Dishing the Dirt

The Secret History of Meat

PART ONE: THE HUMAN COST OF DIRTY MEAT

Some say meat is murder. In the long term for human beings, it may be more like suicide. Meat causes death, disease and environmental destruction. Agricultural techniques have contributed to the growth of antibiotic-resistant bacteria (“superbugs”), the spread of food-borne illness and the emergence of lethal conditions like new variant CJD. Our appetite for meat has partly led to the prevalence of the fatal diseases of affluence in our society – cancer, diabetes and cardiovascular disease – and contributed to hunger in the developing world by demanding land and resources be devoted to feeding our farmed animals instead of human beings. Reliance on meat and livestock proved disastrous for the United Kingdom when BSE wiped out our export markets and foot-and-mouth decimated our countryside and the tourist industry on which it depended. As the nations most recently affected by bird flu have learned, meat is not something that you can ever rely on. Not as a commodity, not as a way of life – and certainly not as a food.

This report cannot examine all the ills that derive from meat: instead it will focus simply on the product on our plates – how it gets there, where it comes from and what comes with it. As meat sales have declined and vegetarianism grown, so the vested interests reliant on meat have worked harder and harder to reinforce the idea that the dead flesh of slaughtered animals is a healthy, wholesome and desirable product. Marketing men and women, advertisers, package designers and lifestyle editors have done their very best to disguise the true nature of meat and position it as something modern, fresh and clean – to make a silk purse out of this sow’s ear. The reality is anything but.

Of Meat, Microbes and Men

95% of food poisoning is caused by animal products – either directly or through their contamination of other foods [1] - and the Government’s Food Standards Agency estimates that there are 5.5 million cases in the UK every year.[2] Food poisoning is a disease we simply do not take seriously enough – in the words of the former head of the FSA, “it is a real illness which kills people” [2]. The people it kills also tend to be the most vulnerable - the old and the very young. All of the 21 people who died as a result of the infamous outbreak of E.coli 0157 in Scotland in 1996 were over 65 [3]. In fact, over 500 people became ill in that single incident and 149 required hospitalisation, including children. The cause? Inadequate precautions taken in a single butcher’s shop.

Food poisoning is the illness that results from the contamination of food with harmful bacteria and a relatively small number of types of bacteria are responsible for almost all the serious food poisoning in this country (see table below). Symptoms of food poisoning are generally the same, whatever the bug – abdominal cramps, diarrhoea and vomiting. Patients become dehydrated and for those who are already vulnerable, the resulting disturbance in their body chemistry can lead to kidney and even heart problems. E. coli 0157 is so dangerous because it produces a specific toxin which attacks the  bowel and kidneys. This ‘verotoxin’ causes such severe damage to the lining of the gut that haemorrhage and bloody diarrhoea result. Its damage to kidneys is even worse, leading to haemolytic uraemic syndrome (HUS) which leads in turn to kidney failure. Infection with E. coli 0157 is now the leading cause of acute kidney failure in children.

E coli 0157 is of concern because it is so dangerous once infection takes hold but other bacteria cause more deaths because they infect more people. Between them, salmonella and campylobacter account for millions of cases of food poisoning each year (see table below) and kill hundreds. Because most people do not report symptoms or do not have lab samples taken if they do, confirmed cases hugely under-represent the number of people who become ill across the country – hence the FSA’s estimate of 5.5 million. Other illnesses which are not diagnosed as food poisoning may also be caused by infected food – this is certainly the case with many staphylococcus aureus infections, for instance.

TABLE: Food poisoning bacteria

Notes for table:

a. 2000 figure (no 2003 figure available)

Confirmed cases from Health Protection Agency data, diagnosed by laboratory testing.

