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

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

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.

Rabies

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.

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.

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

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.

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

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.

Prescottella (rhodococcus) equi