Equine vaccines

Equine vaccines

There are more than 3.6 million horses in the United States, 2.5 million in Argentina, and up to 1.2 million in the United Kingdom, Germany, and France. Infectious diseases are of significant concern in all these animals, although the specific threats they face differ according to their use and location. As with other species, travel and intermingling of animals from multiple sources greatly increases infectious disease risk. Unlike other species, horses travel internationally on many occasions, especially in the racing industry. Well-considered vaccination is the most efficient method of preventing disease spread (Box 15.1). Owners should be reminded that vaccination is cheap compared with the value of a horse. In the United States, the five core equine vaccines include: tetanus, rabies, Eastern and Western encephalitis, and West Nile encephalitis.

BOX 15.1 ■

Equine Vaccination Guidelines

The guidelines for vaccinating horses in North America have been produced by the American Association of Equine Practitioners (AAEP). They are available at www.aaep.org/info/vaccination-guidelines-265.

Antibacterial vaccines


Clostridium tetani is found in the intestinal tract of horses and is abundant in the soil on many horse farms. Its spores may persist in the environment for many years. Cl. tetani grows in the anaerobic environment of deep puncture wounds, surgical incisions, umbilical wounds in foals, and in the uterus associated with retained placenta or other trauma. It should be noted that the size or severity of the wound is not always predictive of tetanus development. As the organism grows it secretes a potent neurotoxin called tetanospasmin that is responsible for the disease.

Tetanus vaccines consist of purified, formalin-inactivated toxoids. Tetanus toxoid is a good antigen, especially when adjuvanted and it stimulates a strong, protective antibody response. Circulating antibodies alone can neutralize tetanus toxin. All horses are at risk of tetanus, and tetanus toxoid is a core vaccine for all horses. The duration of immunity is at least one year, so annual revaccination is required. It takes about two weeks for immunity to develop after vaccination. It is also essential to vaccinate pregnant mares four to eight weeks before foaling. This not only protects their foals through colostral antibodies, but also protects them against foaling related tetanus. Tetanus immune globulin should also be administered to any unvaccinated horse that requires immediate immunity as a result of a wound (Chapter 12).


Botulism results from exposure to the neurotoxins of Clostridium botulinum. These toxins cause a flaccid paralysis by inhibiting the release of acetylcholine from motor neurons. Cl. botulinum can produce seven different neurotoxins. Types A, B, and C are associated with botulism outbreaks in horses, but type B accounts for more than 85% of equine botulism cases in the United States. This organism is found in soil so it can contaminate wounds. Cl. botulinum can also cause a rapidly fatal shaker foal syndrome (toxicoinfectious botulism) as a result of ingestion of spores on vegetation. Likewise forage poisoning occurs when preformed toxin is ingested with improperly baled hay or contaminated feed.

A formalin-inactivated toxoid against botulinum toxin type B is licensed for use in horses in the United States. There are no toxoids available for types A or C. Vaccination is warranted for all horses because they may move into recognized endemic areas. It is especially recommended for horses that reside in the endemic areas in Kentucky and the Mid-Atlantic states. The horses at greatest risk are those fed baled hay, haylage, and silage in addition to foals born to unvaccinated mares. Shaker foal syndrome is a significant problem in endemic areas in foals two weeks to eight months of age.