Estimated figures based on multiplication of confirmed cases to reflect under-reporting, eg x10 for salmonella, x3 for listeria etc (after Lacey)

Death figures: GK Adak, SM Long SJ O’Brien (2002) Trends in indigenous foodborne disease and deaths 1992-2000 Gut51; 832-841

Salmonella, campylobacter, listeria and E.coli are picked up by animals on farms, transmitted through their faeces (see Part Two) and frequently spread further at slaughter (see Part Three). Unfortunately, while strenuous (if only partially successful) measures have recently been undertaken to reduce the incidence of contamination of meat products, any progress in this area may be nullified by the emergence of increasingly dangerous antibiotic-resistant strains of these bacteria. According to the head of the US Centre for Disease Control’s Infectious Diseases branch, “increasing antimicrobial resistance is [a] general trend among the foodborne bacterial pathogens”.[5]In other words, the antibiotics used to treat all of these infections have become increasingly ineffective in recent years. So far, there has always been another line of defence but – as will be detailed below – the ranks of effective antibiotic treatments are being thinned down further every year. The growth of antibiotic resistance in these infections is directly linked to farming techniques.

Food poisoning also has an impact beyond the health sphere. One estimate put lost working days in the UK at 23 million per year [6] and costs including health care are thought to run between £750m [7] and £1bn [8] every year. And it isn’t just working lives which are disrupted: 4,000 cases of food poisoning were reported to the FSA in December 2002 [9] – and that’s just the reported cases. How many other Christmases were ruined by infected turkeys – up to two-thirds of whom carry campylobacter? [10]

BSE: Made in Britain

The first case of Bovine Spongiform Encephalopathy (BSE) was diagnosed in England in 1986, although it may have been present in the national herd since the 1970s. Since then, over 180,000 British cattle have caught the disease on over 37,000 farms.[11] Although BSE has disappeared from the headlines, it has not disappeared from our cows and over 500 cases were detected in the UK in 2003.[12] The Government claims to be confident that no infected cattle or material from them is now being eaten by the public. The problem is, the Government has reassured us before.

Variant Creuzfeld-Jacob Disease (vCJD) is the human version of BSE and it has killed 143 people in the UK since the first recorded case in 1995 (Source: CJD Surveillance Unit). vCJD has the same devastating effect on human beings as it has on cattle, directly damaging the tissue of the brain causing dementia, incapacity and death. Diseases of this kind commonly have very long incubation periods between infection and the development of symptoms – in human cases measured in decades. Scientists knew this when BSE was discovered in 1986 and knew that if BSE was infecting human beings there would be no evidence one way or the other for years. Despite this uncertainty, throughout the 1980s and early 1990s, the Government maintained that there was no health risk to human beings from eating beef. They were wrong.

The Government did take action over BSE. As a precaution, they ordered that infected cattle should be slaughtered and their carcases disposed of but by the time this order came into force – almost 2 years after the first diagnosis - at least 600 cattle with the disease had already entered the human food chain and the number of infected cattle showing no symptoms is unknown. The problem was compounded by the Government initially offering farmers just half the value of each cow in compensation, little incentive for honesty. In 1989 a ban was introduced on “high-risk” parts of the animal (such as brains and spinal cords) entering the human food chain – although the official inquiry into BSE later concluded that it was poorly enforced.

At every step on this escalating process, the Government reassured the public that they had done enough.  In 1990, the Chief Medical Officer Sir Donald Acheson informed the public that beef was “safe to eat”, despite evidence that it had been contracted by a cat – presumably from meat in cat food and proving beyond doubt that the disease could infect species other than cattle. A few months later – in a publicity stunt that remains one of the most brazen and ill-considered ever undertaken by any politician - agriculture minister John Gummer reinforced the “beef is safe” message by feeding a burger to his 4 year-old daughter before the cameras of the press.

While the Government and industry (see below) maintained that all was well, behind the scenes scientists and officials were trying to find out what was really going on. Suspicions about the original source of the disease quickly focused on its similarity to the well known sheep disease, scrapie. Scrapie had been known for hundreds of years and until that point had never been implicated in disease in any other animal, including humans. Scientists speculated that it may now have passed to cattle because of one of livestock agriculture’s most widespread and – until then – little known practices: feeding rendered animal protein to farmed animals, including members of their own species. While the general public fondly imagined that sheep and cattle grazed in the summer and ate straw in the winter, the reality was that commercial feeds were – and still are - universally used in livestock production. To the agricultural industry – like every business – waste is anathema and slaughtered animals still carry a great deal of material after meat for human consumption has been removed. Recycling that protein in the form of so-called meat-and-bone meal (MBM) seemed like a crafty way of putting it to use – even though it was being fed to animals which were, and had always been, entirely herbivorous. It was thought that cattle had contracted BSE as a result of eating feeds containing  scrapie-infected sheep’s brains: in fact, the scientists were wrong about the specific cause but right about the problem. Cattle caught BSE from the infected brains of other cattle – it wasn’t just meat and bone that was being recycled in that feed. As the Official Inquiry into BSE put it:

BSE developed into an epidemic as a consequence of an intensive farming practice - the recycling of animal protein in ruminant feed. This practice, unchallenged over decades, proved a recipe for disaster.[13]

When, in March 1996, the Spongiform Encephalopathy Committee announced the discovery of vCJD, they pointed the finger at BSE-infected meat as the likely source of this new infection. With this announcement, the Government’s previous attempts to defend the UK cattle industry from the inevitable economic consequences of beef being associated with a fatal illness were blown out of the water: the EU imposed a ban on the export of all British cattle and beef products within days. In October 1996, researchers at St Mary’s hospital announced that traces left behind by the distinctive protein which causes BSE were also present in vCJD. The link was now unequivocal: vCJD was caught by eating BSE-infected cattle and no one knew how many human beings had been infected. Thanks to that long incubation period, we still don’t.

With the benefit of hindsight, it is clear that the Government of the time failed to do all they could to contain the risk of vCJD. Once the horse had bolted, they worked hard to bring BSE under control and to overturn the export ban but it still took the incoming Labour administration until December 1997 to ban beef “on the bone”. The official inquiry described the Government’s initial response as

preoccupied with preventing an alarmist over-reaction to BSE because it believed that the risk was remote. It is now clear that this campaign of reassurance was a mistake. [13]

The Government gambled that BSE did not present sufficiently grave a problem to risk potential economic damage to the British beef industry. Instead they waited for more evidence and more research and told the British public that everything was just fine. Whether one interprets this as a cynical calculation or indecisive wishful thinking, the BSE debacle confirms that relying on politicians to safeguard public health is a very dangerous game.

Right at the Government’s side, the meat industry also played a part in reassuring the public of the safety of British beef. In its submission to the BSE Inquiry the Meat & Livestock Commission (MLC) claimed “The MLC has always firmly believed that the promotion of greater efficiency in the livestock industry and the livestock products industry is entirely compatible with, indeed promotes, the interests of consumers.”

In examining the consequences of feeding cattle to cattle, that compatibility is hard to detect. The MLC was (and still is) also responsible for the marketing of all British red meat and while they may have disingenuously claimed that there was no contradiction between their role and the interests of consumers, their behaviour does not support that claim. Within days, for instance, of the announcement of the discovery of BSE in a cat, the MLC ran full-page advertisements promoting the safety of beef and held a press conference to reinforce the message. In their 1997/8 Annual Report, the MLC bragged how they had increased minced beef consumption by 18% with targeted advertising. [14]

The BSE Inquiry later concluded that the MLC was guilty of running a campaign in which “hyperbole replaced accuracy” and that they produced “inaccurate statements to the public . . . which exaggerated the safety of beef”. In the absurdly gentlemanly language of official reports the Inquiry concluded that

The MLC was particularly assiduous in seeking to counter the suggestion that it might be dangerous to eat beef. Regrettably this enthusiasm led on occasion to statements which were not scientifically correct. [13]

BSE Today

Cattle are still being diagnosed with BSE at a rate of about 5 a week in the UK. The Government assures us that all infected cattle are caught and that existing precautions – the tracing of cattle, the removal of Specified Risk Material (SRM) and so on – protect those who still eat beef. But are the precautions in place the right precautions and do we know they are being adhered to?

