Swine flu (otherwise known as swine influenza H1N1) has now been confirmed in seven countries across the North American, European, Middle Eastern and Asia-Pacific regions. In response, the World Health Organization has raised their pandemic alert to Phase 4, characterized by clear evidence of human-to-human transmission. This is one phase below the WHO designation that a global pandemic is “imminent”. As of today the number of confirmed cases is relatively low, with the estimated number of deaths in the worst hit country (Mexico) at 149 with nearly 2,000 hospitalizations. There have been many fewer cases outside of Mexico and no reported deaths (UPDATE: First non-Mexican fatality has occurred in Texas.) At this point there is no reason for public concern other than reducing the potential for exposure in high-risk areas and seeking treatment at the first signs of the common symptoms. However, the outbreak raises serious concerns about how quickly a new disease can cross the globe given the ease of travel in the modern world. For this reason, just as it was in London of the 1850s, it’s important to understand what the origin for this current outbreak may be and consider strategies for preventing pandemics before they begin.
The most likely origin, given the high number of infections and the fact that they were the first country with confirmed cases, is Mexico. According to Mexico’s Health Minister, Jose Angel Cordova, the virus “mutated from pigs, and then at some point was transmitted to humans.” Recent reports suggest that the state of Veracruz, specifically the mountain region of La Gloria, is the origin for the first cases. In a region of only 3,000 people it’s estimated that 60% of the population fell ill with swine flu symptoms as early as February of this year. As the Guardian newspaper reported yesterday, the H1N1 virus was confirmed in this area when a sample from a four-year old boy was sent for analysis earlier this month. As of now, this is the earliest confirmed case of swine flu in the world.
What is also significant about the location is that the area around La Gloria is home to one of the largest industrial pig farms in all of Mexico. As reported in The Times of London:
The facility, Granjas Carroll de Mexico, is partly owned by Smithfield Foods, a Virginia-based US company and the world’s largest producer and processor of pork products. Residents of La Gloria have long complained about the clouds of flies that are drawn to the so-called "manure lagoons" created by such mega-farms, known in the agriculture business as Confined Animal Feeding Operations (CAFOs).
According to Smithfield’s website, the facility in Veracruz has 56,000 sows and produced 950,000 hogs in fiscal year 2008 for brands like Weight Watchers and Butterball. While Smithfield denies that the virus could have begun at Granjas Carroll, the conditions of Smithfield’s Mexican subsidiary are appalling. In photos published yesterday on the Mexican website Enlace Veracruz 212 (with commentary in Spanish), leaky pipes are shown transporting pig excrement to a dumping spot the size of a small lake, a dead hog lays rotting in the heat, and piles of diseased animals are stacked onto a cart. There has been no confirmation that swine flu had its origin at Granjas Carroll, but the timing and the location of the earliest reported case is highly suggestive. According to La Gloria resident Erasto Bautista, “We have been fighting this disease for months now and complaining about the pig waste for years,” he said in an interview with the Daily Telegraph, “We are glad to see that the world is finally listening to us.”
Currently, Smithfield has stated it is cooperating with genetic tests of animals from Granjas Carroll to determine if the virus is detected. However, if any of their animals turn out to be positive, it needs to be emphasized that this would not simply be a case of impoverished conditions in Mexico resulting in a global pandemic. Rather, this would be the predictable result of standard policies in modern industrial farming. Smithfield is the current global leader in hog production and, according to a 2006 expose in Rolling Stone, the alleged conditions at Granjas Carroll are just a drop in the bucket. The details are worth quoting at length:
Smithfield's pigs live by the hundreds or thousands in warehouse-like barns, in rows of wall-to-wall pens. Sows are artificially inseminated and fed and delivered of their piglets in cages so small they cannot turn around. Forty fully grown 250-pound male hogs often occupy a pen the size of a tiny apartment. They trample each other to death. There is no sunlight, straw, fresh air or earth. The floors are slatted to allow excrement to fall into a catchment pit under the pens, but many things besides excrement can wind up in the pits: afterbirths, piglets accidentally crushed by their mothers, old batteries, broken bottles of insecticide, antibiotic syringes, stillborn pigs -- anything small enough to fit through the foot-wide pipes that drain the pits. The pipes remain closed until enough sewage accumulates in the pits to create good expulsion pressure; then the pipes are opened and everything bursts out into a large holding pond.
The temperature inside hog houses is often hotter than ninety degrees. The air, saturated almost to the point of precipitation with gases from shit and chemicals, can be lethal to the pigs. Enormous exhaust fans run twenty-four hours a day. The ventilation systems function like the ventilators of terminal patients: If they break down for any length of time, pigs start dying.
