On-farm Factors and Health Hazards

2 On-farm Factors and Health Hazards

2.1 Principles of Epidemiology as Applied to VPH


Epidemiology is a way of thinking and analysing problems with a view to increasing the knowledge of risks, risk factors, pathways of infections and contamination along the food chains, animal populations and environment, and is aimed at enabling community actions. VPH aims to apply veterinary knowledge to improve public health; thus, epidemiology is a building block in this endeavour.

To give a few examples of epidemiology applied to further public health it might be useful to start with John Snow’s study of cholera in London in the Victorian era. John Snow worked as a doctor (anaesthetist) in Victorian London from 1840 to 1850. His pioneering studies were on the cholera epidemic in 1849, on which he published his studies in 1854. Today, we know cholera is a water-borne disease caused by the bacterium Vibrio cholerae. The organism harbours genes for producing cholera toxin, which is transmitted by sewage into water (rivers or lakes) subsequently used for consumption. In brief, the faecal–oral pathway of transmission can result in explosive epidemics, once the bacterium is introduced into the water system. It appears that certain crayfish can harbour the bacteria on their bodies, thus creating reservoirs for the cholera bacteria. In Snow’s era, the prevailing wisdom specified miasma (foul air) or other vehicles to be the causes of cholera. Snow observed that during cholera outbreaks there were large differences in the number of cases (today one would say incidence or attack rate, i.e. the frequency of new cases during an outbreak) during cholera outbreaks in two similar areas of London. Two water companies supplied these separate areas. The water companies were supplying water for households through public pumps (outlets). During his investigations, Snow discovered that the water companies had their water intakes in the river Thames upstream and downstream of the sewage pipe into the river. The company upstream had the lower cholera incidence. Snow deduced that cholera was connected to the water being contaminated with sewage. This was several years before bacteria were recognized as a source of disease. To test his hypothesis, he removed (illegally) the handle of the water outlet associated with suspected cholera risk during the next outbreak. It appeared that the cholera incidence was reduced in the previous high-risk area. To sum it up; Snow did not know what caused the disease, but by applying principles of epidemiology comparing exposed with non-exposed populations he verified the hypothesis that cholera was connected with sewage contamination of drinking water. By intervention aimed at removing the exposure he could prove his hypothesis, albeit there was no prevailing knowledge of the true cause of the disease. This illustrates that epidemiology enables us to assemble enough knowledge to intervene in containing public or animal health risks long before we know all the relevant facts. The principles of comparison either of exposed versus not exposed with regard to disease incidence (cohort studies) or of the exposure rates in cases versus controls, produce ideas about the exposure risks. Interventions aimed at reducing exposures may confirm, or rather gather, further supporting evidence for the disease risks. Consequently, epidemiology is the cutting edge of medicine and public health activities, enabling prevention before the exact causes are identified, as was illustrated by John Snow’s work.

With mad cow disease or bovine spongiform encephalopathy (BSE) the same story could be told in a modern setting (see MAFF, 2000). During 1984 in the UK, a new syndrome emerged in cattle, with symptoms such as behavioural changes (losing rank in cow herd), sound sensitivity, ataxia and weight loss, with no response to treatments whatsoever. During the next 2 years more cattle with similar symptoms appeared in dairy herds in the UK. Wells et al. (1987) described the histopathological symptoms of BSE as being similar to those of scrapie. At that time, BSE was defined as a combination of clinical syndrome and histopathological findings. Then, to assess the risk factors, the usual suspects were rounded up and investigated including:

• contacts with sheep and goats; the risk factor was scrapie, which was known to be transmitted between animals;

• exposure to insecticides, i.e. organophosphates and pyrethrins;

• exposure to meat and bone meal;

• imported animals;

• vaccines;

• genetic mutations;

• unknown factors.

The challenge was now to assess the available evidence using sound epidemiological reasoning to sift through all possible hypotheses for the risk from BSE.

Disease Control Strategies With Regard to Veterinary Public Health

Disease control strategies could be seen as the aim of disease control efforts. By conventional wisdom they are grouped into three broad strategies:

• control strategy is when the aim is to live with the disease agent(s) but to keep the prevalence or concentration below an acceptable level;

• eradication strategy is when the aim is to eliminate the disease agent(s) within a geographical area or population, a primary production system and/or a part of the food chain;

• prevention strategy is when the aim is to prevent the introduction of disease agent(s) into a population and a food chain.

Veterinary public health is often defined as veterinary activities aimed at protecting and/or improving public health in a broad sense by employing one or a combination of these strategies.

Food safety is a veterinary public health activity employing all three strategies. With the advent of meat inspection during the last century, several zoonoses such as tuberculosis, and parasites such as trichinosis, could be controlled. However, it was soon recognized that food safety could not be assured by end product testing alone. This insight led to the development of the HACCP (hazard analysis critical control points), to supplement Good Agricultural Practice (GAP), Good Hygiene Practice (GHP) and Good Manufacturing Practice (GMP).

The HACCP system was conceived by the Pillsbury Company, together with the National Aeronautics and Space Administration (NASA), and the US Army Laboratories at Natick developed this system to ensure the safety of astronauts’ food during the 1960s (WHO, 2003). In the 40 years since then, the HACCP system has become the generally accepted method for food safety assurance. The recent growing worldwide concern about food safety by public health authorities, consumers and other concerned parties – and the continuous reports of food-borne outbreaks – have given further impetus to the application of the HACCP system. The HACCP system achieves process control by identifying hazards and critical control points in the process and establishing critical limits at these control points for the identified hazards (i.e. microbiological criteria), establishing systems for monitoring the critical control points and indicating suitable corrective actions if the critical limits are exceeded, and establishing suitable verification and documentation procedures.

The purpose of a critical control point (CCP) might be to control the growth of bacteria by keeping the food cold stored or frozen, e.g. Salmonella spp. or VTEC O157, and to have procedures to ensure that the cold-chain integrity is kept. Another purpose might be to eradicate pathogens from the food, e.g. pasteurization of milk.

The food chain could be seen as a consequence of the HACCP approach. Many HACCP plans had as their first critical control point the raw material – how to ensure that the raw material was safe. Thus, food processors and food safety authorities started to require that farmers and feed producers also had food safety assurance programmes. At the end of the day it appeared that there were critical control points both in primary production and in feed production, as well as in processing.

Instead of thinking of feed production, animal husbandry and production, abattoirs, cutting, dairying and other processing as separate and independent activities aimed at processing raw materials that might end up on the plate, the modern approach is that everybody along the food chain is producing food. Previously, for example, milk on the farm was considered as a raw material that was transported and changed into a foodstuff only after pasteurization. Now, it is regarded as a food that must be protected all the way from the pastures to the consumers. Consequently, the quality and safety requirements and the supervision along the food chain should be seamless and integrated. The slogans ‘farm to fork’, or ‘from the fields to the plates’ were used to illustrate this new thinking. Inevitably, this has changed the way veterinary surgeons work. Previously, our main goal was to cure sick animals. This is still our main task today but now, in addition, we must ensure that healthy animals produce healthy foods and that our cures for sick animals will not harm the safety of any food produced.

The BSE and dioxin crises within the EU originated due to problems in feed production: in particular the rendering practices in regard to the BSE epidemic, and the raw materials used for feedstuff production in regard to the dioxin crisis. Both crises contributed to this radical overhaul of how we work in food safety. The European Commission (2000) outlined this new approach in its White Paper (http://europa.eu.int/comm/dgs/health_consumer/library/pub/pub06_en.pdf). In the new EU general food law regulation (Council and Parliament Regulation 178/2002/EU) it is stated that all food business operators are responsible for producing safe food. Food business operators are defined as all those involved, from feed producers, farmers and food processors to caterers and supermarkets. Another challenge is to regard animal health and public health as two sides of the same coin.

In the food chain one might apply the same tool but be pursuing different strategies. For example, vaccination will be used to control some diseases (like Salmonella in layers), to control and eradicate other diseases like pseudorabies (Aujeszky’s disease) and to prevent introduction of Newcastle disease into a poultry flock.

