Canine influenza A H3N8 Canine influenza A subtype H3N8 was initially noted as a respiratory syndrome that affected racing greyhounds in 2004. (Crawford et al., 2010) During this initial disease outbreak, large numbers of affected greyhounds died peracutely; affected dogs showed evidence of significant respiratory pathology and hemorrhage. (Iowa State University, 2022) Between 2003 and 2005, outbreaks of respiratory disease were observed at 20 different greyhound racetracks in eight states. (Crawford, 2005) By 2010, canine influenza virus had spread to the pet dog population and had been identified in 30 states. The virus quickly became enzootic in some communities, most notably Florida, Pennsylvania, New Jersey, New York, and Colorado. (Crawford, 2006) (Dubovi, 2008) At the start of the initial 2004 outbreak, there was significant uncertainty regarding the origin of this virus. Even after the respiratory cases were determined to be caused by canine influenza, questions remained as to whether this was a spillover infection of equine H3N8 into greyhounds, or whether equine influenza had established itself in canines and was capable of horizontal transmission. (Moyer, 2011) Further examination of banked greyhound sera demonstrated that canine influenza H3N8 had actually been present in the racing greyhound population as early as 2000. (Moyer, 2011) Based on this information regarding Canine influenza A H3N2 In March and April 2015, an outbreak of respiratory disease captured the attention of veterinarians practicing in the Chicago area. Initially, veterinarians thought these dogs were presenting with kennel cough. However, these veterinarians soon began noting high fevers and explosive spread of illness, both of which suggested the possibility of influenza. (Fiala, 2015) Many dogs in this outbreak tested positive for influenza. However, instead of the H3N8 strain that had been previously documented and was known to be still circulating, these dogs were found to be infected with an H3N2 influenza strain of avian origin. (Richardson, 2015) In the following months, canine influenza H3N2 spread throughout the Midwest and into other areas of the United States. (American Veterinary Medical Association, 2015) Canine influenza H3N2 was originally identified in China in 2006 and was noted in South Korea in 2007. (Richardson, 2015) This virus appears to have been initially acquired from birds, and it incorporates gene segments from multiple different avian influenza viruses. (Iowa State University, 2022) Further testing has demonstrated that canine influenza H3N2 originally entered the canine population in or around 2005. Most cases reported in Asia were severe, but further testing demonstrated that a number of healthy dogs also tested positive for antibodies to H3N2. This finding led researchers to realize that a milder, subclinical form of the disease also existed, in addition to the severe form of canine influenza illness that had been previously noted. (Iowa State University, 2022) In addition to affecting dogs, canine influenza virus H3N2 has been documented to spread among felines in Asia. A feline respiratory disease outbreak in 2010 affected shelter cats that were housed with sick dogs, and canine influenza H3N2 was isolated from the lung tissues of these affected cats. (Song, 2011) Clinical signs of H3N2 canine influenza among affected shelter cats included lethargy, tachypnea, and dyspnea, although co-infection with Bordetella bronchisepti ca may have played a role in the severity of illness noted. (Iowa State University, 2022) Mortality rates
the initial appearance of canine influenza antibodies in greyhound sera, and further genetic analysis of the H3N8 strain, researchers have demonstrated that this initial canine virus derived from a single transfer of equine virus (of the Florida 1 strain) to dogs during 1999-2000. (Parrish, 2012) All cases of H3N8 canine influenza spread from this single introduction of equine influenza in racing greyhounds. The specific mechanism of introduction has not been determined. Since this initial 2004 outbreak, canine influenza H3N8 has continued to circulate in the United States canine population as a separate lineage, with no evidence of being transferred back to horses. (Parrish, 2012) (Rishniw, 2015) Experimental studies have demonstrated that the virus is no longer capable of efficient replication within horses, with naïve horses failing to acquire infections from infected dogs or experimentally infected horses. (Iowa State University, 2022) In other words, this canine influenza strain is now separate from the equine influenza strain from which it initially arose. Cases of H3N8 canine influenza are now reported sporadically throughout the United States. Outbreaks periodically occur, but these outbreaks tend to flare up and resolve relatively rapidly. (Iowa State University, 2022) of up to 40% were observed among affected cats in these shelter outbreaks. (Song, 2011) Experimental induction of canine influenza H3N2 in cats has been documented to cause less severe clinical signs. Signs associated with experimental infection include elevated rectal temperatures, nasal virus shedding, and pulmonary lesions (e.g., suppurative bronchopneumonia). (Song, 2011) Experimental studies have also induced mild clinical signs of H3N2 canine influenza in a small portion of experimentally infected ferrets; sneezing is the most common manifestation of H3N2 canine influenza in ferrets, with mild lethargy and anorexia also noted in some cases. (Iowa State University, 2022) When the H3N2 strain was detected in the United States, leading influenza researcher Edward Dubovi stated, “My concern all along was that someday this virus might make its way here. We don’t know how it happened, but it certainly could have come from a dog or a cat. There are multiple international groups who are rescuing dogs from the meat market in Korea and shipping them into the United States, and we have sketchy quarantine requirements if any at all. Restrictions on the movements of companion animals across borders are somewhat nonexistent.” (Fiala, 2015) This was speculation, however, as there was no direct evidence to confirm that the disease was introduced in this manner. (American Veterinary Medical Association, 2015) The true means by which H3N2 canine influenza was introduced to the United States will likely never be definitively determined. As of August 8, 2015, within six months of its introduction, cases of H3N2 had been confirmed in every state in the continental United States. The largest case clusters in those first six months were seen in Chicago, Atlanta, Asheville, Philadelphia, and New York City. (Cornell University College of Veterinary Medicine, n.d.) Nationwide, the numbers of positive tests peaked in early April of 2015, coinciding with the initial Chicago outbreak. (Cornell University College of Veterinary Medicine, n.d.) In any given week, however, only about 20% to 30% of submitted tests during this initial outbreak were positive
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