Factory farming and human health

Factory farming and human health

June 1, 2001 The Ecologist by Tim O'Brien
It is not small food production, but large-scale factory farming, that presents a threat to our health.

Mad cow disease (BSE) and vCJD (`human BSE'), with its potential to lead to the deaths of thousands of people in the UK, and who knows how many more around the world, are the terrible consequences which have followed from the apparently innocuous practice of feeding dead cows to live ones. The disaster has brought home the impact that 'industrial' animal husbandry - viewing animals as production machines - can have on human health.

And one only has to scratch the surface of life down on the factory farm, to see that BSE may well be only the tip of the iceberg. In a range of areas, from feeding regimes, to animal housing, to the use of drugs in the pursuit of productivity, human health may be threatened by factory farming. Imposing industrial demands on farm animals may, quite literally, be producing fatal flaws in the end product - our food.

It is no surprise that, faced with the BSE disaster and escalating incidence of food poisoning, in particular from Salmonella, Listeria, Campylobacter and E. coli 0157, the UK Government's reaction has been to tighten hygiene regulations. But given the underlying nature of the problem - animals being reared in appallingly cramped conditions, frequently without access to fresh air, clean litter, and sunlight - the measures are unlikely to prove effective. Paradoxically, they may even make our food less safe, by ensuring that livestock production and slaughter become ever more centralised in the hands of a small number of large industrial-scale operators, better able to bear the costs of regulation than small-scale producers.

Life, death and disease, down on the factory farm

Consider the conditions which prevail on factory farms - for example, in intensive boiler chicken sheds. Animals are so crowded together that the floor is scarcely visible, and where it is visible, it can been seen to be covered with excrement, and the atmosphere is full of dust, and scarcely any sunlight. Would one be surprised if disease was rampant? Of course not. Yet these are the conditions in which many animals are reared as food.


The UK Government's Advisory Committee on the Microbiological Safety of Food has stated that: `Raw poultry is a significant carrier of pathogens, particularly Salmonella and Campylobacter.'1 Their 1996 Report on Poultry Meat found that one in three chilled, raw UK- produced chickens on retail sale was contaminated with Salmonella; an even greater proportion (41 per cent) of frozen birds was contaminated 2. The type of Salmonella which most commonly infects chickens is Salmonella enteritidis, but there are several thousand other strains in all types of farm animals.

As one might expect, the environments in which farm animals are confined can also be significantly contaminated. A survey of litter and dust samples from commercial turkeys in Canada, for example, found Salmonella at 86 per cent of flocks.'3

Between 1981 and 1987 there was a 13-fold increase in the rate of isolation of Salmonella enteritidis from layer chickens in England and Wales',4 and in 1991, a report in Which? magazine claimed that up to 7,000 of the 30 million eggs eaten in Britain each day carry the Salmonella bacterium.'5

Although Salmonella-infected animals sometimes show few, if any, symptoms, this is by no means always the case. Many animals suffer considerably as a result of Salmonella infection, just as humans do. A report in The Veterinary Record, in 1995, described a batch of layer replacement chicks, bought in at a day old: `They were soon seen to be huddled together with drooping wings', and ' by six days old 70 of 100 had died.' The chicks were found to be infected with Salmonella pullorum.6

So how is it that Salmonella infection of farm animals is so common, and how is it spread? According to scientists at the Central Veterinary Laboratory: `Bacterial infections can be spread by the airborne route in farm animals, particularly when reared intensively. For example, poor ventilation in poultry houses can cause high concentrations of ammonia to develop and irritate the respiratory tract, predisposing to infection."7

Airborne infection of chicks, calves and laying hens with Salmonella bacteria has been reported and in the case of the latter, within two days of exposure the hens were found to have a generalised infection. Their lungs, liver, spleen, kidneys, ovaries and oviducts were all infected.'8 These airborne-- infected laying hens excreted Salmonella bacteria for up to 28 days. With laying hens confined so closely in battery cages, the possibility of cross-contamination between animals must surely be very high.

