A Critical Moment in Influenza’s History

Featherless ChickensI gave the following presentation last night at Give & Take, a show and tell for adults held at Intermedia Arts in Minneapolis. The organizers ask all presenters (and audience members) two questions: What do you know about? What do you want to know about? A lot of fun and a great learning experience. Other than the photo of the featherless chickens I show none of my slides here, but I think you’ll get the picture.

We begin with a visceral abomination. We recoil at the sight of these chickens bred for baldness. But we recoil for reasons other than those for flinching at mystery meats, for instance. We’re repulsed by the meat because we can’t connect our food to something identifiably organic.

Our featherless friends, on the other hand, seem a violation of temporality. We don’t expect the finished broiler—leg, breast, wings—to be walking about on its own. The sequence is all wrong.

You can imagine these as stars of your own personal Latourian nightmare. You’re dreaming you’re in your local supermarket—maybe only in your underwear, maybe not—and you watch these two birds walk down aisle 6 and hop right into a meats freezer. You look down into the freezer. Shivering birds “Hello, bok, bok, bok, I’m a red dot special! I’m a red dot special!” You wake up in a cold sweat with feathers from your pillow floating everywhere.

In actuality you probably couldn’t spot the difference between our featherless friends once processed and your typical supermarket poultry. Its breeding isn’t in the consumers’ interest—feathers have long been plucked at the factory anyway. Instead, it’s in the interest of the producer. They can now remove plucking from poultry processing, cutting production costs. The cost is also pushed back onto the living bird, which now expresses another attribute that would make it incompatible with living in a natural or ancestral environment. The bird has become further wedded to the industrial process.

We could consider bird baldness the anatomical equivalent of what agribusiness has imposed more broadly on livestock ecologies: thousands of poultry and swine housed atop each other, densities that could never persist in nature because of the disease costs they incur, but that allow more animals to be raised and processed faster.

Among a variety of complications, there is growing evidence that such ecologies are selecting for a greater diversity of virulent influenzas:

  • Such populations are characterized by little genetic diversity, offering few immune firebreaks against an outbreak.
  • Larger populations facilitate viral transmission.
  • Immune systems are likewise depressed under such densities.
  • And the high turnover rate of the poultry process—the duration from birth to processing has been reduced to 40 days—likely selects for more virulent strains able to reach their transmission threshold before their host is killed for food.
  • By increasing the throughput speed, the livestock industry may also be selecting for strains able to transmit in the face of more robust immune systems. Not a good sign for those of us 20-45 years of age.

How did this industrialization of biology came about in the first place?

The Livestock Revolution

Industrial poultry emerged in what is now called the ‘Livestock Revolution’.

Here is a map of poultry across the US in 1929. Each dot represents 50,000 chickens and we see wide dispersion across the country—300 million poultry total at an average flock size of only 70 chickens. In other words, poultry was largely a backyard operation.

That changed after WWII and companies like Tyson, Holly Farms, and Perdue vertically integrated the broiler filiere, buying up other local producers and putting all nodes of production under one company’s roof. By 1992 poultry production is concentrated in a few states, but each dot now represents 1 million broilers, 6 billion in total, with an average flock size of 30,000 birds.

By the 1970s this production model was already so successful that it was producing more poultry than people typically ate. How many roasted chickens were families prepared to eat a week? You can only take your patriotic duty so far.Food science and marketing came to the rescue and repackaged chicken in a mind-boggling array of new products, including chicken nuggets, strips of chicken for salads, cat food, and so on. A market developed large enough to absorb the production.

The poultry market also spread geographically. In the 1970s the vertical model was exported to Asia and companies such as Charoen Pokphand set up vertical filieres in Thailand and, soon after, elsewhere in Asia. We see an explosion in the number of chickens produced in China from the 1980s on. Industrial poultry’s rise in China went hand-in-hand with the country’s economic liberalization.

The result worldwide? The globe is circled by cities of poultry and more recently by cities of pig: largely concentrated in China, the U.S. and Western Europe, but expanding elsewhere.

What are the effects of a globalized livestock on influenza’s evolution?

  • First, more confined livestock, more infections and greater standing diversity.
  • Within any one country the region hosting farms for one type of livestock often hosts other types too, permitting greater reassortment of influenza’s genomic segments across species.
  • In geographically expanding, intensive agriculture destroys wetlands on which many waterfowl typically stop during migration. These birds aren’t stupid. With wetlands destroyed, they now go to where the food is—and that’s the very farms that helped destroy their wetlands, increasing reassortment of influenzas across waterfowl and livestock.
  • Finally, for now, livestock are increasingly shipped and traded across greater geographic extents, increasing the likelihood previously isolated influenza serotypes can trade genomic segments. That’s exactly what happened with this year’s swine flu H1N1. It collected together genetic segments from influenzas previously circulating among Eurasian and North American pigs.