From Smithfield's point of view, the problem with this lifestyle is immunological. Taken together, the immobility, poisonous air and terror of confinement badly damage the pigs' immune systems. They become susceptible to infection, and in such dense quarters microbes or parasites or fungi, once established in one pig, will rush spritelike through the whole population. Accordingly, factory pigs are infused with a huge range of antibiotics and vaccines, and are doused with insecticides. Without these compounds -- oxytetracycline, draxxin, ceftiofur, tiamulin -- diseases would likely kill them. Thus factory-farm pigs remain in a state of dying until they're slaughtered. When a pig nearly ready to be slaughtered grows ill, workers sometimes shoot it up with as many drugs as necessary to get it to the slaughterhouse under its own power. As long as the pig remains ambulatory, it can be legally killed and sold as meat.
The drugs Smithfield administers to its pigs, of course, exit its hog houses in pig shit. Industrial pig waste also contains a host of other toxic substances: ammonia, methane, hydrogen sulfide, carbon monoxide, cyanide, phosphorous, nitrates and heavy metals. In addition, the waste nurses more than 100 microbial pathogens that can cause illness in humans, including salmonella, cryptosporidium, streptocolli and girardia. Each gram of hog shit can contain as much as 100 million fecal coliform bacteria.
Smithfield's holding ponds -- the company calls them lagoons -- cover as much as 120,000 square feet. The area around a single slaughterhouse can contain hundreds of lagoons, some of which run thirty feet deep. The liquid in them is not brown. The interactions between the bacteria and blood and afterbirths and stillborn piglets and urine and excrement and chemicals and drugs turn the lagoons pink.
Still enjoying your BLT? What makes this situation worse is that Smithfield isn’t solely responsible for these practices; they are merely the industry leaders pursuing a policy that is standard operating procedure for factory farming. This has all been well documented and a series of studies over the last few years have emphasized the problems, and the potential dangers, of creating these enormous breeding grounds for pollution and disease.
An early study, in 2000, by epidemiologists Steve Wing and Gary Grant in the journal Environmental Health Perspectives found that groundwater contamination is widespread at CAFO facilities and mostly affects poor and minority citizens that live in rural areas (which may explain why little has been done to address the problem).
Most hog operations, which use waste pits that can contaminate groundwater, are located in areas with high dependence on well water for drinking. Disproportionate impacts of intensive hog production on people of color and on the poor may impede improvements in economic and environmental conditions that are needed to address public health in areas which have high disease rates and low access to medical care as compared to other areas of the state.
The Centers for Disease Control and Prevention issued a warning in 2004 highlighting that “the nation’s 238,000 feeding operations produced 500 million tons of manure” and that “a small percentage of those facilities—called concentrated animal feeding operations (CAFOs)—accounted for more than half of the manure.” They further warned that:
In studies of CAFOs, CDC has shown that chemical and infectious compounds from swine and poultry waste are able to migrate into soil and water near CAFOs. . . Pollutants possibly associated with manure-related discharges at CAFOs include: Antibiotics, which may contribute to the development of antibiotic-resistant pathogens [and] Pathogens, such as parasites, bacteria, and viruses, which can cause disease in animals and humans.
In 2008 the Pew Commission on Industrial Farm Animal Production issued their report in which they warned of:
Numerous known infectious diseases can be transmitted between humans and animals; in fact, of the more than 1,400 documented human pathogens, about 64% are zoonotic [transmitted from animals to humans]. . . For this reason, industrial farm animal production facilities that house large numbers of animals in very close quarters can be a source of new or more infectious agents. Healthy or asymptomatic animals may carry microbial agents that can infect and sicken humans, who may then spread the infection to the community before it is discovered in the animal population.
Most recently, just last week in fact, the Union of Concerned Scientists released their report, CAFOs Uncovered, in which they highlighted that:
High-density confinement means that animals may be exposed to their own manure, which is typically collected within the stocking facilities, often after dropping through slatted floors. The manure can harbor and spread disease-causing organisms, and gases such as ammonia and hydrogen sulfide emitted from the manure can be harmful to both animals and workers. CAFOs also release these harmful products into the surrounding air and water, causing problems far beyond the facility itself.
In the last few years researchers have been warning of the potential that CAFOs represent for the incubation and dissemination of dangerous new diseases. Just to cite a sample from the UCS report:
- Chapin et al_. (2005) writing in "_Environmental Health Perspectives":http://www.ehponline.org/docs/2004/7473/abstract.html determined that substantial levels of antibiotic-resistant pathogens or indicator species (bacteria that are not themselves pathogenic, but are often found together with pathogens) have been isolated from the air in swine CAFOs.
- Green et al_. (2006) writing in the "_Journal of Occupational and Environmental Hygiene":http://www.ncbi.nlm.nih.gov/pubmed/16482973 found potentially pathogenic bacteria—especially Staphylococcus aureus—up to 150 meters downwind from swine CAFOs, suggesting that there is significant risk from airborne pathogens close to CAFO sites.
