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Equine influenza, an outbreak of probable

. Introduction-agent causal —
Equine influenza (EI) is caused by a type A Orthomyxovirus. Viruses are between 80 and 120 nanometer (nm) in diameter, and consist of a core of eight separate segments of ribonucleic acid in a single chapter (RNA), surrounded by a needle agreement of glycoproteins. These viruses are classified based on the relative number of hemagglutinin (H) and neuraminidase (N) glycoproteins in the lipid outer layer. Strains (or subtypes) of influenza viruses are described formally according to their type (A, B or C), host species, location of first isolation (city or country), strain number (if applicable), year of first isolation and antigenic subtype (H and N designation); shorthand identification methods limited to the H / N Description. The two main varieties are known to cause disease in horses is 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. Sub lineages of the two major strains (eg A/eq/Newmarket/2/93 [H3N8], A/eq/Kentucky/92 [N3H8]) have emerged due to antigenic drift (redistribution of the genome that result in genetic alteration) and antigenic drift (point mutations in the genetic code causing alterations in the glycoproteins H and N).
Natural distribution
Equine Influenza affects horses, donkeys, mules and other equines. The virus is widespread with only Iceland, New Zealand and Australia, considered to be free of the virus. The H7N7 subtype is thought to be extinct or present at very low levels. The subtype H3N8 appears to be a mutated bird flu outbreak virus.An participation of a modified H3N8 subtype (designated A/eq/Jilin/89 [H3N8]) occurred in China in 1989. Added morbidity (80%) and mortality (20%) were observed. Other major subtype H3N8 outbreaks have occurred worldwide, including in Trinidad (1979), Argentina (1985), South Africa (1986) and Jamaica (1989). Most of the confirmed outbreaks occurred at racetracks, and as a result, the activities of the races were suspended for long periods of time, resulting in marked economic losses. In Nepal, the disease was reported in the year 1988/1989.Same Nepalganj outbreak years of illness have occurred in many parts of India too. Australia recently registered the outbreak of the disease, in part, many of the countries. As mules and horses are being used as draft animals, remote in hand, many countries. These days everyone is talking about the bird flu how much we are aware it.
Transmission
Equine influenza is spread via aerosols of 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 in 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 the virus in their secretions breathing during the incubation period, and continue to excrete the virus for four to five days after clinical signs are observed. It is also possible that a infected animals shed the virus for 7-10 days after the animal appeared to recover. Viral shedding is believed to reach its peak during the first 24 to 48 hours the animal is febrile. Infectious droplets can spread up to 50 meters. Virtually 100% of the horses that are prone to be infected. Almost 20% infected horses show no clinical signs of disease, but still shed virus and can transmit the infection, morbidity and mortality
Morbidity associated with EI in naïve population is estimated at 60 to 90%, to date, mortality in horses with confirmed infection has ranged from 1% to 20%. The higher mortality rates seen in foals, malnourished or immunocompromised horses and burros.
. Clinical signs —
Equine influenza virus causes the disease clinical upper respiratory tract. The virus spreads rapidly, and naïve or immunocompromised horses have a higher risk of developing the disease. Signs Clinical features are fever, cough, serous to mucopurulent nasal discharge, depression, muscle pain, anorexia, and enlarged lymph nodes. Colic (pain abdominal) and edema of the legs and scrotum have also been observed with influenza infection.In the absence of secondary complications of healthy adult horses usually recover EI within a week or two, however, coughing may persist for a longer period. Colts youth lack sufficient maternal antibodies are at risk of develop rapidly fatal viral pneumonia. The recovery of IE is complicated and prolonged by the development of secondary bacterial infections. Deaths have been reported as caused by secondary bacterial pneumonia and pleurisy. Purple hemorrhagic life-threatening immune-mediated disease, has also developed secondary to infection of EI. Fatal interstitial myocarditis (inflammation of heart muscle) can occur during or after infection.
Diagnosis
A tentative diagnosis of EI is often based on clinical signs. The diagnosis can be confirmed by the detection of virus in samples from the nose swabs. Traditionally, the diagnosis of EI was confirmed by inoculation of embryonated chicken eggs with material from nasopharyngeal swabs and then isolate the virus. Alternatively, paired acute and convalescent serum samples can be presented for inhibition of the hemagglutinin of EI, an increase of four times or more in antibody titer is for the diagnosis of IE. Other diagnostic methods include reverse transcriptase chain reaction (PCR) and nested reverse transcription chain reaction of polymerase. Reverse transcription PCR is more rapid and sensitive serological tests, and more rapid and specific sample isolation.Preferred virus for diagnostic tests are fresh nasopharyngeal swabs that are sent overnight to room temperature. If you want to do serological testing with 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
For viral diseases, treatment is largely supportive. Proper management and nutrition can help the horses to mount an effective immune response. Rest reduce viral shedding. Because the removal rates of the trachea (an indication of the capacity of the airways to remove particles, mucus and infectious organisms) are reduced to one month after infection, the rest is also recommended after resolution of clinical signs. Antipyretics It is recommended for horses with a fever over 105 ° F (40.5 C) and / or severe depression and anorexia. Pneumonia in most affected horses respond best to a combination broad spectrum bactericidal and maintaining hydration through intravenous fluids.
Prevention and control
The inactivated vaccines administered by intramuscular and intranasal are commercially available for prevention of influenza in the horse. The American Association of Equine Professionals (AAEP) has developed guidelines for outbreaks of infectious diseases, these guidelines state that the administration of flu vaccine to booster apparently healthy animals in the face of an outbreak may be valuable. For animals that were vaccinated before the outbreak, the use of a modified live intranasal vaccine may be preferable, because it can induce protective immunity in 5 days. The EI virus is an enveloped virus that appears to be easily killed by common disinfectants used in facilities veterinary medicine, such as quaternary ammonium compounds, bleach solutions and 10%. The most common source of infection is the introduction of a new animal in the herd, therefore, isolation of newly acquired animals is recommended. Isolation protocols should be rigorously applied to horses with signs of respiratory disease, and must be kept for 21 days after the last horse appears to recover from infection. Clothing, equipment, surfaces and hands should be washed and disinfected after exposure to horses known or suspected to be infected.

About the Author

Dr.Kedar Karki M.V.St. Preventive Veterinary Medicine