Scientific research demonstrates very clearly that BSE can infect animals from mice to sheep to pumas. A new BSE-like illness has recently been found in sheep [15] while some scientists suggest that BSE may have infected thousands of sheep before the ban on feeding animal protein to sheep and cattle was introduced.[16] An EU inspection in 2002 (fourteen years after the regulations on SRM were introduced) found workers in a sheep abattoir contaminating carcases on the removal of SRM [17] and an audit by the Meat Hygiene Service in 2004 discovered that hundreds of so-called “casualty” cattle may be slipping through the testing net [18] (problems in slaughterhouses will be examined in more depth in Part 3). Meanwhile, the House of Commons Public Accounts Committee has described the system used to track cattle  - the system on which the detection and control of BSE depends - as "inefficient, overly burdensome and based on obsolete technology".[19] Increasingly sensitive tests have also revealed that prions (the microscopic infective agents which cause BSE, vCJD and scrapie) can be found in muscle, not just the nervous tissue removed as SRM. Following the recent discovery of a scrapie prion in a sheep’s leg, a researcher in the field predicted: "Within the next year, somebody will make a big splash by finding it [the BSE prion] in the muscles of cattle, and the beef industry will go crazy". [20]

A still greater concern, however, is the global trade in animals, meat and feed. Meat and bone meal was widely exported from Britain and other EU countries in the ‘80s and ‘90s and authorities acknowledge that BSE was exported with it. [21] In fact, after “high risk” SRM was banned from MBM exported to Europe, feed manufacturers were keen to include it in feed exported to other destinations – in 1991, Thailand bought over 6,000 tonnes of it.[22] When the UK finally stopped exporting MBM in 1996, other countries – proudly and wrongly asserting their BSE-free status – took over the business. Live animals are still exported from the EU all over the world.

Foreign governments and producers learned a great deal from Britain’s trauma. Unfortunately, one of the lessons they learned was that BSE is bad for business and the response of some was to protect their industries at any cost. Despite the fact that it had imported both live cattle and MBM from the UK in the 1990s, the US Government denied the possibility that BSE could have infected American cattle and only banned the feeding of cattle to cattle in 1997 (although, incredibly, they still allowed animals that had been fed on cattle to be fed back to cattle). The US cattle industry, meanwhile, unsuccessfully sued the talk show host Oprah Winfrey for discussing the risk of BSE on her TV show. The US grudgingly introduced testing for the disease in 2002, but tested only 5,000 cows in the first instance. Despite Canada announcing that it had discovered BSE in May 2003, the US Government continued to offer reassurances until its own first case was diagnosed in December 2003. It has now introduced new precautions and testing but so far on a voluntary basis: only 20,000 of the 35 million slaughtered each year in the US will be tested randomly and beef producers have little incentive to volunteer cattle for testing. In the words of New Scientist magazine “if any cow looks suspicious there is bound to be a temptation to shoot, shovel and shut up” – in other words, dispose of the cow and say nothing about the potential infection in others in the herd. [22]

In France – the country most enthusiastic about banning British beef – the national testing programme officially checked only obviously unwell animals and uncovered just a handful of cases in the 1990s. Recent research and modeling now shows that 300,000 cases of the disease must have gone undetected between 1991 and 2001 while 50,000 severely infected animals may have entered the food chain. [23] Each individual cow, of course, feeds a far larger number of human beings.

In total, 24 countries have now declared cases of BSE – but not until they had no other choice. Even more alarmingly, not all countries in the beef business have a free press or an accountable political system to pressure leaders into disclosure. China exported $55m-worth of beef in 2002 [22]: if its cattle are infected with BSE, would anyone bet their health on the Chinese government being frank about it?

Learning Our Lesson

BSE has not gone away – and nor has the risk of vCJD. It does appear likely that the most apocalyptic predictions of the extent of CJD in the UK will not come to pass but if that is the case, it is no grounds for complacency. The global extent of BSE/vCJD infection has yet to emerge and the conduct of many Governments – including our own – in response to it gives no cause for confidence that it will be managed effectively or even competently. As the management of bird flu also shows (see Part Two), in a global market for meat and livestock, national problems are now everyone’s problems.

BSE was caused by intensive farming practices and if we have escaped a human epidemic, that is a product of good luck, not good judgment. It is true that the specific risk of BSE/CJD was impossible to predict when cattle were first fed to cattle but with hindsight it is utterly clear that ignorance is no excuse: the intuitive repulsion that rational people feel for turning herbivores into cannibals turned out to be a far more reliable judgment on its wisdom than the financial calculations of the farming industry. BSE reinforces the message: ultimately, farming is about putting money in pockets, not food on the table.

