INTRODUCTION
In July 1987, the Central Veterinary Laboratory, GB, announced that, within a herd of cattle
from West Sussex, GB, a new brain disease had been identified that was histopathologically related
to the scrapie disease of sheep. It was called bovine spongiform encephalopathy (BSE). Subsequently,
it was made public that, as early as 1983 in Malmesbury, Wiltshire and 1984 in Pitsham farm, West
Sussex, GB, diseases in cows had arisen that clinically had retrospectively to be classified as
BSE. Whether, in former times, such diseases had occurred sporadically, remains unclear. In sheep
and in goats, scrapie disease has been known since the 18th century. Similar
transmissible spongiform encephalopathies (TSEs) had been recorded since 1947 in mink and
particularly were observed in the 1990s in zoo animals (puma, tiger, lion, ocelot) and in moose
and deer in Canada. Focussing on the use of slaughterhouse waste material as a fodder ingredient
as being a probable transmission pathway, this feeding practice was banned for ruminants in GB in
1988 and in the EU in 1994, and for general animal feeding in GB in 1990, and temporarily in the
EU in 2000. On July 14, 1993 in GB, the 100,000th BSE case in cattle was announced and,
up to now over 180,000 have been reported. In Germany, 7 cases up to the year 2000 and a further
101 BSE cases up to September 18, 2001 were registered (The BSE Inquiry Report, 2000;
Bundesministerium für Verbraucherschutz, Ernährung und Landwirtschaft, 2001).
On March 20, 1996, the Chief Medical Officer of
Great Britain announced that a new variant of Creutzfeldt-Jacob disease (vCJD), a degenerative
brain disease in humans, is probably causally linked to BSE (Confidential Report, 1987). By the
beginning of September 2001, 106 probable and confirmed cases of vCJD had been announced in Great
Britain (Department of Health, GB, 2001). Outside the United Kingdom, further three cases have been
proven in France and one in Ireland. In Germany, no case has been confirmed to date.
Since February 2001, Great Britain has had to fight
another animal epidemic, i.e., foot-and-mouth disease (FMD) of the type O, strain Pan Asia.
Subsequently, isolated cases have also been detected in some countries on mainland Europe (France
and the Netherlands). FMD is endemic in southeastern countries, in particular the east of Turkey,
from where this economically important disease is sporadically introduced into other parts of
Europe. However, because of increasing mobility, including that of live stock transport, the ways
of spreading the disease are no longer limited to this route. The last outbreak in Germany was in
1988 in the proximity of Hannover, whereas the last time that Great Britain suffered a large
epidemic was in 1966.
This article describes the illnesses, the
occupational risk while handling infected animals and biological materials and the preventive
measures for dealing with these diseases as proposed for Germany.
BOVINE SPONGIFORM ENCEPHALOPATHY
(Epidemiologisches Bulletin 2001, Bundesgesundheitsblatt 2001, Zobeley and Glocshuber, 2001)
BSE belongs to TSEs. TSE illnesses of humans include CJD, approximately 80% of which appears to be sporadic and 20% hereditary, Gerstmann-Straeussler-Scheinker syndrome (GSS), fatal familiar insomnia (FFI) and the kuru disease, which arose in Papua New Guinea in connection with ritual cannibalism. vCJD is of special importance, as it is regarded as the human analogue of the cattle epidemic BSE.
New data from the reference laboratory for spongiform encephalopathies in Goettingen, Germany show that the incidence of CJD has remained almost constant over the last few years with 1 to 1.5 cases per million. In a few cases, iatrogenic CJD arose in recipients of dura mater or cornea transplants and through contaminated neurosurgical instruments.