Streptococcus equi subspecies equi causes strangles in horses, donkeys, and mules. Clinical disease includes abrupt pyrexia, pharyngitis, and dysphagia, so that horses have difficulty swallowing and develop anorexia. Lymphadenopathy then develops, leading to abscess formation in the submandibular and retropharyngeal lymph nodes. When these abscesses burst, their contents contribute to a copious purulent and highly infectious nasal discharge. Metastatic strangles is characterized by abscesses in other lymph nodes, especially in the abdomen and thorax. Although most severe in weanlings and yearlings, horses of any age can develop the disease. As of 2017, strangles is a reportable disease in the United States. Recovery from clinical disease results in prolonged immunity that lasts for at least five years. This immunity is associated with the production of antibodies against S. equi M protein. Strains of S. equi show little genomic diversity and strangles vaccines should offer cross protection against all circulating strains of the bacteria. Vaccination is recommended where strangles is a persistent endemic problem or for horses at a high risk of exposure. Several cell-free vaccines are available in some countries. These inactivated injectable S. equi bacterins are associated with a relatively high prevalence of injection site reactions (soreness or abscesses at the injection site and occasional cases of purpura hemorrhagica). In addition, any protection conferred by these vaccines is short-lasting. A purified Streptococcal M-protein (Strepvax II, Boehringer Ingelheim) vaccine given intramuscularly is available in the United States. This vaccine will not prevent the disease. It will, however, reduce the severity of clinical disease and reduce disease prevalence by about 50%.

Strangvac 4 (Intervacc) is a subunit vaccine, currently under development, that contains a mixture of eight soluble recombinant streptococcal fusion proteins. The proteins were identified by analysis of the bacterial genome and studies in mice. They consist of a combination of surface and secreted proteins. The cloned proteins are generated in Escherichia coli, purified, and then combined. A saponin based adjuvant, Matrix C is subsequently added. This vaccine is administered intramuscularly. Strangvac 4 has DIVA (differentiate infected from vaccinated animals) capability, because none of the antigens included in diagnostic ELISA (enzyme linked immunosorbent assay) tests are present in the vaccine.

Several attenuated live vaccines are available globally. For example, a live intranasal vaccine containing a nonencapsulated strain of S. equi (Pinnacle, Zoetis Animal Health) is available in the United States and New Zealand. After administration, attenuated bacteria should ideally reach the lingual and pharyngeal tonsils where they stimulate local immunity. They can be isolated from vaccinated horses up to 46 days after vaccination. In some cases, the attenuated bacteria may cause the slow development of mandibular or retropharyngeal abscesses, a nasal discharge, and occasional cases of purpura hemorrhagica. These may be severe in young foals. Because this attenuated organism retains the ability to infect wounds, no other vaccines should be delivered concurrently and no invasive procedures performed at the same visit. This vaccine was generated by treating a wild-type isolate with a mutagen. It differs from the original strain by about 68 mutations, but it is not known which of these are responsible for its attenuation. Its activity depends on the production of nasopharyngeal mucosal immunoglobulins (IgG and IgA) directed against the M protein.

A second modified live vaccine (MLV), Equilis StrepE (MSD Animal Health), is available in Europe. This contains a live attenuated aroA deletion mutant (Strain TW928) that lacks 932 base pairs of the aroA gene. This vaccine is administered by submucosal injection into the inside of the upper lip, but painful reactions at the injection sites may occur. Immunity to experimental challenge persists for about three months. This vaccine is not DIVA-compatible. Because of the risk of purpura, horses known to have had strangles within the previous year and horses with high antibody levels (Titers>1:3,200) should not be vaccinated.


Anthrax is a fatal septicemia caused by Bacillus anthracis. The infection can be acquired by ingestion, inhalation, or wound contamination. It is restricted to certain areas in North America associated with alkaline soils. Vaccination is not required outside these endemic areas. The anthrax vaccine, the Sterne strain, is an attenuated nonencapsulated spore vaccine. It may cause injection site swelling in young foals and should not be used in pregnant mares. Anthrax is a zoonosis, therefore a physician should be consulted if the vaccine is accidentally injected or gets into human skin wounds or eyes. Because this is a live bacterial vaccine it is important to ensure that antibiotics are not given to the horse at the same time.


Leptospirosis is a sporadic disease of horses. The leptospires cause equine recurrent uveitis, abortions, and renal disease. The bacteria are spread via the body fluids of infected horses, especially their urine. The most common serovars in horses in the United States are Leptospira interrogans, serovar Pomona type kennewicki, and Leptospira kirchneri serovar Grippotyphosa. A killed whole cell monovalent bacterin against serovar Pomona is approved for use in horses.