The fundamentally unhygienic conditions of intensive boiler chicken production have been described many times. In fact, Salmonella contamination of poultry houses can be so severe that pressure washing or steam cleaning of the house between the rearing of separate batches of chicken can actually lead to an increase in levels of bacteria.'9

Another way in which Salmonella infection can be introduced and spread is via contaminated feed. According to the Advisory Committee on the Microbiological Safety of Food: `Animal feed is an important potential vector for the transmission of microbiological infection to poultry flocks,'10 and, `we regard animal feed as an important potential vehicle for the transmission of Salmonella infection.'11

What's more, contaminated feed may produce elevated levels of Salmonella in farm animals even though Salmonella is not the contaminating agent. In 1994, an outbreak of Salmonella choleraesuis was reported in pigs fed material contaminated with aflatoxin and vomitoxin (poisons present in feed contaminated with certain fungi), which seemed to compromise the immune and metabolic systems of the pigs, predisposing them to Salmonella infection.'12

The emerging picture is one of practices that are designed to cut production costs to the bone; processes where cost is the overriding concern, and quality and compassion are secondary. Recycling of dead animals as feed for ones of the same species is the most extreme example of this 'industrial' approach.

In 1979, ahead of the BSE crisis, the Royal Commission on Environmental Pollution warned against the dangers of feeding dead farm animals to live ones, highlighting the possibility of recycling disease-causing agents.'13 And yet, even now, more than twenty years after the warning from the Royal Commission, and more than ten years after the farming industry became aware that the BSE crisis was triggered by feeding dead animals back to live ones, we continue to make cannibals of farm animals: poultry can still be fed with hydrolysed feather meal, and the `off-cuts' and waste blood from poultry abattoirs.


According to the UK Government's Advisory Committee on the Microbiological Safety of Food, Campylobacter has been reported to be the most common cause of infectious intestinal disease in humans in England and Wales'14 - more common even than Salmonella. Symptoms typically include nausea, headache, backache, fever, abdominal pain and diarrhoea. In some cases, illness can be severe and prolonged, leading to arthritis and even neurological complications: since the eradication of polio, Guillain-Barre Syndrome is the most feared cause of paralysis in the Western world, and its most common cause is Campylobacter infection.

In the UK, Campylobacter has been detected in 48 per cent of fresh chickens,'15 and in 11 out of 12 turkeys following processing and before sale.'16 A study in Northern Ireland found Campylobacter in 94 per cent of fresh chickens examined'17; another study found 64 per cent of chicken wings on retail sale contaminated with the bacterium.

The organism is surprisingly resilient: it has been found to survive on chickens frozen for three months.'18

Given the prevalence of Campylobacter in chicken carcases, it is not surprising that a survey by the Central Veterinary Laboratory found that nearly half of those broiler flocks examined were colonised with Campylobacter.'19

Animal feedstuffs are not thought to be significant source of Campylobacter infection as they are of Salmonella. Instead, it is the environment of the intensive boiler house that is believed to represent the most significant reservoir of infection.'20 The Advisory Committee on the Microbiological Safety of Food, in its 1996 Report on Poultry Meat, said: `We recommend that industry gives attention to the improvement of the broiler farm environment at the earliest opportunity.'21

Poultry are not the only potential source of Campylobacter. In Holland, 85 per cent of pigs sampled were found to be infected with Campylobacter.21

A report in The Veterinary Record in 1996 noted the spread of resistance to the antibiotic erythromycin in Campylobacter, and suggested that `the spread of these resistance traits may be due to genetic exchange of material between strains among animals under intensive production techniques. These conditions could vastly increase the occurrence of very rare genetic events'. The authors went on to note: `Modern production methods and slaughter of young susceptible animals have created a heterogeneous population of Campylobacter species in pigs, which may allow the transfer of genetic resistance factors... to human pathogens.'23

This is a very serious deve\lopment. Effectively, the Veterinary Record report is warning that factory farms could represent an uncontrolled experiment in bacterial genetic engineering, allowing the emergence of new strains of bacteria capable of resisting treatment with antibiotics.

Escherichia coli

The possible emergence in farm animals of new, especially dangerous strains of bacteria has also been raised in connection with the 1996/97 outbreaks of Escherichia coli 0157 in Scotland, which killed one in twenty of the people infected.24

The bacterium E. coli is a normal inhabitant of the gastrointestinal tract of humans and livestock. It colonises the newborn's colon within hours of birth, and serves important intestinal physiological functions for the rest of the host's life.

