Submitted to: Western Poultry Disease Conference
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2014
Publication Date: 3/23/2015
Citation: Kapczynski, D.R., Pantin Jackwood, M.J., Spackman, E., Suarez, D.L., Swayne, D.E. 2015. Update on H7N3 highly pathogenic avian influenza in Mexico [abstract]. In: Proceedings of the Western Poultry Disease Conference, March 23-25, 2015, Sacramento, California. CDROM.
Technical Abstract: In June of 2012, an H7N3 highly pathogenic avian influenza (HPAI) virus was identified as the cause of a severe disease outbreak in commercial laying chicken farms in Jalisco, Mexico. This region is responsible for approximately 55% of the eggs produced in Mexico, and infection with this virus severely affects the reproductive tract resulting in misformed or shell-less eggs. The HPAI virus had high sequence similarity of greater than 97% to wild bird viruses from North America in all eight gene segments examined indicating a wild bird source for the low pathogenic (LP) to highly pathogenic (HP) outbreak. Because of high sequence similarity to the HPAI virus, the Mexican government immediately identified a 2006 Cinnamon Teal H7N3 (A/CT/2006) isolate to use as part of a vaccine control program. Originally, three commercial laboratories were authorized to produce the inactivated vaccine, which was distributed by the Mexican authorities. At the end of 2012, with no new outbreaks reported, there were hopes of eradication. However, by early 2013, multiple Mexican states reported new outbreaks of the virus. Many of the new outbreaks were from states outside of Jalisco, indicating the virus had escaped the original containment zone. In 2014, further H7N3 HPAI outbreaks were reported in Guanajuato, indicating the virus continues to persist. The government has subsequently increased the number of commercial vaccine companies authorized to produce the vaccine to approximately ten. Currently, vaccination schedules for layer type birds in these H7N3 affected regions range from 6-15 individual injections over the life of the bird, with swab samples submitted each month for flock surveillance testing. Thus, it does not appear that this virus will be eradicated from the region and represents a clear and present danger to the U.S. poultry industry. Research performed on the H7N3 HPAI virus at the Southeast Poultry Research Laboratory (SEPRL) has demonstrated that the hemagglutinin gene of the HPAI virus contained a 24 nucleotide insert at the hemagglutinin cleavage site which had a 100% sequence identity to chicken 28s ribosomal RNA, suggesting the insert was through non-homologous recombination with the chicken genome. In vaccine studies, both U.S. and Mexican H7 avian influenza virus (AIV) were tested as antigen in experimental vaccines and injected into chickens three weeks prior to challenge. All H7 vaccines tested provided >90 % protection against clinical disease after challenge and decreased the number of birds shedding AIV and the titers of viral shedding. In a second experiment, 26 week-old egg-laying hens were vaccinated either singly or doubly with the A/CT/2006 vaccine and challenged against the HPAI virus. All vaccinated birds reduced shedding of virus compared to sham vaccinated birds and were protected against drops in egg production. These studies demonstrate origins of the 2012 Mexican H7N3 HPAI virus and provide support for vaccination of poultry as part of an eradication program against this virus.