# 4609
Today, another entry in the ever increasing list of animals that can serve as hosts for the influenza A virus. This time it happens to be a variety of striped skunk (Mephitis mephitis), 8 of which died on a mink farm in Canada last December and January.
Initial necropsy and testing results indicated a mixed bacterial pneumonia (Streptococcus dysgaslactiae subsp. equisimilis, Staphylococcus aureus, and Hafnia alvei) as the cause of death, but further testing revealed the pneumonia to be secondary to a viral infection by pandemic H1N1 2009.
Further complicating matters, the skunks also tested positive for ADV (Aleutian Disease Virus), a common virus carried by minks, that may have contributed to the severity of the skunk’s infections.
First some excerpts from the CDC EID Journal article (It’s relatively short, so follow the link to read the whole thing), then some commentary.
Volume 16, Number 6–June 2010
Letter
Pandemic (H1N1) 2009 in Skunks, Canada
Ann P. Britton, Ken R. Sojonky, Andrea P. Scouras, and Julie J. Bidulka
<SNIP>
During mid-December 2009–mid-January 2010, eight striped skunks (Mephitis mephitis) died on a mink farm near Vancouver, British Columbia, Canada. On January 12, 2010, two of the skunks were brought to the Animal Health Centre in Abbotsford, British Columbia, for postmortem examination.
One skunk exhibited purulent nasal exudates. In both skunks, investigators observed splenomegaly and severe pneumonia, characterized by heavy, dark red to purple, lung lobes involving >70% of the lung field. Microscopic examination showed moderate rhinitis and severe bronchopneumonia with intralesional bacteria, areas of interstitial pneumonia, and occasional nematode larvae.
<SNIP>
Detection of influenza A virus nucleoprotein and matrix genes and hemagglutinin and neuraminidase typing was performed with real-time reverse transcription–PCR. Organ samples were positive for pandemic (H1N1) 2009, which was confirmed by sequence analysis of DNA fragments obtained in the hemagglutinin, neuraminidase, and matrix gene testing.
<SNIP>
In view of the detection of pandemic (H1N1) 2009 virus in 2 striped skunks with fatal pneumonia, this species should now be regarded as a potential source of influenza A virus.
Wild animals participate in the transmission of influenza A viruses between species, and the presence of wildlife on farms is known to be a risk factor for infection of poultry (7). Similar to raccoons, skunks express both α2,3 and α2,6 sialic acid receptors for avian and human influenza viruses in the respiratory tract (M. Shrenzel, San Diego Zoo, pers. comm.), which is believed to create the opportunity for mixed influenza infections with potential for genetic reassortment (8).
Skunks, like raccoons, are highly mobile animals with large home ranges in rural and urban areas, which provides numerous opportunities for influenza A virus exposure and transmission to poultry, livestock, pets, and, ultimately, humans. The inclusion of striped skunks in wildlife influenza surveillance programs may be warranted.
Influenza viruses must reside in a living host in order to replicate and survive. Outside of a suitable host environment, the influenza virus can only survive for a limited amount of time.
In order to infect a host, a virus must attach itself to cells in the host’s body. Influenza viruses have an affinity for either the alpha 2,3 receptor cell or the alpha 2,6 receptor cell.
Avian adapted influenza viruses bind preferentially to Alpha 2,3 receptor cells, which are commonly found in the digestive tract of birds. This explains why most avian flu viruses are gastrointestinal infections in birds.
Human adapted viruses have an affinity for the alpha 2,6 receptor cell, which populate the upper airway and lungs. This is why influenza is a respiratory virus in humans.
There are some crossovers in receptor cells, and humans have some avian-like alpha 2,3 receptor cells, particularly deep in the lungs. It is harder for avian influenzas to reach those cells, but not impossible.
Some species, like pigs, have an abundance of both types of receptor cells, and thus make good mixing vessels for human and avian adapted viruses.
If a pig (or any other host) is simultaneously infected with two different flu viruses, it is possible for the viruses to swap genetic material (via reassortment) and create a new, hybrid virus.
For more on how influenza viruses are thought to bind to cells, you might wish to revisit:
Study: H1N1 Receptor Binding
RBD: Looking For The Sweet Spot
Receptor Binding Domains: Take Two
Last January I wrote a blog entitled Mixing Vessels For Influenza which mentioned research done by two wildlife disease experts from the San Diego Zoo - Mark Schrenzel and Bruce Rideout – that identified the North American Striped Skunk - along with a handful of other small carnivores - as a potential host for influenza reassortment.
The striped skunk, like the pig, has both types of receptors cells.
Over the past few years we’ve seen reports of H5N1 (bird flu) infections among dogs, cats, civets, raccoons, martens, and – of course – humans. Additionally, researchers have successfully infected cattle with the H5N1 virus, along with ferrets and mice for testing.
Pandemic H1N1 flu has been documented in humans, swine, turkeys, skunks, ferrets, cats, and dogs. For a listing of animal pandemic flu reports you can visit the AVMA Pandemic Flu page.
The fact that skunks, and civets, and raccoons are susceptible to influenza may seem inconsequential, but small mammals that can carry influenza viruses can become difficult biosecurity problems on poultry farms, and may serve as a conduit for bird flu viruses.
Additionally, they provide yet another reservoir, and perhaps another opportunity for flu viruses to mutate or reassort.
While successful reassortments (biologically competitive and `fit’) don’t happen very often, when they do, they pose a significant threat to a variety of species, including humans.
Reason enough to ramp up our surveillance in farmed animals and wildlife.
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