However, there is a sub-set of strains of E. coli which can cause a wide variety of diseases. For example, around one-third of mastitis cases in cattle are caused by E. coli, and 35 per cent of the UK's cows contract mastitis every year - a painful disease of the udder25 affecting cows subjected to the stresses of intensive dairy farming.

Recently, most attention has focused on those strains which produce toxins harmful to cultured Vero cells (African green monkey kidney cells). These bacteria are known as verocytotoxin-producing E. coli, or VTEC.

E. coli 0157 is one such strain which frequently (but not always) produces verocytotoxins. It is thought to have acquired the ability to produce these toxins by a process of genetic exchange with another bacterium.

The strain has received close attention because, in 1983, it was found that in humans VTEC infection can lead to haemolytic uraemic syndrome (HUS), a form of kidney failure. This can be fatal in 10 per cent of cases, and those who recover may have serious long-term impairment of kidne function. Even if HUS does not develop, E. coli 0157 commonly results in severe abdominal cramps, bloody diarrhoea, and in some cases sometimes vominting. The infectious dose appears to be very small - ingestion of less than 100 bacteria can produce illness.26 No specific treatment exists, and the effectiveness of antibiotics remains unclear.

Outbreaks of VTEC infection in England, Scotland and Wales have shown a steady increase over the years. Whilst there was one single outbreak in 1987, which affected 26 people, by 1994 the figure had increased to 6 outbreaks, affecting 130. In 1996/97 in Scotland, more than 20 people died and over 400 others were affected, in two separate E. coli outbreaks in Lanarkshire and Arbroath.

E. coli outbreaks in humans have been linked to a variety of foods - turkey roll sandwiches, minced beef products, even milk. In January 1993, an outbreak occurred across four states in the USA, affecting 732 people, four of whom died. One child excreted the organism for 72 days. The outbreak was linked to hamburgers consumed at multiple outlets of a single restaurant chain.

A US National Animal Health Monitoring System study found E. coli 0157 in faecal samples from 63 per cent of cattle feedlots examined.17 As well as being present in the intestinal tract of cattle, E. coli 0157 can also be present in the udder," which may explain why people have become ill following the consumption ofmilk, or milk products.

VTEC strain of E. coli other than 0157 are known to cause cattle illness, particularly in calves. Oedema disease in pigs (which can result in convulsions, paralysis and sudden death) is also associated with verocytotoxin-producing E. coli.

E. coli 0157 has also been found in UK sheep.29 And colisepticaemia in poultry, caused by E. coli, has increased with the development of intensive boiler production.30

Abattoirs dealing with very large numbers of animals, contaminated externally with manure, whose gastro-intestinal contents are dispersed during slaughter can be expected to offer a route for E. coli to enter the human food chain.

As noted earlier, evidence is emerging of surprisingly high rates of mutation in those food poisoning organisms found in large numbers in our farm animals.

A study reported in the journal Science, in November 1996, found `alarmingly high' incidences of mutation in E. coli 0157 and Salmonella. The study also found that these bacteria seemed to bel able to mutate easily by horizontal transmission of genes, from one bacterium to another. It was suggested that this could confer antibiotic resistance, from a reservoir of pathogenic bacteria in the environment, allowing the bacteria to `to escape immune surveillance or elude therapeutic intervention.'31 With the emergence of such highly mutable food poisoning bacteria, the confinement of farmed animals in crowded and unhygienic conditions is simply asking for trouble.


Listeria can cause miscarriages, still births, and serious illnesses in newborns. Between 1987 and 1989, 26 babies in the UK died from listeriosis. In response, in 1989 the UK Government issued a warning to vulnerable groups, such as pregnant women, to avoid high- risk foods, such as soft cheeses and meat pates.

Listeria continues to be associated with farm animals, and a wide range of food products derived from these animals. Listeria monocytogenes has been found to contaminate up to 66 per cent of fresh and frozen chicken products.32 Other research has found the body surfaces of pigs to be contaminated by Listeria in 58 per cent of cases.33

Listeria also seems to be a significant contaminant of abattoirs. One Dutch study found Listeria in 100 per cent of environmental samples taken from the conveyor in an abattoir.34 Sheep are also known to harbour Listeria, where it causes increases in abortions, and nervous disease.

