The Other Influenza: Equine Flu
Is your horse feeling under the weather, running a temperature and coughing? Think your horse may of caught the flu? You could be right! In fact equine influenza, an Orthomyxovirus, is the most frequently diagnosed cause of viral respiratory disease in the horse. This virus is endemic all over the world except in Iceland and in New Zealand. Influenza A viruses can infect a wide variety of species including humans, wild and domestic birds, pigs, sea mammals, dogs, cats, and even ferrets. Viruses of one host will occasionally mutate and become capable of infecting additional species. For example, in 1989 a severe equine outbreak occurred in China. This epidemic was the result of an influenza virus which incorporated avian-like genetic features with the traditional equine virus. In 2004 an equine-linage influenza jumped to dogs in the United States causing an influenza pandemic with high morbidity and mortality in infected dogs. Think this couldn’t happen again? Unfortunately history has a habit of repeating itself.
Influenza viruses are classified on the basis of their antigenic properties. Based on their hemagglutinin (HA) glycoprotein they are divided into 16 subtypes (H1 to H16). The HA, or viral hemagglutinin glycoprotein, is important in determining the host specificity by serving as the receptor-binding protein. This protein is necessary for the virus to bind to the host cell, thereby allowing the viral particle to fuse with the host cell, inject its genetic material, and essentially take over the protein manufacturing centers. The cell becomes a factory for additional virus assembly until the cell itself is finally destroyed. The second component is neuraminidase (NA), which facilitates the release of newly formed viral particles from the host’s cell creating subtypes (N1 to N9).
In horses the primary type of influenza seen is H3N8 or Influenza A/equine/2 subtype. A severely virulent form of influenza, H7N7 or the A/equine/1 subtype, has not been isolated from the equine population since the late 1970’s, although some feel it may still be circulating at low levels in the equine populations of Central Asia and Eastern Europe.
The Influenza H7 equine virus is important, for it is the H7 serotype that traditionally has the highest mortality rates. Influenza H7 can invade not only cells of the lungs but also other parts of the host’s body including cells of the brain. This is why the H7 serotype is so dangerous and lethal. Researchers have identified one stretch of amino acids that are unique to this subtype of the influenza virus and believe them to be responsible for the virus’ unique ability to invade tissues other than those in the lungs. The H7 variety is prevalent in birds, and birds are now believed to be the source of the highly virulent H7 of horses. The H7 subtype is what gives public health officials the greatest concern with a possible human epidemic.
The H3N8 virus is the primary influenza seen in horses since the 1980’s. Since then it has mutated into two distinct lines: European and American. The American lineage has developed into three distinct antigenic lines of its own known as the South American, Kentucky, and Florida subtypes. The rate of genetic mutation in the equine viruses is believed to be low compared with the genetic diversions of the human, avian, and swine influenza viruses but it still impacts vaccination, which is the foundation of influenza control.
Just as with the human flu, outbreaks of equine influenza are associated with the congregation of large numbers of horses. The virus is transmitted through direct contact with an infected animal, via airborne transmission through the formation of droplets, and by way of contact with contaminated fomites. The virus may survive up to 48 hours on dry surfaces and longer on moist or wet surfaces.
The incubation period for equine influenza is short, requiring only 2 days following exposure to the virus.
Horses with influenza are anorexic (have a poor appetite), lethargic, and run high temperatures (pyrexia) in conjunction with nasal discharge and cough. In uncomplicated cases, recovery takes place in 7 to 14 days with appropriate supportive care. Complications of infection include secondary bacterial pneumonia, myositis, myocarditis, and edema of the limbs. Following recovery the cough may persist for months and make the horse more susceptible to heaves. Fatalities are rare, except with the H7N7 variety which may result in mortality rates of up to 35%. Following natural infection a horse is considered to be immune from reinfection for approximately one year.
Diagnosis may be confirmed through viral isolation from nasal swabs or the demonstration of seroconversion following infection on paired serum samples.
Control is achieved through good husbandry and vaccination, of which both modified-live and killed varieties are available. An intranasal modified-live vaccine manufactured by Intervet has been shown to be effective for up to 12 months, although the manufacturer suggests vaccinating every six months. Foals under 6 months of age are not vaccinated due to the neutralizing effects of maternal antibodies. Killed vaccines are typically given on a 3-dose protocol with revaccination occurring at 6-month intervals. Booster vaccinations should be given 1 to 2 weeks before a horse is stressed or has the potential for exposure. Precise vaccination guidelines are available at http://www.aaep.org.
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