Potomac horse fever

Equine neorickettsiosis, (Potomac Horse Fever), is caused by an obligate intracellular bacterium, Neorickettsia risticii. It is transmitted by the accidental ingestion of insects harboring the metacercaria of an infected trematode. The infection results in abortion in mares in addition to depression, fever, leukopenia, enterocolitis with profuse diarrhea, and laminitis. A killed adjuvanted whole cell vaccine is available. It may be beneficial in endemic areas but N. risticii is genetically very heterogeneous, and as a result, the vaccine does not protect against all strains. Vaccination should be timed for the spring in advance of the trematode/snail season in summer and fall.

Antiviral vaccines

Eastern and western equine encephalitis

Both Eastern equine encephalitis (EEE) and Western equine encephalitis (WEE) are caused by alphaviruses in the family Togaviridae. These viruses are maintained in the environment by circulating through birds and mosquitos. They are not common diseases but do occur sporadically in mid-summer and fall across the United States. Outbreaks may be especially common in very wet years when pools of stagnant water form and mosquitos thrive. Clinical EEE cases are primarily restricted to the Eastern coastal plains and the Gulf coast. Conversely WEE primarily occurs in Western and Midwestern states and the southeast. A variant of EEE (Madariaga virus) occurs in South America. Thus these diseases can be considered endemic across both North and South America. Both diseases present with fever, anorexia, and depression. Severe cases can result in blindness, ataxia, behavioral changes, convulsions, and death within two to three days. EEE is nearly always fatal in horses (75%–80% mortality) whereas WEE causes about 30% to 40% mortality. Recovered horses likely have lifelong immunity. Combined vaccines against EEE and WEE are core vaccines that should be boosted annually. In areas with a prolonged mosquito season it may be appropriate to give two doses annually, one in the spring and one in the fall. Likewise, horses that were not vaccinated in the previous year should receive two doses three to six weeks apart.

All currently available EEE/WEE vaccines are formalin-inactivated whole viral products. It has not yet been possible to produce effective modified live vaccines. These vaccines may be combined with vaccines containing antigens from tetanus, influenza, and West Nile Virus.

Venezuelan equine encephalitis

Venezuelan equine encephalitis (VEE), as its name implies, is endemic in tropical wet forest areas of South and Central America. It is caused by an Alphavirus, maintained in a rodent reservoir, and transmitted by mosquitos. It can cause debilitating and potentially lethal encephalitis in horses and humans. VEE has not been diagnosed in the United States since 1971. It is therefore a reportable foreign animal disease. Should VEE recur, an inactivated vaccine may be given to horses in a two dose primary series, three to four weeks apart with annual revaccination. However, there have been outbreaks of disease associated with incomplete inactivation of formalin-treated vaccines. Vaccination against EEE and WEE will induce antibodies that cross-react with VEE and may provide partial protection.

A modified live vaccine strain of VEE, C-84, is also used in horses. The vaccine must be kept cold and given as a single dose to horses over three months of age. Once reconstituted it must be used immediately. Horses should be revaccinated annually. This vaccine has been conditionally approved in the United States. Obviously, it cannot be used in the United States at the present time but would be released should a VEE outbreak occur.

West nile virus

West Nile virus (WNV) is the most significant insect borne encephalitis virus in North America. It is classified as a Flavivirus. WNV is now found across the entire United States and most of Canada and Mexico. WNV affects birds, humans, and horses, but horses are by far the most susceptible species, representing over 95% of clinically affected mammals. Affected horses develop ataxia and motor deficits ranging from mild symptoms to an inability to walk. Fever is not a consistent feature. About 30% of infected horses die and the survivors may show residual effects including altered gait and abnormal behavior. Because of its distribution and significance, WNV vaccination is considered essential (core). At the present time in the United States there are two licensed inactivated tissue culture adjuvanted whole virion vaccines, a canarypox recombinant vectored vaccine, an inactivated yellow fever chimera vaccine, and a DNA-plasmid vaccine.

