Since its initial identification in Mexico and the United States, concerns have been raised that the novel H1N1 influenza virus might cause a pandemic of severity comparable to that of the 1918 pandemic. In late April 2009, viruses phylogenetically related to pandemic H1N1 influenza virus were isolated from an outbreak on a Canadian pig farm. This outbreak also had epidemiological links to a suspected human case. Experimental infections carried out in pigs using one of the swine isolates from this outbreak and the human isolate A/Mexico/InDRE4487/2009 showed differences in virus recovery from the lower respiratory tract. Virus was consistently isolated from the lungs of pigs infected with A/Mexico/InDRE4487/2009, while only one pig infected with A/swine/Alberta/OTH-33-8/2008 yielded live virus from the lung, despite comparable amounts of viral RNA and antigen in both groups of pigs. Clinical disease resembled other influenza virus infections in swine, albeit with somewhat prolonged virus antigen detection and delayed viral-RNA clearance from the lungs. There was also a noteworthy amount of genotypic variability among the viruses isolated from the pigs on the farm. This, along with the somewhat irregular pathobiological characteristics observed in experimentally infected animals, suggests that although the virus may be of swine origin, significant viral evolution may still be ongoing.

Epidemiologic, serologic, and molecular phylogenetic methods were used to investigate an outbreak of highly pathogenic avian influenza on a broiler breeding farm in Saskatchewan, Canada. Results, coupled with data from influenza A virus surveillance of migratory waterfowl in Canada, implicated wild birds as the most probable source of the low pathogenicity precursor virus.

The 2009 pandemic H1N1 (pH1N1), of apparent swine origin, may have evolved in pigs unnoticed because of insufficient surveillance. Consequently, the need for surveillance of influenza viruses circulating in pigs has received added attention. In this study we characterized H1N1 viruses isolated from Canadian pigs in 2009. Isolates from May 2009 were comprised of hemagglutinin and neuraminidase (NA) genes of classical SIV origin in combination with the North American triple-reassortant internal gene (TRIG) cassette, here termed contemporary SIV (conSIV) H1N1. These conSIV H1N1 viruses were contiguous with the North American αH1 cluster, which was distinct from the pH1N1 isolates that were antigenically more related to the γH1 cluster. After the initial isolation of pH1N1 from an Alberta pig farm in early May 2009, pH1N1 was found several times in Canadian pigs. These pH1N1 isolates were genetically and antigenically homogeneous. In addition, H1N1 viruses bearing seasonal human H1 and N1 genes together with the TRIG cassette and an NA encoding an oseltamivir-resistance marker were isolated from pigs. The NS gene of one of these seasonal human-like SIV (shSIV) H1N1 isolates was homologous to pH1N1 NS, implicating reassortment between the two strains. Antigenic cross-reactivity was observed between pH1N1 and conSIV but not with shSIV H1N1. In summary, although there was cocirculation of pH1N1 with conSIV and shSIV H1N1 in Canadian pigs after May 2009, there was no evidence supporting the presence of pH1N1 in pigs prior to May 2009. The possibility for further reassortants being generated exists and should be closely monitored.

The first North American outbreak of highly pathogenic avian influenza (HPAI) involving a virus of Eurasian A/goose/Guangdong/1/1996 (H5N1) lineage began in the Fraser Valley of British Columbia, Canada in late November 2014. A total of 11 commercial and 1 non-commercial (backyard) operations were infected before the outbreak was terminated. Control measures included movement restrictions that were placed on a total of 404 individual premises, 150 of which were located within a 3 km radius of an infected premise(s) (IP). A complete epidemiological investigation revealed that the source of this HPAI H5N2 virus for 4 of the commercial IPs and the single non-commercial IP likely involved indirect contact with wild birds. Three IPs were associated with the movement of birds or service providers and localized/environmental spread was suspected as the source of infection for the remaining 4 IPs. Viral phylogenies, as determined by Bayesian Inference and Maximum Likelihood methods, were used to validate the epidemiologically inferred transmission network. The phylogenetic clustering of concatenated viral genomes and the median-joining phylogenetic network of the viruses supported, for the most part, the transmission network that was inferred by the epidemiologic analysis.

Bluetongue is a non‐contagious, haemorrhagic, Culicoides‐borne disease of ruminants. The causative agent, bluetongue virus (BTV), is a member of the Orbivirus genus of the Reoviridae family. So far, 26 BTV serotypes have been identified worldwide. The global distribution of bluetongue has been expanding, and rapid detection of BTV, preferably in the field, is critical for timely implementation of animal movement restrictions and vector control measures. To date, many laboratory‐based, molecular assays for detection of BTV have been developed. These methods require the samples to be shipped to a central laboratory with sophisticated instruments and highly skilled technicians to perform the assays, conduct analyses and interpret the results. Here, we report the development and evaluation of a rapid, portable, user‐friendly, pan‐BTV reverse transcription‐insulated isothermal polymerase chain reaction (RT‐iiPCR) assay that can potentially be used in low‐resource field conditions. The total length of the assay was <60 min, and at the end of the assay, the results were automatically displayed as ‘+’ or ‘−’ without the need for data interpretation. The RT‐iiPCR assay detected 36 BTV isolates and two in vitro transcribed RNA samples representing all 26 BTV serotypes. The assay did not cross‐react with other animal viruses tested, including two closely related orbiviruses. The analytical sensitivity of the assay was as low as nine copies of in vitro transcribed double‐stranded BTV RNA. Analysis of BTV‐infected whole blood samples showed that the BTV RT‐iiPCR assay was as sensitive as real‐time RT‐PCR. The assay can potentially be used for rapid screening of animals for BTV in routine diagnostics and for monitoring bluetongue outbreaks both in ruminants and in Culicoides vectors in the field and in the laboratory.

All reports of avian influenza virus infections in poultry and isolations from wild bird species in Canada, the United States, and Mexico between 2009 and 2011 involved low pathogenic avian influenza. All three countries reported outbreaks of low pathogenic notifiable avian influenza in poultry during this period. The reports involved outbreaks of H5N2 among commercial turkeys in Canada in 2009 and 2010; outbreaks of H5N3 in turkeys in 2009, H5N2 in chickens in 2010, H7N3 in turkeys in 2011, and H7N9 in chickens, turkeys, geese, and guinea fowl in 2011 in the United States; and multiple outbreaks of H5N2 in chickens in Mexico in 2009, 2010, and 2011. Outbreaks of pandemic H1N1 infections in turkey breeder flocks were reported in Canada in 2009 and in the United States in 2010. Active surveillance of live bird markets in the United States led to the detection of H2, H3, H4, H5, H6, and H10 subtypes. Despite the fact that wild bird surveillance programs underwent contraction during this period in both Canada and the United States, H5 and H7 subtypes were still detected.