Tuesday, November 03, 2015

That Touch Of Mink Flu (H9N2 Edition)


Credit Wikipedia




Just over six years ago, in That Touch Of Mink Flu, we looked at a story out of Denmark, where at least 11 mink farms in the Holstebro were reported to be infected with a variant of the human H3N2 virus.  In 1984,a rather large outbreak in Swedish mink farms was found to be due to the H10N4 avian virus, while in 2006 CIDRAP reported a European Mink had H5 flu virus.


Mink are a member of the Mustelidae family of carnivorous mammals, which also includes otters, badgers, weasel, martens, ferrets,  and wolverines. A number of these species are affected by flu viruses – most notably ferrets – which are often used in influenza research.

Also in 2009, an H3N2 Swine Influenza was detected in Canadian Mink, reported in a Journal of Clinical Microbiology report called  Characterization of a Canadian Mink H3N2 Influenza A Virus Isolate Genetically Related to Triple Reassortant Swine Influenza Virus.   The authors noted:


The transmission of the virus from swine to mink seems to have occurred following the feeding of animals with a ration composed of uncooked meat by-products of swine obtained from slaughterhouse facilities. 


This is a route of infection we’ve seen before, and with tragic results, as hundreds of tigers in Thailand and China have been infected with HPAI H5N1 (and died) since the middle of the last decade after being fed infected raw chicken carcasses (see HPAI H5: Catch As Cats Can).


The farming of mink in China has become big business, with more than 60 million raised in 2012.  In China, raw poultry or poultry meat products are routinely fed to mink raised in captivity, raising concerns that mink could become infected with one of the many avian flu subtypes found in Asian poultry.


Yesterday we looked at  EID Journal: Replication Of Avian H9N2 In Pet Birds, Chickens, and Mammals, Bangladesh, and concerns over H9N2’s pandemic potential – either as a primary threat, or as a contributor of genes to another reassorted  subtype  – of this ubiquitous, yet lowly pathogenic avian flu virus.

Over the past few years we’ve seen increasing signs of mammalian adaptation of H9N2 viruses (see 2010 Study: The Continuing Evolution Of Avian H9N2  & Molecular characterization of mammalian-adapted Korean-type avian H9N2 virus and evaluation of its virulence in mice), raising additional red flags.


Today – via the Virology Journal -  we get a serological survey of antibodies to H9N2 (along with H5 & H7 viruses) in Chinese farmed minks, along with the results of experimental infection of minks with the H9N2 virus. Given their raw poultry diet, it isn’t surprising that serological evidence of exposure to both H5 and H9 viruses was quite common, although none showed signs of H7.


Considering that the blood samples were drawn in Shandong Province between March and October of 2013 – very early in the initial outbreak of H7N9 – the lack of H7 antibody detection is not all that surprising.


Mink inoculated with the H9N2 subtype replicated the virus in their lungs (and to a lesser extent) heart, brain, and kidney. While H9N2 infection was non-fatal for mink, they developed lung lesions, edema, and shed the virus through their respiratory tract.


Both findings illustrate the potential for minks to help bridge the gap between avian species and mammalian adaptation of H9N2 (and other) avian flu viruses.


Avian influenza virus H9N2 infections in farmed minks

Chuanmei Zhang12, Yang Xuan2, Hu Shan2, Haiyan Yang2, Jianlin Wang2, Ke Wang2, Guimei Li2 and Jian Qiao1*

Virology Journal 2015, 12:180  doi:10.1186/s12985-015-0411-4

Chuanmei Zhang, Yang Xuan and Hu Shan contributed equally to this work.

Published: 2 November 2015

© 2015 Zhang et al.


The prevalence of avian H9N2 viruses throughout Asia, along with their demonstrated ability to infect mammals, puts them high on the list of influenza viruses with pandemic potential for humans. In this study, we investigated whether H9N2 viruses could infect farmed minks.


First, we conducted a serological survey for avian influenza virus antibodies on a random sample of the field-trial population of farmed minks. Then we inoculated farmed minks with A/Chicken/Hebei/4/2008 H9N2 viruses and observed the potential pathogenicity of H9N2 virus and virus shedding in infected minks.


H9 influenza antibodies could be detected in most farmed minks with a higher seropositivity, which indicated that farmed minks had the high prevalence of exposure to H9 viruses. After infection, the minks displayed the slight clinical signs including lethargy and initial weight loss. The infected lungs showed the mild diffuse pneumonia with thickened alveolar walls and inflammatory cellular infiltration. Influenza virus detection showed that viruses were detected in the allantoic fluids inoculated supernatant of lung tissues at 3 and 7 days post-infection (dpi), and found in the nasal swabs of H9N2-infected minks at 3–11 dpi, suggesting that H9N2 viruses replicated in the respiratory organ, were then shed outwards. HI antibody test showed that antibody levels began to rise at 7 dpi.




We provide serological and experimental evidence that strongly suggests farmed minks are susceptible to H9N2 virus infection, strongly suggesting that feeding raw poultry meat is a risk factor for cross-species transmission of influenza A virus from avian to farmed raised small mammals like minks, which could lead to eventual adaption of avian origin new influenza A virus to mammals, and reminding us to pay more attention to detecting its onset in minks.

It is very important to do epidemiological surveillance of influenza virus not only within common susceptible animals, like avian populations, but also for all other species where intensive production and high geographic densities of animals may favor the appearance of new influenza virus isolates. Furthermore, through monitoring AIVs in other animal can not only prevent and control new influenza viruses pandemic prevalence, and provide more information for people’s public health.

(CONTINUE . . . )

1 comment:

Fred de Vries said...

This is a route of infection we’ve seen before, and with tragic results...

Yes, we did, because Bovine Spongiform Encephalopathy (or Mad Cow disease) was caused by cattle - normally herbivores - being fed the remains of sheep in the form of meat and bone meal (MBM), which caused the infectious agent to jump from sheep - where it causes scrapie - to cattle - where it causes BSE.