As the genetic origins of the novel strain of H1N1 influenza A become better understood (it takes time for a layman like me), it’s increasingly clear that there are serious and urgent questions over the role of intensive livestock farming – as practised in CAFOs – in the development and transmission of potentially pandemic flu viruses.
Patient zero, pig zero, farm zero?
This isn’t just about the now-notorious Granjas Carroll de Mexico farm (part-owned by Smithfield, the world’s largest pork producer) near La Gloria, in the province of Veracruz, Mexico. This CAFO may or may not be the direct source of the virus, whose first human sufferer may have been four-year-old local villager Edgar Hernández Hernández.
However suggestive the circumstantial evidence, the Smithfield connection is, for now, mere conjecture. Smithfield has stated that it has submitted samples from the farm for testing:
I am also pleased to reconfirm that there is no evidence at this time that the hogs at Veracruz, or anywhere else, have been infected with A(H1N1) influenza.
This notwithstanding and so the public can have full confidence in the health of our Mexican pig herd, yesterday we submitted samples from our farm in Veracruz for further testing under the direction of Mexican governmental authorities, including genetic sequence analysis that will determine what, if any, strains of flu are present. The results will enable us to conclude with certainty that the A(H1N1) strain is not present in our hogs. These tests will take approximately twelve days. [Emphasis added]
There seems to be some stalling for time here, with an extraordinary 12 days to wait for the results (an earlier press release suggested results in “a few days”) and the sampling process has been questioned as apparently carried out by Smithfield itself.
Never mind the final link, what about the rest of the chain?
But even if the virus is ultimately conclusively linked to the Granjas Carroll CAFO, it would only make it the last link in a complex process of virus mutation, reassortment and transmission that’s played out on pig farms over the last 10 (or even 90) years.
The key question for pig producers (and consumers) is whether and to what extent modern methods of pig production, including CAFOs, have exacerbated the development and transmission of new virus strains, including the novel H1N1 virus that now threatens a human pandemic.
Prevalence of swine flu in pigs
There’s no denying that swine flu is a common illness of pigs across the world. The FAO’s recent briefing on swine influenza states:
SI is widespread and endemic in pig populations worldwide and is responsible for one of the most prevalent respiratory diseases in pigs. In the US, Studies have shown that 30% of the entire US swine population have been exposed to H1N1 since 1930.
… The disease in swine has a strong economic impact on the pig industry in industrial farming systems in the UK alone, SI costs have been estimated at up to £7 per pig [emphasis added]
It’s therefore rather surprising that Smithfield Foods, who produce over 25% of all US pork, are able to claim in a recent press release:
Smithfield Foods, Inc. (NYSE: SFD) today reaffirmed that there is no evidence of the presence of A(H1N1) influenza in any of the company’s swine herds or in its employees at any of its worldwide operations, including those in the United States. (Smithfield, Va., May 3, 2009 /PRNewswire-FirstCall via COMTEX News Network/) [emphasis added]
To be fair, Smithfield is probably talking about the novel strain of A(H1N1) influenza here, but it’s at least misleading to suggest that pig herds don’t routinely suffer from closely related viruses. And there’s little forthcoming information on recent prevalence and spread, as reported by New Scientist:
Smithfield Foods, in a statement, insists there are “no clinical signs or symptoms” of swine flu in its pigs or workers in Mexico. That is unsurprising, as the company says it “routinely administers influenza virus vaccination to swine herds and conducts monthly tests for the presence of swine influenza.” The company would not tell New Scientist any more about recent tests. USDA researchers say that while vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus. [emphasis added]
Pigs as “mixing vessels” for the flu virus
DEFRA, amongst others, describes pigs as “mixing vessels” for strains of influenza of different origin, confirms the prevalence of swine influenza in the global herd, and touches on the dangerous implications:
Swine influenza is a disease of pigs caused by a virus (influenza virus). Influenza viruses exist as various types and the most common type found in pigs is Type A.
The virus is present in all pig producing countries, including the UK. Type A strains can also infect other species, including people, although the strains of virus involved are usually different. However pigs have been described as ‘mixing vessels’ for the various influenza virus strains (including the strains causing avian influenza). This means that they may have a role in the spread of influenza viruses between species or in the development of new strains of virus. [emphasis added]
When two different strains of flu virus occupy the same cell, these viruses are able to swap genes, creating a new “reassortant” strain, possibly containing genetic components originating from viruses associated with different species. These reassortant viruses may behave differently from their parent strains, creating the possibility of human pandemic if they can be transmitted to, and then directly between, humans.