- Sayah et al_. (2005) in "_Applied and Environmental Microbiology":http://aem.asm.org/cgi/content/abstract/71/3/1394 determined that water sources near CAFOs may also act as vectors of infection for the nearby population. Antibiotic-resistant bacteria or resistance genes that originated at swine and other CAFOs were detected in both ground and surface water.
- Sapkota et al. (2007) found fecal indicator bacteria (Enterococci and coliforms) in test wells 250 and 400 meters downgradient from swine CAFOs (i.e., where groundwater is at a deeper level than directly below the CAFO), at concentrations that were higher than EPA safe drinking water guidelines. This was especially disturbing considering that groundwater supplies 97 percent of rural drinking water and, since individual wells are often untreated, exposure from these sources could be significant.
- Koike et al. (2007) found tetracycline-resistant bacteria (an antibiotic famous for helping stamp out cholera and now used to ward off disease in factory farms) as much as 250 meters downgradient from a swine CAFO and determined they had survived there for over three years. Soil-dwelling bacteria found in the groundwater downgradient from CAFOs carried identical tetracycline-resistance genes as those found in swine manure lagoons, while bacteria from upgradient sites did not. This strongly suggests that gene transfer had occurred between CAFO bacterial species and those better adapted to surviving and spreading in soil. This means that highly virulent bacteria that are adapted to the manure lagoons could infect other bacteria that are adapted to different environments (like your bathwater).
What this collected information represents is a potential blueprint for why swine flu is the main topic for discussion on the 6 o’clock news. Even if the source for this current outbreak remains inconclusive after additional testing, it is clear that there is a disaster waiting to happen. Currently, American politicians are more concerned with protecting the pork industry by renaming swine flu than with addressing the root of the problem. For the last thirty years we have chosen a policy that has concentrated our food industry into a highly unstable structure that is not so much “too big to fail” but so big it must fail. We may have been able to buy slightly cheaper pork chops, but we’ve also created a perfect system for manufacturing highly-virulent disease organisms that can be disseminated quickly into a world without walls.
Fortunately, the solution is a simple one. We’ve allowed our food production to become concentrated into an industry with a large number of animals at just a few facilities and now we must do the opposite. Supporting local food production, the closer to home the better, will help to spread our food sources away from a few enormous mega-farms and into smaller, regional farms with fewer animals at each. Many locally-owned grocery stores, food co-ops and farmers markets will carry these products. Then, since government subsidies have supported the concentration of this industry, we need to insist that only small farms be given these subsidies (or that farm subsidies be ended altogether). The process may take some time, but that’s entirely dependent on what we decide is important. We’ve been priming the pump of food industry concentration for more than three decades. If we want to prevent the future spread of disease pandemics we only need to follow John Snow’s advice from 160 years ago: remove the handle.
For more see: Capitalist Pigs and the ‘NAFTA Flu’
UPDATE 1: Nature now has special coverage of swine flu related news and research. Click here for more.
UPDATE 2: Interview with CDC Chief Virologist Ruben Donis by the journal Science confirms that H1N1 is derived from hogs and may have originated in US production facilities. Donis questions Smithfield’s claim that Granjas Carroll could not be the source: “The only suspicious thing in that story is this is the largest farm in Mexico. The fact that the index case also is from the area makes it interesting.”
UPDATE 3: H1N1 influenza virus has now been confirmed in eleven countries and the WHO has raised their pandemic level to Phase 5. The confirmed number of deaths in Mexico from H1N1 is 7 with 97 infections. There have been 257 confirmed cases worldwide and only one other death (a child in Texas, whose family was visiting from Mexico). These numbers are almost certainly low, as these are only the cases confirmed by laboratory tests.
UPDATE 4: This is a rapidly changing event, so for further updates I recommend the following websites:
UPDATE 5: The New York Times reports on Smithfield’s role in Romanian swine flu: “[Smithfield] moved with such speed that sometimes it failed to secure environmental permits or inform the authorities about pig deaths — lapses that emerged after swine fever swept through three Romanian hog compounds in 2007, two of which were operating without permits. Some 67,000 hogs died or were destroyed, with infected and healthy pigs shot to stanch the spread.”
Last updated:
Wednesday, 29 Apr
2009 - 06:00 UTC
Brilliant post, Eric! And an excellent reminder of how our (in the US) demand for cheap food and inexpensive products negatively impacts thousands of people elsewhere, including our close neighbor, Mexico.
A lot of our produce here in Texas comes from Mexico – in fact, for some of us, it could be considered “local”. In addition to the issue of pesticide use, there’s also the problem of bacterial contamination with runoff from intensive livestock farming operations. A backyard vegetable garden becomes all the more attractive.
