control of abortion caused by EHV-1.

Please check with your state or provincial animal health office on what diseases are reportable.


Inactivated vaccines

A variety of inactivated vaccines are available, including those licensed only for protection against respiratory disease,  and two that are licensed for protection against both respiratory disease and abortion,. Performance of the inactivated respiratory vaccines is variable, with some vaccines outperforming others. Performance of the inactivated abortion/respiratory vaccines is superior, resulting in higher antibody responses and some evidence of a cellular response to vaccination.

Modified live vaccine

A single manufacturer provides a licensed modified live EHV-1 vaccine.  It is indicated for the vaccination of healthy horses 3 months of age or older as an aid in preventing respiratory disease caused by equine herpesvirus type 1 (EHV-1).


None of the available vaccines have a label claim to prevent the neurologic form of EHV-1 infection. It has been suggested that vaccines may assist in limiting the spread of outbreaks of EHM by limiting nasal shedding of EHV-1 and dissemination of infection. For this reason some experts hold the opinion that there may be an advantage to vaccinating in the face of an outbreak. If this approach is pursued, only afebrile and asymptomatic horses should be vaccinated and protection against clinical EHM should not be an expectation.  The vaccines with the greatest ability to limit nasal shedding and viremia of the neuro virulent strain include the vaccines licensed for control of abortion (Pneumabort-K® & Prodigy®), the MLV vaccine (Rhinomune® & Calvenza®).

Vaccination schedules:

Adult, non-breeding, horses previously vaccinated against EHV:  Frequent vaccination of non-pregnant mature horses with EHV vaccines is generally not indicated as clinical respiratory disease is infrequent in horses over 4 years of age. In younger/juvenile horses, immunity following vaccination appears to be short-lived. It is recommended that the following horses be revaccinated at 6-month intervals:

  • Horses less than 5 years of age.
  • Horses on breeding farms or in contact with pregnant mares.
  • Horses housed at facilities with frequent equine movement on and off the premises, thus resulting in an increased risk of exposure.
  • Performance or show horses in high-risk situations, such as racetracks. More frequent vaccination than at 6 months intervals may be required in certain cases as a prerequisite for entry to the facility.  See here for USEF Vaccination Rule.

Adult, non-breeding horses unvaccinated or having unknown vaccinal history:  Administer a primary series of 3 doses of inactivated EHV-1/EHV-4 vaccine or modified-live EHV-1 vaccine. A 4 to 6 week interval between doses is recommended.

Pregnant mares: Vaccinate during the fifth, seventh, and ninth months of gestation using an inactivated EHV-1 vaccine licensed for prevention of abortion. Many veterinarians also recommend a dose during the third month of gestation and some recommend a dose at the time of breeding.

Vaccination of mares with an inactivated EHV-1/EHV-4 vaccine 4 to 6 weeks before foaling is commonly practiced to enhance concentrations of colostral immunoglobulins for transfer to the foal. Maternal antibody passively transferred to foals from vaccinated mares may decrease the incidence of respiratory disease in foals, but infection is common in these foals and may result in clinical disease and establishment of the carrier state.

Barren mares at breeding facilities: Vaccinate before the start of the breeding season and thereafter based on risk of exposure.

Stallions and teasers: Vaccinate before the start of the breeding season and thereafter based on risk of exposure.

Foals: Administer a primary series of 3 doses of inactivated EHV-1/EHV-4 vaccine or modified-live EHV-1 vaccine, beginning at 4 to 6 months of age and with a 4 to 6 week interval between the first and second doses. Administer the third dose at 10 to 12 months of age.

Immunity following vaccination appears to be short-lived and it is recommended that foals and young horses be revaccinated at 6-month intervals.

The benefit of intensive vaccination programs directed against EHV-1 and EHV-4 in foals and young horses is not clearly defined because, despite frequent vaccination, infection and clinical disease continue to occur.

Outbreak mitigation:

In the face of an outbreak, horses at high risk of infection, and consequent transmission of infection, may be revaccinated. Administration of a booster vaccination is likely to be of some value if there is a history of vaccination. The simplest approach is to vaccinate all horses in the exposure area—independent of their vaccination history. If horses are known to be unvaccinated, the single dose may still produce some protection.  It is essential to understand that strict quarantine, isolation, and monitoring protocols are more effective at controlling outbreaks than any vaccination protocol.

Controversy persists among experts regarding possible association between frequent vaccination against EHV and the risk of developing EHM.  The absence of any controlled challenge studies designed to examine this question makes it unwise to offer any definitive conclusion

Horses having been naturally infected and recovered: Horses with a history of EHV infection and disease, including neurological disease, are likely to have immunity consequent to the infection that can be expected to last for 3 to 6 months (longer in older horses). Booster vaccination can be resumed 6 months after the disease occurrence.