The remit of veterinary public health activities is wide – which makes this field the most satisfying in which to work in veterinary medicine. There are always new challenges awaiting. One interesting development is the issue of conservation medicine (Daszak et al., 2004), where one links the prevention of zoonoses with the conservation of wildlife and ecosystems, with sustainability of agriculture and economic and social development all based on as sound an epidemiological knowledge as possible. The conservation medicine approach to emerging diseases integrates veterinary, medical, ecological and other sciences in interdisciplinary teams. These teams investigate the causes of emergence, analyse the underlying drivers and attempt to define common rules governing emergence for human, wildlife and plant emerging infectious diseases. The ultimate goal is risk analysis that allows us to predict future emergence of known and unknown pathogens. Then, the disease control strategies can be employed as appropriate.

Many zoonoses normally thought of as food-borne can be transmitted by direct contact with animals or through the environment, or from person to person. One example is E. coli O157 or enterohaemorrhagic E. coli (EHEC) – also referred to as shigatoxinlike (STEC) or verotoxin-producing E. coli (VTEC), as reviewed by Mead and Griffin (1998), and also verotoxigenic E. coli (VTEC) in foodstuffs, in the opinion of the Scientific Committee of Veterinary Public Health (2003). Hence, any disease control strategies employed must take a holistic view of the disease problem. To prevent person-to-person transmission the public health authorities may require that children in kindergartens with diarrhoea stay at home until the clinical symptoms cease. When visiting farms or herds visitors are obliged to wash their hands to avoid transmission of EHEC after direct animal contacts.

For some years it has been recommended in Sweden that children under 5 years of age should not visit farms during the summer, when the risk of catching EHEC is highest. EHEC poses a challenge since it can be eradicated at the processing stages of the food chain using heat treatment, while in the primary production stage the challenge is to control the bacteria and to prevent the clinical disease in humans.

I hope this and the following chapters will induce readers to pursue a career in veterinary public health. Although no promises about gold and glory can be given, your professional life will not be boring.


Daszak, P., Tabor, G.M., Kilpatrick, A.M., Epstein, J., Plowright, R. (2004) Conservation medicine and a new agenda for emerging diseases. Annals of the New York Academy of Sciences 1026, 1–11.

European Commission (2000) http://europa.eu.int/comm/dgs/health_consumer/library/pub06_en.pdf

MAFF (2000) The BSE Inquiry. http://www.bseinquiry.gov.uk

Mead, P.S., Griffin, P.M. (1998) Escherichia coli O157: H7. Lancet 352, 1207–1212.

Scientific Committee of Veterinary Public Health (2003) http://europa.en.int/comm/food/fs/se/sev/out58_en.pdf

Wells, G.A., Scott, A.C., Johnson, C.T., Gunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. (1987) A novel progressive spongiform encephalopathy in cattle. Veterinary Record 121, 419–420.

WHO (2003) http://who.int/fsf/Micro/haup.htm

2.2 Zoonotic Diseases in Farm Animals

Basic Parameters for Describing Disease

Disease is an abnormal status that can be detected in clinical form by our senses (vision, palpation, smell, etc.) or in sub-clinical form only by specific tests. Zoonoses are diseases infecting animals that also can be naturally transmitted to humans.

With respect to their frequency of occurrence, zoonotic diseases can occur in the following forms:

• epidemic: a sharp increase in occurrence above the status that is, under given conditions, considered as ‘normal’;

• pandemic: a worldwide epidemic;

• endemic: regularly present in a given population;

• outbreak: a sudden epidemic affecting ≥2 or a high number of related individuals; and

• sporadic: a disease occurring as single cases in unrelated individuals.

To describe general disease patterns, some basic parameters can be used:

• incidence: number of new cases of a disease, expressed as a proportion of the ‘at-risk population’ within a given period;

• at-risk population: part of a population particularly susceptible to a given disease; and

• prevalence: diseased individuals as the proportion of the total population at a given time.

Information needed about a given disease often includes whether it is present or absent. Absence of disease can be proved only by testing all susceptible animals; this normally poses numerous practical difficulties. Rather, this is commonly handled through testing of a sample of the animals in the location. The sample size chosen will depend on the particular circumstances, such as size of the animal population and nature/prevalence of the disease, but the most important factor is which confidence level is expected from the results (most commonly 95%). Sampling and testing programmes can be:

• monitoring: ongoing testing to detect changes in disease prevalence; and

• surveillance: continuous testing, often of the same population section, to detect early cases for disease control purposes.

Notifiable Diseases

Notifiable disease are those designated in official lists issued by national (e.g. UK Government, Table 2.1) and/or international regulatory authorities (e.g. OIE; Table 2.2) and which, immediately after their detection or suspicion, must be reported to the authorities. Therefore, a given disease can be notifiable internationally, nationally or both. There are several reasons for inclusion of a disease in the ‘notifiable’ category:

• it can cause significant economic damage (the most common reason), e.g. foot and mouth disease;

• it can cause severe illness or death in humans, e.g. rabies, tuberculosis;

• it cannot be differentiated from another disease, e.g. swine vesicular disease;

• it is a newly introduced disease with expected significant, or yet to be assessed, impact – e.g. caseous lymphadenitis in the UK; and

• it is important for tradition – or public opinion-related reasons.

Understandably, in practice, notification of a given disease is useful only if it is diagnosable by an appropriate test, and is controllable.

Table 2.1. Notifiable diseases in the UK (from DEFRA, 2005).

Notifiable Disease

Species affected

Last occurence

African Horse Sickness



African Swine Fever




Cattle and other mammals


Aujeszky’s Disease

Pigs and other mammals


Avian Influenza (Fowl plague)




Sheep and Goats


Bovine Spongiform Encephalopathy (to BSE home page)



Brucellosis (Brucella abortus)



Brucellosis (Brucella melitensis)

Sheep and Goats


Classical Swine Fever



Contagious agalactia

Sheep and Goats


Contagious Bovine Pleuropneumonia



Contagious Epididymitis (Brucella ovis)

Sheep and Goats


Contagious Equine Metritis






Enzootic Bovine Leukosis



Epizootic Haemorrhagic Virus Disease



Epizootic Lymphangitis



Equine Infectious Anaemia



Equine Viral Arteritis



Equine Viral Encephalomyelitis



Foot and Mouth Disease

Cattle, sheep, pigs and other



cloven-hooved animals


Glanders and Farcy



Goat Pox



Lumpy Skin Disease



Newcastle Disease



Paramyxovirus of pigeons



Peste des Petits Ruminants

Sheep and Goats



Dogs and other mammals


Rift Valley Fever

Cattle, Sheep and Goats


Rinderpest (Cattle plague)



Scrapie (on DEFRA’s BSE website)

Sheep pox



Swine Vesicular Disease



Teschen Disease (Porcine enterovirus






Tuberculosis (Bovine TB)

Cattle and deer


Vesicular Stomatitis

Cattle, pigs and horses


Warble fly

Cattle (also deer and horses)


West Nile Virus



Table 2.2. Diseases notifiable to the OIE (from OIE, 2004).

Multiple species diseases

Cattle diseases


Bovine anaplasmosis

Aujeszky’s Disease

Bovine babesiosis


Bovine brucellosis


Bovine cysticercosis

Foot and mouth disease

Bovine genital campylobacteriosis


Bovine spongiform encephalopathy


Bovine tuberculosis

Lumpy skin disease

Contagious bovine pleuropneumonia

New World screw-worm (Cochliomyia hominivorax)



Enzootic bovine leukosis

Old World screw-worm (Chrysomya bezziana)

Haemorrhagic septicaemia


Infectious bovine rhinotracheitis/infectious pustular vulvovaginitis


Q fever

Malignant catarrhal fever



Rift Valley fever




Vesicular stomatitis

Trypanosomosis (tsetse-transmitted)

Sheep and goat diseases

Equine diseases

Caprine and ovine brucellosis (excluding B. ovis)

African horse sickness


Contagious equine metritis

Caprine arthritis/encephalitis


Contagious agalactia

Epizootic lymphangitis

Contagious caprine pleuropneumonia

Equine encephalomyelitis (Eastern and Western)

Enzootic abortion of ewes (ovine chlamydiosis)

Equine infectious anaemia


Equine influenza

Nairobi sheep disease

Equine piroplasmosis

Ovine epididymitis (Brucella ovis)

Equine rhinopneumonitis

Ovine pulmonary adenomatosis

Equine viral arteritis

Peste des petits ruminants


Salmonellosis (S. abortusovis)

Horse mange


Horse pox

Sheep pox and goat pox

Japanese encephalitis

Swine diseases

Surra (Trypanosoma evansi)

