Influenza Viruses in Dogs
Canine influenza virus
The first outbreak of canine influenza virus (CIV) was detected in racing greyhounds in the United States of America (USA) in 2004. The virus was determined to be an influenza type A virus, subtype H3N8.
The virus’s emergence as a respiratory pathogen in dogs has been linked to the H3N8 equine influenza virus (EIV) ‘jumping’ species from equine to canine and adapting to its new host. In the USA, studies have shown that the canine H3N8 influenza virus has diverged considerably from the H3N8 EIV from which it originated. It appears to belong to a separate lineage1. More studies are being undertaken to determine the timing of this interspecies virus transfer, especially as retrospective studies provided serological evidence that CIV was already circulating in USA greyhound populations as early as 19991.
In the past few years, there has been sufficient evidence to confirm that CIV has become established in its new host and is capable of being transmitted between dogs, with such transmission being sustained. Initially thought to be confined to greyhounds, it is now considered that all dog breeds are susceptible to the virus.
After the initial outbreak of CIV in Florida, more than 10 outbreaks of the CIV have been identified, affecting over 30 states between 2004 and 2010. Most recently in September 2011, Texas experienced another outbreak, indicating that CIV is still persisting in the USA.
Other influenza viruses in dogs
Recent events and studies have demonstrated evidence of other h4 and h2 influenza viruses in dogs, suggesting that dogs may be more susceptible to influenza A viruses than previously suspected.
H3N8 – United Kingdom, Japan and Australia
Interspecies transmission of the EIV H3N8 subtype into dogs has also been demonstrated in the United Kingdom (UK), Japan and Australia during outbreaks of equine influenza in horses.
However, unlike the situations in the USA, the virus did not become established in the canine host, and there was no evidence of horizontal transmission of the influenza virus between dogs. These cases appeared to be strictly EIV infections in dogs rather than the adapted CIV infections experienced in the USA.
In 2008, UK researchers conducted a retrospective study2 following a respiratory disease outbreak in foxhounds in the UK in 2002. Antibodies to EIV H3N8 were detected in serum samples, and polymerase chain reaction (PCR) testing done on lung tissues confirmed that the virus had 100% identity with the UK’s EIV H3N8 strains. It was thought that the foxhounds were infected through aerosol spread (as they were housed near infected horses). However, the foxhounds had been fed horsemeat the week prior to clinical signs and the oral route of infection could not be ruled out. The mechanism of transmission was unclear, but the study demonstrated transmission of EIV to dogs in the UK, independent of that in the USA.
In an experiment conducted by Japanese researchers3, three dogs which were in close contact with EIV H3N8 infected horses seroconverted. Two out of the three dogs also shed virus. All dogs remained asymptomatic, but it was shown that dogs can be infected after close contact with EIV–infected horses. This finding has implications for the management of an EIV outbreak.
Following the 2007 EIV H3N8 outbreak, some dogs housed at racecourses where EIV occurred developed respiratory signs. Serum and nasal samples were collected from dogs at Warwick Farm, Rosehill and Randwick racecourses in New South Wales. Of 29 dogs exposed to infected horses, 20 showed seroconversion, and the virus was isolated from 1 sample.
Pandemic (H1N1) 2009 – China and USA
In late 2009, China and the USA confirmed cases of dogs being infected with the pandemic (H1N1) 2009 influenza virus. There was no evidence of sustained dog–to–dog transmission of the virus in these cases and it is likely that, as is the case with pigs and other animals, these isolated canine cases are due to human infections spilling over into animals.
H3N2 – South Korea and China
From May to September 2007, cases of severe respiratory disease occurred in animals at 3 veterinary clinics located 10–30 kms apart in the Kyunggi Province and one kennel located in Jeolla Province (South Korea).
Clinical signs observed included fever, cough and nasal discharge. CIV was suspected and serology, including antigen testing, was performed on samples from infected dogs. Nasal swabs were positive for three strains of an influenza virus and negative for other pathogens. Subsequent phylogenetic analysis indicated that the influenza isolates from South Korea belonged to a different cluster of Influenza A viruses than those of equine and canine influenza H3N8 viruses4.