In animals, the following TSE illnesses are well known: scrapie in sheep and goats, with related illnesses in mink, deer (North American moose) and exotic hoof animals, such as certain antilopes, a spongiform encephalopathy in cats and BSE in cattle. Although the BSE epidemic reached its peak in 1992 with more than 85,000 infected cattle in GB, one must expect rising numbers of cases in other European countries such as France, Portugal, Republic of Ireland, Switzerland and, in addition, Germany. The feeding of cattle with sheep carcasses and offal materials that were at least partly contaminated with the scrapie pathogen is regarded as the cause for the emergence of the BSE epidemic in GB. It is assumed that this feeding practice has spread a previously unknown pathogenic factor/organism of a specific encephalopathy in the cattle. This hypothesis is supported by the fact that, 5 years after the prohibition of the feeding of meat and bone meal to ruminants (1988), the number of BSE cases in GB has decreased strongly.
As a possible cause for the BSE cases appearing in Germany since November 2000, it is assumed that the use of high-risk materials [brain, spinal marrow] together with insufficient pathogen inactivation in bone-meal production have led to the spreading of the BSE pathogen. Estimates at the end of 2001 suggest that 150–500 BSE cases can be expected in Germany.
All past investigations into the etiology of TSEs point to certain proteins, so-called prions (proteinaceous infectious particle) as being responsible for these illnesses. The prion protein is an endogenous protein, which occurs in most cells of all mammals but is particularly produced by neurons. The normal cellular form of the prion protein is denoted PrPc. The infectious prion protein, which is called PrPSc, is
a misfolded prion protein that possesses the same amino acid sequence and the same covalent linkages as the normal PrPc and differs from the PrPc only in its tertiary and quaternary structure. It is assumed that during the course of a prion disease, infectious PrPSc can convert, directly or indirectly, normal PrPc to PrPSc by forcing it to take up the misfolded structure of PrPSc. This so-called “protein only hypothesis” demands that an organism that does not contain the normal prion protein PrPc must be resistant to structurally altered infectious prion protein. This has been elegantly demonstrated in experiments by the group of Charles Weissmann: PrPc – knockout mice, in which the gene for the prion protein is missing, remain healthy after infection with prions, unlike wildtype mice, and are also unable to multiply prions (Bueler et al., 1993). In contrast, transgenic mice, raised to produce PrPc particularly strongly, are substantially more susceptible to the pathogenic factor/organism than are the wildtype.
With regard to the process of infection and the course of the illness, it is accepted that, after the ingestion of a sufficient quantity of the pathogenic factors/organisms via food, the prions first arrive at the lymphoid tissue adjacent to the digestive system and infect the neural tissue that supplies these lymphoid organs. The pathogenic factor/organism can infect the brain along the splanchnic or vagus nerve. Following marked pathogen multiplication in the central nervous system, the misfolded prion proteins lead to the formation of amyloid, which is responsible for the symptoms of the illness and the activation of glia cells.
Pathogen transmission
Several studies have shown that scrapie and BSE or CJD in humans is transferable to a variety of other animal species, e.g., to rodents, to carnivores such as cats and mink, to pigs, to various monkey species and, above all, to ruminants. Of special public interest is whether BSE infections can also occur in other domestic animals such as sheep, pigs, poultry and fish through the feeding of potentially infectious meat and bonemeal. High doses of infectious prion proteins administered intracerebrally can cause an infection in the pig. However, so far, no infection has been obtained by oral transmission. With poultry and fish, the species barrier is obviously so impervious that, at least by food, no pathogen transmission with subsequent illness occurs. In contrast to this, sheep and goats can experimentally be infected via food with BSE pathogens.
It has to be borne in mind that during the transition of the pathogenic factor/organism from one species to another infections may occur in which the prions may multiply without being recognized because of the absence of clinical symptoms. Here, further investigations are necessary in order to identify those domesticated animals that are non-affected carriers of infectious prion proteins.
