Causative agent
Equine influenza (EI) is caused by a type A Orthomyxovirus. The viruses are 80 to 120 nanometers (nm) in diameter, and consist of a core of eight separate segments of single-strand ribonucleic acid (RNA) surrounded by a spiked arrangement of glycoproteins. These viruses are classified based on the relative numbers of hemagglutinin (H) and neuraminidase (N) glycoproteins in the lipid outer layer. Strains (or subtypes) of influenza viruses are formally described according to their type (A, B, or C), host species, location of first isolation (city or country), strain number (if any), year of first isolation, and antigenic subtype (H and N designation); shorthand methods of identification are limited to the H/N description. The two major strains known to cause disease in equids are H7N7 (A/eq/Prague/56[H7N7], type A influenza, equine, first isolated in Czechoslovakia in 1956) and H3N8 (A/eq/Miami/2/63[H3N8], type A influenza, equine, first isolated in Miami, strain 2, isolated in 1963). The two subtypes are immunologically distinct. Sublineages of the two major strains (e.g., A/eq/Newmarket/2/93[H3N8], A/eq/Kentucky/92[N3H8]) have emerged due to antigenic shift (reassortment of the genome resulting in genetic alteration) and antigenic drift (point mutations in the genetic code causing minor alterations in the H and N glycoproteins).

Natural distribution
Equine influenza affects horses, donkeys, mules, and other equidae. The virus is widespread with only Iceland, New Zealand, and Australia considered to be free of the virus. The H7N7 subtype is believed to be extinct or present at very low levels. The H3N8 subtype appears to be a mutation of an avian influenza virus.

An outbreak involving a modified H3N8 subtype (designated A/eq/Jilin/89[H3N8]) occurred in China in 1989. High morbidity (80%) and mortality (20%) were observed. Other important outbreaks of the H3N8 subtype have occurred worldwide, including in Trinidad (1979), Argentina (1985), South Africa (1986), and Jamaica (1989). Most confirmed outbreaks occurred at racetracks; as a result, horseracing activities were suspended for prolonged periods of time, resulting in marked economic losses.

Transmission
Equine influenza is spread via aerosolized respiratory secretions and fomites, including contaminated inanimate objects and people moving between infected and uninfected horses. The most common source of infection and outbreak is the introduction of a new animal into the herd. The incubation period is usually one to three days. Incubation periods approaching seven days have been observed, but are less common. Infected horses shed virus in their respiratory secretions during the incubation period, and continue to excrete the virus for four to five days after clinical signs are observed. It is also possible for an infected animal to shed the virus for 7-10 days after the animal has appeared to recover. Viral shedding is thought to reach its peak during the first 24 to 48 hours the animal is febrile. Infected droplets may be able to spread as far as 50 yards. Virtually 100% of horses that are exposed become infected. Nearly 20% of infected horses do not exhibit clinical signs of disease, but still shed virus and can spread the infection.

Clinical signs
Equine influenza virus causes clinical disease of the upper respiratory tract. The virus spreads rapidly, and naïve or immunocompromised horses are at higher risk of developing disease. Clinical signs include fever, coughing, serous to mucopurulent nasal discharge, depression, muscle soreness, anorexia, and enlarged regional lymph nodes. Colic (abdominal pain) and edema of the legs and scrotum have also been observed with influenza infection.

In the absence of secondary complications, healthy, adult horses usually recover from EI within one to two weeks; however, coughing may persist for a longer period. Young foals lacking adequate maternal antibodies are at risk of developing a rapidly fatal viral pneumonia. Recovery from EI is complicated and prolonged by the development of secondary bacterial infections. Deaths have been reported as caused by secondary bacterial pneumonia and pleuritis. Purpura hemorrhagica, a potentially fatal, immune-mediated disease, has also developed secondary to EI infection. Fatal interstitial myocarditis (inflammation of the heart muscle) can occur during or after infection.

Diagnosis
A tentative diagnosis of EI is often made based on clinical signs. Diagnosis can be confirmed by detection of the virus in samples from nasal swabs. Traditionally, a diagnosis of EI was confirmed by inoculating embryonated hen eggs with material from nasopharyngeal swabs and subsequently isolating the virus. Alternatively, paired acute and convalescent serum samples can be submitted for EI hemagglutinin inhibition; a fourfold-or greater increase in antibody titer is diagnostic for EI. Other diagnostic methods include reverse transcriptase polymerase chain reaction (PCR) and nested reverse transcriptase polymerase chain reaction. Reverse transcription PCR is more rapid and sensitive than serologic testing, and more rapid and specific than virus isolation.

Preferred samples for diagnostic testing are fresh nasopharyngeal swabs that are shipped overnight at room temperature. If serologic testing is desired, a minimum of 2 ml of whole blood should be collected in an EDTA (lavender top) or ACD (yellow top) tube and shipped overnight at room temperature.

Treatment
As for all viral disease, treatment is largely supportive. Good husbandry and nutrition may assist horses in mounting an effective immune response. Rest reduces viral shedding. Because tracheal clearance rates (an indication of the ability of the respiratory tract to eliminate particles, mucus, and infective organisms) are reduced for up to one month after infection, rest is also recommended after resolution of clinical signs. Antipyretics are recommended for horses with fevers exceeding 105°F (40.5 C) and/or severe depression and anorexia. Pneumonia in more severely affected horses responds best to a combination of broad-spectrum bactericidal antibiotics and maintenance of hydration via intravenous administration of fluids.

Currently available antiviral drugs are approved for use in humans only and little is known about their use in equids. Often their cost precludes their use. Veterinarians who use approved drugs in a manner that is not in accord with approved label directions (e.g., use of an antiviral drug only approved for use in humans) must follow the federal extralabel drug use regulations of the Animal Medicinal Drug Use Clarification Act (AMDUCA).

Morbidity and mortality
Morbidity associated with EI in naïve populations is estimated at 60 to 90%; to date, mortality of horses with confirmed infection has ranged from 1% to 20%. Higher fatality rates are observed in foals, malnourished or immunocompromised equids, and donkeys.

Prevention and control
Inactivated intramuscular and intranasal vaccines are commercially available for prevention of influenza in equids. The American Association of Equine Practitioners (AAEP) has produced Guidelines for Infectious Disease Outbreaks; these guidelines state that the administration of booster influenza vaccines to apparently healthy animals in the face of an outbreak may be of value. For animals that were unvaccinated prior to the outbreak, the use of a modified live intranasal vaccine may be preferred because it can induce protective immunity within 5 days. The Guidelines are available to AAEP members through the AAEP website (www.aaep.org) or the AAEP office (aaepoffice@aaep.org).

Vaccination is not always effective in preventing infection, but it appears to reduce severity of clinical signs. The AAEP has produced "Guidelines for Vaccination of Horses" that can be obtained by contacting the AAEP at aaepoffice@aaep.org.

The EI virus is an enveloped virus that appears to be easily killed by disinfectants in common use in veterinary facilities, such as quaternary ammonium compounds and 10% bleach solutions. The most common source of infection is the introduction of a new animal into the herd; therefore, isolation of newly acquired animals is recommended. Isolation protocols should be rigorously applied for horses showing signs of respiratory disease, and should be maintained for 21 days after the last horse has appeared to recover from the infection. Clothing, equipment, surfaces, and hands should be cleaned and disinfected after exposure to horses known or suspected to be infected.

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