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Information from the Baker Institute on Canine Influenza

Background:

Influenza viruses are important pathogens of mammals and birds. The main reservoir of influenza A viruses (fig.1) is in aquatic birds. Migrating birds carry the virus between continents and play a key role in the process of virus evolution. For many years it has been known that other animals susceptible to influenza include humans, domestic fowl, pigs, horses, mink, ferrets, seals, and whales. As of late, an equine influenza virus has spread to dogs where they are causing new diseases.

Virion Properties and Replication:

Fig. 2 avian hemagglutinin (courtesy of www.accessexcellence.org.)

The viruses are pleomorphic enveloped particles that may be spherical or filamentous, 80-130nm in diameter. Virions are enveloped and surrounded by peplomers, and their genomes are made up of 8 segments of negative sense RNA and have two important surface proteins -- hemagglutinin (HA) (fig. 2) which bind to sialic acid on the surface of cells, and neuraminidase (NA) (fig. 3) that cleaves the sialic acid allowing the release of the bound virus. The viruses are sensitive to heat, acid, and lipid solvents and detergents. Viruses replicate in the nucleus, but bud at the plasma membrane.

Prevention and Control:

Fig. 3 neuraminidase ribbon diagram (courtesy of answers.com)

Prevention is the best approach to controlling equine influenza. Early recognition and immediate isolation of sick horses reduce exposure of other horses to the virus. Any training or work done by individual horses should be stopped when clinical signs are recognized in that animal. New horses brought into a stable or farm should be quarantined for up to 6 weeks to avoid the possibility of introducing equine influenza or other viruses. Control involves isolation and vaccination. Stables and courses where outbreaks have occurred may be put under quarantine for 4 weeks.

Vaccination is done with inactivated vaccine containing A/equine (H7N7) and A/equine (H3N8), with the latter preferably containing viruses that match the current field viruses. Inactivated vaccines are given with adjuvant, and the number of vaccinations depends on the risk — some race horses are vaccinated every 3-9 months. Vaccines may protect animals from clinical disease but not prevent transmission. Modified live intranasal vaccines are available (Flu Avert), which appear to be more effective.

(Influenza A viruses are named by their host, geographic origin, strain number, and year number as well as the HA and NA types. For example, influenza virus A/equine/Miami/1/63)

Canine Influenza Virus:

Canine influenza virus or 'dog flu' is a new disease in dogs caused by a H3N8 influenza virus strain. It was first observed in greyhounds in Florida in January 2004. Retrospective testing of stored viruses showed that there were positive samples in greyhounds in 2000, suggesting that the virus had been circulating in the greyhounds since at least that time. In the January 2004 outbreaks, dogs had fevers of 39.5°C - 41.5°C (103.1°F - 106.7°F), a soft gagging cough for 10-14 days, and then recovery. A smaller proportion of dogs died suddenly with hemorrhage from the nose and mouth.

Multiple outbreaks of respiratory disease were subsequently seen at greyhound race tracks in many regions of the country, including Florida, Texas, West Virginia, Colorado, Iowa, Kansas, Massachusetts, and Wisconsin. Subsequently, respiratory disease was also observed in pet household and shelter dogs in Florida, in animals with ages between 3 months and 9 years. Another outbreak occurred in household dogs after boarding at a veterinary clinic which contained a dog from a shelter with respiratory disease. Some of the affected dogs developed severe signs of the virus, including temperatures of 40°C - 41°C and pneumonia.

The virus isolated from the dogs showed the closest antigenic cross-reactivity in HA inhibition assays with the H3 of equine influenza, and the closest genetic relationship was with recent isolates of H3N8 equine influenza. In June 2004 and in early 2005 approximately 100% of the greyhounds at tracks in Florida were serologically positive for H3 influenza, with evidence of active seroconversion suggesting that there was active infection underway. Many dogs with respiratory disease in Florida proved to be seropositive for the virus infection, and there were also infections in other regions of the country, including New York.

At present there are no licensed vaccines for dogs, but those are in active development.

Clinical Disease and Pathogenesis:

Fig 4. respiratory epithelial cells (courtesy of Keele University

The pathogenesis of the canine disease is still being examined, but it is likely to be similar to that seen for other influenza viruses. In those cases, the virus primarily infects the epithelial cells (fig. 4) of the respiratory tract, resulting in a fever lasting 4-5 days, with reddening of the nasal mucosa and serous or mucopurulent discharge. Secondary bacterial infections can occur — leading to brochopneumonia and purulent exudates. Normally, the disease is self-limiting and complete recover occurs in 2-3 weeks.

Immunity is likely to be partly antibody mediated, with an important role for secretory IgA at the epithelial surfaces, and IgG prevents secondary spread. Cellular immunity (T cells) is important in clearing virus-infected cells.

Diagnosis:

Can be diagnosed based on symptoms, although it can be confused with other causes of kennel cough such as Bordetella brochiseptica. Nasal swabs taken early in the course of the disease can be used for virus isolation. Virus can be detected by hemagglutination. Isolates are indentified by specific reference to antisera adn HA inhibition assays. Serological diagnosis can be performed by hemagglutination inhibition (HI) assays with paired sera from acutely infected and convalescent dogs, looking for an increase in specific titer.

Epidemiology and Control:

Influenza viruses are highly contagious and spread rapidly. Virus is often shed early after infection before they develop clinical signs, and also are shed for several days after clinical signs begin. The viruses are clearly transmitted by close contact and by housing animals in shelters, boarding kennels, and the like. The shipment of greyhounds to tracks likely helped in the widespread dispersal of the virus in the USA.