Equine Influenza

Equine influenza, caused by the H3N8 orthomyxovirus, equine influenza A type 2 (A/equine 2), is one of the most common infectious diseases of the respiratory tract of horses. The influenza A/equine 1 virus (H7N7) appears to have been extinct in nature for many years. Since the early 1980s, the equine influenza A/equine 2 viruses have diverged into two distinct evolutionary lineages, Eurasian and American, of which the American lineage predominates and has been responsible for almost all outbreaks worldwide in recent years. Continued antigenic drift has resulted in three distinct American sub-lineages, a South American lineage, a Kentucky lineage (also known as classic American lineage), and a Florida lineage. The latter has been responsible for most of the outbreaks in North America, Europe and elsewhere in the world during the last decade. Further genetic evolution of the Florida sub-lineage has resulted in two groups of viruses referred to as Florida sub-lineage clades 1 and 2. Clade 1 representatives include Ohio 2003, South Africa 2003, Japan 2007 and Australia 2007 viruses. Clade 2 representatives are present in Europe, India and China and include Richmond 2007. 

Influenza is endemic in the equine population of the United States and throughout much of the world, with the notable exceptions of New Zealand and Iceland. Australia has also regained its equine influenza-free status after the extensive outbreak of 2007. Equine influenza virus does not typically circulate asymptomatically within large groups of horses. Sporadic outbreaks of EIV result from the introduction of an infected horse. This epidemiologic finding and the rapid elimination of the virus by the equine immune response suggest that infection can be avoided by preventing entry of the virus into an equine population by the quarantine of newly arriving horses for at least 14 days, and by appropriate vaccination before exposure. All horses should be vaccinated against equine influenza unless they live in a closed and isolated facility.

To date, the most important factors associated with increased risk of infection have been identified as:

1) Age: Horses 1 to 5 years old are more susceptible, although a recent study demonstrated an increased incidence of EIV among older horses (6-10 years old) and horses previously vaccinated against EIV within the previous 12 months. These results help support the belief that 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 strains contributing to incomplete clinical protection.

2) Serum concentrations of influenza virus-specific antibody, particularly HA-specific antibody, are a correlate of protection stimulated by vaccination and / or natural infection. Low concentrations of HA-specific neutralizing antibody titers and / or a mismatch between antibody and virus causing the infections may increase risk of infection.  Local mucosal protection, although difficult to quantitate, also plays an important role in protection against viral infection.

3) Frequent contact with large numbers of horses.

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, among other factors. Horses that are partially immune can become subclinically infected and shed virus. Immunity to the same (homologous) strain of virus following natural infection persists for approximately one year. Immunity following vaccination with inactivated influenza vaccines can be short-lived, allowing recently vaccinated horses to become infected and shed virus, thereby contributing to maintenance and spread of infection within the equine population. For these reasons, only vaccines of proven efficacy should be selected for use.

Although influenza is endemic in many countries and circulates continuously in the equine population, explosive outbreaks occur at intervals of several years when the immunity of the equine population wanes, and sufficient antigenic drift in the virus has occurred, allowing the virus to evade vaccinal immunity. Antigenic drift, by generating antigenically heterologous viruses, reduces the degree and duration of protection conferred by previous infection or vaccination using vaccines that confer protection primarily by generating protective concentrations of neutralizing antibodies targeting the surface glycoproteins of influenza. Although antigenic drift of equine influenza virus is slower than that of human influenza virus, it is still recommended that equine vaccines contain killed viral antigens from clinically relevant isolates obtained within recent years. The 2010 and 2014 OIE Expert Surveillance Panels on equine influenza vaccine composition had a number of findings and recommendations:

  • All equine influenza virus isolates between 2008 and 2014 were H3N8 viruses of the Florida sub-lineage, and comprised two sub-lineages, clades 1 and 2. The viruses identified in the USA in 2014 were characterized as clade 1 viruses, whereas those detected in France, Germany, Ireland, Sweden and the UK were clade 2 viruses.  Global surveillance is likely insufficient to assure that these geographic restrictions are absolute but it seems likely that the equine influenza viruses circulating in North America are all from Clade 1: i.e. A/South Africa/2003-like or A/Ohio/2003-like.
  • Because of the antigenic differences between Florida Clade 1 and Clade 2 it is possible that vaccination with only one of these antigens will not fully protect against disease caused by the other. However, at this time there is no evidence of a vaccine failure resulting from this phenomenon. This means that North American horses vaccinated with a Clade 1 virus, such as A/Ohio/2003-like, should be protected from current circulating North American influenza viruses, but may not be fully protected if they travel overseas, or in the event that Clade 2 viruses are introduced to North America, for example in a horse transported here for competition.
  • The OIE panel recommended that vaccines contain examples of both Clade 1 (e.g. A/South Africa/2003-like or A/Ohio/2003-like) and Clade 2 (A/Richmond/2007) viruses particularly for horses traveling internationally.
  • The absence of any isolation of Eurasian lineage influenza virus or the A/equine 1 virus for many years means that these viruses no longer need to be included in vaccines.