Despite warnings during the 1980s, Listeria continues to be a significant health-hazard. In May 1995, brie cheese was the source of 17 cases of listeriosis in France. Nine pregnant women were infected, two of whom had miscarriages, and another two of whom had stillborn babies.35

A contributory factor to the dangers of Listeria may be the peculiar ways in which the bacteria respond to storage and cooking. Unusually, vacuum packing seems to enhance recovery of the bacteria, compared with cells packaged in air,36 while exposure to low temperatures appears to enhance the potential for the organism to cause disease. Listeria has also been found to be able to survive microwave cooking.

According to the Oxford Concise Veterinary Dictionary: `The organism is widespread in nature and very resistant to physical and chemical agents. Infected materials, such as faeces and silage, can harbour the organism for many years.'37 In view of the fact that Listeria monocytogenes appears to be so widespread among intensively reared poultry, the practice of spreading untreated litter from boiler chicken sheds (often containing dead birds, many of which may be contaminated) onto fields seems highly unwise.'

Poisoned Food

With so many bugs associated with farm animals, is it any surprise that we are being poisoned by our food? Year after year in the UK, people in their thousands are being poisoned by the food they eat. Survey after survey has found unacceptably high levels of food- poisoning organisms in meat, and a relentless increase in reported cases of food poisoning.

Which? magazine surveys, in the mid-1990s, found the presence of Salmonella in up to 36 per cent of chickens and Campylobacter in more than 40 per cent of chickens.38 In other research, Campylobacter was isolated from 48 per cent of fresh chickens examined in the UK39, and in a staggering 94 per cent of fresh chickens examined in Northern Ireland.40 Campylobacter has also been found in 11 out of 12 turkeys, examined following processing and before point-of-sale.41 Verocytotoxin-producing strains of E. coli have been found in 22 per cent of raw beefburgers42 and in 25 per cent of raw pork sausage43 obtained from retail outlets in north and north-west London.

Even for milk and milk products, the levels of bacterial contamination considered 'acceptable' are surprisingly high. For ground-water drinking water, a typically acceptable level of contamination might be 10-20 bacterial cells per ml.44 But for cows' milk which is to be used for the manufacture of raw milkbased products whose manufacture does not involve any heat treatment, up to 100,000 bacterial cells per ml is considered an 'acceptable' level of contamination.45

Food poisoning is increasing relentlessly

just as levels of food-poisoning bacteria in meat are unacceptably high, so too are the levels of food poisoning itself. According to figures from the Communicable Disease Surveillance Centre, laboratory reports of faecal isolates of Campylobacter in England and Wales increased from 28,761 in 1988 to 44, 414 in 1994. For Salmonella, the increase was from 27,478 in 1988 to 30,411 in 1994. This represents a total increase, for the two pathogens, of 33 per cent in six years. It must also be born in mind that not all cases of food poisoning are reported. Estimates suggest that only around 1 in 30 to 1 in 40 cases are reported.46,47

This would mean that in 1994, in England and Wales alone, there were somewhere between 1.5 million and 3 million cases of food poisoning, from Salmonella and Campylobacter - one case for every 17- 34 people in the population. Based on these numbers, and further data from the Public Health Laboratory Service, food poisoning in England and Wales can reasonably be predicted now to be costing industry (in lost time) and the taxpayer (in health-care costs) well over L1 billion, perhaps nearer L3 billion every year.

And there are, on average, four deaths for every 1,000 reported cases of Salmonella infection in humans in England and Wales.48 In terms of the financial and human cost, this is like having a brand new BSE epidemic every couple of years.

The situation in Scotland likewise shows an accelerating incidence of food poisoning. A report in The Guardian newspaper, on 31 December 1996, qu\oted Scottish Office figures which showed that confirmed notifications of food poisoning rose from 858 in 1970 to 6,510 in 1990. By 1 November 1996 (that is, prior to the devastating E. coli 0157 outbreaks), Scotland had already recorded 8,408 cases of food poisoning for that year.49

A report in the Financial Times, on 5 March 1997, noted that, according to the Office of National Statistics, food poisoning in England and Wales increased six-fold over the previous 15 years.50 One of the reasons for this huge increase was said to be: 'more intensive rearing of chickens and farm animals under conditions that can spread germs.'

