Effect Measure

Dogs, cats and swine flu’s promiscuity

Swine flu started in pigs (although we don’t exactly when or where), adapted to and passed to humans who returned the favor and passed it back to pig herds. Then we heard that turkeys in Chile had contracted the virus, followed by ferrets and a house cat. We can infect animals cross species with flu in the laboratory, but all of these are cases acquired in the natural world by animals interacting with humans. Once cats were on the menu, the next question was dogs, another population “companion animal” (aka, pet) in the US and Western Europe (and literally a menu item in many parts of Asia). In recent years there have been periodic outbreaks of “dog flu,” an H3N8 subtype that didn’t seem to infect humans but produced “kennel cough” like symptoms in dogs. Now we get reports out of China that the family dog can also be infected with swine flu — by us:

Two dogs in Beijing have tested positive for swine flu in the second case of animals catching the disease in China along with pigs in the northeast, Chinese media said Sunday.

The A(H1N1) virus detected in the dogs was 99 percent identical to the one circulating in humans, the state-run Beijing Times reported, quoting China’s agriculture ministry.

The news comes 10 days after four pigs in China’s Heilongjiang province were diagnosed with the virus, which specialists said might have been caught from humans, the report said.

Countries including the United States, Canada and Chile have already reported cases of animals being infected with the A(H1N1) virus.

A cat in the US state of Iowa was diagnosed with swine flu at the beginning of the month in the first known case in the world of the new pandemic strain spreading to the feline population. (iafrica.com; h/t Chen Qui)

The Chinese news service Xinhua is reporting that the virus was found in 2 samples of 52 taken from sick dogs at the China Agricultural University College of Veterinary Medicine and genetic analysis showed it to be 99% homologous to virus from cases of human swine flu.

What strikes us about this is not the danger to dogs specifically but the amazing promiscuity this virus is showing. We have always thought of influenza virus subtype strains to be relatively host species specific, although exceptions do exist. Humans occasionally get the devasting (to us) H5N1 bird flu, which can also infect cats, ferrets and a few other animals, but all rarely. This virus doesn’t seem to care if you are a human, pig, turkey, dog, cat, ferret or who knows what else. Maybe that’s too strong, because while all those infections have been reported we still don’t know how easy it is to transmit. But nothing so far suggests it’s extremely rare. On the contrary, the evidence suggests if we start looking for infections in other species we will start to find them.

I don’t see why we should be thinking only of mammals and birds. Could the influenza virus also infect insects or reptiles or amphibians? (NB: a new vaccine production method in caterpillar cells doesn’t use the flu virus but an insect virus with the gene for the flu HA protein spliced into it; our post here). Maybe there’s a good biological barrier to that but if there is, I don’t know what it is and I don’t think we’ve done much looking outside of birds, humans and pigs.

The species promiscuity of this virus raises still another issue. Influenza viruses not only have species preferences but tissue preferences (called tropisms). Rabies virus infects nervous tissue but not kidneys while flu mainly (although not exclusively) likes cells in the respiratory tract. But if this virus is so indifferent to what species it is infecting, might it not also develop a wider palette of tissue tropisms? Nothing we see in the genetic sequences predicts the striking host non-specificity or what’s allowing it and we are still pretty vague on the distribution of viral receptors in different body tissues, assuming we even know how to characterize those receptors (the conventional story of the 2,3 versus 2,6 sialic acid linkages seems now to be much more complicated; see our posts here and here for more about this).

The dog and cat story may mean a lot more than our pets are at risk. Right now these are just questions. How hard it will be to get the answers and how long it will take is anyone’s guess.


  1. #1 melbren
    November 30, 2009

    Hi Revere-

    As far as “tropisms” are concerned, could this possibly explain why some people seem to get the stomach version, and others seem to get the respiratory version of this flu? For example, several months ago, CNN’s Dr. Sanjay Gupta and Anderson Cooper seemed to have simultaneously contracted the swine flu while on assignment in Afghanistan. Dr. Gupta described his symptoms as more G.I., and Anderson Coopers’ symptoms were described as more respiratory in nature.

    Also, would influenza be able to infect people differently based partially on a person’s haplogroup/type?