Historically, equine influenza vaccines have been administered at intervals as short as 3 months to horses considered at high risk of infection. All currently marketed equine influenza vaccines are likely to provide protection of at least six months duration. This is true for both of the modified live vaccines on the market today, and for inactivated vaccines. This performance depends on the quality of currently marketed vaccines, and maintaining this performance will depend on the inclusion of any new antigenically distinct equine influenza viruses that may appear in the horse population in the future.

 See here for USEF Vaccination Rule.


There are three types of equine influenza virus vaccine currently marketed:

Inactivated vaccines 

Each of these has been shown to be efficacious in providing protection against clinical disease and viral shedding when used appropriately. These vaccines frequently include multiple strains of equine influenza virus A2 representing the major circulating strains; however, none contain strains isolated during the last 5 years. The majority of these vaccines require two-dose priming regimens, although a three-dose priming regimen is recommended here as described below; a 3-dose regimen is required for at least one of the most effective inactivated vaccines. These vaccines are well suited to pre-foaling boosters designed to increase colostral antibody levels against influenza virus.

Modified-live (MLV) cold-adapted equine influenza /A2 vaccine

This product is administered intranasally. The vaccine has proven to be very safe and a single administration to naïve horses is protective for up to 12 months, although only a 6-month claim is made on the product data sheet. Circulating antibody responses in naïve horses post-vaccination are minimal, suggesting that other factors, such as local protection at the nasal mucosa may be enhanced by this vaccine. The product is licensed for vaccination of non-pregnant animals over 11 months of age using a single dose of vaccine, followed by boosters at 6-month intervals. Generally, horses shed vaccinal virus for less than 1 week after vaccination. However, the amount and duration of shed vaccinal virus is so minimal that other horses in contact with them will not be vaccinated. Incorporation of the MLV vaccine into a program that previously used inactivated vaccine can be easily accomplished by substituting the MLV when routine boosters are scheduled.

Experience strongly supports the safety of the MLV intranasal vaccine when administered to foals less than 11 months of age. Similarly, the vaccine is protective when administered to foals six months of age or older. The onset of protection in previously unvaccinated naïve horses has been documented as early as seven days after vaccination. The vaccine is not recommended for vaccination of mares in late pregnancy to boost colostral antibodies, as data available to date suggest that circulating antibody responses to vaccination are low.

Canary pox vector vaccine 

This product is to be administered by intra-muscular injection and has been shown to provide protection of at least six months duration. A two dose priming regimen is recommended, with boosters at a six month interval. The vaccine is safe to use in foals as young as four months of age, and there is some evidence of efficacy in the face of maternal immunity. Because this vaccine induces high levels of antibody, it is likely to be suitable for pre-foaling boosters.

Vaccination Schedules:

Adult horses, previously vaccinated:  Mature performance, show, or pleasure horses constantly at risk of exposure should be revaccinated at 6 month intervals. Other adult horses could be vaccinated as infrequently as once a year.

Adult horses, unvaccinated or having an unknown vaccination history: Either one dose of the MLV intranasal vaccine or a 2-dose series of canary pox vector vaccine at a 4 to 6 week interval (revaccinate semi-annually) or a primary series of 3 doses of the inactivated-virus vaccines is recommended. The ideal intervals between these vaccinations are three to four weeks between the first and the second vaccination, followed by an interval ideally as long as three to six months before the third vaccination. This regimen generally induces higher and more persistent antibody titers than those induced by use of the previously recommended 2-dose initial series. Subsequent revaccination should be at intervals of 6 to 12 months, depending on the age of the horse as well as the degree and duration of risk of acquiring infection. 

Pregnant broodmares, previously vaccinated: Vaccinate 4 to 6 weeks before foaling using an inactivated-virus vaccine or the canary pox vectored vaccine.

Pregnant broodmares, unvaccinated or having an unknown vaccination history:  Use a 3-dose series of the inactivated-virus vaccines, with the second dose administered 4 to 6 weeks after the first dose and the third dose administered 4 to 6 weeks pre-partum.  With a canary pox vector vaccine, a 2-dose series is recommended with the second dose administered 4 to 6 weeks after the first dose but no later than 4 weeks pre-partum.


Foals of vaccinated mares:  Administer either a single dose of the MLV intranasal vaccine (2 doses are recommended if foal is less than 11 months of age, 1st dose at 6 to 7 months of age and second dose at 11 to 12 months of age) or a primary series of 2 doses of canary pox vector vaccine at a 5 week interval or a 3-dose series of inactivated-virus vaccine beginning at 6 months of age. The recommended intervals between these vaccinations with an inactivated-virus vaccine are 4 to 6 weeks between the first and the second vaccinations. The third dose should be administered between 10 and 12 months of age.