Animal welfare and food safety - inextricably linked

Scientists at the University of East Anglia found that when the average monthly temperature exceeded 7 deg C, the number of food poisoning cases increased - a 7 per cent increase in food poisoning for each degree rise in temperature. However, food poisoning did not appear until a month after the temperature rise." As a researcher pointed out: `This shifts the emphasis of responsibility for food poisoning away from the consumer and onto the producer'.52 Another of the researchers said that further investigations had shown that the infections began on farms, usually those employing intensive methods 53

Other researchers have noted that because poultry have a habit of pecking the ground, pathogens shed in faeces and present in litter will be ingested.54 Also, feet become contaminated from faeces, and skin and feathers can readily become contaminated in the dust-laden environment.55 A study of Salmonella contamination in French poultry houses found samples of the pathogen on walls, drinkers, feeders, floor, insects, in water, in feed, and of course on the chickens themselve.56 Similarly, Campylobacter was found in the air, litter and drinking water containers.57 It was stated that: `Intensive rearing of fowl where thousands of birds are kept together is conducive to the spread of Salmonellae, and probably other pathogens.58 Under such conditions, one infected bird, contaminated feed or other sources of contamination in the environment can easily spread pathogens to many birds.'

Further evidence for the on-farm origin of food-poisoning organisms comes from a large study conducted in England in 1985 and 1986. This research identified similar strains of Campylobacter, from a boiler farm, through a processing plant to wholesaler, catering college and retail outlet to consumers. About 31 per cent of Campylobacter isolates from patients were the same strain as 91 per cent of the chicken isolates from the affected farm. Elimination of infection at the farm was reflected in a major reduction in prevalence of the Campylobacter strain in the local population.59

Furthermore, a higher incidence of Campylobacter infection occurs in people who have occupational exposure to poultry and cattle than in others in farming communities,60 and employment in poultry processing may predispose workers to campylobacteriosis.61 A serological survey has found that 27-68 percent of personnel in poultry and red meat plants have antibodies to Campylobacter jejuni, compared to 3 per cent of arable workers. This increased resistance to campylobacteriosis suggests that the carcasses being processed are significantly contaminated by the time the arrive at the abattoir.

Work by the Food Microbiology Research Division of the Department of Agriculture for Northern Ireland, in 1994, found that: `The manner in which animals are housed will directly affect the microflora of their exterior, whilst the age at slaughter will have a major effect on the microflora of the gastro-intestinal tract ... Those animals which are intensively reared and slaughtered young will have the greatest potential for carrying pathogens'.62

As an example, the Department of Agriculture compared the microbial count of hides from cattle in summer (cattle slaughtered in summer will have spent some months in open fields) with hides from cattle in winter (which will have spent months indoors in pens), and found that the winter hides showed around 100,000 times more microbial contamination than the summer hides.

The same author considered the effect of long journeys to abattoirs, and noted: `The travel can be stressful ... Further stress can be applied when animals with a social hierarchy, such as cattle, are mixed. These animals will then attempt to reassert their social position and the consequent fighting causes stress which can increase susceptibility to gastro-intestinal infections ... Whilst the time period required for full-scale infection will not be available, the animals will be able to contaminate their exterior surfaces. This is especially so where tiered transport systems are used, e.g. the `double-decker' carriers for cattle and 'triple-decker' carriers for sheep.'

All of this strongly bears out comments by David Statham, Chairman of the Chartered Institute of Environmental Health's (CIEH) Food and General Health Committee. At the CIEH's Annual Congress in 1995, he said that a concerted effort is needed at farm level to attempt to eradicate the infective organisms from food animals and that: `This requires careful control of feedstuffs, and good animal husbandry to attempt to eliminate infection at source.