Great post, Eric. However, I am still puzzled about the connection between intensive pig farming (unpleasant though it is) and swine flu. As far as I recall, H5N1 avian flu came from the opposite kind of establishment – small, family-run flocks that lived with humans close by. In some way, one might argue that huge, centralized hog warehouses, while horrible for the pigs, would make disease outbreaks simpler to control. Here in Norfolk, loads of pigs are reared free-range in fields … the containment problems are too complicated to think about, and would no doubt have to result in the effective shutdown of the entire country, as happened in the foot-an-mouth outbreak a few years back.
In the meantime, the Gee flock of six bantams, undoubtedly the most spoiled chooks in Cromer, is just about to move from one of these
to one of these
… a massively intensive facility that can in principle house ten
egg production unitschickens.Henry, I’m glad you brought up avian flu. The evidence that factory farming is the source of H5N1 is fairly strong, the difference is that avian flu can infect migratory birds making the original source difficult to pinpoint. Pigs don’t yet have that kind of range, notwithstanding reports by the Walrus and the Carpenter.
According to The Lancet (Vol 6., 2006) the idea that migratory birds were the cause was widely circulated but with relatively little evidence.
The Lancet editors recommend the 2006 GRAIN report “Fowl Play: The poultry industry’s central role in the bird flu crisis” and I highly encourage people to look through it.
To cite just one study they refer to in their report please see Chen et al. (2006) in PNAS. After they tested more than 13,000 wild birds in marshes within bird flu infested provinces in China, researchers only identified six pathogenic bird flu viruses in six ducks. The study’s conclusion was that: “Transmission within poultry is the major mechanism for sustaining H5N1 virus endemicity in this region.”
However, I fully support your “intensive” farming practices. I’m sure your kids love it too.
As for the argument that small, family run flocks are the most likely source for avian flu, let me quote the GRAIN report (page 8):
thank you Eric for coming by Watergate Summer, and I did add a link to this…really brilliant article , thank you for your research and sharing..
Fantastic post, Eric. I don’t have anything to add, but have sprinkled the link around a bit… this is important stuff to know for everyone.
Eric – thanks again for these replies. I consider myself informed. When I have finished groping underneath chickens for eggs, I shall riff on this in another place
Fascinating post Eric – many thanks. I am by no means an expert in this area but I have a couple of questions/observations.
First about the PNAS report that you mentioned. I had a quick glance at it and spotted that out of the >13000 samples tested they only found 44 that contained influenza virus (though I thought is was more or less endemic in wild fowl); of these 44, 6 were the H5N1 strain. 6/44 is obviously a bigger ratio than 6/13000 suggesting that infection of wild fowl is a not insignificant factor in the spread of disease, though of course intensively farmed poultry populations are clearly an important reservoir (and the major factor sustaining the outbreak in southern China, as the authors conclude).
Second – the assertion that the virus pathogenicity increases during infection among intensively farmed populations is very interesting. Do you know of any peer-reviewed reports that have demonstrated this (for ‘flu or any other virus)? I didn’t spot a reference in the GRAIN report but may have skimmed too fast.
Eric> Let me start by saying that I am not a fan of industrial farming, in the pig factories we see (or the milk factories with milking hours in three shidts to fully utilize the milking machines). However, all of the conclusions/suggestions you make that this industrial farming is the source of this outbreak of swine flu is a bit quick.
Why do i state that? Mainly because it is the pig in itself that is the “problem” when it comes to human adaptation of the influenza virus. It has a good thrachea where different viruses can replicate and exchange information. Actually even small farms, or back yard poultry and pig keeping (as very common in Asia) has been looked at as a problematic area when it comes to having a H5N1 strain present and then add on a human taking care of the animals and poultry kept in a cage on top of the pigs’ pen (bird manure is high in protein and can be used as food source for pigs sometimes). It is in conditions like these that the H5N1 has clamed human fatalities, without industrial farming…
That’s not saying that industrial farming hasn’t got big problems and is looking at animals in a very “economical” and non animal friendly way.
For the last thirty years we have chosen a policy that has concentrated our food industry into a highly unstable structure that is not so much “too big to fail” but so big it must fail. We may have been able to buy slightly cheaper pork chops, but we’ve also created a perfect system for manufacturing highly-virulent disease organisms that can be disseminated quickly into a world without walls.
It might be important to point out that the last 40 years people in the industrial worlds have grown used to and is expecting to be able to eat meat almost every day – in contrast to earlier times when meat consumption was limited to the rich… It is a need to remember that it might be interesting to find a middle ground here where not only rich people can eat the correctly produced meat?!
Supporting local food production, the closer to home the better, will help to spread our food sources away from a few enormous mega-farms and into smaller, regional farms with fewer animals at each.
