Think your dog may have a bad case of Infectious Tracheobronchitis? You may not be dealing with a run-of-the-mill kennel cough. Canine Influenza virus, or CIV, has become an important emerging infectious disease in dogs. The virus responsible for the condition is H3N8 influenza A virus.

According to a University of Florida study, the canine flu has been circulating in the United States canine population at least since 1999. Even though the canine flu was first identified in 2004, antibodies to the influenza A H3N8 virus date back to 1999 and possibly earlier. The first cases of canine influenza were reported among racing greyhounds in the state of Florida. Since 2004, outbreaks of CIV have been reported in at least 27 states.

The canine influenza virus is closely related to equine (horse) viruses. The canine flu is believed to have originated from the introduction of an equine influenza into the canine population. Now the virus is easily transmitted from dog to dog. The virus may also undergo airborne transmission through coughing or sneezing and may additionally be spread by contaminated fomites. Infected bedding, contaminated food, grooming equipment, or infected clothing from caretakers all serve to harbor the virus. The virus is believed to survive 48 hours in the environment. Most outbreaks to date have been limited to shelters or kennels. Outbreaks among individual pets have not yet been described.

Viral shedding begins as early as two days following exposure to the virus, and peaks around four days following exposure. Viral shedding persists for 7 to 10 days. Dogs may shed virus before the onset of clinical signs. Infected dogs will typically discontinue shedding virus ten days to two weeks following infection.

Morbidity rates may run as high as 90% in exposed animals since there is little natural immunity in the greater canine population. It may be helpful in distinguishing canine influenza from the more commonly seen infectious tracheobronchitis, especially in animals vaccinated for Bordetella bronchiseptica, parainfluenza, and canine adenovirus.

Canine influenza was initially reported as a peracute hemorrhagic pneumonia with a 36% mortality rate. Fortunately, hemorrhagic pneumonia is a rarely seen clinical syndrome with canine influenza. More commonly, canine influenza will develop clinically as a lower respiratory disease often confused with infectious tracheobronchitis, or kennel cough. Clinical signs include an elevated temperature, mucopurulent nasal discharge, and a productive cough. These animals are often lethargic and anorexic. Dogs with significant respiratory disease are likely to suffer from secondary opportunistic bacterial pneumonias and sinus infections. When bronchopneumonia develops, a 10% mortality rate is characteristic.

Treatment consists of broad spectrum antibiotics for complicating bacterial pneumonias. Theses animals may also benefit from nebulization, oxygen therapy, and supportive care. The efficacy of an antiviral drug, oseltamivir or Tamiflu®, available from Roche, has yet to be determined but may prove to be beneficial when treating individual cases.

Conformation of an outbreak may be obtained by demonstrating the presence of the virus through virus isolation or by paired serologic tests, which test for antibodies to the virus. Ideally, two serum samples should be submitted, with the first being collected one week after the onset of clinical signs and the second 2 to 3 weeks later. A fourfold increase in the antibody titer suggests that there has been a recent infection. Other possible confirmatory tests include ELISA-based antigen and PCR-based tests.

There is no currently licensed vaccine for the prevention of canine influenza.

Kennels, hospitals, and shelters need to be depopulated and thoroughly disinfected in order to minimize further risk of exposure.

References:
Basilio, Paul. “CIV on the Rise”. Veterinary Forum. August 2008. P. 8.
Bonagura, John and David Twedt, Editors. Kirk’s Current Veterinary Therapy XIV. Saunders/Elsevier. 2009. Pp. 1291-1294.
“Canine Flu is Traced to 1999.” DVM Newsmagazine. April 2008. P. 16S.