Inactivated vaccines may not prevent infection, but they do reduce disease severity and prevent the development of a viremia.

A recombinant canarypox vectored WNV vaccine is available that will not replicate in vaccinated horses but persists for a sufficient period to stimulate a protective response. It is administered with a carbopol-based adjuvant (Chapter 7).

A chimeric vaccine, (EquiNile, Merck Animal Health) also incorporates a carbopol-based emulsion adjuvant. This vaccine consists of a vaccine strain of yellow fever (17D) with inserted West Nile premembrane (prM) and envelope (E) proteins to generate a chimeric virus-like particle. The remaining nucleocapsid proteins in addition to the nonstructural proteins and untranslated gene termini are those of yellow fever 17D virus.

A DNA-plasmid vaccine (West Nile-Innovator DNA, Fort Dodge Animal Health) has also been developed. The vaccine consists of a plasmid vector engineered to express high levels of the virus premembrane (prM) and envelope (E) proteins. In addition, the plasmid contains gene promoters and marker genes (see Fig. 6.2). Upon injection, together with a biodegradable oil adjuvant, this plasmid enters cells and causes them to express the WNV proteins.

Antibodies to WNV are detectable by 21 days postvaccination and reach maximal titers by about 4 weeks. WNV antibody titers may be somewhat lower in response to combined vaccines when compared with single antigen vaccines. Recovered horses probably develop life-long immunity.

Equine rhinopneumonitis

Equid herpesvirus type 1 (EHV-1) and type 4 (EHV-4) cause respiratory and neurologic disease, and abortion. They are endemic in horse populations worldwide. Many foals become infected in the first weeks or months of life, but infections also occur in when horses from different sources are mingled. Both viruses cause upper respiratory tract disease with fever, lethargy, anorexia, nasal discharge, cough, and mandibular lymphadenopathy. Both EHV-1 and EHV-4 can cause abortion in naïve mares, weak nonviable foals, or a relatively infrequent paralytic neurologic disease (equine herpesvirus myeloencephalopathy, EHM). EHV-4 causes especially severe abortion outbreaks.

Like other herpesviruses, these viruses establish latent infection in horses, which then become asymptomatic carriers. Most horses are therefore re-infected multiple times during their lifetime, usually subclinically. Viral reactivation occurs when horses are stressed, resulting in a viremia and short-term viral shedding. If this reactivation occurs in pregnant mares, they may abort.

Vaccination is required for the prevention of abortion and to reduce the severity of rhinopneumonitis in young or other at-risk horses. Although horses develop antibodies after infection, these antibodies are not correlated with protection. There is no evidence that vaccines prevent the development of EHM.

Many different inactivated vaccines are available for the control of EHV-1 and -4. These include some licensed for protection against respiratory disease alone, and two that are used for protection against both rhinopneumonitis and abortion. One inactivated vaccine is given intramuscularly for two doses, but the third dose may be given intranasally. Not all these vaccines are equally protective and immunity is generally short lasting.

A modified live EHV-1 vaccine is also available (Rhinomune, Boehringer Ingelheim). It is used for protection against rhinopneumonitis. Like other live herpesvirus vaccines, it causes rapid onset of protection as a result of interferon production. Because immunity is relatively short lasting, multiple doses may be administered annually. Even infected, recovered horses probably only remain immune for up to six months. Horses younger than five years of age, horses in contact with pregnant mares, horses that come into extensive contact with frequently moved horses, and show horses in high-risk environments should receive EHV-1 vaccines. Equestrian organizations may require such vaccination. (See section “International Vaccine Requirements”.)


Although not a common disease in horses, equine rabies is invariably lethal and is of public health significance. Rabies vaccine should therefore be considered a core requirement in horses. There are five licensed rabies vaccines currently approved for use in horses in the United States. All are inactivated and tissue-culture derived. They are given intramuscularly and are highly effective.