It might furthermore be interesting to point to the studies that have been made on organic farming and looking at the potential and confirmed pathogens that are present in soil/environmental samples which are spreading to the animals. For example,Trichinella spiralis, causing Trichinosis has been appearing in free range pigs. Again, this is not a problem IF you cook your meat properly but if you shift from eating pork (from industrial farming) where this risk is very low and go back to the better farming (for the pig) with free range, this is a risk we need to inform about so people don’t get harmed. Again, back in the good old days people knew lots more about handling meat and animals in order to have good meat/produce. Today I am not so sure.
And on that note, I will leave veal production out of the debate. But I think this disucission about pig farming and industrial farming really needs to make a note about the key thing; why we ended up with industrial farms and how we should solve that issue in case price is not the distinguisher?!
(and I buy organic meat, am not a fan of egg production or poultry plants which in my opinoin is in quite a bad state too. And not mentioning the amount of antibiotics that are put in animals in the US … nor how bad it can get for a cow, in an organic milk production, who gets sick and might need treatment for that.)
… another thing (sorry about the lenghty post) One of the big problems with big industrial farms is that the animals in there are more susceptible to disease due to high concentration of individuals as well as being genetically alike and therefore, once a virus gets hold of the population it can spread throughout the population of animals quickly. This is one of the reasons why all the birds had to be slaughtered when H5N1 was suspected in some industrial settings in Europe. Also one of the reasons farmers are weary of letting people enter their farms since if they get one sick pig, more are likely to follow. (It is therefore a slightly sensitive setting, and often the dosage of antibiotics increase the bigger the population of animals, by need. Then again, there are countries that doesn’t allow antibiotics as a addative in the food as a precaution but rather allows it when and only when sickness is determined.)
Stephen – (It appears that Åsa addressed some of what I was just preparing to post – Thanks for the insight!) I didn’t see anything about virus pathogenicity specifically in the GRAIN report and the UCS report emphasized the economic costs and the potential transmission of virulent pathogens but didn’t specify that this had occurred before (thankfully!).
I think the logic in this case is remarkably similar to the cases of multidrug resistant tuberculosis (MDR-TB) that were incubated in Russian and central Asian prisons. It’s not so much that pathogenicity increases as the result of close proximity, merely that once a mutant strain develops it has easy access to hundreds or thousands of additional hosts and can spread rapidly. Those strains that survive in fecal material are then flushed out to manure lagoons where they can contaminate ground water.
For examples of MDR-TB see Stuckler et al. (2008) or this recent story in Scientific American.
This has also been documented for pigs in the peer-reviewed Journal of Swine Health and Production that may have what you’re looking for. Desrosiers et al. (2003) report on a herd of previously healthy pigs that saw the introduction and rapid spread of swine influenza virus (SIV).
They also cite additional papers that demonstrate explosive epidemics of swine influenza associated with factory farm CAFOs:
While there’s no way to completely protect animals from developing deadly viruses, it would seem that preventing large concentrations of animals would be a good safeguard against spreading a virulent strain once it does arise. Of course, in the case of MDR-TB the cause was from not finishing a complete series of antibiotics. It would be interesting to know what potential effects the large amount of antibiotics administered to factory farm animals are having in the creation of virulent diseases?
Thanks for that Eric but I don’t think it directly addresses the assertion made in the GRAIN report. As you quoted them:
This is a pretty strong statement so I was wondering what was the evidence. I can certainly imagine that high-density herds provide an easy target for an invading virus and that the virus population might evolve rapidly because it quickly passes between hosts. But why would it necessarily evolve towards increased pathogenicity? I guess that, having spent some time in domesticated animals, when it comes into contact again with wild populations of birds, it might have changed sufficiently to result in more severe disease in these animals. Equally however, once it has passed around the wild population (and changed again), re-introduction to domestic animals could well be dangerous. So the problem may be more one of the virus jumping back and forth between different populations.
But this is all speculation on my part – I was hoping someone who knew what they were doing had done a rigorous study. Not that I wan to impugn GRAIN, but they seem to have an agenda that may make them a less than impartial source of information.
Åsa – I think you are correct that caution needs to be taken to accurately identify the origin of the current swine flu outbreak (about to be classified as a Phase V pandemic as I write this). I specifically mentioned in my post that it’s currently unknown if CAFOs are the cause of this H1N1 virus, but that the epidemiological argument is quite strong and should be an issue of concern.
As for your concern about cost, it’s true that (as of right now) locally raised animals are more expensive than factory farm animals, thanks largely to the money companies save on feed and infrastructure by dealing in such high volume. It’s also true that governments subsidize factory farms much more than localized farms. However, I don’t think your argument stands that reducing the number of factory farms and promoting local food production means that only rich people will be able to eat meat.
In 2007 Elanor Starmer and Timothy Wise of Tufts University published their study (Living High on the Hog – Factory Farms, Federal Policy, and the Structural Transformation of Swine Production) and found that, thanks to government subsidies as part of the 1996 Farm Bill, factory farms were able to save an average of $947 million each year between 1996 and 2005. Small and mid-sized farms would be better able to compete if these subsidies were eliminated (and potentially able to provide a cheaper product if the subsidies went to them instead).
