Orthomyxoviridae, Type A (based on core proteins), Subtype H3N8 (based on surface glycoproteins); strains identified by geographic origin, host, year of isolation, and serial number.
Etymology
Greek ' orthos' (straight) and ' myxa' (mucus).
Distribution
Serologic evidence indicates Influenza Virus H3N8 appeared in dogs in 2000/2001. It was first identified in 2004 in racing Greyhounds in Florida.
It has also been identified in many states in the USA with greyhound racetracks. Distribution in pet dogs is currently restricted to less than a dozen states.
Significance
Associated with respiratory tract disease; may resemble kennel cough ; has the potential to contribute to or cause severe hemorrhagic pneumonia.
It has been identified in pet dogs and shelter dogs in addition to dogs at racetracks.
Envelope glycoproteins hemagglutinin (H) and neuraminidase (N) important in antigenicity and virulence. These proteins are important as targets for antibodies following exposure or vaccination when one becomes available.
Taxonomy
Orthomyxovirus Type A, subtype H3N8 (from horses).
Tolerances
Temperature
Stable at -70C for long periods; stable at cool ambient temperatures (0-15C) for days, less stable at higher environmental temperatures (25-35C).
Humidity
Stable at high humidity.
Other
Sensitive to detergents (lipid solvents).
Stable at pH 7-8.
Development
Growth
Replicates in epithelia of respiratory tract of dogs; spread from dog to dog via aerosol droplets and fomites.
Longevity
Can persist in the environment for hours to days; may last longer in humid, cool environments.
Obligate parasite of dogs; survives for hours to days outside of the dog.
Lifecycle
Replicates in respiratory tract epithelia; shed in aerosol droplets.
Transmission
Spread dog-to-dog via aerosol, direct transmission, and indirect spread via fomites.
Pathological effects
Because this is a new virus in dogs, all dogs are immunologically naive and susceptible to infection. Approximately 20% of dogs will not develop clinical signs following infection; most will experience mild disease. Most severe disease is seen in young or those with secondary bacterial infections.
Infection and replication in respiratory epithelia leads to the destruction of these cells. Resultant inflammatory response contributes to tissue damage. Secondary infection with bacteria may occur, and may contribute to more severe disease.
Incubation period of 2-5 days; virus is shed from the respiratory tract for approximately one week following appearance of clinical signs.
Other Host Effects
Most affected dogs present with fever and moist cough that may persist for two weeks or longer. It is nonresponsive to antibiotics. Some dogs will exhibit a purulent nasal discharge that is usually due to secondary bacterial infection. A small percentage of dogs may experience more severe disease with evidence of pneumonia, including high fever, labored breathing, and evidence of lung consolidation on radiographs. Persistent cough is indicative of damaged respiratory epithelium and not of continual virus shedding.
Control
Control via animal
Currently, no vaccine is commercially available.
Infected dogs should be strictly isolated.
Control via chemotherapies
Supportive care, including maintenance of hydration.
Antibiotics if secondary bacterial infection is suspected; cases with pneumonia should use broad-spectrum antibiotics.
Influenza antivirals for use in humans are not approved for use in dogs; according to the AVMA, veterinarians who use approved drugs in a manner that is not in accord with approved label directions (eg 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).
Control via environment
Routine recommendations for hygiene should be applied for canine influenza virus; routine disinfection will inactivate the virus. Hand washing after handling dogs, disinfection of equipment and supplies such as bowls, and avoiding aerosolization during cleaning are recommended.
Nasal swabs, tracheal wash, lung post mortem for virus detection.
Specimen storage
Refrigerate.
Transport of samples
Ship on cold packs; ship serum by 2-day, samples for virus detection generally overnight.
Isolation
Virus may be isolated from nasal swab, tracheal wash, or lung tissue if collected early in the infection, generally within 48 hours of onset of signs.
Field diagnosis
Clinical signs, history of exposure to dogs with respiratory disease, nonresponsive to antibiotics; must rule out canine parainfluenza , canine adenovirus , canine distemper , mycoplasma , and Bordetella bronchiseptica.
Laboratory diagnosis
Virus detection - isolation may take 1-2 weeks; immunoassays including immunofluorescence and ELISA for type A influenza; PCR ; PCR most sensitive; virus detection assays may be unrewarding, especially if not in the acute phase.
Serology - since dogs are not currently vaccinated, presence of antibodies indicates exposure; paired samples with evidence of rising titer indicate active infection and are diagnostic.
Crawford P C, Dubovi E J, Castleman W I, Stephenson I, Gibbs E P J, Chen L, Smith C, Hill R C, Ferro P, Pompey J, Bright R, Medina M J, Influenza Genomics Group, Johnson C M, Olsen C S, Cox N J, Klimov A I, Katz J M & Donis R O (2005) Transmission of Equine Influenza Virus to Dogs.Science310 (5747), 482-485 PubMed.
Edward J Dubovi PhD, Professor of Virology, Director-Virology Section, Department of Population Medicine and Diagnostic Science, College of Veterinary Medicine, Cornell University, Ithaca NY 14853, USA.
Melissa Kennedy DVM PhD DipACVIM , Department of Comparative Medicine, University of Tennessee, PO Box 1071, Knoxville, TN 37901-1071, USA.