  2. #2 MattK
    November 30, 2009

    Since birds are reptiles (phylogenetically) I don’t know why other reptiles couldn’t be infected as well unless metabolism or body temp end up being important.

    As an aside, does anyone know what the deal is with the adjuvanted vaccine in Canada? We have experienced around 148 serious adverse events after 8.24 million doses distributed but the US has 177 for 46 million doses. A lot of ours seem to be anaphylaxis (but only 6 from the “bad batch”). I’m not sure how much of this is attributable to differences in reporting and the fact that a lot of our vaccination has been run by public health authorities who are all networked together. Anyone know if there tends to be a systemic difference between Crates of Canadian and American reporting?

  3. #3 revere
    November 30, 2009

    melbren: We’ll probably eventually find that there are a lot of things in the mix we haven’t been taking into account (e.g., where the viral envelope came from). The new science of epigenetics is rewriting a lot of what we thought we knew about “genetic” differences between people and the whole question of tissue tropism is up in the air. Influenza is an intestinal disease in birds and the human intestinal tract and blood vessels have the right kind of receptors, so obviously there is a lot we don’t know (posts here and here).

    Matt: We’re probably not going to understand a lot of this for a while (after this is all over). The process of assembling the needed information, analyzing it (if it exists) and interpreting it will take time. You point to one of the issues that has to be sorted out: reporting differences. So, no instant answers.

  4. #4 K
    November 30, 2009

    It seems to me that the biggest danger is in species that are multitudinous and closely confined with others of their own species. Chicken houses and CAFO’s for cows and pigs of course but humans self confine themselves together with others of their species in school’s, businesses, opera houses, theaters etc. I wouldn’t even worry so much about dogs and cats but certainly not insects and reptiles. They all keep a fair distance between each other compared to a chicken house or school classroom.

  5. #5 phytosleuth
    November 30, 2009

    Let’s hope insects can’t get this flu.

  6. #6 R
    November 30, 2009

    I don’t see how it’s possible that the ‘promiscuity’ of H1N1 isn’t the top story of this pandemic.

    Eventually, this bug is going to reassort with a flu in some other species.

    If it retains its infectiousness in humans after said reassortment, all hell breaks loose.

    WHY isn’t this being discussed anywhere?

  7. #7 Jonathon Singleton
    November 30, 2009

    Thank you for this posting. Indeed, Effect Measure has been consistent in pointing out and publically discussing the epidemiological fact of swine flu as a cross species pathogen…

    Revere, “[Transgenic swine flu] doesn’t seem to care if you are a human, pig, turkey, dog, cat, ferret or who knows what else… [Evidence] suggests if we start looking for infections in other species we will start to find them.”

    May I ask an historical question of you Revere? Has there ever been a virus like swine flu, with a high species promiscuity, before now? As you no doubt are aware, I’m unsurprised by the evolution of this transgenic virus vis a vis the context of environmental pollution — all genetically modified products are manufactured using technically unstable viral or bacterial agents which can escape-transfer-evolve across-into-within other organisms.

    Anyway, I really am starting to feel like a detective who asks the cancer patient that pesky question, “So, when you tv watched those cowboy smoking adverts in a smoke filled room all those years ago, would you have believed then the tobacco companies were Nixon-lying to the public about their carcinogenic products!?!”

    D225G RBD mutation in swine flu… Henry Niman’s concerns have prompted me to ask a poignant question at Crof’s blog (see below). What about the other species currently being infected? Will D225G RBD mutation in human swine flu evolve within other species?

    Crof’s H5N1 Blog — Hong Kong seeks information on mainland dog flu reports (November 29, 2009)

    Reader posting by Jonathon Singleton…

    Secretary for Food & Health Dr.York Chow said: “The other thing is whether the viral genetic structure has changed after the [inter-species] transmission. So there are many questions that need to be answered before we can make a judgement of the implication of these transmissions.”

    I would like to say Dr York Chow is asking sensible questions. I am becoming increasingly angered by many so called medical and science professionals who appear to be “clueless” about the definition of a transgenic virus like swine flu.

    Apparently, analysis of genetic composition found the virus detected in the dog samples and those found on human A/H1N1 flu cases were 99 percent homologous. I’m sure these sobering results also match the other species contracting swine flu.