Foals of nonvaccinated mares: Administer either a single dose of the MLV intranasal vaccine (2 doses are recommended if foal is less than 11 months of age, 1st dose at 6 to 7 months of age and second dose at 11 to 12 months of age) or a primary series of 2 doses of canary pox vector vaccine at a 5 week interval or a 3-dose series of inactivated virus vaccine at 6 months of age (see above), unless there is an unusual threat that warrants earlier vaccination. Because some maternal anti-influenza antibody is still likely to be present, a complete series of primary vaccinations should still be given after 6 months of age.

Outbreak Mitigation:

Vaccination to boost immunity in the face of an outbreak may be a valuable strategy if the outbreak is detected early enough. In previously vaccinated horses, any vaccine can be used for this purpose. In unvaccinated horses, or horses with an unknown vaccination history, the early onset of immunity after administration of the intranasal product (protection within 7 days), may recommend it for use. The use of a canary pox vectored vaccine may also be considered for this purpose. (View AAEP Infectious Disease Control Guidelines on Influenza)

Equine Viral Arteritis

Equine viral arteritis (EVA) is a contagious disease of equids caused by equine arteritis virus (EAV), an RNA virus that is found in horse populations in many countries. While typically not life-threatening to otherwise healthy adult horses, EAV can cause abortion in pregnant mares; uncommonly, death in young foals; and establish a long-term carrier state in breeding stallions. While various horse breeds appear equally susceptible to EAV, the prevalence of infection can vary widely, with higher seropositivity rates occurring in Standardbreds and Warmbloods.

Historically, outbreaks of EVA have been relatively infrequent. However, the number of confirmed occurrences appears to be increasing, likely attributable to increases in:

  1. Global movement of horses
  2. Accessibility of carrier stallions
  3. Utilization of shipped cooled or frozen virus-infective semen

Transmission most frequently occurs through direct contact with virus-infective respiratory secretions leading to widespread dissemination of the virus among susceptible horses in close proximity. Venereal transmission by infected stallions has a significant role in virus spread on or between breeding farms. Equine arteritis virus can be very efficiently spread through artificial insemination and the use of fresh-cooled or frozen semen. There is limited evidence that virus can also be transmitted via embryo transfer where the donor mare is bred with infective semen from a carrier stallion. The virus has been shown to remain viable for considerable periods of time in raw, extended or frozen semen held at temperatures equal to or less than 4°C. Indirect transmission, though less significant, can occur through contact with virus-contaminated fomites.

The majority of primary EAV infections are subclinical or asymptomatic. EVA can vary in clinical severity both between and within outbreaks. EVA cannot be diagnosed based on clinical signs alone, as case presentation is similar to various other infectious and non-infectious equine diseases. Laboratory confirmation is required for diagnosis.

Clinical signs, if they occur, typically develop 3 to 7 days post-infection and are variable but may include any combination or all of the following: fever; depression; anorexia; dependent edema (lower limbs, scrotum and prepuce or mammary glands); localized or generalized urticaria; supra or periorbital edema; conjunctivitis; lacrimal discharge and serous to mucoid nasal discharge. Abortion is a frequent sequel to infection in the unprotected, pregnant mare. When pregnant mares are exposed to the virus very close to term, they may not abort but give birth to a congenitally infected foal, affected with a rapidly progressive and fulminant interstitial pneumonia. Foals infected with EAV during the first few months of life can develop a life-threatening pneumonia or pneumoenteritis.

A carrier state can develop following EAV infection in the post-pubertal colt or stallion. The virus can persist in the reproductive tract of stallions for many years and may result in lifelong infection. The carrier stallion is widely accepted as the natural reservoir of EAV and the source of diversity among naturally occurring strains of the virus.


The current licensed vaccine in North America is a highly attenuated, modified live virus product. It has been shown to be safe and effective in stallions and non-pregnant mares. Mild post-vaccinal febrile reactions with transient lymphopenia have been observed in a small percentage of first-time vaccinated horses. Primary vaccination provides clinical protection against EVA but does not prevent re-infection and limited replication of challenge virus. However, in first-time vaccinates, the frequency, duration, and amount of vaccine virus that is shed via the respiratory tract is significantly less than that observed with natural infection.

Vaccination in the face of an EVA outbreak has been successful in controlling further spread of the virus within 7 to 10 days. Immunization with the MLV vaccine stimulates a rapid protective response, which in turn restricts development of the cell-associated viremia and viral shedding via the respiratory tract in horses naturally exposed to infection. As a consequence, the amount of EAV in circulation is greatly decreased, limiting further spread of the virus.