African swine fever

Venezuelan equine encephalomyelitis

Atrophic rhinitis of swine

Avian diseases

Classical swine fever

Avian chlamydiosis

Enterovirus encephalomyelitis

Avian infectious bronchitis

Porcine brucellosis

Avian infectious laryngotracheitis

Porcine cysticercosis

Avian mycoplasmosis (Mycoplasma gallisepticum)

Porcine reproductive and respiratory syndrome

Avian tuberculosis

Swine vesicular disease

Duck virus enteritis

Transmissible gastroenteritis

Duck virus hepatitis

Lagomorph diseases

Fowl cholera


Fowl pox

Rabbit haemorrhagic disease

Fowl typhoid


Highly pathogenic avian influenza


Infectious bursal disease (Gumboro disease)


Marek’s disease


Newcastle disease


Pullorum disease

Fish diseases

Bee diseases

Bacterial kidney disease (Renibacterium salmoninarum)

Acarapisosis of honey bees


American foulbrood of honey bees

Channel catfish virus disease

European foulbrood of honey bees

Enteric septicaemia of catfish (Edwardsiella ictaluri)

Tropilaelaps infestation of honey bees


Varroosis of honey bees

Epizootic haematopoietic necrosis

Mollusc diseases

Epizootic ulcerative syndrome

Infection with Bonamia exitiosus

Gyrodactylosis (Gyrodactylus salaris)

Infection with Bonamia ostreae

Infectious haematopoietic necrosis

Infection with Candidatus xenohaliotis californiensis

Infectious pancreatic necrosis


Infectious salmon anaemia

Infection with Haplosporidium costale

Oncorhynchus masou virus disease

Infection with Haplosporidium nelsoni

Piscirickettsiosis (Piscirickettsia salmonis)

Infection with Marteilia refringens

Red sea bream iridoviral disease

Infection with Marteilia sydneyi

Spring viraemia of carp

Infection with Mikrocytos mackini

Viral encephalopathy and retinopathy

Infection with Mikrocytos roughleyi

Viral haemorrhagic septicaemia

Infection with Perkinsus marinus

White sturgeon iridoviral disease

Infection with Perkinsus olseni/atlanticus

Crustacean diseases

Other diseases

Crayfish plague (Aphanomyces astaci)


Infectious hypodermal and haematopoietic necrosis


Spawner-isolated mortality virus disease


Spherical baculovirosis (Penaeus monodon-type baculovirus)


Taura syndrome


Tetrahedral baculovirosis (Baculovirus penael)


White spot disease


Yellowhead disease


Actions Following Disease Notification

Management of a number of notifiable diseases in the UK (and EU) is covered by related EU policies, and can include:

• isolation of affected or suspect animals;

• declaration of an infected premises and possibly an area;

• control of the movement of animal, people and vehicles;

• killing (slaughter) of all affected and in-contact animals (with compensation) within a certain geographical radius, for disease eradication purposes e.g. foot and mouth disease;

• slaughter of an infected animal with compensation, e.g. tuberculosis, BSE;

• treatment, e.g. anthrax in pigs;

• vaccination, e.g. rabies, Newcastle disease; and

• related cleaning and sanitation regimes.

Understandably, necessary pre-conditions for successful management of notifiable diseases include individual and/or herd identification of animals and records of movement for relevant farm animal species. However, it should be noted that different countries may manage diseases differently. If a country declares (and proves) freedom from a given notifiable disease, then it can decide to import animals only from those countries that apply compulsory notification of that disease.

Principal zoonotic notifiable diseases in farm animals


This is a contagious, usually chronic disease, characterized by nodular lesions – tubercles with necrosis, caseation and calcification in lungs, lymph nodes or other organs. The infectious route is either mainly inhalation (e.g. cattle) or ingestion (e.g. pigs). Disease is caused by three different types of mycobacterium. Mycobacterium tuberculosis causes infections mostly in man, rarely in dogs, parrots and non-human primates. M. bovis causes tuberculosis mostly in cattle, but can also infect humans, goats and pigs; sheep and horses have high resistance. M. avium is found mostly in birds, and also in pigs, but it is still debatable whether can it infects humans. The main sources of infection of cattle appear to include wildlife, e.g. badgers in the UK – although this is still a controversial and debatable explanation – and opossums in New Zealand and Australia. In the EU, some countries are declared free from bovine tuberculosis, whilst in others prevalence of infected herds varies between <1% and 8%. In the UK at the beginning of 2001, around 900 animals were found to be reactors out of approximately 372,000 tested.

Diagnosis of bovine tuberculosis in live animals can be based on:

• culturing of respiratory tract secretions, but this gives positive results only in <20% of naturally infected animals;

• detection of antibodies, but antibody responses vary in magnitude and often cannot be detected until a few months after infection;

• cellular immune responses; infection stimulates strong responses, with delayed-type hypersensitivity reactions detectable 3–4 weeks after infection;

• tuberculin skin test; based on intradermal injection of a crude protein extract from supernatants of M. bovis and M. avium injected at two separate sites on the neck and measurement of the skin thickness after 72 hours. Sensitivity (% of infected animals correctly identified) of the tuberculin test is around 90%, and specificity (% of uninfected animals correctly identified) is around 99.9%;

• interferon-γ test (IFN-γ test); whole blood is cultured with PPD from M. bovis and M. avium and IFN-γ production is measured by ELISA after 24 hours. A field trial in Northern Ireland showed an IFN-γ test sensitivity of 84.3% whilst parallel tuberculin sensitivity was 83.1%.

Positive findings of tuberculous lesions (caseous lymphadenitis) at postmortem meat inspection of tuberculin-positive slaughtered cattle can vary (40–70%). This variability can be affected by the interpretation criteria used for the tuberculin skin test, as well as by how detailed the meat inspection was. Tuberculous lesions in reactors are found mainly in lymph nodes draining the head and lungs (around 40 and 70%, respectively), but are found much less frequently in lung tissue or mesenteric lymph nodes (<10%). With respect to microbiological isolation of the pathogen, most lesions that are visible yield positive results. However, several weeks is required to obtain culture results. Carcass meat from cattle with only localized lesions found and removed is used for human consumption as in such cases there are no tuberculous lesions in muscles. However, the entire carcass is condemned in the case of spread or generalized tuberculous lesions. To date, there is not yet clear evidence of human M. bovis infection via meat or meat products.

Bovine tuberculosis had much higher implications for human health in the first half of 20th century, when neither herd testing nor milk pasteurization measures were implemented. For example, in the 1930s in the UK, 40% of cows were infected and 0.5% produced contaminated milk, leading to roughly 2000 human deaths per annum. However, since milk pasteurization and herd testing were introduced (1940s–1950s), the prevalence of positive herds decreased to 1.6–2.5% and human cases decreased to 32–34/year. Hence milk pasteurization prevents, to a large extent, the risks from food-borne tuberculosis, but it should be kept in mind that dairy products from unpasteurized milk dairy products are available on the market. Therefore, nowadays, occupational exposure to M. bovis, e.g. farmers, may represent a higher public health risk.

Mycobacterium paratuberculosis (M. avium subspecies paratuberculosis, M. johnei) causes Johne’s disease (paratuberculosis) in cattle. Disease is characterized by enteritis and/or enlargement of mesenteric lymph nodes, often with haemorrhages. Diagnosis of paratuberculosis by blood tests (AGIDT, ELISA, CFT) is possible. Human infection with this pathogen (Crohn’s disease) may be acquired primarily via contaminated milk, although the question of whether association between Johne’s disease and corresponding Crohn’s disease actually exists is still being debated.

Bovine Spongiform Encephalopathy (BSE)

This disease, caused by a proteinaceous agent called a ‘prion’, primarily affects cattle, in which it was first recognized in the mid-1980s in the UK. However, a single case of BSE in a goat was confirmed in France in 2004; the implications of caprine BSE for overall BSE epidemiology have yet to be determined. Bovine BSE infections have been registered in a number of countries since the 1990s (Table 2.3). It is generally accepted that the initial source of infection was feeding of cattle with meat and bone meal which probably contained carcasses of sheep infected with scrapie in the 1980s. This was preceded by a change (lower temperature) in the rendering process. However, it seems that the vast majority of cases were caused by feeding cattle-derived material to cattle.