Some veterinarians prefer that mares be vaccinated before breeding. Given the potency of these rabies vaccines, the mare’s antibody levels will remain high throughout the pregnancy and still provide sufficient colostral antibodies.

If confronted with foals from mares with an unknown vaccination history one may assume that they have been vaccinated and boost accordingly. An alternative approach is to test their serum for antibodies against rabies about 24 hours after birth at a time when it would be expected that they have received colostral antibodies. If negative, they should be treated as if the mares were unvaccinated, whereas if positive, one must assume that the mare had been vaccinated.

If a vaccinated horse has been exposed to a rabid animal then it should immediately be revaccinated by a veterinarian and then placed under observation for 45 days as directed by the regulatory authorities. If an unvaccinated horse is exposed to a rabid animal it may be euthanized immediately. If this is an unacceptable procedure, then the horse should be monitored for six months under veterinary supervision and with the approval of the appropriate authorities. This may also include isolation and immediate vaccination.

Equine viral arteritis

Equine viral arteritis is caused by equine arteritis virus (EAV), an RNA virus in the genus Arterivirus. It occurs in horses worldwide. EAV can cause abortion in pregnant mares and establish a long-term carrier state in breeding stallions. Foals infected during the first few months of life may develop edema, conjunctivitis, urticaria, and rarely, a severe pneumonia, enteritis, or pneumoenteritis. The majority of primary EAV infections are however subclinical or asymptomatic. Persistent carrier stallions are the natural reservoir of EAV. All horses should be serologically tested and a negative antibody titer should be documented by a US Department of Agriculture laboratory before vaccinating. An inactivated adjuvanted vaccine is licensed for use in certain European countries. It is prepared from virus grown in equine cell culture. This vaccine is used in breeding and nonbreeding horses. Its safety in pregnant mares has not been investigated. Interestingly, another inactivated vaccine has been developed in Japan. It is stored in case an outbreak of EVA should occur in Japan. It is not commercially available.

A modified live EAV vaccine is licensed for use in the United States and Canada. It contains a virus attenuated by multiple serial passages in primary equine and rabbit kidney cells and in equine dermal cells. It is safe and effective in stallions and nonpregnant mares. It should not be given to pregnant mares. Mild febrile reactions and transient lymphopenia do occur. However, in first-time vaccinates, the frequency, duration, and amount of vaccine virus that is shed via the respiratory tract is less than that observed with natural infection. Vaccination in the face of an EVA outbreak has been successful in controlling disease spread. When vaccinating against EVA, it is important to consult with state and/or federal animal health officials to ensure that the program is in compliance with any official control program.

Breeding stallions should receive annual revaccination against EVA no later than four weeks before each breeding season. Before initial vaccination, all stallions must undergo serologic testing and be confirmed negative for antibodies to EAV. All first-time vaccinated stallions should then be isolated for three weeks after vaccination before being used for breeding. Some countries bar entry of any horse that is serologically positive for antibodies to EAV, regardless of vaccination history. Countries that do accept EVA vaccinated horses typically require stallions or colts to have a certified vaccination history and confirmation of prevaccination negative serological status.

Equine influenza

Equine influenza virus (EIV) causes an acute respiratory disease in horses, donkeys, and mules worldwide. This disease, caused by the orthomyxovirus, equine influenza A type 2 (A/equine 2), is one of the most common and important infectious diseases of horses. It is highly contagious and spreads rapidly between horses as a result of coughing. It is endemic in many countries and causes major outbreaks when sufficient antigenic drift occurs and the horse population is no longer immune. It causes high morbidity with significant economic consequences. Mortality is uncommon, but the virus may kill donkeys and colostrum-deprived foals.

EIV, like other influenza viruses, undergoes continuous antigenic change (drift) as a result of mutations in its RNA genome, which result in amino acid substitutions in its hemagglutinin and consequent alterations in its structure and antigenicity. Continuous virus surveillance and characterization are essential for its control. Influenza vaccines only work when they match the circulating strains and they must be updated periodically if failures are to be avoided. This update is based on a formal review of circulating strains by an expert committee of the OIE (The World Organization of Animal Health).