Vaccination Schedules:

In planning a vaccination program against EVA, it is important to consult with state and/or federal animal health officials to ensure that any such program is in compliance with the state's control program for EVA, if one exists.

The indications for vaccination against EVA have been:

1) To protect stallions against infection and subsequent development of the carrier state.

2) To immunize seronegative mares before being bred with EAV-infective semen.

3) To curtail outbreaks in non-breeding populations.

Note: It is not possible to differentiate vaccine-induced antibody response from that due to natural infection. It is strongly recommended that prior to vaccination, serum from all first-time vaccinates be tested and confirmed negative for antibodies to EAV by a USDA-approved laboratory.  Mares intended for export should be similarly tested.


Breeding stallions, previously vaccinated:  Should receive an annual booster vaccination against EVA every 12 months and no earlier than 4 weeks before the start of each breeding season.

Breeding stallions, first-time vaccinates:  Prior to initial vaccination, all stallions shall undergo serologic testing and be confirmed negative for antibodies to EAV. Testing should be performed shortly prior to, or preferably at, the time of vaccination. Negative certification is of importance should a vaccinated stallion be considered for export at a later date. All first-time vaccinated stallions should be isolated for 3 weeks following vaccination before being used for breeding.

Teaserscan play a role in the introduction and dissemination of EAV within a breeding population. Vaccination against EVA is recommended on an annual basis.

Mares to be bred to carrier stallions or to be bred with virus-infective semen should first be tested to determine their serological status for EAV antibodies.

Seronegative mares should be vaccinated against EVA and isolated from any other seronegative horses for 3 weeks. The purpose of the isolation period is twofold:

1) To enable the vaccinated mare adequate time to develop immunity against the disease before being exposed to EAV infection during breeding.

2) To afford ample opportunity for cessation of possible post-vaccinal viral shedding via the respiratory tract.

Following insemination, first-time vaccinated mares must be isolated for an additional 3-week period as they are likely to experience a limited re-infection cycle with the strain of EAV present in the semen. Should such mares fail to become pregnant, they can be bred back to a carrier stallion or with infective semen without the need for revaccination or an additional 3-week isolation period post-insemination.

In the case of embryo transfer, it is recommended that both donor and recipient mare, if seronegative, be vaccinated against EVA if the donor mare is to be bred with virus infective semen.                                                                                                         

Seropositive mares, having tested serologically positive for antibodies to EAV, can be bred to a carrier stallion or with infective semen for the first time without the need for prior vaccination against EVA. After breeding, such mares should be physically separated from unvaccinated or unprotected horses for 24 hours to avoid possible risk of mechanical transmission of infectious virus from voided semen.

Pregnant mares: The manufacturer does not recommend use of this vaccine in pregnant mares, especially in the last two months of pregnancy. Under circumstances of high risk of natural exposure to infection, the vaccine has been administered to pregnant mares in order to control outbreaks of the disease. Based on early experimental studies and field experiences using this vaccine, the last 1 to 2 months of pregnancy represent the time of greatest risk for a possible adverse effect on pregnancy. This was most recently illustrated in the aftermath of the 2006 multi-state occurrence of EVA when a very limited number of abortions associated with the vaccine virus were confirmed in mares vaccinated within the final 2 months of gestation.  

Nurse marescan play a role in the introduction and spread of EAV among resident equine populations and should be vaccinated annually according to recommended protocols.


The manufacturer does not recommend use of this vaccine in foals less than 6 weeks of age unless under circumstances of high risk of natural exposure to infection.

Colt (male) foals

Especially in EAV endemic breeds, colt foals should be vaccinated between 6 and 12 months of age to protect against the risk of becoming carriers later in life. Colts should be confirmed seronegative for antibodies to EAV prior to vaccination as described above and kept isolated for 3 weeks following vaccination. Because foals of EAV-seropositive mares can carry colostrally-derived antibodies for up to 6 months, testing and vaccination should not be performed prior to 6 months of age.

Outbreak Mitigation:

Non-breeding population:  Vaccination is an effective strategy in containing outbreaks, particularly in congregated groups of horses where isolation may be problematic. Serologic testing, as described above, should be performed on intact males and females that may be intended for future breeding purposes and/or export.

Breeding population: Outbreaks of EVA can be complex and can have far reaching implications. Vaccination is a component of outbreak management but should be performed only under the direct supervision of a veterinarian. (View AAEP Infectious Disease Control Guidelines

Vaccination and Exporting of Horses:

In instances where there is uncertainty or concern over whether vaccination against EVA could prevent the export of a horse to a particular country, it is advisable to consult the area federal veterinarian or assistant director in charge in the state to determine the specific import requirements of that country. There are a number of countries that bar entry of any equid that is serologically positive for antibodies to EAV, regardless of vaccination history. Countries that do accept EVA vaccinated horses, regardless of gender, typically require stallions or colts to have a certified vaccination history and confirmation of pre-vaccination negative serological status.