All genes of the South Korean canine isolates were of avian influenza virus origin, and gene sequencnig found the canine isolates to be closely related to those of avian influenza virus (H3N2) from South Korea. It was concluded that the avian influenza virus H3N2 had been transmitted to the dogs at the affected kennels, but there is uncertainty as to the origin of the virus and its mode of introduction. Possible introduction pathways include feeding of uncooked minced duck or chicken meats, or direct aerosol (e.g. dogs sold in live–bird markets). Furthermore, evidence suggested that the South Korean H3N2 virus was transmitted between dogs during the outbreak (though epidemiological data were limited). Horizontal transmission of the H3N2 strain between dogs was experimentally shown in a 2009 study4. This study also indicated that there is the potential for the establishment of another influenza virus within the canine population – separate to the USA CIV H3N8. To date, the distribution of the South Korean H3N2 subtype still seems to be geographically limited and no further outbreaks have occurred.
In China, there were sporadic reports of dogs being infected by subtype H3N2 in 2006 and 2007. Analysis showed that these cases were phylogenetically close to the cases reported in South Korea5.
Currently, CIV is the only known influenza subtype circulating in dogs. It is established in dog populations in USA and outbreaks continue to occur.
The H3N2 influenza subtype in dogs still seems to be geographically isolated, and no further incidents have been reported in South Korea or elsewhere since 2007. It is nevertheless worthwhile to monitor the H3N2 subtype as it was shown experimentally that sustained transmission could occur between dogs.
As the H3N8 and H3N2 influenza subtypes were not known to have been pathogenic in dogs previously, most dogs are na?ve and do not possess innate immunity. This na?ve population means that many dogs are susceptible to these subtypes and these viruses could easily spread from one dog to another. Virtually all dogs are susceptible regardless of age and attack rates of 60 to 80% are not unusual.
Studies done after the 2004 USA CIV H3N8 outbreak concluded that the CIV virus is not breed specific6; the virus spreads efficiently between dogs; and, the infection can often be subclinical.
Clinical signs, diagnosis and management
Incubation period and clinical signs
The incubation period for CIV ranges from two to five days before clinical signs appear, and infected dogs shed virus for four to ten days from the initial day of clinical signs. Nearly one in five dogs remain asymptomatic and are silent shedders and spreaders. In dogs that do exhibit clinical signs, two forms of clinical syndromes occur:
- a mild form with a soft, moist cough that persists for 10 to 21 days or longer despite therapy with antibiotics and cough suppressants. Some dogs have a "kennel cough"–like cough
- a more severe form with high fever and pneumonia. Pneumonia may be due to a secondary bacterial infection. Greyhounds can also have haemorrhagic pneumonia. Case fatality is reported between 1 and 8%, mostly from pneumonia.
To date, the most reliable method to diagnose CIV infection is by antibody detection or demonstration of viral nucleic acid using a PCR test on pharyngeal or nasal swabs. Antigen tests have recently become available, but have not always been useful in detecting the virus, probably because the amount of virus shed is low.
Control and management
Treatment is mainly supportive, based on severity of clinical signs. There is no specific antiviral treatment for CIV, but secondary bacterial infections should be treated with antibiotics and, accordingly, with other supportive care.
Merck Animal Health (USA) has manufactured a vaccine (Nobivac® Canine Flu H3N8) to help control the spread of CIV. The vaccine is only available for use within the USA. It is effective in significantly reducing severity of the disease, associated secondary infections and viral shedding.
Apart from vaccination, hygiene and strict biosecurity control measures (e.g. isolation of sick dogs, wearing disposable clothing) especially in shelters or kennel situations, are still paramount in managing and controlling the spread of CIV.
Implications for Australia
Currently, CIV remains geographically isolated, and despite the prevalence of susceptible hosts, the spread of CIV is reasonably contained. Evidence to date does not indicate any zoonotic potential with CIV. With global animal movements, CIV could potentially enter Australia through importation of animals, but this risk is being managed by current quarantine arrangements.
As canine, and other, influenzas are important emerging infectious diseases, and as influenza viruses have the potential to ‘jump’ species, veterinarians should remain vigilant in examining all influenza–like illnesses such that management measures can be put in place rapidly if needed. Veterinarians should consider influenzas as part of their differential diagnoses for respiratory disease and coughing dogs.
For more information contact the Emergency Animal Disease Watch Hotline on 1800 675 888.
Office of the Chief Veterinary Officer
Australian Government Department of Agriculture, Fisheries and Forestry
3. Yamanaka T, Nemoto M, Tsujimura K, Kondo T, Matsumura T. Interspecies transmission of equine influenza virus (H3N8) to dogs by close contact with experimentally infected horses. Veterinary Microbiology 2009 Nov 18; 139(3–4):351–355.