BSE and the new variant of the Creutzfeldt-Jakob disease
Since 1996 in GB, a new variant of CJD (vCJD) has appeared, which, in contrast to classical CJD, predominantly arises in relatively young patients (average age 27–29 years) and which exhibits a modified clinical course of the disease and a new specific histological set of the brain alterations. To date, 106 proven or probable vCJD cases have arisen in GB, with a further 3 cases in France and 1 case in the Republic of Ireland. Several experimental investigations with transgenic mice have shown that the pathogenic organisms of BSE and vCJD are biologically and biochemically very similar. Because of these results and the temporal and local correlation between the occurrence of BSE and vCJD in GB, it must be assumed with considerable certainty that vCJD is caused by infection with the BSE pathogen and represents an analogue of BSE in humans. vCJD resembles the classical form of CJD in that it is untreatable and leads to the death of the patient. Contrary to CJD, vCJD is characterised by a more protracted course (death occurring 6–12 months after the onset of the illness). It is interesting that all vCJD patients exhibit a specific genotype of the prion protein, which is found in approximately 40% of the normal population. It is possible that persons with a different genotype will fall ill later (longer incubation period) or that they exhibit genuine resistance against the infectious prion protein.
Whether vCJD cases will arise in Germany depends on the probable exposure of the population to BSE pathogens via food, particularly from 1980 to 1996. The problem of whether vCJD can result via other transmission paths remains unresolved. Of special importance is the possible transmission by blood or blood products. An investigation by British scientists has gained attention in which a group of sheep was infected by feeding them with 5 g brain substance from BSE infected cattle; subsequently, the blood of these sheep was transfused into BSE- and scrapie-free sheep (Houston et al., 2000). Only one out of 19 tested animals has developed TSE so far but, according to the data of the researchers, it has not developed the typical scrapie illness that naturally occurs in sheep. However, these results remain to be confirmed. In general, the transmission of prion diseases via blood or blood products seems improbable; nevertheless, the task force on the safety of blood in Germany has recommended the intensified employment of leucocyte depletion and the exclusion of blood donors who resided for more than 6 months in GB during the period from 1980 to 1996.
Because of the occurrence of the infectious prion protein in lymphatic tissues in vCJD, an important point that is being discussed at present is whether medical items, e.g., surgical instruments that have come into contact with potentially vCJD-pathogen-contaminated organs or tissue must be submitted to a special disinfection/sterilisation procedure.
Diagnosis of BSE and vCJD
Because of the absence of a detectable immune response in the infected organisms, diagnostic possibilities are limited. Those procedures used at present as “BSE rapid tests” are based on the identification, by means of Western blot or ELISA techniques, of the proteinase K-resistant misfolded form of the prion protein in the brain tissue of cattle. For this, however, brain tissue of the killed animal must be present and these tests are only able to detect the illness in infected animals at later stages. Diagnosis of the disease is confirmed by histopathological and immuno-histochemical investigations.
In vCJD patients, diagnosis can be made on the basis of the clinical course, on investigation of cerebrospinal fluid, by characteristic EEG alterations and by nuclear magnetic resonance (NMR). A specific intra vitam diagnostic possibility is the identification of the infectious prion protein in, e.g., a tonsillar biopsy. It is to be hoped that, in the near future, tests will be developed that can detect the pathogenic factor/organism specifically and that are sufficiently sensitive during the incubation phase.
Prevention strategies at work (slaughtering)
BSE-positive cattle have been found in the Federal Republic of Germany. The pathogen is suspected to be able to cause TSE in humans. Thus, this BSE agent is regarded as a biological working material as specified in the Regulations of Security and Health Protection at Work involving contact with biological working materials ("Regulation of Biological Materials” = Biostoffverordnung BioStoffV). In connection with the German law on industrial safety and health (Arbeitsschutzgesetz) BioStoffV represents EU guideline 90/679/EWG of the Council of November 26, 1990 concerning the protection of employees against occupational hazards from biological working materials.