When we factor in the “externalized” costs associated with factory farm COFAs (see the reports mentioned in my post) the logic of continuing our current policy would seem to be as economically irresponsible as it is medically dangerous.
Stephen – I can’t speak for GRAIN as an organization other than to assess the quality of their research. However, it turns out that they do discuss this question of increased pathogenicity in avian influenza and I simply missed it. On this question they cite three papers and I will link to them along with their associated abstracts:
Suarez et al_. (2004) in the journal "_Emerging Infectious Diseases":http://www.cdc.gov/ncidod/EID/vol10no4/03-0396.htm:
Suarez, DL (2000) in Veterinary Microbiology:
Ito et al_. (2001) in the "_Journal of Virology":http://jvi.asm.org/cgi/content/abstract/75/9/4439:
My goodness Eric, you are thorough! I had a quick scan of the papers. Part of the difficulty in addressing this question seems to be down to problems with keeping track of virus populations circulating in the wild. It’s obviously easier to track virus evolution within a domesticated population on a farm.
I’ve linked to this post here
Stephen:
I can certainly imagine that high-density herds provide an easy target for an invading virus and that the virus population might evolve rapidly because it quickly passes between hosts. But why would it necessarily evolve towards increased pathogenicity?
It wouldn’t necessarily evolve into more pathogentic but since it’s in its nature to exchange the segment(reassort)/mutate the sequence it would probably change and evolve and the only viruses we would see would probably be the more pathogenic ones. (or more transmissiable ones that would be persistent in the population).
I guess that, having spent some time in domesticated animals, when it comes into contact again with wild populations of birds, it might have changed sufficiently to result in more severe disease in these animals. Equally however, once it has passed around the wild population (and changed again), re-introduction to domestic animals could well be dangerous. So the problem may be more one of the virus jumping back and forth between different populations.
Key thing would be that if the virus moves from one type of population (wild birds) to another one (poultry for example) the new population might not have any antibodies against the strain since they never had encountered the virus before. THat is partly why the species jumping viruses are so disturbing. (Partly why the humans who lived in the 1968 would be more protected against a new strain of 1968 Hong Kong flu if that came around again… )
And yes, it is hard to sequence and keep track of all the strains in the wild since there are quite a few of them, always changing and evolving. The primers wouldn’t always work with new ones etc…
Eric:
As for your concern about cost, it’s true that (as of right now) locally raised animals are more expensive than factory farm animals, thanks largely to the money companies save on feed and infrastructure by dealing in such high volume. It’s also true that governments subsidize factory farms much more than localized farms. However, I don’t think your argument stands that reducing the number of factory farms and promoting local food production means that only rich people will be able to eat meat.
I agree that large money saving in big feeding is probably one of the savers for industrial farming and that we never should’ve expanded into the industrial farming thjs much. It a huge problem, and as you state in the beginning, maybe more to do with manure and all the waste very centralized than much of the other concerns.
I am sorry but I fail to see how the current cost of production of especially pigs meat and what the farmer get and the cost in the store is to be maintained if we shift into “more locally produced” as well as “better farming”. I haven’t seen the fact the government subsidize industrial farms more than local farms (it might be very different here in the US compared to Europe) however, the amount of meat production we currently have is enough to keep the prices low for the consumer. If it shifted into less industry, more locally production of happy pigs in smaller populations there will be less amount of meat (it will be better most likely) and thus the price will go up, mainly because it is more expensive to keep happy pigs.
I don’t think that we will end up with only rich people eating meat but but there is going to be a need to discuss this since we now have (too) cheap meat/eggs in contrast to what kind of animal welfare we have. I haven’t seen any studies that state that the prices would stay this, however it might not be changed into 50dollars/pound pork but I don’t think it is likely it would stay at the 4dollars/pound as it might be now. And a change into say 9dollars/pound might be enough for people to not understand why we would have to do this “since I can’t have meat every day and why isn¨’t it as cheap as it was before” (answering that it was too cheap and not realistic might not do the trick in this group?). And letting the government subsidize even more for locally produced meat (or any farming in general) might not be the solution either if you look at the heavy subsidized European union and their overproduction of plenty of the food items.
Hopefully, all this will be on the agenda soon…. but I think it would be from the point of view that we have realised that we can’t keep this up and it has to change. Then we also probably have to change our view on meat and food in general.
This is a pretty strong statement so I was wondering what was the evidence. I can certainly imagine that high-density herds provide an easy target for an invading virus and that the virus population might evolve rapidly because it quickly passes between hosts. But why would it necessarily evolve towards increased pathogenicity?