Further controls must not stop at the farm gate. Strict controls must be implemented to prevent animals being crammed together in dirty, overcrowded conditions during transportation. This is more than just a hygiene problem. It is an important animal welfare issue, too.63

Farm animals would be infected with fewer disease-causing organisms if, for example, they were reared in less overcrowded, more open environments - where broiler chickens, for instance, were not pressed up one against the other, where they were not forced to live next to the dead bodies of their companions, where they had access to direct sunlight, and were not condemned to spend their brief lives blistering their feet in their own excrement, and their lungs by breathing an atmosphere heavy with ammonia fumes, dust and bacteria.

Antibiotics - saviour or suicide?

With disease-causing organisms so prevalent on factory farms, it is not surprising that farmers have resorted to the widespread use of antibiotics. The routine use of antibiotics is particularly attractive to farmers as many of these substances have an as-yet poorly understood ability to promote the growth-rate of the animals to which they are administered.

So farmers, in a desperate battle to contain the bug-explosion on factory farms, and in order to maximise profits by pushing growth- rates ever faster and faster, are routinely dosing farm animals with a whole range of different types of antibiotics.

But evidence is emerging that several of these antibiotics, used in vast quantities in farming, are jeopardising the effectiveness of similar antibiotics vital in human medicine. Factory farming is pushing the world ever further into the post-antibiotic era, with all the crises that this may bring for human health.

Where do we go from here?

It is surely inevitable that in order to provide a safe food supply, we must dispense with factory farms, and other intensive food production enterprises, and return to small-scale, cruelty-free food production geared to local demand.

We have to do it anyway - these monster, industrial-scale food enterprises are too socially and ecologically destructive.

And it's time to stand up and declare, simply and straightforwardly, that it is also morally unacceptable to keep hundreds of millions of sentient animals imprisoned for life in our sordid concentration camps.

Visualise Factory Farming

It is hard to visualise the typical scale on which factory farms operate: 20,000-30,000 'boiler' chickens are crowded inside a building up to 400 feet long. Individual buildings house more than 100,000 laying hens, and keeping one to two million birds on a single site is becoming increasingly common. As many as 12,000 pigs may be kept in a completely enclosed building no longer than a football field.

In the US, well over 8 million farm animals are killed for food every year. Yet even in the face of such staggering size and pollution, factory farm operations continue to pursue even more massive operations and profits. 'Circle Four Farms' in Milford, Utah, a venture of the four largest US pork companies, is reported to produce hog waste that amounts to the yearly equivalent of 1.8 million people - an amount just below that generated by Utah's entire population of 2 million.

Circle four Farms is aiming to increase its production to 2.5 million hogs, expanding to a 25 mile stretch of 'farms'.

Virtually all growers of 'boiler' chickens are under contract to huge corporations who control even the smallest details of how they raise their birds. The top four boiler companies now produce nearly 50 per cent of America's boiler meat. Independent hog farmers are following suit, with the number of US hog farms dropping by nearly 75 per cent over the last 15 years. just four corporations control over 50 per cent of the hog slaughter in the US. and 2 percent of cattle feeding operations account for 40 per cent of all cattle sold.

1 Advisory Committee on the Microbiological Safety of Food. 'Report on Poultry Meat'; HMSO, London: p.17.1996.

2 Ibid. p. 12.

3 Irwin, R.J. et al. 'A national survey to estimate the prevalence of Salmonella species among Canadian registered commercial turkey flocks'; Canadian Journal of Veterinary Research 58/4: 263-267, 1994.

4 Cox, J.M. 'Salmonella enteritidis: the egg and I'; Australian Veterinary Journal 72: 108, 1995.

5 'The Chicken and the Egg Story' Which? Magazine: pp82-83, February 1992. 6 Veterinary Record 137 (14): 336. 30 September 1995.

7 Cooper, G.L. et al. `Airborne challenge of chickens vaccinated orally with the genetically defined Salmonella enteritidis

8 Wathes, C.M. et al. `Aerosol infection of calves and mice with Salmonella typhimurium'; Veterinary Record 123: 590-594. 3 December 1988.

9 Davies, R.H. & Wray C. 'Observations on disinfection regimens used on Salmonella enteritidis infected poultry units'; Poultry science 74 (4): 638-647,1995.

10 Advisory Committee on the Microbiological Safety of Food. `Report on Poultry Meat'; HMSO, London: p51, 1996.

11 Ibid. p. 56

12 Pfeifer, CW. 'Association between aflatoxicosis and Salmonella: a case study'; Swine Health and Production 2(5):20-22,1994.

