Fall 2015 Avian Influenza Background and Update

Fall 2015 Avian Influenza Background and Update

Early in the history of influenza science, it was recognized that influenza viruses have the potential of crossing species barriers. In the late 1920s, it was established that the “filterable agent,” which later would be identified as influenza, could cause illness in both people and swine. Then the first human influenza isolate was identified in 1933 by inoculating human throat washings into the nostrils of ferrets. It was also recognized early on that chicken embryos were excellent tissues for virus amplification, and bird influenza, or fowl plague, was documented in 1955. However, not until the late 1970s did we gain a clearer understanding of the true One Health implications of influenza and the wide variety of strains found in animals, particularly in aquatic birds (1).

Although two influenza types (A and B) cause the majority of human infections, influenza A is particularly important due to its many host animals and its ability to cause pandemics. Influenza A viruses are divided into subtypes on the basis of two proteins on the virus surface: hemagglutinin (HA) and neuraminidase (NA). There are 18 known HA proteins and 11 NA proteins. The influenza A virus genome has 8 segments that are easily exchanged (reassorted) between viruses. As a result, influenza A viruses are a genetically and antigenically diverse group of viruses which continuously evolve. As the viruses exchange HA and NA genes, a large number of different virus subtypes (e.g. H1N1, H10N2, H5N2) are formed. Aquatic birds can be carriers of all influenza A subtypes except subtypes H17N10 and H18N11 which have only been detected in bats. Influenza A H1N1 and H3N2 are currently the most important subtypes in humans, influenza A H3N8 and H7N7 cause illness in horses and influenza A H3N8 and H3N2 are causing disease outbreaks among dogs.

The global spread of the Asian-origin Highly Pathogenic Avian Influenza (HPAI) A H5N1 subtype generated concerns about wild birds migrating across continents introducing the virus to the United States (US). Thanks to heightened avian influenza surveillance in US wild birds from 2006-2011, experts learned that influenza in wild birds has a seasonal pattern peaking in late summer to early fall. Influenza virus prevalence decreases during the fall and is at its lowest during the over wintering period. The surveillance data also show dabbling duck species such as Mallard, Wood Duck, and American Green-Winged Teal as the primary reservoir for avian influenzas in this country. These birds generally don’t get sick but carry the viruses in their respiratory and intestinal tracts. Avian influenza viruses are likely spread from infected to uninfected birds via shared water bodies. The avian influenza prevalence is less in watersheds at southern latitudes, especially during the hot breeding season (2).

Depending on the pathogenicity in domestic poultry, avian influenza viruses are divided into highly pathogenic (HP) and low pathogenic (LP) avian influenza (AI) strains. Highly pathogenic strains are always H5 or H7 subtypes, however, all H5 and H7 subtypes are not HP. While HPAIs often cause serious illness in poultry, the strains are often not particularly pathogenic to wild birds or mammals. Circumstantial evidence has implicated wild birds as the most important source of HPAI in domestic poultry for some time. However, the recent global spread of the Asian-origin HPAI A H5N1 subtype in wild birds at a time when we are able to follow the evolution of the virus through molecular sequencing has helped bring our understanding of the ecology of avian influenza viruses to a new level.

The Asian H5N1 was first recovered from geese in China in 1996. The virus was recognized as a potential human health concern after 18 people became ill and 6 people died as a result of influenza A H5N1 infections in Hong Kong in 1997. This was the first time influenza H5N1 infections had been identified in people. All ill had close contact with infected poultry and 1.5 million chickens in Hong Kong were culled to prevent further disease transmission (3). The Asian H5N1 virus reappeared in Hong Kong in 2003 when two people were found infected with the virus.  Strains that have evolved from the Asian HPAI A H5N1 virus (Eurasian HPAI H5 viruses) have since been detected in wild birds and poultry in more than 50 countries in Africa, Asia, Europe and the Middle East. At this time, six countries (Bangladesh, China, Egypt, India, Indonesia and Vietnam) are considered endemic for the virus. A number of reassortant HPAI viruses have been detected as the H5N1 viruses continue to evolve. Most influenza genes have been exchanged but the specific H5 HA gene continues to be present in all highly pathogenic isolates. Scientists have agreed on a nomenclature system to follow the evolution and spread of these H5 virus genotypes and have divided the strains into clades depending on the phylogenetic characterization and sequence homology of the H5 gene (4).

One such clade, the 2.3.4.4 HPAI A H5N8 virus was originally detected in China in 2010. The virus subsequently caused an HPAI outbreak in South Korea in January 2014, which resulted in the culling of 14 million poultry. By September 2014, the H5N8 virus had been detected in Japan, China and Russia. By November 2014, it had reached Germany, the United Kingdom and the Netherlands and by December 2014, it had been recovered in Italy.

An H5N2 reassortant that contained the Eurasian clade 2.3.4.4 H5 gene discussed above, was detected in domestic chicken and poultry in British Columbia, Canada in November 2014. Heightened surveillance by US Departments of Agriculture and Interior as a result of this finding resulted in the detection of an H5N8 strain in Washington State in December 2014 (5). The virus was almost identical to the H5N8 virus circulating in Eurasia; in other words likely spread by wild birds from Eurasia to North America. The wild bird surveillance efforts in Washington State also yielded a Eurasian clade 2.3.4.4. reassortant HPAI A H5N2 that was highly similar to the virus recovered from Canada the previous month and a reassortant clade 2.3.4.4 H5N1 virus containing genes from both Eurasian and American influenza viruses.

Subsequently, the HPAI H5N8 has been detected in wild and domestic birds along the Pacific flyway.  Influenza A H5N2 reassortants have also been detected along the Central and Mississippi flyways (6) causing large outbreaks on poultry farms affecting more than 48 million birds in 9 Western and Midwestern states during the spring of 2015 (7). The poultry industries in Minnesota, where 9 million birds (primarily turkeys) were culled, and Iowa where 32 million birds died, many of them layer hens, were particularly impacted with an estimated economic loss of more than $1 billion and 8,400 lost jobs in Iowa alone (8). Avian influenza is very contagious among poultry and it is believed that the rapid spread of viruses resulted both from wild bird introductions and human movement between farms. USDA has worked closely with state agriculture agencies to improve biosecurity measures and stamp out the virus in domestic bird populations. To date, no human illness has been associated with the 2.3.4.4 HPAI viruses found in the US.

Wild bird influenza surveillance efforts continue to identify HPAI H5 viruses. It is anticipated that transmission among waterfowl will increase in the late summer and early fall when temperatures cool and a new generation of birds join older waterfowl at the migration staging areas. When migration gets under way, these birds may yet again introduce HPAI H5 viruses to domestic poultry along their migratory flyways.

References

This and other articles were published in Volume 8 Issue 3 of the One Health Newsletter.
Article written by: Carina Blackmore, DVM, PhD, Dipl. ACVPM