Like bird flu, BSE also illustrates the way in which Governments have a conflict of interests between protecting public health and promoting commercial interests. The litany of farmed animal epidemics from foot-and-mouth through BSE to bird flu is an object lesson in the risks inherent to livestock farming: the history of the management of risks to human beings from those illnesses shows that our own health is at stake. The unanswerable question is: what’s next?

The conventional rubric in response to crises like the BSE disaster is that “lessons were learned”. Today, the Government argue that rules have been tightened, new systems are in place and old mistakes will not be repeated. The fact remains that the institutions on which we relied to assure our safety let us down. Perhaps they have learned their lesson but the more important question is - has the public learned its lesson? Are we going to continue to rely on government and officials to protect us?

Antibiotic-resistance: a self-inflicted wound?

Antibiotics transformed the treatment of infections and infectious diseases when they were discovered in the middle of the 20th Century. Today, the emergence of antibiotic-resistant bacteria threatens a return to the days when simple infections could prove fatal. The most famous of these so-called “superbugs” is MRSA, UK cases of which have multiplied 25-fold in the last ten years,[24] but concentration on this one organism has sometimes masked the breadth of this problem: according to Professor Peter Collignon, Direcor of Infectious Diseases at Canberra hospital “Overall, there are almost no bacteria where there is not resistance to more antibiotics then there were 10 or 15 years ago”.[25] Dr Sandy Macara of the British Medical Association went even further: "there is a real prospect that the majority of our antibiotics could become impotent for the purposes on which we have relied upon them for 40 years.”1 

Underlying this frightening development is a simple law of nature: the survival of the fittest. Antibiotics (also known as antimicrobials) are drugs which destroy or inhibit the growth of bacteria (bacteria which are killed or controlled by a certain antibiotic are said to be “sensitive” to it). Different antibiotics target different bacteria but even within a single species or strain, bacteria are not identical. Some will have mutations which allow them to survive treatment and so when antibiotics are used, these resistant bacteria will multiply. So, although mutations providing resistance to antibiotics are rare, each use of the antibiotic will cause the resistant strains to increase in number. Over time, the resistant bacteria completely replace the sensitive forms and the result is that the antibiotics become ineffective. The irony is, each time we treat an illness with antibiotics, we are encouraging this process to take place.

Unfortunately, the bacteria which infect animals are the same as or very similar to those which infect human beings and so the antibiotics used to treat human diseases and those used to treat farmed animals are also similar and in some cases identical. Thus, each time we treat farmed animals with antibiotics we create antibiotic-resistant bacteria which have the potential to infect us too. In the words of the European Agency for the Evaluation of Medicinal Products, “Animals undoubtedly represent a source of antibiotic-resistant microorganisms for humans”. [26]

A classic example of this kind of antibiotic resistance is found in a bacteria we have already discussed and whose name will recur in this report many times: salmonella. There are over 2,000 strains of this particular bacteria but in general salmonella infections in both animals and humans used to respond to treatment with “simple” antibiotics. Over the last few years, however,  important disease-causing strains have become resistant to a range of antibiotics including ampicillin (a close relative to penicillin), chloramphenicol, trimethoprim and, most recently, a class of antibiotics known as fluoroquinolones, of which the most common in use in human beings is ciprofloxacin. When researchers in Taiwan encountered the first ciprofloxacin-resistant salmonella strains they uncovered both the frightening pace at which this problem can emerge and its origin. Samples from patients taken in 1997 were all sensitive to ciprofloxacin – by 2001, half of all samples were resistant. When the researchers then studied the DNA of the resistant bacteria, they were able to trace it back to pigs. Pigs had been treated by fluoroquinolones and so the salmonella carried by them had become resistant. When humans handled and ate their meat, they became infected with the new resistant strain and the human fluoroquinolone, ciprofloxacin, no longer worked.[27] Fortunately, one last line of antibiotics, third generation cephalosporins, were still effective. Alarmingly, salmonella strains resistant to those have now emerged in the USA.[28]