The occupational handling of animals and biological products also belongs to the activities under BioStoffV, if, by these activities, biological working materials (such as infectious agents) are set free and employees can come into direct contact with them. According to BioStoffV, activities can be differentiated into disclosed (if the employee is aware of the presence of the biological material, the infectious agent) and not disclosed activities. Activities in the slaughtering of cattle, sheep and goats rank among the activities that are not disclosed under BioStoffV.
Depending on the risk of infection, biological working materials are divided into four risk groups. Agents associated with TSE are classified under risk group 3*. By definition, it includes biological working materials that can cause a serious disease in humans and thus present serious hazard to employees. Danger of spreading the disease within the animal population exists, but effective prevention or treatment is possible. The marking of the risk group with an asterisk points to a limited risk of infection for employees, since infection via the air route is not normally regarded as possible.
According to BioStoffV (§ 6 and 7), the employer must evaluate the occupational hazard and define necessary preventive measures for each activity with biological working materials. A substantial basis for hazard evaluation is the adequate acquisition of information.
For consultation regarding all questions of industrial safety involving biological working materials, a “Board for Biological Working Materials” (ABAS) has been formed at the Federal Ministry for Work and Social Order consisting of experts from the public and private sectors, trade unions, governmental authorities, legal accident insurance, universities, and science.
To reinforce BioStoffV, ABAS has defined certain measures for the protection of employees from infections by TSE pathogenic factors/organisms of domestic animals (cattle, sheep, goats) (Resolution 602, 2001). The resolution serves as a provisional aid for employers and supervisory authorities and is regularly updated.
Risk materials
Resolution 602 (2001) assumes that health hazard is present only on contact with so-called specified risk materials. Risk materials are defined as those organs and tissues in which the TSE pathogenic factor/organism can be determined in very high concentrations in infected or diseased animals. The list of risk materials is continuously updated.
Risk materials are (Resolution 602, last up-date: March 20, 2001):| a) | skulls including brain and eyes, tonsils, spinal cord and spinal column, excluding tail vertebrae, but including the ganglia of spinal nerves of cattle older than twelve months and the intestine independently of age; and |
| b) | skulls including brain and eyes, tonsils and spinal cord of sheep and goats older than 12 months or from those with a permanent breakthrough of a foretooth, and the spleen of any sheep and goat. |
Possible contacts during slaughtering
Persons employed in slaughterhouses and who undertake slaughtering in butchers' shops may come into contact with risk materials in particular when carrying out the following jobs: pin shot anaesthetisation, exarticulation of the head, bisecting of the animals, and removal of spinal cord and meninx. Whether additional jobs are affected has to be examined by the employer in the context of hazard evaluation. This may be the case, for example, during the packing and preparation of risk materials for transport.
The usual slaughtering process of cattle covers critical stages during which there is a risk of transmission of risk material (brain, spinal cord) to meat and/or organs (Troeger, 2001). This includes the anaesthetisation by means of the pin shot, the exarticulation of the head and, most importantly, the sawing of the bodies into two halves along the spinal column.
During the longitudinal splitting of the animal body along the centre of the spinal column, the vertebral channel is opened and the spinal chord is split over its entire length. Nerve tissue can contaminate not only the instruments being used, but also the adjacent meat. Therefore, from April 1, 2001, meat containing vertebral bones, e.g., complete roast beef and T-bone steak from animals over 12 months old, may not be offered to consumers. The spinal column or parts of the spinal column including the spinal ganglia must be dyed after removal and stored until they can be eliminated innocuously.
A practical alternative for cattle being slaughtered in small slaughterhouses involves the removal of bones from the whole body, either while still warm or once cooled. The individual meat portions are separated by different butchering methods without the longitudinal splitting of the spinal column. If necessary for legal reasons of meat hygiene, longitudinal splitting of the spinal column can take place later, when no more meat for the consumer is adhering to the carcass. In the field of industrial cattle slaughtering, the sucking off of the spinal cord from the whole slaughtered body by means of negative pressure and subsequent conventional sawing or the complete removal of the whole spinal column including the spinal ganglia by sawing appear to be the most promising methods (Troeger, 2001).
