Equine influenza is highly contagious and spreads rapidly among naive horses. Horses 1–5 yr old are the most susceptible to infection. Orthomyxovirus A/equine-2 was first recognized in 1963 as a cause of widespread epidemics and has subsequently become endemic in many countries, except for New Zealand and Iceland. China, Japan, and Australia experienced devastating epidemics of equine influenza affecting tens of thousands of horses in 2007. Equine influenza had not been reported in China since 1993, in Japan since 1972, and had never been reported in Australia.
Endemicity is maintained by sporadic clinical cases and by inapparent infection in susceptible horses introduced into the population by birth, through waning immunity, or after movement from other areas or countries. A carrier state is not recognized for equine influenza. The clinical outcome after viral exposure largely depends on immune status; clinical disease varies from a mild, inapparent infection to severe disease in susceptible animals. Influenza is rarely fatal except in donkeys, zebras, and debilitated horses. Transmission occurs by inhalation of respiratory secretions. Epidemics arise when one or more acutely infected horses are introduced into a susceptible group. The epidemiologic outcome depends on the antigenic characteristics of the circulating virus and the immune status of a given population of horses at time of exposure. Frequent natural exposure or regular vaccination may contribute to the degree of antigenic drift seen with specific strains of A/equine-2 virus in some parts of the world.
The incubation period of influenza is ~1–3 days. Clinical signs begin abruptly and include high fever (up to 106°F [41.1°C]), serous nasal discharge, submandibular lymphadenopathy, and coughing that is dry, harsh, and nonproductive. Depression, anorexia, and weakness are frequently seen. Clinical signs usually last <3 days in uncomplicated cases. Influenza virus replicates within respiratory epithelial cells, resulting in destruction of tracheal and bronchial epithelium and cilia. Cough develops early in the course of infection and may persist for several weeks. Nasal discharge, although scant and serous initially, may become mucopurulent due to secondary bacterial infection. Mildly affected horses recover uneventfully in 2–3 wk; severely affected horses may convalesce as long as 6 mo. Recovery may be hastened by complete restriction of strenuous physical activity. Respiratory tract epithelium takes ~21 days to regenerate; during this time, horses are susceptible to development of secondary bacterial complications such as pneumonia, pleuropneumonia, and chronic bronchitis. Complications are minimized by restricting exercise, controlling dust, providing superior ventilation, and practicing good stable hygiene. Primary complications of vasculitis, myositis, and myocarditis are seen infrequently.
The presence of a rapidly spreading respiratory infection in a group of horses characterized by rapid onset, high fever, depression, and cough is presumptive evidence of equine influenza. Definitive diagnosis can be determined by virus isolation, influenza A antigen detection (patient-side kit), or paired serum samples (hemagglutination inhibition). Nasopharyngeal swabs are obtained for virus isolation and antigen detection. These samples should be obtained soon after the onset of illness. Virus isolation in chick embryos is highly specific but less sensitive for detection of influenza because of bacterial contamination of the sample. Antigen detection is performed using a human influenza A kit, which provides immediate results that are not affected by bacterial contamination.
Horses that do not develop complications require rest and supportive care. Horses should be rested 1 wk for every day of fever, with a minimum of 3 wk rest (to allow regeneration of the mucociliary apparatus). NSAIDs are recommended for horses with a fever >104°F (40°C). Antibiotics are indicated when fever persists beyond 3–4 days or when purulent nasal discharge or pneumonia is present.
Prevention of influenza requires hygienic management practices and vaccination. Exposure can be reduced by isolation of newly introduced horses for 2 wk. Numerous vaccines are commercially available for prevention of equine influenza. An intranasal modified-live influenza vaccine, designed to induce mucosal (local) antibody protection, has demonstrated protection against natural challenge. This vaccine is temperature sensitive and is not capable of replicating beyond the nasal passages (ie, inactivated by core body temperature). Most commercially available influenza vaccines are inactivated, adjuvanted vaccines recommended primarily for IM administration. A recombinant canarypox-vectored influenza vaccine has also been shown to be effective against influenza challenge. Because the duration of protection provided by current vaccines is limited, booster injections for at-risk adult horses should be administered every 6 mo. Sedentary horses can be vaccinated annually. Foals should be vaccinated with a single modified-live intranasal vaccine or a series of three inactivated vaccines beginning at 6 mo, with booster vaccination in 3–6 wk and again between 10 and 12 mo of age. Broodmares should be vaccinated 4–6 wk before foaling.