In fact, as early as 1997 The World Health Organisation (WHO) identified salmonella as one of four kinds of infection in which antibiotic resistance had already been transmitted from animals to man. The other bacteria were campylobacter, E. coli and enterococci (a kind found in animal intestines): it is no coincidence that these are all common causes of food-poisoning. Food poisoning is normally caused by th transfer of bacteria carried by animals to humans. When ingested, antibiotic-resistant bacteria from animals can either infect humans directly or transfer the genes providing their resistance to similar bacteria. Either way, eating animal flesh is the simplest and most direct way of introducing animal infections into our bodies. According to the head of the US CDC’s Infectious Diseases branch, in the case of the disease-causing bacteria commonly found in animals, “the principle driver of increasing resistance is the use of antibiotics in agriculture”.[5]

Antibiotics in Agriculture

The use of antibiotics is not simply common in agriculture but underpins the intensive farming techniques which are used for over 90 per cent of farmed animals in the UK. We shall examine the reasons for this in a moment but the scale of agricultural antibiotic use is simply staggering: in the UK 433 tonnes of antibiotics were sold for farmed animal use in 2002 [29] – roughly the same amount as was used in human medicine. Bearing in mind that the normal dose of antibiotics is measured in milligrams, the amount of treatments this represents is astronomical. Over the last 30 years, agricultural use of penicillin-type antibiotics has increased by over six times and tetracyclines by 15 times while a Government report in 1998 found that some pig farms used up to 10 different antibiotics simultaneously to dose pigs of various ages and conditions.[1]

There are three reasons for this massive scale of antibiotic use. Firstly, and obviously, hundreds of millions of farmed animals are bred in the UK each year. Most, however, live only a few weeks or months before slaughter, theoretically reducing their chances of contracting disease and requiring medication. In practice, however, farmed animals are at particular risk of infectious disease because of the conditions in which they are kept and so require medication with antibiotics on a scale quite disproportional to their numbers and physical size. Thirdly, antibiotics are used not simply to treat or prevent disease but as so-called “growth promoters” – additives to feed which help animals put on weight more quickly and so enhance profits.

Added Extras

When we eat animals, we eat what they ate – and that includes the drugs that were fed to them. Clearly, all drug residues in meat have the potential to pose risks in their own right but residues of antibiotics may also contribute to antibiotic resistance in organisms living naturally in the human gut. For this reason, there are rules in place which are supposed to prevent us from taking a dose of the drugs animals are given before their deaths. In theory, animals are given no active medications before slaughter – a “withdrawal period” of days or weeks allowing the residues of medications to be excreted from their bodies. The withdrawal period does not guarantee that their flesh will be free from residues – simply that they will be at what is judged to be an acceptable level. In the UK, the Veterinary Medicines Directorate, a branch of Government, monitors these residues. Their Veterinary Residues Committee’s report in 2003 found 89 contaminated products out of 35,399 analyses – a level of 0.0025%.[30] 71 residues were of the poultry feed additives, nicarbazin and lasacolid and were thought to be due to non-medicated feed becoming contaminated with medicated feed at the production stage. The committee bluntly stated: “this continued occurrence of feed additive residues in poultry products is unacceptable”.

While the level of contamination appears low, replicated on a national scale it provides frightening evidence of the prevalence of food residues: if we estimate that 40 billion meat meals are eaten in the UK each year, around 100 million meals are likely to be contaminated with residues. While residues are not an important component in the development of antibiotic resistance, this level of contamination is an alarming indication of poor procedures and inadequate regulation.

Stop Press: Batches of organic chicken sold by – among others – Waitrose and Tesco have been withdrawn from sale after being found to be contaminated with the banned feed additive, nitrofuran. Nitrofuran was banned in 1995 because long term exposure was thought to increase cancer risk.[151]

Factory Farming

Antibiotics are not simply helpful in factory farming – they are essential to it (see Part Two). Intensive farming emerged in the later 1940s at precisely the time that antibiotics became widely available. Previously, the inevitable consequences of dirt and overcrowding had prevented intensification of livestock agriculture. Antibiotics provided a solution: they opened the door to the system we have today.

