Tuesday, May 12, 2015

Taking HPAI To The Bank (Vole)

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Bank Vole – Credit Wikipedia

 

# 10,041

 

For more than a decade a debate has raged on as to how HPAI viruses – like H5N1 – manage to get into so many commercial poultry operations, particularly in South Korea and Japan where farm biosecurity is heavily embraced. 

 

One possibility (as yet unproven) has been that small mammals – like dogs, cats, mice, or voles – are somehow vectoring the virus into commercial poultry flocks.

 

We’ve seen evidence that dogs and cats are both susceptible to H5N1, and of H5N8 Antibodies Detected In South Korean Dogs.  Additionally, we’ve seen H5N1 infections among   civets, raccoons, martens, and – of course – humans.  Scientists have experimentally infected cattle, along with ferrets and mice for testing.

 

A couple of years ago, in H7N9 Transmission and Replication In The Guinea Pig Model, and in 2012’s EID Journal: Guinea Pigs As Reservoirs For Influenza, we saw that the common guinea pig is susceptible to a wide variety of human and avian flu strains.

 

But avian viruses are thought to only rarely jump to mammals. 

 

Avian adapted flu viruses bind preferentially to the alpha 2,3 receptor cells found in the gastrointestinal tract of birds, while mammals typically have mostly alpha 2,6 receptor cells in their upper respiratory tract.   Some mammals – like pigs – have both types of receptor cells, and are therefore more likely to be infected by an avian virus.

 

Frankly,  there’s not been a whole lot of research on the ability for HPAI viruses to infect, replicate, and spread via small wild mammals. But we have a study, published today in the journal Veterinary Research, that undertakes just an experiment using bank voles.

 

Why bank voles, you ask?

 

Well, wild bank voles are likely to inhabit the same areas that wild and migratory birds regularly visit, they have a habit of inserting themselves into barns and farm settings looking for food, and they are already a known vector in Europe for the Puumala virus, a milder form of hantavirus (see Hantaviruses: Of Mice And Men).

 

As we learn from this study, bank voles were not only susceptible to two types of avian flu viruses (H5N1 & H7N1), most were able to carry the virus asymptomatically, shed the virus in copious amounts, and were able to pass on the virus to naïve co-housed sentinel voles.

 

I’ve only included some excerpts from a much longer, fascinating study.  Follow the link to read it in its entirety.

 

Susceptibility to and transmission of H5N1 and H7N1 highly pathogenic avian influenza viruses in bank voles (Myodes glareolus)

Aurora Romero Tejeda1, Roberta Aiello1*, Angela Salomoni1, Valeria Berton1, Marta Vascellari2 and Giovanni Cattoli1

Published: 13 May 2015

© 2015 Romero Tejeda et al; licensee BioMed Central.

Abstract

The study of influenza type A (IA) infections in wild mammals populations is a critical gap in our knowledge of how IA viruses evolve in novel hosts that could be in close contact with avian reservoir species and other wild animals. The aim of this study was to evaluate the susceptibility to infection, the nasal shedding and the transmissibility of the H7N1 and H5N1 highly pathogenic avian influenza (HPAI) viruses in the bank vole (Myodes glareolus), a wild rodent common throughout Europe and Asia.

Two out of 24 H5N1-infected voles displayed evident respiratory distress, while H7N1-infected voles remained asymptomatic. Viable virus was isolated from nasal washes collected from animals infected with both HPAI viruses, and extra-pulmonary infection was confirmed in both experimental groups. Histopathological lesions were evident in the respiratory tract of infected animals, although immunohistochemistry positivity was only detected in lungs and trachea of two H7N1-infected voles. Both HPAI viruses were transmitted by direct contact, and seroconversion was confirmed in 50% and 12.5% of the asymptomatic sentinels in the H7N1 and H5N1 groups, respectively.

Interestingly, viable virus was isolated from lungs and nasal washes collected from contact sentinels of both groups. The present study demonstrated that two non-rodent adapted HPAI viruses caused asymptomatic infection in bank voles, which shed high amounts of the viruses and were able to infect contact voles. Further investigations are needed to determine whether bank voles could be involved as silent hosts in the transmission of HPAI viruses to other mammals and domestic poultry.

<SNIP>

Discussion

The aim of this study was to investigate the susceptibility of the bank vole to infection with two HPAI strains, the H5N1 A/turkey/Turkey/1/2005 (Tk/H5N1) and the H7N1 A/ostrich/Italy/2332/2000 (Os/H7N1) isolates, and to establish whether those avian viruses are transmitted by infected animals to naïve co-housed sentinel voles.

<SNIP>

The present study demonstrated that the bank vole is susceptible to infection with highly pathogenic H5N1 and H7N1 viruses of avian origin without prior adaptation, shedding viable virus in the environment, and transmitting the virus to contact voles. Interestingly, infection with the same HPAI strains demonstrated high pathogenicity and 100% of mortality in BALB/c mice [38], while infected voles were more resistant to the clinical condition and displayed zero or very low mortality rate.

These important findings may suggest that wild rodents could play a role as silent hosts in IA virus epidemiology, contributing to the spread of HPAI virus infections during an outbreak. If this occurs under natural conditions, the circulation of IA viruses in these rodents may provide opportunities for the acquisition of mammalian adaptive mutations, which could minimize the barriers to interspecies transmission of these viruses. However, the study of synanthropic wild mammals, and in particular wild rodents, is a critical and important gap in our knowledge of how IA viruses may evolve in new hosts [22], considering that these species share the same ecological habitats as waterfowl and live commensally around domestic poultry farms [32], thus running the risk of being exposed to IA viruses.

(Continue . . .)