    I’m concerned forward thinking scientists such as Henry Niman (Recombinomics), who is trying to alert the world to the dangers of a recent mutation (D225G) in swine flu, are being childishly ignored by the “establishment”!

    I cannot understand why organisations such as WHO blatantly ignore the implications of the D225G RBD mutation in swine flu vis a vis interspecies spread and infection. And, of course, as Dr York Chow suggests — continued transgenic evolution… It’s like the WHO and others are operating in a different paradigm!?!

    Henry Niman wrote a simple explanation of D225G: “[It’s] signifcance is pretty straight forward. The change leads to a targeting of the lung leading to high levels of virus leading to cytokine storm, hemorrhaging, and rapid death…”

  8. #8 revere
    November 30, 2009

    Jon: I am not fixated on “transgenic” (by which I suppose you mean genetically engineered?). At any rate, there are a lot of genetically promiscuous organisms (your gut is full of them), exchanging genetic material across bacterial and probably eukaryotic cells and species. How promiscuous is flu? We’ve never looked systematicaly at a lot of other animals, but it probably depends on how much contact they’ve had with aquatic birds. If we found it in fish, molluscs, amphibians, etc., it wouldn’t surprise me, but then it wouldn’t surprise me if that was biologically impossible for some reason, either. It’s flu. Nothing about flu is straightforward, certainly not its epidemiology or clinical manifestations. But I guess not everybody feels that way.

  9. #9 Don S
    November 30, 2009


    Please see today’s ECDC update – http://im.ly/f54c5/

    “Mutations in the haemagglutinin HA1 gene D222G
    Following initial reports from Norway, WHO has noted that a spontaneous mutation in the haemagglutinin gene
    D222G has been observed in at least seven countries world-wide (1). These spontaneous mutations have been
    detected retrospectively following genetic sequencing. They were first detected in April and were seen in Mexico
    and the USA and so are not a recent phenomenon (1,2). Finnish and French virologists reported another three
    cases last week (3). As in a number of the cases the viruses were reported from two patients with very severe
    illness who died. WHO and ECDC are currently assessing the public health significance of this mutation (1,2). It is
    unclear whether the mutation is especially pathogenic or whether it is somehow selected for in very ill patients.
    However there is no evidence that the virus is transmitting, none of the patients are reported to be connected to
    each other and the mutation is not spreading in Europe. As further sequencing is undertaken reports of its
    detection in other European countries can be expected.”

    So they have now analyzed older samples and confirmed that this mutation has been part of the mix from the start. If it is transmitted it is doing it “under the radar” (which I would not rule out) and has been doing so in its low level way from the beginning of Pandemic A/H1N1’s appearance.

    The “simple” and “straightforward” explanation just doesn’t seem to jibe with the fact that it is present in samples from early in Mexico forward without any significant clusters of serious pathology associated with it. The clinical face of Pandemic A/H1N1 with this mutation is what we have been seeing from the start. Which doesn’t rule that “simple” hypothesis completely out but does make it seem a lot less likely. And many other hypotheses exist.

    Just off the top of my head I can come up with several others … one hypothesis that seems most attractive to me is that it has been part of the mix in multiple individuals from the start but that it is a minority member in most individuals’ influenza populations and missed in the consensus sequence process. In most people it reproduces only a little, causes little pathogenicity, and has low transmissibility to the next individual. Enough though that it continues to slowly and widely show up. In a few people it gets a chance to take off. Maybe there is something host related. Maybe some bacterial process that facilitates it. Who knows. Those people get identified with it as it is in those people that it becomes enough of the mix to be seen and it is in those people that the more complete analyses get done. OTOH those people do not seem to be able to transmit it any better than most and it fails to spread.

    Will the the multiple mixes in multiple organisms allow this mutation to be more uniformly pathogenic and/or more tranmissible as it trades other supporting players out for new ones? Maybe, maybe not. Maybe another mutation will. Maybe a bit picked up from another organism – or two. This bug is out there now having one night stands with every influenza that exists; some surprises are to be expected – unsurprisingly. We are just like Inspector Clouseu, never knowing when or when Cato will attack, even as we know that the attack WILL come.

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