Thursday, November 20, 2014

Eurosurveillance: Avian H10N7 Influenza In Harbor Seals



# 9352


Just about a month ago, in Avian H10N7 Linked To Dead European Seals, I wrote about the recent die off of seals in Denmark and Germany and the determination that their deaths were the result of a combination of avian H10N7 influenza, pneumonia, and bacterial infection.


In 2011 a similar die off of seals in New England made headlines, which was eventually linked to a different avian flu virus (see New England Seal Deaths Tied to H3N8 Flu Virus). In 2012, in mBio: A Mammalian Adapted H3N8 In Seals, we saw further evidence that this virus had recently adapted to better bind to alpha 2,6 receptor cells, the type found in the human upper respiratory tract.


Although known human infections with avian H10N7 are limited, we’ve discussed them previously on several occasions . 


Admittedly there are fewer opportunities for interaction between seals and humans than say with pigs or poultry, but suddenly seals being viewed as potential `mixing vessels’ for flu.  


This report today from journal Eurosurveillance.



Avian influenza A(H10N7) virus involvement in mass mortality of harbour seals (Phoca vitulina) in Sweden, March through October 2014

S Zohari ()1, A Neimanis2, T Härkönen3, C Moraeus3, J F Valarcher1

We provide the first scientific report of influenza A virus involvement in a mass mortality event among harbour seals (Phoca vitulina) off the west coast of Sweden. Avian influenza A (H10N7) virus was detected in the lungs of two affected animals. This subtype has not been reported in seals to date, nor has influenza A-associated mortality been reported in seals in Europe. Circulation of avian influenza viruses in mammals may have implications for public health.

Increased numbers of dead harbour seals (Phoca vitulina) from the west coast of Sweden were first noted in March 2014. From March through October, 425 carcasses were detected in several seal colonies in the Kattegat and the Skagerrak seas (Figure 1). This unusually high mortality contrasted with the typical annual number of 30 to 40 dead seals reported from this area. Although most seals were too decomposed for examination, influenza A virus (IAV) subtype H10N7 was detected in the lungs of two animals. According to media reports [1], H10N7 virus has recently been detected in dead seals in Denmark, Germany and the Netherlands in association with die-offs of seals first observed in July in Denmark and currently ongoing in Germany and the Netherlands [2,3].



Although IAV infection has been reported in a variety of species of marine mammals including seals [10-12], this is, to our knowledge, the first published report of AIV isolation from seals in Europe and the first time that the H10 subtype has been detected in seals anywhere. It provides evidence that the H10N7 subtype was associated with an outbreak of seal mortality in Europe. Although we detected the virus in only two affected seals, media reports support H10N7 involvement in seal mortality events in Denmark, Germany and the Netherlands, as the virus was isolated from numerous dead seals [1-3].

As in AIV-associated mortality events in seals in the United States (US), Seal 1 suffered from a concurrent bacterial pneumonia [10]. Viral damage to physical components of the respiratory immune system is thought to allow secondary invasion of opportunistic bacteria. Limited quantity and quality of material from Seal 2 precluded investigation of bacterial infection.

Through phylogenetic analyses, we showed that this virus is genetically closely related to Eurasian AIVs from wild and domestic birds (Figure 2 and 3). IAVs are known to be circulating at high prevalence in European aquatic birds [13], supporting initial introduction of the H10 virus in seals from aquatic birds in Europe. The seals probably contracted the virus through direct or indirect contact with wild birds or their droppings. Interspecies transmission from birds to seals requires concurrent alignment of numerous factors and although it occurs, it is not likely to occur often. There was an interval of 4.5 months between Seal 1 and Seal 2, suggesting that the virus was circulating among the seal population during this entire time.

From a public health perspective, extended circulation within a mammalian host not only demonstrates that this strain is capable of infecting and circulating in mammals, but it increases the opportunity for mutations to occur that may facilitate human infection. For example, the H3N8 strain from harbour seals in the US had recent mutations that are known to make influenza viruses more transmissible and cause more severe disease [12]. It also has the ability to target the SAα-2,6 receptor found in the human respiratory tract, an adaptation known to increase transmission and virulence in mammalian hosts [12]. In addition, some avian H10 viruses, including those isolated from farmed mink (Mustela vison) (H10N4), humans (H10N7, H10N8) and pigs (H10N5) (Figure 2) had the unique ability to cause severe disease in mammalian species without prior adaptation in poultry, supporting the hypothesis that these viruses in particular might pose a threat to human health [14-20].

Outbreaks of diseases among marine mammals can also involve interaction with humans and wild and domesticated animals, therefore, circulation of AIVs in mammals may have potential implications for public health. Management of dead marine mammals is challenging and especially difficult when they carry a new pathogen with unknown infectivity for humans. We lack information on the zoonotic potential of this particular strain of AIV and highlight the need for further assessment and research regarding risks for public health. Handling and disposal of carcasses may expose people to any number of potential zoonotic pathogens. This necessitates applying the precautionary principle as well as close collaboration and sharing of responsibility and resources between agencies at the local and national level for situations in which jurisdictional boundaries are often poorly defined.

(Continue . . .)

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