Abstract
In August 2015, Malaysia experienced an outbreak of acute respiratory disease in racehorses. Clinical signs observed were consistent with equine influenza (EI) infection. The index cases were horses recently imported from New Zealand. Rapid control measures, including temporary cancellation of racing, were implemented to minimize the impact of the outbreak. By November, the disease outbreak was resolved, and movement restrictions were lifted. The aim of this study was to confirm the clinical diagnosis and characterize the causal virus. A pan-reactive influenza type A real-time RT-PCR was used for confirmatory diagnosis. Antigenic characterization by haemagglutinin inhibition using a panel of specific ferret antisera indicated that the causal virus belonged to clade 1 of the H3N8 Florida sub-lineage. The genetic characterization was achieved by the whole genome sequencing of positive nasal swabs from clinically affected animals. Pylogenetic analysis of the haemagglutinin (HA) and neuraminidase (NA) genes demonstrated ≥99% homology with several EI strains that had recently circulated in the USA and Japan. The antigenic and genetic characterization did not indicate that the current World Organisation for Animal Health (OIE) recommendations for EI vaccine composition required modification.
Highlights
Equine influenza virus (EIV) can cause acute respiratory disease in horses, and lead to economically punitive disruptions within the equine industry [1,2,3]
This equine influenza (EI) outbreak commenced in August 2015
The samples collected between the 7 September and the 8 October from horses at the three turf clubs tested negative for EIV, respiratory disease was reported at Selangor in late September
Summary
Equine influenza virus (EIV) can cause acute respiratory disease in horses, and lead to economically punitive disruptions within the equine industry [1,2,3]. EIV contains an octameric segmented genome encoding 12 proteins. Evolution of EIV typically occurs by mutations occurring within the antigenic epitopes of the strongly immunogenic HA protein, resulting in the evasion of the host immune response [4,5]. All 12 proteins are involved in EIV proliferation and host interaction, and should be taken into account to achieve a thorough analysis. The H3N8 subtype of EIV has been in persistent circulation in endemic countries since the 1960s, and a gradual genomic evolution in the interim years has resulted in several antigenically distinct lineages. In the 1990s, the American lineage further drifted antigenically into the South America, Kentucky and Florida sub-lineages [7]. In the early 2000s, the Florida sub-lineage
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