13 Royal Commission on Environmental Pollution. 'Seventh Report: Agriculture and Pollution'; HMSO, London: p.150.1979.

14 Advisory Committee on the Microbiological Safety of Food. 'Report on Poultry Meat'; HSMO, London: p.25.1996

15 Hood, A.M. et al. 'The extent of surface contamination of retailed chickens with Campylobacter jejuni serogroups', Epidem. Inf. 100:17-25. 1988.

16 Simmons, N. A. & Gibbs, FJ. `Campylobacter spp. in oven-ready poultry'; Journal of Infection 1: 159-162.1979.

17 'Campylobacter food surveillance studies in Northern Ireland '; Food Safety Northern Ireland Surveillance Bulletin NoA. Editor: Dr. E. Mitchell. Published by the Department of Health and Social Services, The Department of Agriculture for Northern Ireland and Department of Environment (Northern Ireland). Spring 1996.

18 Svedhem, A. et al. 'The occurrence of Campylobacter jejuni in fresh food and survival under different conditions'; J. Hyg., 87:421- 425.1981.

19 'Campylobacter in half of surveyed UK boilers'. Animal Pharm, 8 December 1995.

20 Advisory Committee on the Microbiological Safety of Food . 'Report on Poultry Meat'; HMSO, London: p 49.1996.

21 Ibid. p.92.

22 Weijtens, M.J.B. et al. `Prevalence of Campylobacter in pigs during fattening: an epidemiological study'; Veterinary Quarterly 15 (4):138-143.1993.

23 Moore, J.E. et al. 'Erythromycin-resistant thermophilic Campylobacter species isolated from pigs'; Veterinary Record 138: 306- 307. 30 March 1996.

24 Coghlan, A. 'Killer strain raises urgent questions'; New Scientist, 25 January 1997. 25 'Mastitis in 35% of UK cows says IAH'. Animal Pharm, 20 December 1996.

26 Advisory Committee on the Microbiological Safety of Food. 'Report on Verocytotoxin-- Producing Escherichia coli'; HMSO, London: p.15. 1995.

27 'E. coli 0157 in US feedlot cattle'. Animal Pharm, 20 December 1996.

28 Childers, A.B. & Walsh, B. 'New meat inspection technology for prevention of Escherichia coli 0157:HT; Meat Focus International: 318- 319. September 1996.

29 Chapman. PA. et al. 'Sheep as a potential source of verocytotoxin-producing Escherichia coli 0157% Veterinary Record 138: 23-24. 6 January 1996.

30 Ashton, W.L.G. 'Enterobacteriaceae'; in 'Poultry Diseases', editor FT W. Jordan. Published by Bailliere Tindall, London: p. 38.1990.

31 LeClerc, J.E. et al. 'High Mutation Frequencies Among Escherichia coli and Salmonella Pathogens'; Science 274: 1208-1211. 15 November 1996.

32 Advisory Committee on the Microbiological Safety of Food. 'Report on Poultry Meat'; HMSO, London: p 16. 1996

33 Takeshige K. et al. `Epidemiological studies of Listeria monocytogenes from dressed carcasses at a slaughter house'; Journal of the Japan Veterinary Medical Association 48 (2): 131-135. 1995

34 Elzen, A.M.G. van den & J.M.A. Snijders 'Critical points in meat production lines regarding the introduction regarding the introduction of Listeria monocytogenes'; Veterinary Quarterly 15 (4): 143-145. 1993

35 '17 cases of Listeria in France'. Animal Pharm, 23 June 1995.

36 Kim, K.T. et al. `Heating and storage conditions affect survival and recovery of Listeria monocytogenes in ground pork'; Journal of Food Science 59 (1): 30-32.1994.

37 Concise Veterinary Dictionary; Oxford University Press, Oxford: p 477. 1988. 38 'How safe is chicken?' Which? Magazine: pp. 8-9, October 1996.

39 Hood, A.M. et al. 'The extent of surface contamination of retailed chicken with Campylobacter jejuni serogroups'; Epidem. Inf. 100:17-25.1988.

