● 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.
● killing (slaughter) of all affected and in-contact animals (with compen- sation) 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
Tuberculosis
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. boviscauses tuberculosis mostly in cattle, but can also infect humans, goats and pigs; sheep and horses have high resistance. M. aviumis 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. bovisandM. aviuminjected at two sep- arate 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-␥ test (IFN-␥ test); whole blood is cultured with PPD from M. bovis and M. avium and IFN-␥ production is measured by ELISA after 24 hours. A field trial in Northern Ireland showed an IFN-␥ test sensitivity of 84.3% whilst parallel tuberculin sensitivity was 83.1%.
Positive findings of tuberculous lesions (caseous lymphadenitis) at post- mortem 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. aviumsubspecies 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 ⱕ2.7%).
Table 2.3. Incidence of BSE in cattle at the end of 2003 (adapted from OIE data).
First recorded Total
Countries case cases
EU
Ireland 1990 1,360
Portugal 1993 862
France 1991 897
Switzerland (non-EU) 1990 417
Germany 1994 298
Spain 1990 897
Belgium 1997 118
Italy 1994 119
Netherlands 1997 71
Denmark 1992 13
Luxembourg, Austria, Greece, Finland 1
Slovakia 2001 13
Czech Republic 2001 8
Slovenia 2001 3
Poland 2002 9
United Kingdom 1985? 182,482
Other countries
Israel 2002 1
Japan 2001 9
Canada 1993 2
USA 2003 1
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 ani- mals other than ruminants, and (under specified conditions) non- ruminant 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 con- sumption 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).
Year Deaths
1995 3
1996 10
1997 10
1998 18
1999 15
2000 28
2001 20
2002 17
2003 (up to 6 May) 8
Anthrax
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).
Brucellosis
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 post- mortem 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 haveB. abortus orB. 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.
Glanders
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, Aedesmosquitoes 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 sub- clinical 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