I’m not an expert on this, but my PhD was on the evolution of more pathogenic genotypes of feline leukemia virus during in vivo infection, so I might make a few comments — even though I’m by no means a flu expert. It is not in a virus population’s advantage to become so pathogenic that it kills off the host reservoir, but there could indeed be a selection pressure for increased replication, which can manifest as increased pathogenicity in some cases. I don’t have access to journals here, but the J Virol paper cited above, from the abstract, looks like a highly artificial situation — I assume the “passaging” was done via human intervention? I have no doubt you can force a virus to change genotypes, but would it happen the same way under the actual mingling and selection pressure that goes on? That’s the paper I’d like to see.
The Vet Micro paper, from the abstract, doesn’t look as if it’s addressing pathogenicity per se, unless I’m missing something.
The first paper shows one example of pathogenicity appearing to evolve in a more natural cohort. But the question would be, and I think Asa mentioned this – is this also happening in other settings, and what is the relative frequency? Is it truly more common in intensive situations? I think you’d need to look at a lot more cohorts, and compare them to wild cohorts, to get a clearer idea. Those would be great experiments, and hopefully there are lots of scientists now scrambling to make those sorts of studies in the current outbreak.
Again, apologies if I’m missing something because I can’t access the full papers. But I’m not sure GRAIN’s statement, though it may represent truth, has entirely been backed up by the three studies it cites. If I was refereeing it for a peer-reviewed journal, I’d probably ask the authors to qualify their statement somewhat — or find a lot more references.
Hi.
Another thread sent me here with my question about an article from The Journal of Virology. The article can be found here. Just click the link for the small .pdf:
Experimental infection of pigs with the human 1918 pandemic influenza virus
Some of the wording in this document is distressing:
“Viruses used in this study were rescued using reverse genetics….”
“Swine have been proposed as an intermediate host in the indirect transmission of influenza A viruses from an avian reservoir to humans … The presence of the avian and human receptors in the swine respiratory tract can enable the pigs to become infected with either avian or human influenza A viruses, setting the stage for reassortant events between swine, avian, and human viruses, or for adaptation of an avian virus to a mammalian receptor….”
I was wondering if you folks are aware of this article, and I’d be interested to know what you think of it. Am I right that the 1918 flu was brought back through genetic reconstruction and that it was intentionally re-introduced into the world through the experiments described in the article? If so, can the strains described in the article be compared to the strain which caused the recent outbreak?
Thanks.
@Michael – Thanks for sending this over. It’s very interesting. You’re right that the 1918 virus (or “Spanish flu” as it was called back then) was reconstructed and given to pigs in this study. However, it wasn’t “re-introduced to the world” as you say. They inoculated 18 piglets with the virus and state that “Pathological changes were evaluated in all major organs of all piglets at the time of necropsy.” In other words, they were all killed and examined to see what the virus did to them. Poor little piggies.
It’s been hypothesized for many years that the 1918 flu was originally transferred to pigs from humans and has never really gone away. This study gives support to that argument. There have been several flare ups of various forms of swine flu over the last 90 years in pigs and now a mutated version (the H1N1 flu we all know and love today) has been introduced to humans and caught us completely off guard. So, in other words, humans gave the flu to pigs which “remixed” it and gave it back to us. Seems sort of fair actually.
There’s nothing particularly nefarious about what they describe in the paper (other than murdering Wilbur and his family). The research was publicly financed so there was a great deal of control and oversight required in order for them to do the experiment. My concern in the article I wrote here is that the mutant version of swine flu had a higher chance of infecting humans because of the huge number of pigs forced together in factory farm COFAs (for more on that see Farming Pathogens).
A similar study to the one you linked to was released recently looking at avian flu (H5N1). Check out their review over at Science Daily and if you have any other questions please feel free to ask.
Thank you for your response, Eric. That helps clarify things. But if the 1918 flu already existed, why reconstruct it? Technically, I guess I should have said the PURE strain of the 1918 flu was reintroduced to the world.
Something I forgot to mention about the recent flu scare were the reports that the strain had no pedigree…couldn’t be traced back to a previous strain. Isn’t that impossible, unless the new strain is, well, new?
What I’m getting at is, there seems to be a chance that this flu strain was created in a lab. If that’s the case, shouldn’t it be easy to find out where it came from? With all the govt oversight and registry requirements, that should be a walk in the park, right? Like tracing the Ames strain of anthrax used in the “anthrax attack.” Can’t the Mexican flu be traced back to its source?
Thanks again.