Equine leptospirosis is typically a sporadic disease. The primary leptospiral-associated equine clinical disease presentations include; recurrent uveitis, late-term abortion and acute renal failure. Infection is acquired through exposure to the organism via the mucous membranes or abraided skin. The leptospiral organisms are shed in the urine of infected horses (additionally the placenta, fetal fluids and urine of the mare in abortion cases) and a number of wildlife hosts which can shed Leptospira spp. in the urine. 

Seroprevalence data from healthy horses indicate that it is common for horses to carry titers to multiple serovars. Multiple serovar titers can result from direct exposure to these serovars, cross-reactivity of the MAT (microscopic agglutination test) between different serovars or both. In diseased horses, Leptospira interrogans serovar pomona is the most commonly incriminated pathogen/serovar in the U.S.


There is currently one vaccine approved for use in horses. It is a killed, whole cell bacterin. 

The product is labeled for vaccination of healthy horses 6 months of age or older as an aid in the prevention of leptospirosis caused by Leptospira interrogans serovar pomona.
The vaccine has demonstrated safety in foals as young as 3 months of age. Efficacy of this product was demonstrated utilizing an intraperitoneal Leptospiral challenge model. Vaccinated horses did not develop leptospiremia or leptospiuria as compared to controls.

The duration of immunity of this product has not been determined. 

Vaccination Schedule:  

Horses 6 months of age or older: Initial two dose series, 3 to 4 weeks apart. Annual revaccination. 

Pregnant mares: The product has demonstrated safety in pregnant mares during the 2nd trimester. Additional safety studies in pregnant mares are ongoing.

Potomac Horse Fever

Equine neorickettsiosis is caused by Neorickettsia risticii (formerly Ehrlichia risticii). Originally described in 1979 as a sporadic disease affecting horses residing in the eastern United States near the Potomac River, the disease has since been identified in various other geographic locations in the United States and Canada. The disease is seasonal, occurring between late spring and early fall in temperate areas, with most cases in July, August, and September with the onset of hot weather.

Clinical signs are variable but may include: fever, mild to severe diarrhea, laminitis, mild colic, and decreased abdominal sounds. Uncommonly, pregnant mares infected with N. risticii (usually in the middle trimester between 90 and 120 days) can abort due to fetal infection at 7 months of gestation.

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. Foals appear to have a low risk of contracting the disease. Vaccination against this disease has been questioned because field evidence of benefit is lacking. Proposed explanations for this include lack of seroconversion and multiple field strains whereas only one strain is present in available vaccines.


The currently available commercial vaccine is a killed, adjuvanted product, which is also available combined with rabies vaccine. The current vaccine does not carry a label claim for the prevention of abortion.

Vaccination Schedules:

Due to the seasonal incidence of disease, vaccination should be timed to precede the anticipated peak challenge during the summer months or fall.

Adult horses, previously vaccinated:  Manufacturers recommend revaccination at 6- to 12-month intervals. However, veterinarians may consider an interval of 3 to 4 months for horses in endemic areas because protection following vaccination can be incomplete and short-lived.

Adult horses, previously unvaccinated or with unknown vaccinal history:  Administer a primary series of 2 doses, at a 3- to 4-week interval. Peak protection occurs 3 to 4 weeks after the second dose.

Pregnant mares previously vaccinated against PHF:  Vaccinate semi-annually to annually. Schedule 1 dose to be administered 4 to 6 weeks before foaling. To date no studies have been published that examine the efficacy of PHF vaccines to prevent N. risticii induced abortion.

Pregnant mares unvaccinated or with unknown vaccinal history:Administer a primary series of 2 doses, at a 3- to 4-week interval. Schedule so that 2nd dose is administered 4 to 6 weeks before foaling.

Foals:   Due to the low risk of clinical disease in young foals and the possible maternal antibody interference, primary immunization for most foals can begin after 5 months of age. The manufacturer’s recommendation is for a 2-dose series administered at a 3 to 4 week interval. However, as with other killed products, a third dose at 12 months of age is recommended. If the primary series is initiated when foals are less than 5 months of age, additional doses should be administered at monthly intervals up to 6 months of age to ensure that an immunologic response is achieved.

Horses having been naturally infected and recovered: Administer a primary series (as described above) or booster vaccine (if previously vaccinated) 12 months following recovery from natural infection.

Rotaviral Diarrhea

Rotavirus, a non-enveloped RNA virus, is a major infectious cause of foal diarrhea and has been documented to cause 50% or more of foal diarrhea cases in some areas.

While rotavirus diarrhea morbidity can be high (50% of susceptible foals), mortality is low (<1%) with veterinary intervention.

