Last January, after waiting for months to see if HPAI H5 would return to the United States, we instead saw APHIS Announce HPAI H7N8 At A Commercial Turkey Farm In Indiana. This was the first detection of a highly pathogenic H7N8 virus, although LPAI H7N8 viruses had previously been detected in wild birds.
Nine farms were affected (1 HPAI & 8 LPAI), but the outbreak was quickly contained, and no other farms or wild birds in the area tested positive for the HPAI virus since then.
Early reports suggested a spontaneous LPAI-to-HPAI mutation occurred at one of the farms after the LPAI virus was introduced into the poultry population (see APHIS: Epidemiology Report On Indiana H7N8 Outbreak).
LPAI viruses are commonly found in wild and migratory birds, often only producing mild symptoms in poultry. The concern is - when LPAI H5 and H7 viruses are not quickly controlled - they have the potential to mutate into highly pathogenic strains.
Hence all H5 & H7 outbreaks are reportable to the OIE, and must be quickly eradicated.
Over the past year we've seen an unusual number of spontaneous LPAI-to-HPAI mutations, particularly in Europe, including:
Also in France, we saw the emergence of HPAI H5N2 and HPAI H5N9, both likely evolved from LPAI viruses, along with emergence of several new `European Lineage' LPAI viruses (see DEFRA: Updated Assessment On France's HPAI/LPAI Outbreak).
Indiana's H7N8 may well turn out to be an aberrant `one-off' event, never to return.
But it - along with the 5 novel flu strains that emerged over the winter in France and the two H7 outbreaks in Germany and the UK last summer - remind us just how quickly avian flu viruses can re-invent themselves.
And why good biosecurity and constant vigilance are required if we are to avoid a repeat of the 2014-2015 epizootic that swept the North American poultry industry.
An analysis of the H7N8 virus, recently published in Genome Announcements, follows:
Outbreak of H7N8 Low Pathogenic Avian Influenza in Commercial Turkeys with Spontaneous Mutation to Highly Pathogenic Avian Influenza
Mary Lea Killiana, Mia Kim-Torchettia, Nichole Hinesa, Sam Yingstb, Thomas DeLibertoc, Dong-Hun Leed
Highly pathogenic avian influenza (HPAI) subtype H7N8 was detected in commercial turkeys in January 2016. Control zone surveillance discovered a progenitor low pathogenic avian influenza (LPAI) virus in surrounding turkey flocks. Data analysis supports a single LPAI virus introduction followed by spontaneous mutation to HPAI on a single premises.
In January 2016, the Indiana State Board of Animal Health (BOAH) veterinarians were notified of increased mortality at a commercial turkey operation (1). Decreased water consumption and recumbent turkeys with pulmonary congestion and edema were reported in one of six barns. Three days following the onset of clinical signs, mortality increased from 100 to 800 birds within 24 h. Birds in the five other barns on the index premises showed no clinical signs. Turkeys from the affected barn tested positive for H7 by PCR, and partial sequencing confirmed H7N8 highly pathogenic avian influenza (HPAI). Additional samples collected within a 10 km zone surrounding the index farm identified eight additional H7-positive premises, none with clinical signs, and partial sequencing confirmed H7N8 low pathogenic avian influenza (LPAI).
This is the first detection of an H7N8 HPAI virus in any species. The virus is not related to the H5 HPAI viruses that caused outbreaks in the United States from 2014 to 2015. Based on full genome sequences representing seven different premises, the index H7N8 HPAI virus and subsequent H7N8 LPAI viruses are of North American wild bird lineage and are highly similar to each other across all eight genes (excluding the multi-basic amino acid insertion at the cleavage site responsible for the mutation to HPAI). The H7N8 HPAI virus contained a 9-nucleotide insertion at the hemagglutinin gene cleavage site translating to basic amino acids (PKKRKTR*G).
The H7N8 virus is also highly similar across six of eight genes (except nucleoprotein and matrix) to a recent H7N8 LPAI virus isolated from a hunter-harvested male lesser scaup (after-hatch year) in Kentucky during November 2015 as part of the national wild bird surveillance effort. This indicates that reassortment likely occurred prior to virus introduction in turkeys in Indiana. However, mutation to HPAI likely occurred during replication of the virus in poultry.
In general, influenza A viruses circulate in wild waterfowl, and the H5 and H7 subtypes have the potential for mutation from LPAI to HPAI which requires the acquisition of a multibasic cleavage site (http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.03.04_AI.pdf).
Mechanisms for acquiring multibasic amino acids include (a) insertion of basic amino acids from codons duplicated at the cleavage site during transcription (2, 3), (b) accumulation of basic amino acids by gradual mutation resulting in amino acid substitutions, and (c) nonhomologous recombination resulting in the insertion of a foreign nucleotide sequence adjacent to the hemagglutinin (HA) gene cleavage site (4).
Additional genetic analysis of eight H7N8 viruses for which whole-genome sequences were obtained suggests a single introduction event was followed by lateral/secondary spread and provides potential insights into virus evolution and the epidemiology of this outbreak. Further studies are required to determine the mode of acquisition of the multibasic amino acid insertion at the HA gene cleavage site for this virus.
Nucleotide sequence accession numbers.The genome sequence of HPAI A/turkey/Indiana/16-001403-1/2016(H7N8), LPAI A/turkey/Indiana/16-001573-2/2016(H7N8), and LPAI A/turkey/Indiana/16-001574-7/2016(H7N8) are deposited in GenBank under accession numbers KU558903 to KU558910, KU585905 to KU585912, and KU585913 to KU585920, respectively.