On anaesthetisation with a pin shot, which is common practice in Germany before slaughtering, a metal pin penetrates the skull bone into the brain. Here, substantial tissue damage (including damage to the blood vessels) occurs in the brain. There is thus a risk of the distribution of fragments of brain tissue via the venous bloodstream into the lung circulation. Possible organs affected include the heart, lungs and the blood itself. At present alternatives to this method of the anaesthetisation are anaesthetisation by an electric shock, by a blunt shot and stroke, the use of lasers and anaesthetisation by gas.
In the past, for safety reasons, a spinal cord destroyer (a plastic rod) was inserted, after anaesthetisation, through the pin shot hole into the spinal cord and then removed. This served as an effective measure to immobilise the animal and to avoid accidents caused by reflex movements of the slaughtered animals, especially whilst attaching them to the metal claw for transport within the slaughterhouse. From January 1, 2001, the use of the spinal cord destroyer has been forbidden to avoid the distribution of spinal cord material via the blood and lymphatic circulation into the animal body. At present, there are two practicable alternatives. In large-scale enterprises with an assembly line, one can immobilise the slaughtered animal by electrostimulation so that safe attachment becomes possible. In small-scale enterprises in which perhaps only one animal is to be slaughtered at a time, the upper foreleg has to be tied up and secured before exsanguination. For attachment of the animal to the metal claw, one must wait until the reflexes in the hind legs have faded away (Schulz, 2001).
General hygiene measures
In the technical rules for working with biological materials in Germany (TRBA 500), minimum requirements regarding general hygiene are specified and have to be implemented according to BioStoffV.
Risk analysis and definitions based thereon are mandatory requirements in the meat industry. Food hygiene regulations require meat-processing enterprises to maintain a system of hazard and risk evaluation aimed at food security. In meat processing, high standards are applied to hygienic conditions in working areas, devices and plants, etc. In the realm of personal hygiene, the usual indispensable precautions are, e.g., appropriate work clothes, clean/disinfected hands, gate systems, etc., which should minimise the transfer of unwanted microorganisms to the product. However, these precautions (e.g., gloves) also shield the employee from the transition of biological working materials. Thus, in practice the requirements resulting from TRBA 500 are already covered by the high requirements of product hygiene.
Special preventive measures while handling risk material
Additionally, the employer has to provide the following personal protection at relevant workplaces where risk material is handled (according to ABAS: Resolution 602, 2001):
| a) | Damp-proof and humidity-rejecting protective gloves. When damaged, gloves have to be changed immediately. When working with cutting tools, such as knives or milling machinery, they are to be worn in addition to and under the gloves preventing cuts and punctures. |
| b) | Suitable face protection (e.g., spraying protection: visor or goggles plus mouth and nose protection), if splashing of risk materials might occur. This applies in particular to the jobs of “animal halving” and “spinal cord withdrawal” and to cleaning, if necessary. To increase the desired acceptance of these protective measures, employees should participate in the selection of face protection. |
| c) | Suitable protective clothing. Protective clothing for hygiene requirements, consisting of hygienic clothing, apron and rubber boots, is sufficient for personal protection. Protective clothing must be worn until the result of the BSE rapid test is known. This does not apply to protective equipment that can be cleaned by water jet (cut-inhibiting gloves, rubber apron and visor). Protection equipment can be cleaned as usual if tests are negative. Single-use protective clothing is to be disposed of in the same way as all risk material. |
Cleaning
On completion of work with risk material, the work area has to be mechanically cleaned with
water (not under high pressure) to remove blood, tissue and other impurities. Subsequently,
decontamination has to take place by foaming with alkaline cleaners under the following conditions:
final concentration of the cleaner 1 mol ´ L–1
NaOH (equivalent 4%), for 30 minutes. The work area must be thoroughly rinsed with water once again
(water jet, not under high pressure).