Clinical symptoms include apprehensiveness, occasional aggression, kicking when milked, high-stepping gait (particularly hind legs), skin tremors and loss of condition. Early studies on BSE looked for, and did not find, evidence that BSE was associated with pharmaceuticals, pesticides, genetic determinants, artificial insemination or direct contact with sheep/cattle.

Trends in the BSE epidemic in the UK are characterized by a sharp increase in new cases until the peak in 1992, when 1% of adult breeding cows per year were infected. Since then, the incidence has been decreasing by approximately 40% per year. The infection was associated primarily with dairy herds; 61% of all dairy herds were affected, comprising 81% of BSE cases. The intra-herd prevalence was relatively low (on average ≤2.7%).

Table 2.3. Incidence of BSE in cattle at the end of 2003 (adapted from OIE data).


First recorded case

Total cases













Switzerland (non-EU)





















Luxembourg, Austria, Greece, Finland






Czech Republic









United Kingdom



Other countries















With respect to the spread of BSE, no evidence has been found either for horizontal transmission or for vertical transmission via the sire. However, vertical maternal transmission could be possible, as scrapie infection proved possible by feeding sheep with placenta from scrapie-positive sheep. Also, the calf offspring of clinical cases had a higher risk of BSE (9.6%), compared to those from non-BSE cases.

Currently available, or under development, diagnostic procedures for BSE (indeed, as well as for scrapie) include:

1. Post-mortem tests:

• histopathology of brain samples, a gold standard against which all other tests are validated (EU Diagnostic Manual);

• antibody-based tests for PrPSc protein: Western blot with brain; Immunocytochemistry (ICC) with brain, tonsil, third eyelid, ELISA with spinal cord, etc.; and

• others.

2. Ante-mortem tests (in live animals):

• clinical signs; however, these produce around 20% false positive diagnoses;

• immuno-capillary Electrophoresis (ICE);

• urine test (for metabolic markers); and

• others.

Control measures for BSE used in the UK have focused on multiple aspects and were implemented both on-farm and on-abattoir:

1. Computerized cattle tracing system (CTS):

• operated by the Government and holding the full history about birth, movement and death of all cattle in the UK since 28 September 1998 (and 1996–1998 retrospectively);

• each animal entering the food chain has a passport; and

• numerical ear tagging from 17 January 2000.

2. Feed controls that include:

• prohibition of all mammalian protein (except milk, gelatin, amino acids, dried blood products, dicalcium phosphate) to ruminants;

• prohibition of mammalian meat and bone meal (MMBM) to any farm stock;

• ban of MMBM at feed-handling premises;

• some exceptions include milk and milk products, fishmeal for animals other than ruminants, and (under specified conditions) nonruminant gelatin for coating of additives, hydrolysed protein and dicalcium phosphate.

3. Slaughter of cattle over 30 months scheme (OTMS):

• slaughter with compensation of bovines >30months;

• only at licensed abattoirs; and

• meat banned for human consumption is incinerated, or rendered and destroyed.

4. Beef Assurance Scheme (BAS):

• animals up to 42 months old can be slaughtered for human consumption under certain conditions;

• these animals are from only herds that have never had a BSE case;

• they are from only specialist beef herds;

• grass-fed only; no feeding of MMBM during the past 7 years, no feeding of concentrates during the past 4 years (unless from a mill not used for MMBM production); and

• animals tested and negative for BSE.

5. Accelerated slaughter scheme: slaughter of animals born between 1989 and 1993) that during first 6 months of life shared contaminated feed with BSE cases.

6. Offspring cull scheme: slaughter of animals born after 1996 (tight feed control), but at risk from infection from their dams.

7. Removal of Specified Risk Materials (SRMs) from the food chain: meat hygiene measures (at abattoir) to remove and destroy specified organs and tissues, potentially containing prions if the animal is infected, from all bovines intended for human consumption. For details, see Chapters 5 and 6.

8. Ban of pithing and, potentially in the future, mechanical stunning of ruminants (see same chapters).

Public health concerns associated with BSE have arisen since recognition of a new variant of the previously known transmissible spongiform encephalopathy in humans (Creutzefeld-Jacob disease: vCJD). Because it resembles BSE characteristics, it has been assumed that it is a result of meat-borne BSE infection. The incidence of vCJD is shown in Table 2.4. However, current knowledge of the possibilities and ways of contracting vCJD from BSE infected foods is insufficient. The main reason is that vCJD cases could not be clustered until relatively recently. Namely, one cluster of five cases of vCJD occurred in a village in the UK, which retrospectively could be linked to a local butcher, whose practices at the time could enable meat contamination by bovine brain tissue. Understandably, further intensive research on BSE–vCJD link is both ongoing and necessary.

Table 2.4. vCJD deaths in the UK (adapted from UK DEFRA data).



















2003 (up to 6 May)



It is caused by Bacillus anthracis, an anaerobic bacterium that sporulates when exposed to air (oxygen), although the spores can survive in the environment for many years. Disease, principally in cattle, is characterized by sudden death with ‘tarry’ blood from body orifices. In pigs, anthrax can take sub-acute form. Anthrax is endemic in semi-tropical countries and sporadic in temperate areas; it is typically a food-borne disease. Diagnosis in animals is mainly based on microscopic identification of polychrome methylene blue-stained, square-ended bacilli in smear samples from blood; suspect dead animals are commonly sampled after cutting off an ear. Controls may include restrictions imposed on infected location, prohibition of certain feeds, moving animals off the premises and vaccination. In humans, anthrax is relatively rare and the majority of cases (e.g. 85% in the UK) are not food-borne but associated with occupational exposure, e.g. handling hides/skins. Human anthrax infections can take different forms: cutaneous anthrax (localized ulceration, black scab, fever, followed by septicaemia), inhalation anthrax (fulminating pneumonia) and intestinal anthrax (acute gastroenteritis).


Other names include: in humans, Malta fever, undulant fever; in animals, Bang’s disease, contagious abortion, epizootic abortion. The causative agent and main occurrence are as follows: Brucella abortus (cattle; worldwide), B. canis (dog; North America), B. melitensis (sheep, goat; Mediterranean, Middle East), B. ovis (sheep; New Zealand, Australia, Americas), B. suis (pig; Latin America, Europe) and B. neotomae (desert rat).

Brucellosis of cattle is caused by Brucella abortus, which also produces disease in humans. Brucellosis of cattle produces no characteristic postmortem signs. Diagnosis is by laboratory testing of blood or milk samples and by laboratory culture of the pathogen from the placenta, vaginal discharge or the milk of infected cows. Since brucellosis of cattle is still present in many countries, including some in the EU, prevention in brucellosis-free UK relies on herd surveillance: monthly testing of bulk milk samples from dairy herds and blood testing of beef breeding herds every two years. All infected cattle and contacts which have been exposed to infection must be slaughtered.

Brucella melitensis infects sheep and goats and can cause a disease in humans known as ‘Malta fever’, usually after ingestion of affected milk. When infection is first introduced into a flock or herd, a very high number of abortions can occur, but signs also include fever, mastitis, arthritis, orchitis or nervous signs in both sheep and goats. There are no lesions which distinguish B. melitensis-affected animals from animals with other diseases which also cause abortion. B. melitensis is prevalent in Mediterranean and Middle Eastern countries, as well as in some areas of Asia, Africa and Central and South America. In the UK, annual surveys for B. melitensis are carried out; blood samples are tested using ELISA and serum agglutination.

Brucella suis infects pigs but has no such public health relevance, as have B. abortus or B. melitensis.

Slaughter of animals infected with brucellosis is permissible only under conditions of special preventive measures (gloves, masks, etc.) to protect abattoir staff from potential infection.


Two forms of this serious disease, mainly of equids (horses, mules and donkeys), are caused by the bacterium Burkholderia mallei. In ‘glanders’ the principal lesions are in the nostrils, submaxillary glands and lungs; in ‘farcy’ the main lesions are on the surface of limbs or body. This disease was eradicated from the UK in 1928, but is still present in parts of Europe, Asia, Asia Minor and North Africa. Glanders is an important zoonosis; humans can be infected from affected horses by inoculation through a wound. Without treatment, the mortality rate can reach 95%. Diagnosis can be made by taking samples from clinical cases and by the ‘mallein’ test, when a dose (0.1 ml) of antigen is injected into the tissue below the eye. Swelling at the injection site, often with a high temperature, often indicates a potential carrier state, and can be an aid to field diagnosis. Controls include immediate slaughter of infected horses and strict isolation of suspected cases and contact animals.