Influenza viruses have two major surface proteins, the hemagglutinin (HA) and the neuraminidase (NA). The HA is the major target of neutralizing antibodies and an essential antigen in influenza vaccines. Equine influenza viruses are classified by their subtype, and also the location and year they were first isolated. For example, H7N7 was first isolated in Prague in 1956, whereas H3N8 was first isolated in Miami, Florida in 1963. H7N7 strains have not been detected since the late 1970s.

The original H3N8 equine influenza virus strain changed very little between 1963 and 1988. In 1989, however it diverged into two antigenically and genetically distinct lineages, one European and one American. The European lineage has not been isolated for many years and is believed extinct. The American lineage subsequently evolved into Kentucky, South America, and Florida lineages. The Kentucky and South American lineages have not been isolated recently. Sometime after 2000, the Florida lineage in turn diverged into two sublineages, clades 1 and 2. These are the dominant EIV lineages currently circulating internationally. Florida clade 2 viruses have predominated in Europe and Asia whereas clade 1 viruses predominate in North America. Florida clade 1 includes A/eq/Ohio/03, A/eq/Wisconsin/03, and A/eq/South Africa/03 viruses. Florida clade 2 includes A/eq/Italy /99, A/eq/Newmarket/03, and A/Richmond/07 viruses. Viruses from these two sublineages are sufficiently different antigenically as to require the presence of both in vaccines. Vaccination against one clade may not fully protect against disease caused by the other. Currently, OIE recommends that horses travelling internationally should receive vaccines containing both Florida clade 1 and clade 2 viruses. Antigenic drift continues to occur, however. and recent isolates are diverging from both clades. Newly emerged strains of clade 2 may be responsible for recent outbreaks of influenza in vaccinated horses in the United Kingdom and France.

It is clear that influenza outbreaks generally follow introduction of an infected horse into a stable where it spreads rapidly through susceptible animals. Thus quarantine of newly arriving horses and timely vaccination are required for disease control. All horses should be vaccinated regularly against influenza with the currently recommended strains. Vaccination reduces both clinical signs and viral shedding, although vaccinated infected horses may still shed some virus. Equine influenza does not infect humans, but the virus has spread to dogs (Chapter 13).

Should an outbreak of influenza occur, it may be necessary to establish a buffer zone surrounding that area. In the 2007–2008 Australian outbreak caused by the Florida clade 1 strain A/eq/Sydney/07, the disease was compartmentalized by ring vaccination that blocked viral spread.

In some countries, vaccination is mandatory for horses participating in equestrian activities under the rules of International Equestrian Organizations. Some of these organizations require biannual rather than annual revaccination because antibody levels appear to drop after four to six months. It is absolutely critical that equine influenza vaccines contain epidemiologically relevant strains because there is minimal cross-strain protection.

There are four types of EIV vaccine currently available: whole inactivated and subunit vaccines, an intranasal modified-live cold adapted vaccine, and a recombinant canarypox vectored vaccine.

The earliest flu vaccine developed consisted of whole, inactivated, products. Inactivated influenza vaccines may contain many different antigens from multiple strains of influenza A clade 2. They contain whole viruses combined with adjuvants such as carbomer, aluminum hydroxide, or ISCOM-matrix. The viruses are first grown in embryonated chicken eggs or in tissue culture and concentrated and purified before they are inactivated with formaldehyde or beta-propiolactone. They induce antibodies against the viral hemagglutinin, neuraminidase, and other conserved viral antigens. However, immunity is often short-lived. Thus most of these vaccines require two injections for priming, although three are better. They are most suitable for vaccination of pregnant mares to boost colostral antibodies.

A subunit influenza vaccine is also available (Equilis Prequenza, MSD Animal Health). It contains the purified HA and NA subunits of the European and Florida clade 1 virus, but not clade 2 virus. It is adjuvanted with ISCOM/ISCOM-matrix. It is not currently available in the United States.