40 'Campylobacter food surveillance studies in Northern Ireland ; Food Safety Northern Ireland Surveillance Bulletin No.4. Editor: Dr. E. Mitchell. Published by the Department of Health and Social Services, The Department of Agriculture for Northern Ireland and the Department of Environment (Northern Ireland). Spring 1996.

41 Simmons, N.A. & Gibbs, FJ.'Campylobacter spp. in oven-ready poultry'; Journal of Infection 1: 159-162.1979.

42 Willshaw, G.A. et al. 'Examination of raw beef products for the presence of Verototoxin producing Escherichia coli, particularly those of serogroup 0157% Journal of Applied Bacteriology 75:420- 426.1993.

43 Smith, H.R. et al. 'Examination of Retail Chickens and Pork Sausages in Britain for Vero Cytotoxin-Producing Escherichia coli'; Applied and Environmental Microbiology 57 (7): 2091-2093.1991.

44 Lloyd, A. Superintending Inspector, Drinking Water Inspectorate. Personal communication. 20 October 1995.

45 'Milk Hygiene: A guide to the diary products (hygiene) regulations for dairy product processors'; MAFF Publications, London: p.14.1995.

46 Roberts, J.A. et al. 'Economic impact of a nationwide outbreak of salmonellosis: costbenefit of early interventon'; British Medical Journal 298:1227-1230.1989.

47 Sockett, P 'Social and economic aspects of food-borne disease ; Food Policy, 110-119. April 1993.

48 Roberts, J.A. et al. 'Economic impact of a nationwide outbreak of salmonellosis: costbenefit of early intervention'; British Medical Journal 298:1227-1230.1989.

49 'Food poisoning inquiry urged'. The Guardian, 31 December 1996. 50 'Food poisoning increases' The Financial Times, 5 March 1997.

51 Bentham, G. & Langford, LH. `Climate change and the incidence of food poisoning in England and Wales'; Int. J. Biometerol 39 (2): 81-86.1995.

52 'Food poison risk will increase with "global warming"'. The Daily Telegraph, 6 January 1996.

53 'Food poisoning linked to farms'. The Guardian, 6. January 1996.

54 Bryan, FL. & Doyle, M.P `Health Risks and Consequences of Salmonella and Campylobacter jejuni in Raw Poultry'; Journal of Food Protection 58 (3): 326-344. 1995. 55 Bryan, FL. 'Poultry and Poultry Meat Products: Initial Microflora'; in 'Microbial Ecology of

Food: Vol II Food Commodities'. Published by Academic Press, NewYork, p. 417, 1980. 56 Lahellec. C. et al. 'Influence of Resident Salmonella on Contamination of Boiler Flocks'; Poultry Science 65: 2034-2039.1980.

57 Shane, S.M. `The significance of Campylobacter jejuni infection in poultry: a review ; Avian Pathology 21: 189- 213.1992.

58 Mc Coy, J.H. 'Trends in Salmonella food poisoning in England and Wales 1941-72'; J. Hyg., Camb. 74: 271-282.1975.

59 Pearson A.D. et al. `Sporadic human Campylobacter: Evidence for transmission from fresh chickens'; 'Epidemic human Campylobacter traced to a single chicken farm in southern England', in 'Campylobacter IV, editors B. Kaijser & E. Fallen. Published by the University of Gotenburg, Gotenburg, Sweden: pp. 307-310, 279-281, 1987.

60 Jones, D.M. and Robinson, D.A. `Occupational Exposure to Campylobacter jejuni infection ; The Lancet: pp 440-441. 21. February 1981.

61 Grados, 0. et al. 'Campylobacter infection: an occupational disease risk in chicken handlers'; in 'Campylobacter If, editors Pearson, A.D. et al .PHLS, London. p 162. 1983. 62 Madden, R.H. 'Microbial hazards in animal products'; Proceedings of the Nutrition Society 53: 309-316. 1994.

63 'Food poisoning too often traced to farms - CIEH'. Farmers Weekly, 15 September 1995. 64 'Infection traced to the farm'. Farmers Guardian, 15 September 1995.

65 Statham D. 'Food Poisoning : Endemic or Growing Epidemic?' Paper presented at the Chatham Institute Environmental Health Annual Congress: pp. 7-9. 1995.

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