West Nile Virus (WNV)

WNV is a flavivirus, one member of a group of Arthropod-borne viruses (Arboviruses), and causes infection of birds, horses and humans. Poultry can be infected but do not usually develop the clinical disease. Although a range of other animal species, such as goats and sheep, can be infected, they develop only low levels of the virus. To date, there have been no reports of cattle having been affected by the virus. Disease is transmitted by the bite of infected mosquitoes, and takes the form of encephalitis or meningitis.

The disease has been recorded in Africa, the Middle East, West and Central Asia and the USA. In Europe, recent outbreaks occurred in Romania (1996), Italy (1998), Russia (1999) and France (2000). Infected humans can have a flu-like illness with fever; a small proportion of cases (less than 1%) develop meningo-encephalitis, which produces nervous signs and may be fatal. However, many infected people show no symptoms. In the USA in 2002, 4161 people were reported to be infected with the disease, with 277 fatalities. In the UK, antibodies against WNV were found in birds, suggesting exposure, but the virus itself has not been identified in horses or in humans.

The main route of transmission of WNV is through mosquitoes, and the risk of food-borne infection of humans via meat/milk from infected animals is considered to be extremely low. The virus is destroyed by normal cooking methods (at <100°C) and pasteurization, and there have been no reports of the virus infecting people following consumption of meat and milk from infected animals. However, it should be noted that a related viral disease, tick-borne encephalitis, has been proved to cause food-borne infection via unpasteurized goats’ milk.

The main control measures are focused on control of the mosquito population, since control of migratory birds is very difficult. In addition, handling dead birds with bare hands should be avoided.

Rift Valley fever (RVF) virus

This virus belongs to the family Bunyaviridae, genus Phlebovirus, and causes disease in wild and domestic ruminants, dromedaries, some rodents, as well as in humans; it is a major zoonosis.

After incubation of 1–67 days, disease in animals is characterized by fever, abortion and diarrhoea; mortality can reach 70% (calves). In humans, infection is flu-like and recovery occurs within 1 week.

Infection is transmitted via many families of mosquitoes, which serve as competent vectors, Aedes mosquitoes are the main host reservoir. Sources of infection for animals are wild animals and mosquitoes; and for humans mosquitoes, blood, nasal secretion and vaginal secretion, but aerogenic and alimentary (meat, milk) routes of infection are also possible.

To date, RVF has been reported only in some African countries, particularly those with a humid climate and large mosquito populations. The only epidemics north of the Sahara were recorded in Egypt (1977, 1993) and in Mauritania (1987). However, few cases of laboratory infection have occurred in other countries; RVF is not yet present in Europe.

Control measures include hygiene and vector control, but so far have not shown a significant efficacy.

Avian influenza (AI) virus

Influenza has three types including type A, for which birds are the natural host. Type A is further divided into subtypes, based on haemagglutinin (HA, 15) and neuroaminidase (NA, 9). Avian influenza (AI) includes a subclinical type (LPAI; low mortality) and a high-pathogenicty type (HPAI; high mortality) which differ with respect to clinical symptoms and genetic characteristics. Although it is known that LPAI can become HPAI, it is unknown whether this is associated with pathogenicity for humans.

Transmission of AI is possible via direct contact, contact with faeces of infected animals (transport, cages), as well as via the airborne route, but it is not certain whether vertical transmission occurs.

When considering the zoonotic potential of AI, it should be stressed that no hard evidence for sustained transmission to humans has been found to date. However, it should also be noted that immunity against this disease (i.e. H5N1) does not exist in human population. Adaptation of H5N1 to human hosts, through close contact between infected animals and humans, would have represented the main potential risk for human population – ultimately enabling efficient human-to-human transmission.

Prevention of AI entering Europe is based on border controls, biosecurity (i.e. prevention of contact with flying wild birds, avoiding livestock markets) and surveillance systems for early detection. In the case of an HPAI epidemic, the contingency plans include slaughter of infected or suspect animals and destruction of the meat. In some cases, preventive slaughter of flocks neighbouring the infected flocks would be possible, as well as emergency vaccination.

Controls related to humans would include public information systems, protection of staff in the infected zone (physical protection, vaccination, antiviral treatments) and monitoring of contact from infected individuals. Poultry products, generally, should not pose a risk even if they contain the virus, because of both its non-alimentary transmission and the fact that only cooked poultry products are normally eaten.

Other zoonotic diseases associated with farm animals: microbial


Erysipeloid (erysipelas, diamonds) is disease, most often seen in pigs, caused by the bacterium Erysipelothrix insidiosa (rhusiopathiae) that is present in soil. Clinical features in animals include high fever, diamond-shaped lesions on the skin (acute form) or enlarged, painful joints and heart disease (chronic form). Transmission to humans occurs via contaminated cuts and abrasions during handling affected animals/meat, usually on the hand or forearm; human disease takes the form of localized erythema with pain or arthritis in finger joints; septicaemia can occur, but very rarely. Prevention measures include keeping pigs on concrete and vaccination of sows (twice yearly, 3–6 weeks before farrowing).


Listeriosis (mononucleosis, circling disease) is a disease primarily of ruminants, but also occurs in humans. It is caused by the bacterium Listeria monocytogenes (sometimes L. ivanovii in sheep), which is widely distributed, excreted in the faeces of healthy food animals and humans, and ubiquitous in the soil/environment and in silage. In animals, listeriosis is commonly in the meningoencephalitis form (circling, paralysis) or the visceral form (abortion, with retained placenta) with fatality rates of 3–30%. Disease can be transmitted to humans directly from animals (rarely), or as food-borne from contaminated foods (see Chapter 1.2). It is characterized by sudden fever, headache, meningitis, pneumonia, septicaemia, abortion and stillbirth; primarily in pregnant and IC individuals.


Orf is an infection caused by a Parapox virus that can survive in environment for up to 20 years. Infection of sheep can occur via cuts and abrasions. Orf is often seen on the mouth, teat and udder; the virus has been isolated from the poll of rams. Can be transmitted to humans via direct contact, i.e. infection of fingers due to sheep milking.


Leptospirosis in humans is caused by Leptospira hardjo (Dairy Worker Fever) via infected cows’ urine, with the organism entering through mucous membranes, cuts and abrasions. Another type of leptospirosis is caused by L. icterohaemorrhagiae (Weil’s Disease) via infected rat urine and contaminated water. The human disease is characterized by flu-like symptoms and causes prolonged debilitation.

Q Fever

Q Fever in sheep and goats is caused by Coxiella burnetti, a rickettsial organism; it is very infectious for humans. Transmission routes include infected urine, faeces and afterbirths, as well as contaminated dust and unpasteurized milk. It is characterized by a general malaise.

Other zoonotic diseases associated with farm animals: parasitic

The main groups of zoonotic parasites relevant to meat hygiene and inspection include:

• nematodes (roundworms), e.g. Trichinella;

• cestodes (flatworms, tapeworms), e.g. Taenia saginata, T. solium, Echinococcus granulosus

• trematodes (flukes), e.g. Fasciola, Fascioloides, Dicrocoelium

• protozoa, e.g. Toxoplasma gondii, Sarcocystis, Giardia/Cryptosporidia;

• arthropoda (insects, lice, mites, bugs, linguatula).


Relevant species of this parasite include T. spiralis (main species affecting mammals), T. pseudospiralis (affecting birds and mammals), T. nativa (present in cold regions of Canada, Russia, Arctic regions) and T. nelsoni (present in Africa, but also in Europe). In food animals, the occurrence of trichinellosis is low (sporadic) in some countries in Europe and in the USA, exceptionally low in other countries such as Norway and Sweden, and the disease is declared eradicated in some countries such as Denmark, UK, Portugal and Canada. The main reservoirs of trichinellosis are numerous wild, meat-eating animals, as well as vermin (rats, mice); disease is transmitted only by ingestion of muscles containing viable encysted Trichinella larvae. Among animals from which meat is eaten by humans, the disease affects domestic pigs, wild boar, horses, bear and walrus.