A modified-live cold adapted intranasal vaccine against H3N8 is also available (Flu Avert, Merck Animal Health). A/Equine 2, Kentucky/91 was attenuated by cold adaptation in embryonated eggs. As a temperature-sensitive agent it can replicate in the upper respiratory tract, but not deeper within the body. It is approved for vaccination of nonpregnant horses over 11 months of age, followed by revaccination every 6 months. As with other live intranasal vaccines horses shed the vaccine virus. However, shedding lasts for less than a week. Onset of immunity occurs by seven days postvaccination. It is best not to use this vaccine in pregnant mares. In addition to safety concerns, this vaccine does not elicit high serum antibody levels so colostral antibodies may not be elevated. This is not entirely surprising because the intranasal immune response is primarily restricted to the mucosa. This vaccine is only available in the United States.

A canarypox-vectored vaccine encoding the hemagglutinin genes from A/eq/Ohio/03 and A/eq/Richmond/1/07 is marketed under the name Recombitek (Boehringer Ingelheim/Merial) in North America and as ProteqFlu in Europe. It contains a carbopol adjuvant and is administered intramuscularly. During the 2007 Australian outbreak it was shown to significantly reduce the severity and duration of disease and viral shedding. An accelerated vaccination schedule with only 14 days between vaccination and boosting was applied in emergency situations. Ideally it should be administered at least 4 weeks before an event. This vaccine induces high antihemagglutinin levels, so it should induce colostral antibodies in pregnant mares. The advantage of this vaccine is that it has DIVA capability. Vaccinated horses only have antibodies against the hemagglutinin whereas infected horses develop antibodies against multiple other viral antigens such as the neuraminidase.

In general, horses receive two priming doses of vaccine four to six weeks apart, followed by revaccination five to six months later. Foals should be vaccinated at six to seven months, and annually or biannually thereafter. If necessary, vaccination of foals at three months may be effective. Antibody levels appear to wane rapidly between the second and third vaccination and if the interval between these boosters is too long there may be an “immunity gap” to EIV lasting several weeks. Horses infected during this time may develop subclinical infection and shed significant amounts of live infectious virus, posing a risk to naïve contacts. Interestingly, there also appears to be a negative correlation between the number of doses of vaccine received by a horse and its antibody titers. The reasons for this are unclear, but it has been suggested that newly formed plasma cells displace older memory plasma cells resulting in a loss of preexisting antibodies. Perhaps there is an overvaccination problem. Mares have significantly higher antibody levels than stallions for reasons unknown.

Strategic vaccination may be appropriate such as timing revaccination to correspond to periods of exposure to other horses. Vaccination in the face of an outbreak may be effective if the outbreak is detected sufficiently early. In unvaccinated horses, the rapid onset of immunity that occurs after the use of the intranasal product suggests that this would be the logical vaccine to use.


Rotaviruses, nonenveloped RNA viruses, are a major cause of foal diarrhea. Morbidity is often high whereas mortality is low. Rotavirus vaccination of pregnant mares results in a decrease in the prevalence and severity of foal diarrhea on infected farms probably as a result of rotavirus antibodies in mares’ colostrum. An inactivated vaccine that contains rotavirus Group A is specifically licensed for use in pregnant mares to induce colostral antibodies.

Other equine vaccines

African horse sickness

African Horse Sickness is an insect-borne disease affecting all Equidae caused by an unenveloped double-stranded RNA Orbivirus related to bluetongue virus. It is transmitted by Culicoides midges and is confined to sub-Saharan Africa. Nine antigenically distinct viral serotypes have been identified. Both monovalent and polyvalent modified live vaccines are commercially available. These contain virus attenuated by growth in Vero cells and most provide good protection, although they have the potential to revert to virulence, undergo reassortment, and possibly be transmitted by their vectors. Some are more reactive than others and protection may be incomplete. Additionally, the currently available vaccines may cause fetal abnormalities when given to pregnant mares. Annual revaccination is required.