The company that released contaminated flu virus material from a plant in Austria confirmed Friday that the experimental product contained live H5N1 avian flu viruses….
http://www.torontosun.com/news/canada/2009/02/27/8560781.html
Fascinating thread on the flu at the link below. Amazing amount of research. Among other points the thread originator makes:
1 Baxter develops re-assorted Swine-Avian-Human virus and gives a sample to Schering-Plough
2 Schering-Plough puts this virus into there farm Swine Flu vaccine distributed to Mexico (they would need to cover there tracks a bit – random lots would contain the virus)
3 Pigs in Mexico spread the new virus to humans
http://forum.prisonplanet.com/index.php?topic=101543.msg678284;topicseen#msg678284
Michael: I was wondering if you folks are aware of this article, and I’d be interested to know what you think of it. Am I right that the 1918 flu was brought back through genetic reconstruction and that it was intentionally re-introduced into the world through the experiments described in the article? If so, can the strains described in the article be compared to the strain which caused the recent outbreak?
The paper you linked to studies what would happen when pigs are infected with the 1918 virus. The virus has been reconstructed in several laboratories over the world, all of them BSL3 (that means, within confinement of air masks for the people and shut off air vents with no possibility of transmission outside of the room – in this case the pen of the pigs). THis means that NO, nothing is reintroduced into the world, but only studied in a very specific room. And all studies are subject to govermental control/security clearance.
The H1N1 that is endemic in pigs in Europe at the time, and also some of the influenza strains we see on a yearly basis, are “relatives” to the 1918 strain. That said, it didn’t just disappear but rather changed into something similar but different.
The strain that caused the recent outbreak, the swine flu H1N1 for lack of better wording, shares the linage of the Spanish flu for the HA and NA (two major proteins on the surface of the influenza virus particle) as in being of HA1 and NA1. The proteins aren’t exactly alike and the other proteins in the virus differ, some are avian, some are swine origin. Hope this helps?!
Thank you, Åsa. You folks have been most helpful. I’m trying to understand how this problem arose. The conclusion I’ve arrived at is that the Mexican flu is manmade. I’ve also come to the conclusion that it was released for depopulation purposes.
Adolph Hitler thanked American and English eugenicists for their groundbreaking work in his book Mein Kampf. After eugenics was tarnished as a “science” in world war 2, it went underground. Today it’s called bioethics, but the goal is the same—to depopulate. The Mexican flu is one of the tools which is being used in this program.
Such is the conclusion I’ve arrived at, and the list of links to support this view would be exhaustive.
On a positive note, the recent Mexican flu outbreak has led to a lawsuit being filed. Jane Burgermeister has recently filed criminal charges with the FBI against the World Health Organization (WHO), the United Nations (UN), and several of the highest ranking government and corporate officials concerning bioterrorism and attempts to commit mass murder. An article regarding her case can be found here:
http://www.naturalnews.com/026503_pandemic_swine_flu_bioterrorism.html
In a nutshell, her case is this:
There exists an international corporate criminal syndicate intent on carrying out a mass genocide against the world population using an artificial (genetic) engineered flu pandemic. This criminal syndicate involves senior individuals at multinational corporations such as Baxter Pharmaceutical, policy think tanks such as the Trilateral Commission and Conference Board, branches of government such as the (U.S.) Executive Branch, and quasi-government organizations such as the World Health Organization (WHO), which have conspired together to commit mass genocide against innocent people using a flu pandemic. The genocide is to take place through human to human spread of increasingly virulent lab created flu, and through contaminated deadly vaccinations intended to be administered in Fall 2009.
Count One—
From in or about 2008 to the present, in the United States of America, and in other countries, including Austria, Switzerland and Mexico, Defendants did conspire with each other and with others to devise, fund and participate in the final phase of the implementation of a covert international bioweapons program involving, among other entities, the pharmaceutical companies Baxter and Novartis, causing death and disease to the people of the United States of America and other countries by first bioenginneering and, then releasing lethal biological agents…
Count Two—
Beginning in or about 2008 to the present, in the United States of America, Defendants have implemented new and/or accelerated the implementation of laws and regulations designed to strip the citizens of the United States of their lawful Constitutional rights to refuse an injection by creating or allowing provisions to remain in place that criminalize the refusal to take an injection against pandemic viruses and by imposing other excessive and cruel penalties such as imprisonment and/or quarantine while barring the citizens of the United States from claiming compensation for injury or death from the above-mentioned forced injection, in violation of laws on federal corruption and the abuse of office and also of the Constitution and Bill of Rights.
Count Three—
Beginning in or about 2008 to the present, the Defendants have been involved in the theft of at least 9 trillion dollars from the people of the United States under the pretext of a bank bailout, and have preplanned the mass murder of the victims of their theft by means of a forced vaccination, also by installing an extensive network of FEMA concentration camps and identifying mass graves in violation of laws on mass murder, federal corruption and Racketeering Influenced Organized Crime.
And so on. Her case is provable, according to legal experts. I just hope none of the nice people here are involved in this nastiness. The employers who promised you immunity (both medically and legally) lied to you. They would despise you if you took part in this and would seek to eliminate you at the earliest possible opportunity. If you have any inside information which will help stop the coming mass murder, I encourage you to make it public now.
Best wishes.
Mike