With regard to washing, it is important to ensure the correct use of personal protection equipment and cleaning agents. Because of the use of gloves, a skin protection plan is particularly important for the avoidance of skin diseases.
Other occupations
Agriculture. ABAS Resolution 602 (2001) comes to the conclusion that, in agriculture at present, there are no activities in which farmers come into contact with specified risk materials. If the slaughtering of cattle is performed on the farm, the same additional requirements apply as those in slaughterhouses.
Institutes for animal body removal. The same resolution states that, in institutes for animal body removal, contact with risk material (organs and tissue of cattle, sheep and goats, or for dead cattle, sheep and goats, when the risk material has not been removed) can occur: a) in the case of transport to the institute for animal body removal, in particular whilst loading and unloading the transport vehicles; b) on cleaning and disinfection work; and c) disturbance elimination during the transportation of the materials within the plant. In these jobs, the following are to be made available to employees: damp-proof and humidity-rejecting protective clothing, including protective gloves, and suitable face protection, if splashing of risk materials might occur.
According to Resolution 602, during the thermal combustion of correctly manufactured meat and bone meal, no special additional preventive measures are necessary apart from the already valid work and health protection regulations (Resolution 602, 2001; Schulz, 2001; Troeger, 2001).
Stability of the pathogenic factor/organism and deactivation options
Infectious prion proteins are extremely resistant to heat, a resistance that far exceeds that of bacterial spores. Ionising or UV irradiation also have little effect in inactivating the pathogenic factors/organisms. Moreover, prion proteins are resistant to many chemical disinfectants, e.g., hydrogen peroxide. Phenol, formaldehyde, biguanide, iodine or chlorine compounds and the ethyl oxide sterilisation procedure are unsuitable for inactivating prion proteins. For the d econtamination of, for example, medical instruments used in patients with CJD, either 1–2 mol ´ L–1 NaOH or 2.5–5% sodium hypochlorite and/or 4 mol ´ L–1 guanidiumthiocyanate is recommended. Following these inactivation measures, sterilisation is necessary at 134 °C for one hour (Bundesgesundheitsblatt, 1998). CDC/NIH (1999) suggest autoclaving potentially infectious material (animal waste, meat and bonemeal) for 4,5 h at 132 °C. Alternatively, combustion is suggested for solid materials and sterilisation with 1N NaOH for liquid materials (Taylor et al., 1995, 1997; CDC/NIH, 1999). It is noteworthy that there are reports regarding the failure of prion inactivation after short-term exposure to temperatures up to 600 °C (Brown et al., 2000).
FMD is caused by an aphthovirus from the family of Picornaviridae. Different serotypes exist but, in Europe, only the types O, A, and C have been proven so far. Cattle, pigs, sheep, goats, chamois deer, camels and elephants and, in rare cases, humans can be infected. The disease is distributed world-wide, with the exception of North America, Australia and New Zealand. The virus strain that arose in GB this year is type O, strain PanAsia. The morbidity of sensitive populations is almost 100%.
Primary infection takes place in the throat; subsequently, after multiplication, the virus can appear in blood, milk and saliva before typical symptoms occur. After an incubation period of usually 3–6 days, fever and later the typical aphthas arise. With the beginning of stomatitis, the animals begin to salivate (“FMD beard”) and to smack their lips in a peculiar way. Because of the pain in the feet, tripping and twitching/raising of the feet are noticeable. The wounds heal within 2–3 weeks. Cattle are the most severely affected (apathy, milk decrease, loss of hooves) and have the highest mortality (adult cattle 5%, calves up to 95%). Pigs die more frequently because of myocarditis caused by the virus. The symptoms in sheep are mild; the mortality of lambs, however, can amount to 75%. If animals survive the disease, they can remain viral carriers over a long time period (for more than two years).