The life cycle of the parasites comprises: (i) intestinal stage with adult parasites laying live larvae in gut wall; (ii) migration stage with non-infective larvae migrating via blood/lymph circulation or actively from gut to muscles; and (iii) muscular stage with larvae becoming encysted intracellularly in muscles and subsequently infective. The largest numbers of cysts (invisible to the naked eye) are present in respiratory muscles (diaphragm, intercostal), larynx and tongue. Animal hosts usually show no symptoms, whilst in humans the disease in its muscular stage is serious (severe muscle pain, swollen face/eyelids) and, in case of heavy infestation, can be life-threatening.

Modes of transmission in humans include consumption of undercooked meat or, most often, uncooked types of meat products (dried hams, salamis) domestically prepared from non-examined meat, in which the larvae can survive. Modes of transmission in pigs include eating carcasses of infected animals (wildlife, vermin), consumption of raw/undercooked meat containing skeletal/striated muscles, e.g. meat plant offal or uncooked food remains from kitchen (swill), as well as via cannibalism. Modes of trichinellosis infection in herbivores (e.g. horses) are unclear, but may include ingestion of feeds containing remains of infected rodent carcasses. The main controls for trichinellosis in animals can vary between countries, depending on the epidemiological situation and whether the meat will be exported to other countries requesting specified controls to be applied, but can include:

• rearing pigs in a Trichinella-free system, based on biosecurity measures to prevent infection (stock held indoors only, vermin controls, feed controls);

• immunological pre-slaughter (on-farm) testing for the infection (e.g. ELISA);

• examination of muscle samples (diaphragm) of slaughtered pigs and horses to detect larvae (by microscopy following artificial digestion of meat, see Chapter 6); and

• inactivating the larvae in meat by freezing or cooking to 77°C in the centre.

Taeniasis and cysticercosis

Humans infected with taeniasis can be the host for two species of Taenia tapeworms: T. saginata and T. solium. The lifecycles of the two are very similar. Humans carrying tapeworm(s) in their intestines excrete parasite eggs via faeces. T. saginata eggs ingested by cattle via faecally contaminated pasture/feed (defaecating humans, sewage, flooding) develop into the larval form (T. saginata cysticercus, previously called Cysticercus bovis), i.e. cysts (5–9 mm diameter) in the muscles and heart, causing cysticercosis. In cattle, the largest number of cysts is found in mastication muscles, heart and tongue. Similarly, pigs ingest T. solium eggs that subsequently develop into T. solium cysticercus (previously called Cysticercus caelullose) in the muscles. If humans ingest raw/undercooked meat containing either species of cysticerci, the larvae will become free in the intestines and develop to adult tapeworms. Only in the case of T. solium, humans can also become infected by an additional route, via ingestion of tapeworm eggs (faecal–oral route); in such a case humans can develop T. solium cysticercosis as well. T. saginata and bovine cysticercosis are common in Africa, have a low but constant prevalence in New Zealand, in the UK were unknown before the mid-20th century but appear more prevalent since then (many human cases may remain unreported), whilst they are declared as eradicated in some countries (e.g. Germany, Greece). T. solium and porcine cysticercosis have high prevalences in Africa, Mexico and South America; in Europe they are sporadic, and are declared as eradicated in Finland, Greece and Canada. The main control measures for taeniasis and cysticercosis include:

• personal hygiene and related education;

• prohibition of sewage effluent as fertilizer;

• prevention of livestock access to human faeces;

• identification and immediate treatment of infested humans;

• diagnostic testing of animals (e.g. Ag-ELISA methods);

• effective visual meat inspection (cutting and inspection of mastication muscles and heart in slaughtered cattle; carcass muscle surfaces in pigs); and

• effective cooking/freezing of meat to inactivate larvae.

Hydatid disease

The intestinally located tapeworm Echinoccocus granulosus infects dogs and other Canidae, which are definitive hosts. Infected definitive hosts (e.g. dogs) faecally excrete eggs that can contaminate animal feeds or human foods and be ingested. Subsequently, in intermediate hosts (e.g. farm animals, humans), hydatid cysts containing large number of larvae can develop in internal organs (e.g. liver, lungs) and brain, but are rarely in muscles. The cysts can vary in size from a marble to a small football, and in shape which depends on the shape of the organ where they are located. The symptoms and severity of disease depend on the location of cysts, i.e. whether vital organs are affected (e.g. brain). If dogs ingest these cysts, they develop the tapeworm; the disease is zoonotic but not meat-borne for humans. The occurrence of hydatid disease is worldwide; in the UK prevalence in sheep varies from 1% to 50%, whilst in farmers may be up to 30%. The main controls include:

• regular antiparasitic treatment of dogs;

• prevention of contamination (direct or indirect) of animal feeds/pasture and human foods with dog faeces;

• visual examination of organs at meat inspection and subsequent feedback to the farm of origin;

• appropriate disposal (including previous cooking) of rejected infected organs from slaughtered animals to prevent ingestion of viable cysts by dogs and wildlife (Canidae); and

• washing hands after handling dogs.


Fascioliasis (large fluke) is mainly a disease of domestic (cattle, sheep) and wild herbivores caused by the parasite liver fluke Fasciola hepatica. Adult parasites live in the bile ducts and lay eggs which are excreted via faeces. After hatching, the miracidium further develops within an intermediate host (a snail, Lymnaeae trunculata) and cercariae leave the snail to encyst on plants in stagnant waters. Animals can become infected through consumption and humans by inadvertently nibbling contaminated plants. In the duodenum, larvae are freed and develop into fluke in liver. The occurrence of fascioliasis is worldwide. It is quite common in the UK: more than 1 million sheep livers are condemned annually due to liver fluke, and around 30% of cattle are found infected.


Dicrocoeliosis (small fluke; Dicrocoelium dendriticum/lanceolatum) is a similar disease of herbivores with a similar parasitic life cycle but involving two intermediate hosts: a snail and an ant. Infective cysts are formed in ants, and herbivores become infected by ingesting ants with pasture plants. Humans are accidental hosts (small fluke in bile ducts) after ingesting ants on fresh vegetables or occasionally whilst nibbling grass. Both fascioliasis and dicrocoeliosis are zoonotic diseases, but not meat-borne; the severity of these diseases in humans depends on the extent of the liver infestation. The main controls include:

• land management, including control of populations of intermediate hosts (e.g. snails) on pastures/feeds;

• examination of incised livers (bile ducts) at meat inspection of slaughtered herbivores, and feedback to the farms of origin; and

• education of people.


The definitive host for this protozoan parasite (Toxoplasma gondii), cats and wild felines, become infected via ingestion of raw meat or prey (birds/rodents) that contain larval forms (cysts) of the parasite. The infection is transmitted primarily via cat faeces to other mammals, birds and humans, but transmission cycles can involve different routes:

• rodent–vertical transmission–rodent–cat;

• cat–faeces–human;

• cat–faeces–sheep, cattle, horses–contact (placenta)–human;

• cat–faeces–sheep, cattle, horses–meat–human; and

• cat–faeces–pig–cannibalism (tail biting)–pig–meat–human.

In animals, toxoplasmosis does not usually cause symptoms. Cats can sometimes develop encephalitis, hepatitis or diarrhoea, in the case of heavy infestation. In sheep, the main characteristic is abortion later in pregnancy. In humans, the infection can be asymptomatic, but disease can also be vertically transmitted: congenital infection with encephalitis and hydrocephalus. Human toxoplasmosis in the form of cysts in the brain develops mainly in IC individuals (e.g. AIDS patients), whilst in pregnant women it may result in abortion. The occurrence of toxoplasmosis is worldwide, particularly in Africa. It is enzootic in the UK, with prevalence of up to 25% in food animals; some Asian countries declared it as eradicated (e.g. Singapore). The main controls include:

• prevention of contamination of animal feeds (fodder) with cat faeces;

• meat inspection to detect toxoplasmosis lesions such as granulomata in lungs, heart and brain (but they occur rarely) and microscopic meat examination (but this is not routinely conducted);

• freezing and (preferably) cooking of meat to inactivate cysts; and

• advising pregnant women to avoid contact with lambing ewes and cat faeces.


These protozoan, coccidian parasites (sarcosporidia) are in the phylum Apicomplex and affect all animals, birds, reptiles and man. The two most relevant, zoonotic species are Sarcocystis hominis and S. suihominis, affecting cattle and pigs, respectively, as intermediate hosts. For both, definitive hosts are dogs, cats and humans. Transmission routes include:

• dog/cat faeces (sporocysts)–food or water–cattle, pigs–muscle (sarcocysts)–humans or dogs, cats; and

• humans–faeces (sporocysts)–food or water–cattle, pigs–muscle (sarcocysts)–humans or dogs, cats.