Equine rotavirus is transmitted via the fecal-oral route and damages the small intestinal villi resulting in cellular destruction, maldigestion, malabsorption, and diarrhea.

As many as 70% of all foals in the United States will have at least one diarrheal episode prior to weaning. Mare owners need to be aware that strict biosecurity and disinfection during the foaling season also mitigates the morbidity associated with most types of infectious foal diarrhea and other contagious diseases.

Vaccination of mares results in a significant increase in foals’ rotavirus antibody titers. Field trials of rotavirus vaccination in pregnant mares have shown a decrease in incidence and severity of foal diarrhea on farms that historically had annual rotaviral diarrhea cases. Other studies have shown increased rotavirus antibody in vaccinated mares’ colostrum.


The only available vaccine is conditionally licensed, contains inactivated rotavirus Group A, and is indicated for administration to pregnant mares to enhance concentrations of colostral immunoglobulins against equine rotavirus (Group A). The vaccine has been used in mares since 1996 in the USA and is considered to be safe.

Vaccination Schedules:

Pregnant mares (regardless of vaccination history):  Should receive a 3 dose series of intramuscular vaccinations at 8, 9, 10 months of gestation.

Concentrated horse breeding areas in the US routinely use rotavirus vaccine in pregnant mares. Pregnant mares that will be shipped to regions that have had a history of rotaviral diarrhea should also be considered candidates for vaccination.

**It is essential that the newborn foal receives an adequate amount of colostrum and absorbs sufficient anti-rotavirus antibodies from rotavirus-vaccinated mares.

Newborn foals: There are no data to suggest that vaccination of the newborn foal with inactivated rotavirus A vaccine has any benefit for preventing or reducing the severity of infection.

As colostral-derived antibody titers wane at approximately 8 weeks of age, foals may develop rotaviral diarrhea. However, the severity of diarrhea is generally milder and of shorter duration than in foals that become ill within the first 4 weeks of life.

Other adult horses: Vaccination is unnecessary

Snake Bite

Venomous snake bite of equids occurs in certain areas of North America. The risk of rattlesnake envenomation may justify the use of Crotalus atrox (Western Diamondback Rattlesnake) toxoid vaccine in equids. Pre-exposure vaccination may be recommended for those animals in geographic areas or for those traveling to areas where exposure to venomous snakes justifies vaccine usage.


There is one conditionally licensed inactivated (Crotalus atrox Toxoid) vaccine for use in healthy horses 6 months of age or older as an aid in the reduction of morbidity and mortality due to intoxication with Crotalus atrox toxin.

 The label claim for the vaccine is that it may also provide protection against the venoms of the Western Rattlesnake (including the Prairie, Great Basin, Northern and Southern Pacific varieties), Sidewinder, Timber Rattlesnake, Massasauga and the Copperhead. Partial protection may be obtained against Eastern Diamondback Rattlesnake venom. This vaccine does not provide protection against venom from the Water Moccasin (Cottonmouth), Mojave Rattlesnake or Coral Snake. 

Vaccination Schedule: 

Use in healthy horses 6 months of age or older. 

Adult horses: Administer a primary series of three doses at one month intervals. Booster doses are recommended at 6 month intervals. 

Pregnant mares: Manufacturer information claims the product is safe for use in pregnant mares, however this information does not appear on the product label. It is recommended veterinarians contact the manufacturer with questions regarding use in pregnant mares. 

Foals: (6 months of age and older) Administer a primary series of three doses at one month intervals. Booster doses are recommended at 6 month intervals. There is no specific information available regarding the vaccination of foals less than 6 months of age. 


Streptococcus equi subspecies equi (S. equi var. equi) is the bacterium which causes the highly contagious disease strangles (also known as “distemper”).  Strangles commonly affects young horses (weanlings and yearlings), but horses of any age can be infected. Vaccination against S. equi is recommended on premises where strangles is a persistent endemic problem or for horses that are expected to be at high risk of exposure. Following natural infection, a carrier state of variable duration may develop and intermittent shedding may occur. The influence of vaccination on intermittent shedding of S. equi has not been adequately studied.

The organism is transmitted by direct contact with infected horses or sub-clinical shedders, or indirectly by contact with water troughs, hoses, feed bunks, pastures, stalls, trailers, tack, grooming equipment, nose wipe cloths or sponges, attendants’ hands and clothing, or insects contaminated with nasal discharge or pus draining from lymph nodes of infected horses. Streptococcus equi has demonstrated environmental survivability particularly in water sources and when protected from exposure to direct sunlight and disinfectants, and can be a source of infection for new additions to the herd.

Infection by S. equi induces a profound inflammatory response. Clinical signs may include fever (102-106o F); dysphagia or anorexia; stridor; lymphadenopathy (+/- abscessation); and copious mucopurulent nasal discharge.