Hendra virus

Hendra virus is a Henipavirus in the subfamily Paramyxovirinae. It occurs in horses in Australia where it causes a high fever and severe respiratory disease with pulmonary edema. It results in a 58% death rate in humans and a 75% death rate in horses. A vaccine containing the viral G protein (required for cell attachment) is available for use by licensed veterinarians in Australia (Equivac HeV, Zoetis). It should be given to foals over four months with two boosters at three-week intervals followed by annual revaccination.

Crotalid snake bite

The risk of rattlesnake bites with envenomation may justify the use of a Crotalus atrox (Western diamondback rattlesnake) toxoid vaccine in horses. It may provide protection against other species of Crotalid and copperheads, but it does not protect against venom from Mojave rattlesnakes, water moccasins, or coral snakes. Three doses should be administered at one month intervals to horses over six months, and horses should be revaccinated every six months.

Gonadotropin releasing hormone

Gonadotropin releasing hormone (GnRH) controls the pituitary release of follicle-stimulating hormone and luteinizing hormone. These in turn regulate male and female sexual activity. Blocking of GnRH production can be accomplished by vaccination. Antibodies bind to GnRH in the hypothalamic-pituitary portal vessels and prevent the GnRH from binding to its receptor. Thus vaccination can be used to control inappropriate sexual behavior in both stallions and mares. In mares, the reduction in GnRH leads to a decline in estrogen levels so that behavioral estrus ceases. The adjuvanted GnRH conjugated to a foreign protein such as ovalbumin is given as a two dose intramuscular series four weeks apart to suppress ovarian activity and associated estrus behavior in fillies and mares that are not being bred. Antibodies peak about two weeks after the second vaccine dose. Cyclical estrus behavior will start to decline within two weeks after the second dose as the ovaries shrink. This suppression is expected to last for three to six months.

If given to young stallions the presence of antiGnRH antibodies results in decreases in testosterone, libido, sperm production, and sperm quality. Recovery from vaccination is usually complete, should a decision be made to breed with a vaccinated animal. There is however much individual variation in responses. GonaCon is a GnRH vaccine used by the Environmental Protection Agency as a contraceptive and inhibitor of sexual behavior in wild horses and burros (Chapter 20).

Prescottella (rhodococcus) equi

Prescottella equi is a facultative intracellular bacterium that causes lethal bronchopneumonia and pyogranulomatous lung lesions in foals three weeks to six months in age. The organism elicits both antibody and cell-mediated immune responses in foals. (Protection is attributed to a type 1 response mediated by IgG1 antibodies.) Traditional live, killed, and attenuated vaccines have proved to be ineffective. Subunit and DNA vaccines may be somewhat better but they are not yet available. Encouraging results have been obtained when pregnant mares are vaccinated against poly-N-acetyl glucosamine, a highly conserved capsular polysaccharide. It is assumed that this immunity results from transfer of maternal antibodies in colostrum. Passive immunization with hyperimmune serum against whole bacteria or against poly-N-acetyl glucosamine may also be of significant benefit when treating infected foals (Chapter 12).

Adverse events

Allergic reactions, although uncommon, may occur in horses in response to vaccine antigens. In severe anaphylaxis, the major shock organs of horses are the lungs and the intestine. Bronchial and bronchiolar constriction leads to coughing, dyspnea, and eventually apnea. The major mediators of anaphylaxis in horses are probably histamine and serotonin. Anaphylaxis requires prompt epinephrine treatment administered intramuscularly or intravenously (Box 10.2).

Local injection site reactions may occur, especially in response to strangles vaccines and some polyvalent vaccines. Although usually transient, they may be treated with nonsteroidal antiinflammatory drugs and also the use of warm compresses (Fig. 15.1).

Jan 21, 2021 | Posted by in GENERAL | Comments Off on Equine vaccines
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