Infection in animals is normally asymptomatic, but clinical cases can occur in older animals, stall-fed cattle and swill-fed pigs. In humans, infection sometimes causes transient diarrhoea and abdominal pain. Occurrence of sarcosporidiosis is worldwide, but most reports are from North America, UK and Australia, with up to 75% of animals found to be infected. The main controls include:

• prevention of faecal contamination of food and water;

• meat examination (eosinophilic myositis), but it is rarely diagnosed macroscopically, and microscopic examination is not carried out routinely; and

• freezing or (preferably) cooking of meat to inactivate cysts.

Giardia/Cryptosporidia infections

These infections are caused by the protozoan parasites Giardia intestinalis and Cryptosporidium parvum, occuring in most domestic animals (e.g. young cattle) and humans. The occurrence is worldwide; indeed, these are so widespread that the parasites’ oocysts are considered as ‘environmental contamination’. Transmission is faecal–oral with a number of possible routes:

• young ruminants–faeces (oocysts)–animal handling–humans;

• young ruminants–faeces (oocysts)–water–humans;

• young ruminants–faeces (oocysts)–rodents–young ruminants;

• young ruminants–faeces (oocysts)–water–domestic animals; and

• humans–faeces–humans or domestic animals.

Humans most often become infected via contaminated water or raw vegetables (salads), but also via chicken salad, milk drinks and apple cider. Any food that could become faecally contaminated may be a source of infection. Usual symptoms include diarrhoea and possibly loss of weight, but the respiratory system or gall bladder of IC individuals can be infected. The main control measures include:

• treat livestock waste on-farm with raised temperatures and high ammonia levels;

• limit farm run-off into waterways;

• dispose of sewage in a sanitary manner;

• immunocompromised individuals to boil water before consumption; and

• use good personal hygiene measures and exclude infected/carriers from handling food.

Further Reading

Andrewes, C.H. and Walton, J.R. (1977) Viral and Bacterial Zoonoses. Baillière Tindall, London.

Anon. (2001a) Zoonoses and Communicable Diseases Common to Man and Animals, Vols 1–3. Pan American Health Organization, Pan American Sanitary Bureau, Regional Office of the World Health Organization, Washington, DC.

Anon. (2001b) Trends and sources of zoonotic agents in animals, feedingstuffs, food and man in the European Union and Norway in 2001. European Commission, Health and Consumer Protection Directorate-General, Brussels.

Anon. (2003) Tuberculosis in bovine animals: risks for human health and control strategies. The EFSA Journal 13, 1–52.

Anon. (2004) Design of a field trial protocol for the evaluation of new rapid BSE post mortem tests. The EFSA Journal 46, 1–11.

Bell, J.C., Palmer, S.R. and Payne, J.M. (1988) The Zoonoses; Infections Transmitted from Animals to Man. Edward Arnold, London.

DEFRA (2004) Zoonoses Report – United Kingdom 2003. DEFRA Publications, London.

DEFRA (2005) Notifiable diseases in the UK. http://www.defra.gov.uk/animals/diseases/notifiable.index.htm (accessed March 2005).

OIE (2004) http://oie.int/eng/maladies/en_classification.htmListeOIE (accessed December 2004).

Salman, M.D. (2003) Animal Disease Surveillance and Survey Systems. Iowa State Press, Ames, Iowa.

Thrusfield, M. (1995) Veterinary Epidemiology. Blackwell Science, Oxford, UK.

Toma, B., Dufor, B., Sanaa, M., Benet, J.-J., Ellis, P., Moutou, F. and Louza, A. (1999) Applied Veterinary Epidemiology and the Control of Disease in Populations. Maisons-Alfort, France.

2.3 On-farm Factors Affecting Food-borne Pathogens


The main food-borne pathogens causing the majority of food-borne diseases in humans in modern times, e.g. Salmonella, Campylobacter, E. coli O157, originate from healthy farm animals that excrete them faecally. These pathogens enter the food chain by a variety of routes (e.g. guts–environment–contaminated animal coats–carcass–meat) and their control during the post-farm phase is neither easy nor always efficient. Therefore, it is important to understand their spread, and to consider any related controls, of these pathogens on farms. This could minimize further transference of food safety hazards to subsequent phases of the food chain. The significance of the on-farm presence of food-borne pathogens can be illustrated by data on the occurrence of E. coli O157 in healthy cattle: herd prevalence is highly variable and can be anything between 40% and 75%, whilst prevalence in individual animals may be between <1% and >20%. The main route of transmission for food-borne pathogens in farm animals is faecal–oral.

Role of animal diet/feeds

Contaminated feed can be a very important source of food-borne pathogens, e.g. Salmonella spp., particularly in poultry and pigs. Usually, the most persistent contaminants are ‘local’ Salmonella spp., whilst ‘exotic’ Salmonella spp. are often transient and associated with imported feed compounds or components (e.g. protein-based). Feeds can also be contaminated with pathogens excreted by vermin (rodents, birds). Therefore, feeds are sometimes fermented, e.g. liquid feeds for pigs in order to reduce the risk of Salmonella infection. Feeds can also be acidified by the addition of acidulants, or heat treated to reduce or eliminate pathogens. In fermented silage production, rapid fermentation by dominant lactic acid bacteria and suppression of food-borne pathogens is required. It is a two-step process, starting with aerobic fermentation, which consumes available oxygen and produces heat, followed by anaerobic fermentation and accumulation of lactic acid that lowers pH. If air is not properly (or rapidly) excluded, poor-quality silage can result, in which some pathogens such as Listeria monocytogenes can proliferate and be spread to animals.

Also, numerous studies have been published in which effects of the diet type on shedding of pathogens were examined, e.g. the ongoing debate about whether shedding of E. coli O157 is greater in grain-fed or hay-fed cattle. However, because faecal shedding of this or other pathogens is affected by numerous factors other than diet, but acting simultaneously, the actual relevance of diet itself is presently unclear. On the other hand, it had been advocated in the past that the total amount of faeces – and hence the prevalence or levels of food-borne pathogens excreted by animals – could be reduced by total withdrawal of feed for 1–2 days before slaughter. However, some studies have shown that feed withdrawal can actually increase shedding of pathogens, e.g. E. coli O157 in cattle.

With respect to animal diet-based control measures to reduce faecal shedding of pathogens on farms, two approaches have attracted significant attention:

• use of probiotics, which involves feeding animals viable pre-selected microorganisms (usually, lactic acid bacteria) to suppress targeted pathogen(s) within the animal gut either through changing the gut environmental factors or via production of antimicrobial compounds (e.g. bacteriocins); and

• use of competitive exclusion, which involves feeding animals with complex mixtures of bacteria that ‘saturate’ locations on the gut mucosa needed for attachment of pathogens, hence preventing/reducing colonization of the animal gut by the pathogens. For example, Salmonella spp. can be competitively excluded in intensively reared chicks by feeding them with diluted minced gut content of mature hens (anaerobically fermented gut contents).

Unfortunately, both approaches suppress faecal shedding of pathogens in monogastric animals (poultry and pigs) better than in ruminants. In ruminants, it is more difficult to change gut microflora via these oral treatments, due to physiological/microbiological processes occurring in the rumen. Nevertheless, attempts have been made to overcome such difficulties by application of the treatments via rumen-resistant boluses.

Role of stress

The gut microflora of animals start to establish from birth and, once stable and well-balanced, provide good protection against gut colonization by pathogens, e.g. Salmonella spp. However, stress (alone or in combination with antibiotic therapy) can disturb the balance of the microflora and render animals more susceptible to colonization. Therefore, it could be assumed that stress can cause an increase in shedding of pathogens. Stressors include parturition (e.g. calving/farrowing), weaning, sudden changes in diet that alter gut pH and select for particular bacteria, transportation (stress increases with journey length, unloading and reloading) and mixing of animals (on-farm and also at markets, lairage).

Effect of animal age

In some on-farm studies of E. coli O157, gut colonization was more frequent in young cattle. Experimentally infected calves can shed around 1 log higher levels, and also for around 3 months longer, than can adult cattle. Also, it is considered that the biggest reservoir of Salmonella spp. is growers and finishers, but younger animals are more likely to be affected.

