martes, 30 de marzo de 2010

Influenza Virus Transmission from Horses to Dogs, Australia

EID Journal Home > Volume 16, Number 4–April 2010

Volume 16, Number 4–April 2010
Influenza Virus Transmission from Horses to Dogs, Australia
Peter D. Kirkland, Deborah S. Finlaison, Ellie Crispe, and Aeron C. Hurt
Author affiliations: Elizabeth Macarthur Agricultural Institute, Menangle, New South Wales, Australia (P.D. Kirkland, D.S. Finlaison); Warwick Farm Equine Centre, Warwick Farm, New South Wales, Australia (E. Crispe); and World Health Organization Collaborating Centre for Reference and Research on Influenza, North Melbourne, Victoria, Australia (A.C. Hurt)

Suggested citation for this article

During the 2007 equine influenza outbreak in Australia, respiratory disease in dogs in close contact with infected horses was noted; influenza (H3N8) virus infection was confirmed. Nucleotide sequence of the virus from dogs was identical to that from horses. No evidence of dog-to-dog transmission or virus persistence in dogs was found.

Respiratory disease in dogs caused by type A influenza virus was first noted in racing greyhounds in Florida in January 2004 (1). This subtype H3N8 virus has a presumptive but unidentified equine origin. The geographic extent of infection in racing greyhounds and in pet dogs suggest that this virus has become enzootic to the United States (1,2).

In the United Kingdom, pneumonia in dogs and influenza (H3N8) virus have been retrospectively linked, and subtype H3N8 infections have been identified serologically in dogs likely to have been in close contact with horses during the 2003 outbreak of equine influenza (3,4). A 78-bp segment of the hemagglutinin (HA) gene identified in dogs with pneumonia had complete homology with local equine strains (3). Unlike the situation in the United States, no evidence of continuing circulation of an influenza virus of equine origin in the canine population has been found in the United Kingdom.

In Australia, in late 2007, an outbreak of equine influenza virus (EIV) infection occurred in horses. During this outbreak, respiratory disease was noted in dogs of various ages and breeds that were kept near infected horses. Investigations were undertaken to exclude influenza virus infection.

The Study
The first reported case was in a dog near a large stable; the dog became inappetant and lethargic and had had a slight nasal discharge and a persistent cough for several days. Over the next 2–3 weeks, dogs in or near stables with infected horses, including dogs whose owners were handling infected horses or dogs (n = 6) that were only housed with infected dogs, were examined. Samples were also collected from dogs kept with horses at 5 other locations 20–60 km from the first case. Of the 40 dogs, examined, 10 had clinical signs consistent with influenza (anorexia, lethargy, and, for some, a harsh cough that persisted for several weeks). All affected dogs recovered.

Nasal swabs and serum were collected from each of the 40 dogs; 23 were seropositive according to influenza type A blocking ELISA (5) and hemagglutinin inhibition (HI) assay (5) using A/equine/Sydney/2007 virus as antigen (Table). HI titers were 16–256 (geometric mean 122). Results were discordant for 5 dogs: for 2, HI titer was high but ELISA results were negative; for 3, ELISA results were positive but HI titer was negative. These discrepancies may have been resolved had later sampling been possible. Convalescent-phase serum samples were collected 14–16 days later from 26 of the dogs; seroconversion was noted for 4 of the 5 dogs with discordant ELISA and HI results. Testing of 19 dogs 2 years later showed no change in HI titer, although ELISA results were negative for each. Each seropositive dog had been in close proximity to EIV-infected horses but not always in direct contact. No evidence of lateral transmission was found for dogs that did not have contact with horses.

Nasal swabs from 1 clinically healthy dog had a positive result in an influenza A real-time reverse transcription–PCR assay (5) on 2 consecutive days. The dog remained clinically healthy and was seropositive (titer 64) on day 16 after the first positive swab was collected. Attempts to isolate virus from these swabs were unsuccessful.

Nucleic acid sequencing was conducted for the HA, neuraminidase (NA), and matrix (M) genes amplified by PCR from the RNA purified from 2 samples from this dog (A/canine/Sydney/6525/2007 and A/canine/Sydney/6692/2007) and from a nasal swab from an infected horse (A/equine/Sydney/6085/2007) in the same stable (GenBank accession nos. GU045761–GU045769). Sequences were aligned with representative sequences from GenBank by using Clustal W ( before phylogenetic trees with bootstrapping were generated (n = 1,000; random seed n = 111) with MegAlign (Lasergene; DNAStar, Madison, WI, USA). Complete nucleotide homology was found for each of the HA, NA, and M gene sequences from the 2 dogs and the sequence from the infected horse in the same stable (A/equine/Sydney/6085/2007).

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Suggested Citation for this Article
Kirkland PD, Finlaison DS, Crispe E, Hurt AC. Influenza virus transmission from horses to dogs, Australia. Emerg Infect Dis [serial on the Internet]. 2010 Apr [date cited]

DOI: 10.3201/eid1604.091489

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