As Section J also makes clear, farmed animals in the 21st century are at greater risk of infectious diseases than ever before. Their bodies are placed under increasing physical stress in the attempt to enhance “productivity”, be it faster weight gain, more offspring per litter or more litres of milk. Local, national and international trade in live animals mixes animals from different farms and regions, spreading disease (such as foot and mouth) in the process. For this reason, farmers treat their animals with antibiotics or similar medications both when these diseases occur (therapeutic use) and also on a routine basis to prevent them from developing – so long, of course,  as the cost of treatment does not exceed the cost of the disease. This preventative use of antibiotics is known as prophylaxis.

Animals kept outdoors are at risk from infections contracted from their environment – from soil and wild animals for instance, risks which can never be eliminated. Animals kept indoors are at even greater risk of infectious illness, however, because of the dirty conditions in which they are kept, the psychological stress of confinement and, above all else, overcrowding. Up to 30,000 chickens may be kept in a single shed, each with a floor space just centimeters bigger than their own bodies when full grown. Respiratory infections transmitted by droplets in the air spread rapidly because of the physical proximity of every bird to its neighbours. Because chickens are coprophagic (excrement-eating) and kept on litter which is never changed, intestinal infections are passed on through faeces. Ducks and turkeys are kept in almost identical conditions while so-called free-range poultry of all kinds are still kept in flocks numbering in thousands.

Pigs are overwhelmingly kept indoors – on a smaller scale but in equally insanitary and overcrowded conditions. Prophylaxis is widely used to prevent the inevitable respiratory and gut infections – but with, as the Government report in the box makes clear, limited success. Traditionally “free-range” animals such as cattle and sheep are also housed indoors for increasingly long periods.

Infectious diseases by definition strike more than one animal at a time and so in intensive farming, animals are medicated, both prophylactically and therapeutically, en masse – usually by adding medication to their feed or water. The concentration of animals and the administration of multiple doses, however, also multiplies the opportunities for resistant bacteria to spread: one study found that the treatment of a chicken flock in which all campylobacter was sensitive to fluoroquinolones led to 100% resistance within days – in other words, all the sensitive bacteria had been replaced with resistant bacteria.5 Similarly, strains of swine dysentery now exist which are completely resistant to all antibiotics.[28] Not all bacteria respond so dramatically but when this kind of response is replicated on a global scale, it is clear that intensive livestock production is driving the evolution of some resistant bacterial strains on a staggering and unprecedented scale.

Prescribing for Profits

The discovery that antibiotics can enhance the growth of farmed animals was made entirely by chance in 1949, when an American drug company researcher discovered that chickens given a feed containing antibiotic residue gained weight 20% faster than normal.[33] The exact mechanism by which antibiotics achieve this is still not fully understood but it is now thought to be a consequence of two separate actions. Firstly, the antibiotics kill a proportion of the bacteria that are normally found in animals’ guts, allowing more food to be absorbed directly by the animal and reducing the amount of toxins produced by the bacteria themselves (although it should be stressed that having bacteria in the gut is normal for all animals and they do play an important role in digestion overall). Secondly, since growth promoters (GPs) have been banned in some countries (see Timeline) it has been found that they do in fact play a role in suppressing the illnesses that arise from intensification, reducing death rates and farmers’costs.

Needless to say, the industry was not slow to capitalize on this fortuitous discovery and by the 1970s, it was estimated that 40 per cent of all the antibiotics produced in the USA were going into animal feed and the resultant increased growth was adding $2bn a year to US farmers’ profits.[33] Currently growth promoters are estimated to increase growth and feed-conversion ratios by between 3% and 11% depending on the species[34]- the difference between profit and loss for some farmers (an average broiler yields just 3p profit to the producer.[35]

Perhaps most remarkably, this massive exercise in drug administration was originally almost completely unregulated and while restrictions have been introduced over the decades (see below) even today, farmers in the UK obtain antibiotic growth promoters to dose their livestock simply by buying medicated feed. No prescription is required.

