Equine influenza

What it is

Equine influenza is a respiratory disease caused by equine influenza A virus H3N8 (family Orthomyxoviridae). The viruses circulating today belong to the American lineage, in Florida clades 1 and 2, and change gradually (antigenic drift), so vaccine strains must be updated.

It is transmitted by aerosols when horses cough, by direct contact and by contaminated objects, people and vehicles. The incubation period is short, 1 to 3 days, and the virus multiplies in the airway epithelium and destroys it: the epithelium loses its cilia and mucociliary clearance is impaired for weeks, which opens the way to secondary bacterial infections.

It is endemic in almost all of the world; some island countries, such as New Zealand and Iceland, remain free. It is a WOAH-listed disease and notifiable in many countries.

Who it affects

Horses, donkeys and mules of any age. Risk is highest in unvaccinated horses, in young horses and where horses of different origins come together: racecourses, fairs, sales and competitions. Vaccinated horses can also be infected if immunity has waned or the vaccine strain does not match the circulating one well, although they usually become less ill and shed less virus.

Anatomy involved

• Trachea: the virus destroys the ciliated epithelium of the nasal mucosa, pharynx, trachea and bronchi, causing tracheobronchitis. The dry, harsh cough comes from this inflammation, and the loss of cilia explains why the cough lasts weeks after the fever.
• Lungs: the infection can extend to the bronchioles and alveoli and cause viral pneumonia, especially in foals without immunity, in which it can be fatal. More often it is complicated by secondary bacterial bronchopneumonia, mainly due to Streptococcus equi subsp. zooepidemicus.

Clinical signs

• Sudden onset of high fever, depression and inappetence.
• Dry, harsh cough, the most characteristic sign, which spreads quickly through the group.
• Serous nasal discharge that becomes mucopurulent with bacterial infection.
• Enlarged mandibular lymph nodes, muscle pain and sometimes limb oedema.
• Uncomplicated adults recover in 1 to 3 weeks, but cough and exercise intolerance can last longer.

Diagnosis

• PCR on a nasopharyngeal swab taken in the first days of fever, when virus shedding peaks. Rapid antigen tests are also available but are less sensitive.
• Paired serology (haemagglutination inhibition or single radial haemolysis) showing a rise in titre between the acute and convalescent phases.
• Epidemiology helps a great deal: fever and cough in several horses at once after an arrival or an event.
• It must be distinguished from equine herpesvirus 1 and 4, strangles and other respiratory infections.

Treatment and prevention

• Rest: a practical rule is at least one week of rest for each day of fever, to let the epithelium recover and avoid complications.
• Non-steroidal anti-inflammatory drugs for fever and malaise, good ventilation and free access to water and feed. Antibiotics are indicated only for secondary bacterial infection.
• Vaccination: inactivated or recombinant vector vaccines, with strains updated following the recommendations of the WOAH expert panel. They need a multi-dose primary course and frequent boosters, and equestrian federations and racing authorities require them for competition.
• Biosecurity: isolate sick horses, quarantine new arrivals, restrict movements during an outbreak and tighten hygiene of people, equipment and vehicles.
• Drug use in horses is subject to each country's regulations and to withdrawal periods. In the EU the horse is a food-producing species, and its identification document (passport) states whether it is excluded from slaughter for human consumption, which determines which drugs may be given.

Key studies

• Elliott et al. (2023), systematic review of 43 vaccination and experimental challenge articles in equids without prior immunity, with meta-analysis of 38. Efficacy, measured as the reduction in virus shedding, averaged 50.03% (95% CI 23.35–76.71%) with commercial vaccines and 40.37% with experimental ones, ranging from 0 to 100%; only 5 studies achieved complete protection. Most studies come from a few centres and their designs differ widely.
• Cowled et al. (2009), spatial and temporal analysis of the 2007 Australian epidemic, with nearly 10,000 infected premises in a population without immunity. Long-distance spread dropped immediately after national movement restrictions, and the epidemic peak had passed before emergency vaccination could induce immunity. The effective reproduction number between premises was 2.04 in peri-urban areas and 1.99 in rural ones. It is a descriptive study.
• Firestone et al. (2011), case-control study of 200 premises in New South Wales during the first weeks of the 2007 epidemic, before vaccination. Proximity to an infected premises was the factor most associated with infection, and having a footbath in place before the virus arrived reduced the odds of infection (OR 0.27; 95% CI 0.09–0.83), probably reflecting better overall biosecurity. Data were collected by interview about two years later.
• Barquero et al. (2007), study of an outbreak in vaccinated racehorses in Newmarket (UK) in 2003. Two-year-olds were less affected than older horses, mainly because they had been vaccinated more recently, despite similar antibody levels. The data supported vaccinating the whole group as soon as the outbreak is confirmed and suggested that vaccine adjuvanted with aluminium hydroxide alone protected less well. It is a single outbreak.
• Whitlock et al. (2023), descriptive study of the 2019 epidemic in Great Britain: 412 confirmed cases on 234 premises. 72% of cases were unvaccinated and 18% vaccinated; 42% of affected premises had received a new horse in the previous 2 weeks, only 23% quarantined new arrivals and only 57% of resident horses were vaccinated. Data were collected once per premises.