Spread between animals

It is generally believed that indoor farming (i.e. group housing) increases horizontal transmission of pathogens, as compared to outdoor farming, due to closer contacts between animals (including social contact such as licking/grooming) and/or between animals and the contaminated environment. For example, oral secretions and regurgitation of organisms in cattle contribute to the spread of E. coli O157 between neighbouring animals and even between neighbouring pens. Vertical transmission can also occur, but is probably less important due to some protection from maternal antibodies for up to 7 weeks. In addition, introduction of novel shedding-positive animals to established groups increases on-farm spread of pathogens.

Role of vectors

Spread can occur between distant pens or indeed between farms via vermin, wild animals, farm staff and farm equipment. Humans, through their daily activities on-farm, are one of the biggest causes of on-farm spread of pathogens. Rodents (mice and rats) are also very important; a Salmonella-shedding mouse can excrete up to 5–7 logs of the pathogen’s cells in its faeces in one day, which can be sufficient to infect an animal. Some studies found 1–3% of gulls from intertidal sediments harboured E. coli O157. A study carried out in the USA showed that E. coli O157 can be isolated from deer sharing grazing land with cattle.

Survival in the environment

Pathogens can survive for long periods in farm environment-related substrates such as soil, faeces and building materials for extended periods (days to weeks). Pathogens can be attached to dust particles and liquid droplets, and then carried by winds or aerosols (hosing, rain) for considerable distances. Generally, pathogens die off to a large extent when exposed to a combination of higher temperatures and drying, but at lower temperatures and in water (or damp substrates) they survive very well. All water drinkers used by more than one animal can serve as a route for between-animal spread. Water troughs are clearly proven as a source of E. coli O157 infections and re-infections on farms; the pathogen survives in the water for several months and can even multiply in the sediment. This means that the pathogen can survive between two grazing seasons (e.g. over winter).

Recycling of pathogens via organic fertilizers

Animal wastes, such as farmyard manure, slurry and certain abattoir wastes (lairage wastes and gut contents; see Chapter 2.4) often contain food-borne pathogens faecally shed by farm animals. Animal wastes in solid (manure) and liquid (slurry) form can be stored on the farm, transported for use elsewhere, or deposited directly onto land. Storage can reduce levels of pathogens; e.g. appropriate storage of farmyard manure can lead to their ‘auto-heating’ (composting) to pasteurization temperatures (e.g. >60°C), that can destroy vegetative forms of pathogens. Spreading untreated wastes on pasture or agricultural land for crop production can mediate further infections or re-infections of animals with pathogens through either grazing, or feeding contaminated feeds produced on contaminated land. Survival periods of pathogens in soil are variable and affected by numerous factors, but some studies indicate survival periods of >2 years for Salmonella spp. and around 10 months for L. monocytogenes. Pathogens’ survival is better if the organic wastes are applied on land by the injection method (often used for odour control purposes) than by surface spreading; in the latter case, pathogens are more intensively exposed to antimicrobial factors, including drying and sunlight.

Summary of existing on-farm control measures

Presently, the main on-farm control measures for pathogens are based on hygiene and biosecurity incorporated in Good Farming Practices/Good Hygiene Practices (GFP/GHP) – and HACCP-based principles:

• operate an all-in, all-out policy;

• disinfect pens between batches of animals;

• avoid mixing animals (new or by age group);

• use a reliable pathogen-free source of livestock;

• disinfect vehicles used for transportation;

• train staff to disinfect boots and equipment, and keep work clothes on site;

• operate an effective programme for control of vermin;

• clean and disinfect water troughs regularly;

• avoid grazing animals on land newly applied with slurry or manure; ideally store waste for 3 months prior to application onto land;

• restrict access of visitors to units;

• manage feed properly; reliable source, proper production of silage;

• monitor pathogen presence in animals, e.g. ‘ZAP’ Salmonella programme in the UK; and

• vaccinate animals against pathogens, e.g. Salmonella in poultry.

Future on-farm control measures, that are not being routinely used but are under intensive research and development, include in particular: (i) vaccinations against a range of pathogens including such as Campylobacter and E. coli O157; and (ii) bacteriophage therapy based on viruses which attack and targeted pathogenic bacteria.

Further Reading

Anon. (2000) Opinion of the Scientific Committee on Veterinary Measures Relating to Human Health on Food-borne zoonoses. European Commission Health and Consumer Protection Directorate-General, Brussels.

Hinton, M.H. (2000) Infections and intoxications associated with animal feed and forage which may represent a hazard to human health. Veterinary Journal 159, 124–138.

Johnston, A.M. (2000) HACCP and farm production. In: Brown, M. (ed.) HACCP in the Meat Industry. Woodhead Publishing Ltd, Cambridge, UK.

Maunsell, B. and Bolton, D.J. (2004) Guidelines for Food Safety Management on Farms. Teagasc – The National Food Centre, Dublin.

Stanfield, G. and Dale, P. (2002) Assessment of Risk to food Safety Associated with the Spreading of Animal Manure and Abattoir Wastes on Agricultural Land. Final Report to the Food Standards Agency, Report No. UC6029, London.

2.4 Animal By-products, Wastes and the Environment

Animal by-products and wastes produced by abattoirs have not been well regulated in the past; many of them were frequently applied on agricultural land without any treatment. This practice carries the risk of recycling of public health hazards from shedding animals – through the environment – back to grazing animals or those fed by crops harvested from the environment. Additionally, these hazards can contaminate crops grown on the land and intended for human consumption, e.g. root vegetables, salads, etc.

Surveys of abattoir wastes conducted in the UK between 1999 and 2001 indicated that most abattoirs used to discharge effluents and wastes onto agricultural land, either directly or via sub-contraction to secondary companies. Abattoir wastes varied greatly with respect to: (i) types (e.g. lairage manure-based wastes, gut contents, blood, etc.); (ii) volume stored at the premises (e.g. 1–200 tonnes); (iii) conditions of storage (e.g. in tanks, hips, etc.); and (iv) the length of time they were stored on the premises before being disposed of (e.g. between 1 day and 2 years). These variations were much larger among red meat abattoirs, whilst wastes from poultry abattoirs were more uniform. In the surveys, particularly food-borne protozoan pathogens and, to a lesser extent, bacterial pathogens, were found in abattoir wastes, which confirms the public health relevance of abattoir waste handling.

Subsequently, EU regulation EC 1774/2002 has provided health rules concerning animal by-products not intended for human consumption. This new legislation divides animal by-products into three categories, described below.

Category 1 by-products

These by-products represent the highest risk category. The main hazard in Category 1 by-products are TSE-BSE agents, so the controls are designed to target particularly specified risk materials (SRM), i.e. to limit their spread. This category includes:

1. By-products from animals:

• infected by TSE;

• killed for TSE eradication;

• other than farmed or wild (pet, zoo, circus);

• including experimental animals;

• including wild animals suspected of harbouring communicable diseases; and

• with prohibited chemical residues.

2. Animal material collected in waste water treatment from Category 1 processing plants.

3. Catering waste from international transport. This is considered as high-risk material from a public health perspective, since effective, cross-border controls are non-existent.

4. Mixtures of Category 1 with Category 2 or Category 3 materials.

Disposal of Category 1 by-products

1. Directly incinerated in a registered plant.

2. Processed in a plant using any of methods 1 to 5 (Table 2.5) and then incinerated.

3. If the by-products do not contain SRM, those processed in a plant by method 1 must later be buried in a landfill.

4. Catering waste from international transport is disposed of by burial in a landfill.

Category 2 by-products

These by-products represent a medium risk to public health. The category of manure and digestive tract contents must be treated as if they contain organisms pathogenic to humans. If Category 2 by-products are contaminated with category 1 by-products, then their risk level increases and they must be treated as Category 1 by-products. This category includes:

1. Manure and digestive tract contents.

2. Animal material collected in waste water treatment from Category 2 processing plants, or from abattoirs other than those covered under Category 1.

3. Animal products containing residues of veterinary drugs or other contaminants.

4. Animal products other than Category 1, if imported but non-compliant.

5. From animals, other than under Category 1, that died not by slaughter for human consumption.

6. Mixtures of Category 2 and Category 3 materials.

7. Animal by-products other than Category 1 or Category 3.

Table 2.5. Treatment methods for animal by-products.


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Dec 15, 2017 | Posted by in GENERAL | Comments Off on On-farm Factors and Health Hazards

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