Reassortment can occur in any species but is more likely in pigs. The scientific basis for the “mixing vessel” claim is explained by Bruce Janke in a 2008 presentation to the USDA’s APHIS:
Concept [of "mixing vessels"] derived from studies that showed:
• Variation in nucleoprotein in swine greater than in humans or birds
• Pigs have receptors for both avian and mammalian influenza viruses
• Pigs could be infected experimentally with avian viruses of 15 HA subtypes
• Reassortant viruses could be recovered from pigs infected simultaneously with two influenza viruses
What are the novel H1N1 flu virus’s genetic origins?
The genetic make-up of the novel H1N1 virus has been the source of some dispute, focusing on whether it is of entirely swine origin or a triple reassortant of swine, avian and human flu viruses. In fact, it’s both, as virologist Ruben Donis, CDC chief of molecular virology & vaccines, confirms and explains in an interview with ScienceInsider:
Q: Is it of swine origin?
RD: Definitely. It’s almost equidistant to swine viruses from the United States and Eurasia. And it’s a lonely branch there. It doesn’t have any close relatives. [emphasis added]
Donis goes on to explain that these swine viruses already contained genetic components of avian and human flu, which have been present for over 10 years.
Christopher Olsen and others first identified these genes in an H3N2 flu virus found in pigs on US farms in the 1990s. This represented a significant change in the history of influenza in pigs, which was previously restricted almost entirely to the H1N1 virus, itself of avian origin and probably introduced into the pig population during the 1918 Spanish Flu pandemic.
In his presentation to the USDA’s APHIS, Bruce Janke chronicles how the triple reassortant H3N2 swine flu later mixed with H1N1, creating a new reassortant H1N1 with both human and avian genes. This reassortant H1N1 became the dominant strain of swine flu in the US pig herd.
It has also been suggested that the presence in the novel strain of genetic components from both North American and Eurasian swine flu strains indicates that the final reassortment could not have occurred in Mexico. Nonsense, says Professor Vincent Racaniello of Virology Blog:
Q: Mexico’s chief epidemiologist insists this virus did not begin in a Mexican pig farm. “Miguel Angel Lezana, Mexico’s chief epidemiologist, told reporters…. the presence of Eurasian swine flu genes in the H1N1 virus makes it unlikely that the disease originated in a Mexican pig farm.”
A: Chief Epidemiologist? He should be fired. The fact that Eurasian swine flu genes are present in no way makes a Mexican origin more unlikely than any other. [emphasis added]
“A disaster waiting to happen” but are CAFOs more responsible than other pig farms?
It’s hard to avoid the New Scientist’s conclusion that “swine flu was a disaster waiting to happen”. Even if we’re lucky enough to escape a pandemic this time, all the pieces remain in place for further threatening reassortment and mutation.
There’s clear scientific consensus on the role pigs play in harbouring and breeding new strains of flu, but does intensive production, as practised in CAFOs, present higher levels of risk than other methods of pig production?
Various factors come into play in answering this question: the numbers of pigs housed in each unit and their stocking density; the bio-security of units, in avoiding cross-contamination between pigs and both human farm-workers and other species such as poultry.
Bio-security: the gap between theory and reality
At least one expert takes the view that modern CAFOs have an advantage over traditional production in the higher bio-security they offer in relation to other species, particularly poultry. As ScienceInsider reports:
There is much concern that pigs infected with this H1N1 might become infected with a dangerous influenza virus from fowl, like the H5N1 that causes avian influenza, leading to a dangerous superbug.
But Christopher Olsen, a swine influenza researcher at the School of Veterinary Medicine at the University of Wisconsin, Madison says this is unlikely on large hog farms.
“Most modern swine production facilities are single species. The days of a small farmer having pigs and fowl and other animals all mixing together is really unusual in terms of modern commercial swine. My opinion is modern swine facilities have better biosecurity than old-time farms.”