S. equi and S. zooepidemicus are antigenically similar organisms. However, exposure to, or vaccination against, one does not confer reliable immunity to the other.

Following natural or vaccinal exposure to streptococcal antigens, certain individuals may unpredictably develop purpura hemorrhagica, an acute, non-contagious syndrome caused by immune-mediated, generalized vasculitis. Clinical signs develop within 2 to 4 weeks following natural or vaccinal exposure to streptococcal antigens. Clinical signs may 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 may compromise breathing. Immediate medical attention should be sought for individual horses suspected of having purpura hemorrhagica.



Vaccination in the face of an outbreak should be carefully considered, as there is significantly increased risk of adverse reactions in exposed horses.  Purpura hemmorrhagica can be associated with vaccine administration. In a recent retrospective study of 53 horses with purpura hemorrhagica, 5 cases were vaccinated with a S. equi M protein vaccine. Outbreak mitigation and the prevention of spread of S. equi infection are centered on management of horses, personnel, and facilities.

(View AAEP Infectious Disease Control Guidelines—S. equi.; view ACVIM Strep equi consensus statement) 

Killed vaccines:

Killed vaccines are an adjunct to the prevention of strangles. Vaccination with these products should not be expected to prevent disease. However, appropriate pre-exposure vaccination with these products appears to attenuate the severity of clinical signs in affected horses, should disease occur, and has been shown to reduce the incidence of disease by as much as 50% during outbreaks.

All injectable, inactivated S. equi. vaccines, can be associated with an increased rate of injection site reactions as compared to other equine vaccines. Due to the limited variability between commercially available vaccinal bacteria and field isolates, autogenous bacterins are not advocated.

Modified live vaccine: 

An intranasal product has been shown to stimulate a high level of immunity against experimental challenge. The inductive sites are the pharyngeal and lingual tonsils. Vaccinal organisms must reach these sites in sufficient numbers to trigger protective responses; therefore, accurate vaccine delivery is critical to vaccine efficacy. In a small percentage of cases, residual vaccinal organism virulence may result in formation of slowly developing mandibular or retropharyngeal abscesses. The risk of vaccine-associated adverse events is increased when the product is administered to young foals.

Maternal antibody interference with respect to the development of mucosal immunity needs to be studied further.

In order to avoid inadvertent contamination of other vaccines, syringes and needles, it is advisable and considered a good practice to administer all parenteral vaccines or other injectables before the handling and administration of the intranasal vaccine against S. equi.

Vaccination Schedules:

Adult horses previously vaccinated:  Vaccinate every 6 to 12 months based on risk assessment and manufacturers’ recommendations.

Adult horses unvaccinated or having unknown vaccinal history

Killed vaccine:

Manufacturers' recommendations are for primary vaccination with a series of 2 or 3 doses administered at intervals of 2 to 4 weeks, depending on the product used, followed by annual revaccination. Revaccinate at 6- month intervals, regardless of the injectable product used.

Modified live vaccine:

Administer intranasally a 2-dose primary series with a 3-week interval between doses. Semiannual (6-month intervals) or annual revaccination is recommended.

Broodmares previously vaccinated 

Killed vaccine:

Vaccinate 4 to 6 weeks pre-partum with approved products that contain inactivated M-protein. Maternal antibody interference is not known to occur when injectable, M-protein vaccines are administered.

Broodmares previously unvaccinated or having unknown vaccinal history

Administer primary series of killed vaccine containing M-protein (see above, Adult horses unvaccinated) with final dose to be administered 4 to 6 weeks pre-partum.


Killed vaccine:

For foals at high risk for exposure to strangles, administer a 3-dose primary series of an M-protein product beginning at 4 to 6 months of age. An interval of 4 to 6 weeks between doses is recommended.

Modified live vaccine

Administer intranasally at 6 to 9 months of age a 2-dose primary series with a 3-week interval between doses. This vaccine has been safely administered to foals as young as 6 weeks of age when there is a high risk of infection, such as occurs during an outbreak, but the efficacy of its use in very young foals has not been adequately studied. If administered to young foals in this manner, a third dose of the modified live vaccine should be administered 2 to 4 weeks before the foal is weaned to optimize protection during that time of high risk of infection. The risk of vaccine-associated adverse events is increased when the product is administered to young foals.

Horses having been naturally infected and recovered:  Following recovery from strangles, most horses develop a durable immunity, persisting in over 75% of animals for 5 years or longer. This indicates that stimulation of a high level of immunity is biologically feasible given appropriate presentation of protective immunogens. Currently, a diagnostic test is available and may be used to assess the level of immunity conferred by natural exposure or vaccination. Since natural exposure or vaccination can provide variable levels of immunity, use of this test may provide a guideline in determining the need for current or future vaccination. Additional testing information is available from; ACVIM Strep equi consensus statement