In humans, after an incubation period of 3–8 (up to 18) days, fever, weakness, burning aches and redness of the mucous membranes of throat and mouth arise. At the location of the primary inoculation, a so-called primary blister forms; 1–2 days later secondary rashes appear on the lips, cheeks, tongue and throat in the form of painful large vesicles and blisters of various sizes. Simultaneously, strong salivation usually occurs. Sometimes, painful secondary blisters appear on the toes, fingers, hands and soles of the feet and within the genital region. Usually on the 3rd day, defervescence occurs; the mucous membrane alterations heal generally within 10–14 days. The few cases documented so far proceeded in a self-limiting manner.
Transmission of foot-and-mouth disease, inactivation treatments
In animals, transmission takes place via direct contact from animal to animal (e.g., in the
stable, on transport, in cattle markets) and by indirect ways via intermediate carriers (e.g.,
vehicles, persons, animals, animal products, kitchen waste and even through the air). The virus is
inactivated within 48 hours after slaughtering and during the maturation of meat by acidification
at pH values of 6 and less. In meat and/or tissue frozen immediately after slaughtering and in
which therefore no acidifying occurs, the virus can remain infectious for months (at –20 °C, for
years). When dried, the virus may remain for a long time on pasture, hair, walls, covers, clothing
and other articles. Heating to more than 93 °C leads to virus inactivation. The transmission of the
pathogenic organism to humans can take place via direct contact with sick animals, raw milk or
contaminated articles. Skin injuries favour the penetration of the virus into the body.
Transmission from human to human has not been described so far. However, sick persons can infect
sensitive animals by viral shedding.
For the prevention of epidemic propagation,
measures to inactivate the FMD virus and to avoid its spread are essential. The appropriate
procedure is defined in the “Regulation on the Protection against Foot-and-mouth Epidemic (MKS
Verordnung)” of February 1, 1994 (Bundesgesetzblatt, 1994), last changed in March 29, 2001 (Bundesanzeiger 2001) (internet address: e.g.,
http://www.veterinaernetzhessen.de/Tierseuchenbekaempfung/Rechtsvorschriften/mks_verordnung.htm)
together with the appropriate implementation instructions. They refer to restricted areas, stabling, pastures, animals, animal wastes, dung, transport, rodent pest control and protective clothing.
Prevention at work
According to BioStoffV, the FMD virus is classified for humans as risk group 2 (for animals: risk group 4). Risk group 2 comprises biological working materials that can cause a disease in humans and pose a danger to employees; a spreading of the infection within the population is, however, improbable and an effective prophylaxis or treatment is normally possible.
Persons at risk mostly involve those with direct contact with sick animals, e.g., farmers and veterinary staff. Furthermore, there is a risk to all persons involved in killing the infected animals to minimise the spread of the infectious agent. Because of the danger of spreading the virus, culling is carried out directly on the agricultural premises. Personnel should carry damp-proof and humidity-resistant gloves when slaughtering pigs and sheep. This measure prevents possible infection via skin injuries on contact with blood, excrement and saliva of the infected animals. After use, the gloves should be incinerated.
FMD is listed among those occupationally acquired transferable diseases, which compensation can be applied for. However, no cases of chronic infection of humans with FMD contracted during professional activities have been reported so far to the Institution for Statutory Accident Insurance and Prevention in the Meat-processing Industry.
REFERENCES
ARMSTRONG, J., DAVIE, J., AND HEDGER R. S. (1967). “Foot-and-mouth disease in man.” B.M.J. iv:529–530
BAUER, K. (1997). “Foot-and-mouth disease as zoonosis.” Arch. Virol. 13 (Suppl.):95–97.
BECKER, W. (Ed.) (1996). Zoonosen-Fibel. Hoffmann-Verlag, Berlin.
BROWN, P. RAU, E. H., JOHNSON, B. K., BACOTE, A. E., GIBBS, C. J. Jr., and GAJDUSEK, D. C. (2000). “New studies on the heat resistance of hamster-adapted scrapie agent: threshold survival after ashing at 600 degrees C suggests an inorganic template of replication.” Proc. Nat. Acad. Sci. U.S.A. 97:3418–3421.