The “most” causes some concern, as just a single lapse of bio-security can have devastating consequences. Indeed, Caroline Lucas has suggested in The Guardian that the critical reassortment of swine, avian and human influenza strains may have occurred in CAFO(s) where pigs and poultry were housed in close proximity, with workers going between them:
Dr Greger has highlighted how some experts blamed the emergence of the original 1998 virus on intensive farming practices in the US, where pigs and poultry are raised in extremely cramped conditions, in adjacent sheds – and tended to by the same staff. [emphasis added]
Another reported lapse in bio-security is the use in CAFOs of water from ponds frequented by wild fowl:
[...] an unknown pathogen [...] that infected two groups of pigs at separate production facilities in 2006. Both facilities used pond water frequented by migrating waterfowl.
Ellen Silbergeld, professor of environmental health sciences at Johns Hopkins Bloomberg School of Public Health and an expert on pathogen evolution, is stark in her criticism of CAFO’s bio-security, telling David Kirby of the Huffington Post:
CAFOs are not biosecure. They have high rates of ventilation and enormous number of animals that would die of heat stress unless the building was ventilated. We and others have measured bacteria and viruses in the environment around poultry and swine houses. They are carried by flies, too. These places are not bio-secure going in – or going out. [emphasis added]
Numbers and density
Silbergeld goes on to assert that the intensive nature of CAFOs is responsible for a significantly heightened level of risk in the evolution of new flu viruses:
These mixing bowls of intensive operations of chickens and pigs are contributing to speeding up viral evolution. I think CAFOs are contributing.
[But, what about traditional outdoor farms? Aren't those animals even more susceptible to wild type viruses than animals kept indoors, as industry claims?] Well, let’s say that animals in confinement are ten times less likely to be infected by wild animals. But there are 100 times as many of them. You do the math. [emphasis added]
Ruth Watkins – farmer and former lecturer in clinical virology, Imperial College School of Medecine, London – agrees that the numbers and density (and movement) of pigs are critical, stating in an email to Warmwell:
[...] big commercial units with hundreds and thousands of pigs are essential to provide the immune driven mutation, and the mixing, the reassortment opportunities offered by dual or multiple infections and the onward transmission opportunity for newly reassorted viruses.
Successful reassorted viruses do not occur as frequently as you might think. The newly reassorted virus must exit the pig in sufficient quantity to be infectious so that it has competed in the host with the original infecting virus to infect new cells, be competent to infect a new host, to compete with other prevalent influenza viruses. If successful in all these respects it must be spread to new populations and what better route than commercial and globalised trade of piglets.
If one thinks of the small farm with animals outside where are the opportunities for this with influenza? Even if an interesting new virus does emerge it has a small number of animals to infect (influenza viruses give rise to acute infections so that virus is shed for a short period of time only) so where does it go next? It most likely comes to a dead end. [Emphasis added]
The Pew Commission on Industrial Farm Animal Production’s report Putting Meat on the Table: Industrial Farm Animal Production in America stresses a similar point:
While transmission of new or novel viruses from animals to humans, such as avian or swine influenza, seems a rather infrequent event today (Gray et al., 2007; Myers, Olsen et al., 2007), the continual cycling of viruses and other animal pathogens in large herds or flocks increases opportunities for the generation of novel viruses through mutation or recombinant events that could result in more efficient human-to-human transmission. In addition, as noted earlier, agricultural workers serve as a bridging population between their communities and the animals in large confinement facilities (Myers et al., 2006; Saenz et al., 2006). Such novel viruses not only put the workers and animals at risk of infection but also may increase the risk of disease transmission to the communities where the workers live. [Emphasis added]
A desperate need for answers and action
It appears that even the US National Pork Board’s own expert accepts the need for action in response to the virus threat from modern pig production, as David Kirby reports:
The Pork Board’s Dr. Wagstrom said her industry has been working closely with the US Government for nearly a year to set up a new monitoring and rapid animal-identification system for emerging swine flu strains in the U.S. herd. Wagstrom added that the new virus “could have” emerged from a Mexican swine CAFO, though she doesn’t think birds were involved.
There may be no smoking gun (a conclusive demonstration of cause and effect is a tall order), but there’s a large body of evidence suggesting that intensive pig production has some difficult questions to answer. At the very least, vastly improved monitoring is required to track the emergence of virus strains and reduce their potential to spread. Grist’s Tom Philpott reports that the USDA has very recently taken steps to introduce a federal screening programme.
However, further investigation and research is also needed into the role of CAFOs in the evolution of viruses. As a negative externality, alongside the fostering of other pathogens (such as MRSA), animal welfare and pollution issues, it brings into question the very viability of such intensive production.
