Equine influenza virus is a member of the orthomyxovirus family and there are two main subtypes: A/equine/1 (also known as H7N7) and A/equine/2 (H3N8). Like all influenza viruses they mutate rapidly making vaccine manufacture problematic. However the 1 type is less efficient at changing and is not often implicated in outbreaks and only the 2 variant has been isolated from outbreaks since 1980. This is important to know when deciding what vaccine to use.

Technical Reports: More Information on Influenza Strains These reports give an idea of the complexity of the influenza vaccine problem: new strains showing up and old strains still lingering around. Modified from Equine Infections Diseases by Sellon: Outbreaks of a disease resembling influenza have been reported as early as 1751, although the etiologic agent was not isolated until 1956. The virus, designated A/Equine/l/ Prague/56, was isolated during an outbreak of influenza in Czechoslovakia and was characterized as H7N7. H7N7 influenza viruses have not been detected in the horse population since the late 1970s. However, large-scale serologic surveillance demonstrated that these viruses may still be circulating at low levels in the equine population of Central Asia27 and Eastern Europe. In contrast, equine-2 influenza viruses, first isolated in the United States in 1963 (A/equine/2/Miami/l/63), continue to circulate in large parts of the world, except New Zealand, and lceland. Despite intensive vaccination programs, equine H3N8 influenza infections have remained a serious health and economic problem throughout the world. In the late 1980s, severe widespread influenza outbreaks were observed in horses in South Africa, in India, and in the People's Republic of China, where equine influenza viruses were not known to be circulating. The causative agent of the South African outbreak was identified as an H3N8 virus, which was most likely introduced by importation of infected horses from the United States or Europe. The outbreaks in the People's Republic of China have been caused by both conventional strains of equine H3N8 virus and viruses that were antigenic ally and genetically distinguishable from other circulating equine H3N8 viruses. Phylogenetic analysis of the virus causing the 1989 epidemic showed that this virus had evolved independent of the existing equine lineage. Its genetic features were of recent avian lineage, indicating that this virus had probably spread directly to horses from the avian reservoir without genetic reassortment. Since the early to middle 1980s, the equine H3N8 influenza, viruses have diverged into two distinct evolutionary lineages, European and American. Although the circulation of both lineages initially centered largely on the geographic origin, both lineages now appear to be co-circulating in Europe and to a lesser extent in the United States. In the Western Hemisphere, continued genetic divergence appears to have resulted in the formation of three American-like lineages with distinct antigenic characteristics: a South American lineage, a Kentucky lineage, and a Florida lineage. Although the antigenic drift of H3N8 equine influenza viruses is significant in terms of immunization, when compared to human influenza viruses, equine stains have demonstrated relatively little genetic diversion. Sequence comparisons between the prototype reference stains and more recent H3N8 influenza A virus isolates revealed 70% to 90% genetic homology.

More Recent Reports of Outbreak Strains Vet Microbiol. 2007 Mar 31;121(1-2):56-63. An outbreak of equine influenza virus in vaccinated horses in Italy is due to an H3N8 strain closely related to recent North American representatives of the Florida sub-lineage. Martella V, Elia G, Decaro N, Di Trani L, Lorusso E, Campolo M, Desario C, Parisi A, Cavaliere N, Buonavoglia C. Department of Animal Health and Well-being, University of Bari, Valenzano, Bari, Italy. v.martella@veterinaria.uniba.it In December 2005, equine influenza virus infection was confirmed as the cause of clinical respiratory disease in vaccinated horses in Apulia, Italy. The infected horses had been vaccinated with a vaccine that contained strains representatives from both the European (A/eq/Suffolk/89) and American (A/eq/Newmarket/1/93) H3N8 influenza virus lineages, and the H7N7 strain A/eq/Praga/56. Genetic characterization of the hemagglutinin (HA) and neuraminidase (NA) genes of the virus from the outbreak, indicated that the isolate (A/eq/Bari/2005) was an H3N8 strain closely related to recent representatives (Kentucky/5/02-like) of the American sub-lineage Florida, that was introduced in Italy through movement of infected horses from a large outbreak described in 2003 in United Kingdom. Strain A/eq/Bari/2005 displayed 9 amino acid changes in the HA1 subunit protein with respect to the reference American strain A/eq/Newmarket/1/93 contained in the vaccine. Four changes were localized in the antigenic regions C-D and likely accounted for the vaccine failure. Vet Rec. 2006 Feb 11;158(6):185-92. Description of the outbreak of equine influenza (H3N8) in the United Kingdom in 2003, during which recently vaccinated horses in Newmarket developed respiratory disease. Newton JR, Daly JM, Spencer L, Mumford JA. Centre for Preventive Medicine, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU. Between March and May 2003, equine influenza virus infection was confirmed as the cause of clinical respiratory disease among both vaccinated and unvaccinated horses of different breeds and types in at least 12 locations in the UK. In the largest outbreak, 21 thoroughbred training yards in Newmarket, with more than 1300 racehorses, were affected, with the horses showing signs of coughing and nasal discharge during a period of nine weeks. Many of the infected horses had been vaccinated during the previous three months with a vaccine that contained representatives from both the European (A/eq/Newmarket/2/93) and American (A/eq/Newmarket/1/93) H3NN8 influenza virus lineages. Antigenic and genetic characterisation of the viruses from Newmarket and elsewhere indicated that they were all closely related to representatives of a sublineage of American viruses, for example, Kentucky/5/02, the first time that this sublineage had been isolated in the uk. In the recently vaccinated racehorses in Newmarket the single radial haemolysis antibody levels in acute sera appeared to be adequate, and there did not appear to be significant antigenic differences between the infecting virus and A/eq/Newmarket/1/93, the representative of the American lineage virus present in the most widely used vaccine, to explain the vaccine failure. However, there was evidence for significantly fewer infections among two-year-old horses than older animals, despite their having similar high levels of antibody, consistent with a qualitative rather than a quantitative difference in the immunity conveyed by the vaccination.

Influenza infects primarily the cells of the lining of the trachea and bronchi. It spreads rapidly killing the cells of the lining and since these cells are responsible for protecting the lower air way from bacteria and contaminants. This makes secondary bacterial pnemonia a possible complication. Though influenza can cause muscle soreness, swelling in the legs, heart arrythmias, and neurological disease virus isolation from this tissues has been unsuccessful leaving open exactly how influenza causes these changes and it may be a response to the increased circulating inflammatory products rather than infection of these tissues.

Equine flu is most often spread from horse to horse by infectious nasal secretions. The explosive cough can spread infection droplets for long distances throughout a barn. Following infection horses secrete the virus for about a week. This would be for a few days before clinical signs are obvious so these horses may be moved about exposing others before infection is evident. A carrier state of influenza has not been identified however horses with partial immunity from past infection or vaccination may develop subclinical infections and secrete the virus without apparent clinical signs. Influenza can be transmitted by innate objects and people though the virus does not live long off the horse. Moisture may allow the virus to survive up to 3 days off the horse but only for a day or two on dry surfaces.