BUELER, H., AGUZZI, A., SAILER, R., GREINER, R. A., AUTENRIED, P., AGUET, M., and WEISSMANN, C. (1993). “Mice devoid of PrP are resistant to scrapie.” Cell 73:1339–1347.
BUNDESANZEIGER (2001). Letzte Revision der Neufassung der Verordnung zum Schutz gegen die Maul- und Klauenseuche (MKS-Verordnung) March 29, 2001 p. 5797.
BUNDESGESETZBLATT (1994). Neufassung der Verordnung zum Schutz gegen die Maul- und Klauenseuche (MKS-Verordnung) February 1, 1994, p.187.
BUNDESGESUNDHEITSBLATT(1998). Krankenversorgung und Instrumentensterilisation bei CJK-Patienten und CJK-Verdachtsfällen. Bundesgesundheitsbl. Gesundheitsforsch. Gesundheitsschutz 41:279–285.
BUNDESGESUNDHEITSBLATT (2001). “Die bovine spongiforme Enzepahlopathie (BSE) des Rindes und deren Übertragbarkeit auf den Menschen.” Bundesgesundheitsbl. Gesundheitsforsch. Gesundheitsschutz 44:1–11.
BUNDESMINISTERIUM FÜR VERBRAUCHERSCHUTZ, ERNÄHRUNG und LANDWIRTSCHAFT (2001). http://www.bml.de/verbraucher/bse/anzahlbse.htm#01.
CDC/NIH (1999). Biosafety in Biomedical and Microbiological Laboratories. http://bmbl.od.nih. gov/sect7d.htm.
CONFIDENTIAL REPORT(1987) to the director of the Central Veterinary Laboratory from 27. 05.87 http://www.bse.org.uk/files/yb/1987/05/27001001.pdf.
DEPARTMENT OF HEALTH, GB (2001) (http://www.doh.gov.uk/cjd/stats/april01.htm).
EPIDEMIOLOGISCHES BULLETIN (2001). “Die bovine spongiforme Encephalopathie (BSE) – eine Tierseuche mit erheblicher Bedeutung für den Menschen.” Epidemiol. Bull. 4:23–27.
HOUSTON, F., FOSTER, J. D., CHONG, A., HUNTER, N., and BOSTOCK, C. J. (2000). “Transmission of BSE by blood transfusion in sheep.” Lancet 356:999–1000.
RESOLUTION 602 (2001). Beschluss des Ausschusses für Biologische Arbeitsstoffe 602: “Spezielle Maßnahmen zum Schutz der Beschäftigten vor Infektionen durch BSE-Erreger.” Bundesarbeitsblatt 2001 2:96–97. Mit 1. Aktualisierung vom 20.03.2001. http.//baua.prax.abas/entw602.htm.
SCHULZ, N. (2001) “BSE-Ein Thema für den Arbeitsschutz.” FBG-Forum 1:12. http://www.fleischerei-bg.de/infoboard.index.html.
TAYLOR, D. M., WOODGATE, S. L., and ATKINSON, M. J. (1995). “Inactivation of the bovine spongiform encephalopathy agent by rendering procedures.” Vet. Rec. 137:605–610.
TAYLOR, D. M., WOODGATE, S. L., FLEETWOOD, A. J., and CAWTHORNE, R. J. G. (1997). “Effect of rendering procedures on the scrapie agent.” Vet. Rec. 141:643–649.
THE BSE INQUIRY REPORT (2000). http://www.bse.org.uk/report/index.htm TROEGER, K. (2001). “Alternative Methoden stehen zur Wahl.” Fleischwirtschaft 4:62–64.
ZOBELEY, A. and GLOCKSHUBER, R. (2001). “Prionen: Neuartige, immer noch rätselhafte Erreger.” Nachrichten aus der Chemie 49:454–461.