The resulting increase in genetic diversity acts as the fuel for natural selection, including selection for greater transmissibility in humans and greater virulence.

But there appears a problem with our argument.

What About 1918?

If postwar confined animal feedlot operations are to blame, how do you explain the 1918 pandemic, which killed 50-100 million people worldwide? The implication is that because no such industry existed in 1918, livestock intensification need not be to blame for the recent emergence of new influenzas. Something else must explain the recurrence.

But there is an error in reasoning here. The 1918 comparison is an attempt to impose an algorithm upon contingent history, which resists such easy abstraction. Yes, natural selection is on its face an algorithm–propose, dispose, repeat–but the concrete–or rather fleshy–results are dependent on an era-specific mash of previous adaptations and passing ecological circumstances.

In other words, history matters. And pathogens—like humans—have histories. They have their origins, their diasporic migration, their classical eras, Dark Ages, and Industrial Revolutions. And as human pathogens evolve and spread in a world of our own making, these eras often coincide with our own.

For instance, for most of its history the cholera bacterium made its living eating plankton in the Ganges delta. Only once humanity became urbanized and, later, interwoven together by 19th century transport was cholera able to make its way to the world’s cities. The bacterium was able to transform from a marginal bug into a roaring success when municipalities began drawing drinking water from the same place they dumped their shit.

Other pathogens have engaged in similar shifts in epidemiological practice.

Simian immunodeficiency viruses of various stripes infecting monkeys, chimps and other non-human primates likely emerged from sub-Saharan forests when logging broadened the wildlife-human interface. It appears HIV, one of the SIVs, evolved when logging expanded the market for butchered bushmeat. Logging roads also better integrated the deepest forest with regional cities. The virus was thereby able to cross into humans and make its way out onto the global travel network.

So as for influenza. For eons the virus feasted on waterfowl populations that summered on the Arctic Circle. Influenza expanded into humans once we became farmers and our population densities and connections grew enough to support such an acute infection. But since WWII, influenza, as we described, has entered a new phase—its Industrial Revolution: billions of livestock monoculture pressed up against each other, an effort to which we are employed as a major contractor.

So even as livestock feedlots don’t explain 1918, it doesn’t mean they’re not responsible for our current batch of influenzas. That’d be like arguing oil isn’t a cause for war today because the Romans never fought for it. We acknowledge our own historical trajectories. We should be able to acknowledge those of our pathogens as well.

What I Want to Know About

So that’s something of what I think I know. I would like to learn a lot more. For instance,

  • When and how did influenza originate in waterfowl?
  • Is it possible to recover ancient influenza genomes from ice cores?
  • How does an area’s agro-ecological resilience amplify or block the spread of influenza?
  • And finally, how exactly does influenza use agribusiness to its advantage? And what can we do about it?

I’d be curious as to some of your own thoughts about this last question. Let me give you the example that prompted it.

In 2007 the University of Minnesota won a $22.5 million grant from the federal government to study influenza. The University’s partners include a variety of well-respected institutions, among them the Wildlife Conservation Society, the National Wildlife Health Center, the Southeastern Wildlife Disease Study, and the Minnesota Department of Health.

The consortium, however, also includes Cargill, the agribusiness giant, the largest privately owned company in the United States, with $120 billion in revenues in 2008, and poultry and swine operations worldwide. It’s hard to believe that the University’s consortium will ever be willing to address the question whether confined feedlots select for the most virulent influenza strains.

What does one do about that? What does one do about efforts aimed at discovering solutions to the new influenzas backed by those who helped bring about the problem in the first place?

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2 Responses to “A Critical Moment in Influenza’s History”

  1. While it is easy to blame everything on confined feeding operations, there could be other routes of exposure such as sewage. Viruses are shed in fecal material which goes to the sewage treatment plant. Sewage treatment plants concentrates most viruses in sludge while some are released to surface water. Viruses in surface water are picked up and passed through drinking water treatment plants. On the other extreme some virus contaminated sewage effluent is used to irrigated food crops, parks, school grounds and lawns. The concentrated virus contaminated sewage sludge is also used to “fertilize” food crops, grazing land, parks, school grounds, home lawns and gardens. The problem lies with the national policy for using pathogen contaminated sewage products as fertilizer which now includes manures. see,
    http://hartkeisonline.com/2009/08/21/spreading-sewage-sludge-on-us-fields-hidden-cause-of-food-safety-problems/

  2. rgwallace Says:

    A good point, Jim. I’d ask, though, why separate the two? Concentrated animal feedlot operations produce 100 times the waste humans do. And unlike municipalities, agribusinesses are under no statutary obligation to treat their cities of shit.

    I address the point more specifically in the influenza post that follows here.

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