Awareness of the risks associated with prescribing antibiotics to farmed animals is far from new: it was first addressed by a Government committee in the 1960s – examining resistance in salmonella, in fact. Unfortunately, the committee’s recommendations and the subsequent Government action followed the typically conservative, step-by-step approach beloved of all bureaucracies and foot-dragging followed every inquiry and report until well into the 1990s (see Timeline). Finally, in the mid ‘90s, the EU banned a number of growth promoters with the closest similarity to human medicines but all GPs will not be banned fully in the EU until 2006 – fully 20 years since Sweden introduced a total ban. In the USA, powerful business interests are still fighting any such restrictions – indeed, penicillin is still used as a growth promoter in the US, 30 years after its use was banned in the UK. Meanwhile, banning growth promoters has barely appeared on the radar of many significant producers across the world. The importation into the EU of meat derived from animals treated with growth promoters will not be banned.

Banning Growth Promoters: Will it Help?

Considering the growing problem of antibiotic resistance, the use of antibiotics as growth promoters appears to be one of the most reckless and unsustainable applications of medications in agriculture. Because of the low doses used, however, GPs account for only about 10% of total antibiotic usage and because doses are low, they exert less selective pressure on bacteria. In fact, the banning of some growth promoters has so far failed to produce a significant decline in the level of antibiotic resistance found in the human population.[36]  

There is even some evidence that a ban may be counterproductive. In 1998, pig producers stopped using GPs in Denmark. The result was that the sale of therapeutic antibiotics – those used for treating disease – rose dramatically.[37] In the UK, the 1997 ban on the use of tylosin as a growth promoter was marked by increased sales of the drug as a treatment for ileitis (gut inflammation)[37] and use of antibiotics of the category to which it belongs nearly doubled [38] – despite a decline in the number of pigs over that period. This increase in use also reflects the far higher doses that are given when an antibiotic is administered therapeutically rather than for growth promotion.

Similarly, in 2000, it was announced – with some fanfare - that all UK broiler chickens produced under the new Red Tractor farm assurance scheme would be raised without the use of growth promoters – a significant step as the Red Tractor covered about 85% of broiler production. Three years later, the Red Tractor scheme discreetly dropped the policy and the reason they cited was declining bird welfare and increased prescriptions for therapeutic antibiotics.[39] With (at the time of writing) little over a year to go until growth promoters are banned across the EU, the industry appears remarkably complacent about the implications of the ban – perhaps because they anticipate simply administering antibiotics to their animals in other ways.

Cold Turkey

Growth promoters enhance the profitability of intensive farming: prophylactic and therapeutic antibiotics underpin it. Antibiotics allow farmers to crowd thousands of animals together, automate their feeding and pare labour costs to the bone. Organic livestock farming which eschews the use of antibiotics unless absolutely necessary has, as a direct consequence, vastly greater production costs than conventional farming. Currently only a little over two per cent of meat sold in the UK is organic and with prices of organic chicken near double those of conventional broilers, it is clear that organic food production will remain a niche market. Without the administration of hundreds of tonnes of antibiotics, broiler and pig production in the UK would be financially unsustainable. With great reluctance, European regulators have finally accepted that antibiotic growth promoters are unjustifiable and the industry will be forced to change: what no politician or agro-businessman is willing to do is confront the far larger problem of the use of antibiotics in agriculture overall.

No fewer than 20 of the antibiotics used for the treatment of ill human beings in the UK are currently administered to farmed animals (VMD website), while dozens more, virtually identical to human medications, are administered at a rate of over 1000kg per day. The transfer of antibiotic resistance from animals to human beings is now an established fact but while our farming industry remains dependent on antibiotics, they will continue to be applied, regardless of the consequences.

A Selection of Antibiotic-Resistant Bacteria

a. Soil Association press release 18/6/99

b. The European Agency for the Evaluation of Medicinal Products, 1999, Antibiotic Resistance in the European Union Associated with Therapeutic Use of Veterinary Medicines

c. Teale C 2003 Antimicrobial resistance – a threat to sustainable agriculture. State Veterinary Journal  13 (1) 26-29

d. WHO press release 20/10/97 Antibiotic Use in Food-Producing Animals Must be Curtailed

e.Spread of Antibiotic-Resistant E. coli From Animals to People May Be Common, Reuters Medical News, July 17, 2001

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