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A Review of Food Safety and BSE

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Well-known member
Feb 10, 2005
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Montgomery, Al
M.H. Anil - University of Bristol, Department of Clinical Veterinary Science, Division of Food Animal Science.

A. Austin - Fara.Way Research, Oak Farm, Harpsden Bottom, Henley-on-Thames (Formerly a Clinical Neurologist at the Veterinary Laboratories Agency, Weybridge, UK)

Bovine spongiform encephalopathy (BSE) is a member of the group of scrapie-like diseases that are termed transmissible spongiform encephalopathies (TSE). The advent of this new disease in the United Kingdom in the 1980s (Wells et al., 1987) has been followed by a substantial epidemic (Wilesmith, 1996) (Wilesmith, et al., 1988; Wilesmith, et al., 1991) that has produced approaching 200,000 confirmed cases. Since then it has been recognised in many other countries around the world and reports in new countries continue.

One defining feature of the TSEs is that during their pathogenesis affected hosts develop the property of transmissibility within some of their body tissues, so that under certain conditions exposure of fresh hosts to these tissues results in transmission of the diseases. The tissues that display this transmissible property most strongly are the tissues of the central nervous system, but in some TSEs in some species other tissues also come to possess transmissibility.

The routes of exposure through which the diseases can be acquired by fresh hosts include oral ingestion and so there is the potential for food products prepared from affected animals to transmit the diseases to people. Generally, it is more difficult to transmit TSEs inter-specifically than intra-specifically because of a so-called species barrier effect. BSE, however, appears to have the potential to affect a wider host range than is generally the case for other TSEs. There is evidence of its deliberate oral transmission in experiments and unintentionally through food regarding a wide range of species (Bruce et al., 1994; Kirkwood and Cunningham, 1994; Bruce et al., 1997; Hill et al., 1997 Barlow and Middleton, 1990; Robinson et al., 1994; Foster et al., 1993, 1994; Wells et al., 1994, 1998; Bons et al., 1999).

The pathogenesis of TSEs is closely associated with the accumulation in tissues of abnormal isoforms of a host protein, termed PrP, which are derived through a post-translation modification. The transmissible property in tissues is intimately related to these PrP isoforms.

Although the diseases by title are referred to as transmissible, it has become commonplace to call the transmissible property infectivity and to regard the causative agents as unconventional infectious agents. They are considered unconventional primarily because tissue fractions that have been purified to contain no apparent nucleic acid can still transmit the diseases.

Transmission by the transfer of affected tissues, however, does not follow an important characteristic of infections in that generally it shows a dose-dependent effect on pathogenesis in the new host. This is in contrast to infections, which although usually requiring a certain minimum dose to infect a fresh host, do not have a dose-dependent pathogenesis after exposure. The authors prefer the term transmissibility, rather than infectivity, as more appropriate to the phenomenon in TSE.

One of the most prominent characteristics of the TSES is the long latent interval, the incubation period (IP), which elapses between exposure to the causative agents and the development of clinical disease. IP is consistently inversely related to the exposure dose. In inbred lines of small laboratory animal species the response to challenge with specific strains of TSE agents can be very predictable, with standard errors of less than 2% of the mean period (Bruce, 1996). Using well-characterised models, this enables the estimation of the concentration of transmissible agent in tissues by reference to the IP resulting from experimental exposure to the tissues (Kimberlin, Cole and Walker, 1987; Kimberlin and Walker, 1988).

For practical purposes in food safety, the dose of exposure is an important consideration that may influence both the incubation period and the proportion of exposed subjects that succumb, the attack rate. There is scant information on how repeated exposures might influence the dose-dependency.

Concern that BSE was a potential threat to human health through food products derived from affected animals was evident in a number of measures taken by the British Government from the late 1980s onwards. These were designed to remove from the human food chain animal tissues considered likely to contain the transmissible agent. The discovery in Britain of a new human TSE, a variant of CJD, in the 1990s that had characteristics consistent with BSE greatly increased concerns for food safety throughout the world.

Many of the control measures taken had to be adopted with very little available information that was specific to the new disease. A substantial animal research programme was initiated in Britain to provide information. Information that has emerged from this programme and other knowledge is used here to review some aspects of food safety regarding BSE.

An understanding of the pathogenesis of the TSES of food animals, with particular regard to the temporal and spatial development of transmissibility in their tissues, is crucial to the construction of food safety policies

One of the most important requirements was to determine which cattle tissues contained transmissibility and at. what age, or time after exposure, transmissibility developed.

The first study on this ( Fraser and Foster,1994) applied a mouse bioassay to a range of tissues from natural cases of BSE that had been killed in the clinical stage of the disease. Transmissibility was demonstrated in tissues from the central nervous system and the retina, but not in the non-neural tissues that were examined.

Circumstantial and epidemiological evidence from the developing epidemic (Wilesmith, --; Wilesmith, et al., 1988; Wilesmith, et al., 1991) had pointed strongly to cattle acquiring the disease by eating meat and bone meal in commercial rations. An experiment was begun in 1991 with the intention of simulating this exposure through the oral dosing of calves with 100g homogenised brain from clinically affected cows (Wells et al., 1998). The objective was to study the pathogenesis of the disease and the temporal and spatial development of transmissibility. Groups of the calves, three exposed and one unexposed were killed at intervals of four months, starting at two months after exposure, up to 22 months. From 22 months onwards, the kills were altered because too few animals were available to cover the long incubation period.

A range of their tissues was subjected to mouse bioassay for transmissibility, with the individual tissues of the exposed calves in each group kill pooled for a single assay. This revealed that transmissibility was present in the terminal ileum by six months after exposure and this persisted to 18 months, reappearing again at 38 and 40 months. None of the other tissues examined showed transmissibility until the central nervous system and its closely-associated ganglia (the cervical and thoracic dorsal root ganglia ) of two calves killed at 32 months after exposure did so. The trigeminal ganglion showed transmissibility soon after at 36 months.

Previous to the 32-month kill and after the kill at 22 months, only one animal had been killed and tested at 26 months and no transmissibility was found. So, although the study found that transmissibility had been established by 32 months, it did not determine clearly what happened in the months immediately before. In particular, with little or no replication of the results at any time point, no distribution curve for the onset of transmissibility or confidence levels associated with it could be established.

The results from the mouse bioassays in this study have been reinforced by conducting additional bioassays in calves using intra-cerebral inoculation of tissues from the exposed calves, which is a more sensitive method than bioassay in mice.

There was a single indication of transmissibility from bone marrow at 36 months but this remains unconfirmed and possibly may have been a result of cross-contamination of tissues. Apart from this, no evidence has arisen throughout the pathogenesis of this experimental model of transmissibility in a wide range of other tissues.

Besides banning meat and bone meal from commercial diets for food producing animals, an array of measures has been instituted to protect meat consumers from the potential danger of BSE. Initially these were necessarily based upon knowledge of scrapie in sheep, as this was seen as the prototypic TSE. As evidence from research programmes emerged, this was also incorporated into the measures when it was judged appropriate. Some other steps were taken that had little evidential basis, but were implemented to increase consumer confidence in meat. Yet other measures were taken that may have had a mainly political or economic basis, for instance by reducing the amount of beef in the market by carcass disposal measures to support prices, with perhaps only a quasi-scientific justification.

Clinical cases of BSE
In its early clinical stage BSE is often difficult to distinguish from other disorders or behavioural disturbances. For purposes of food safety, it is desirable not to apply a too rigid clinical definition to the disease otherwise cases that do not manifest clear clinical signs may not be classified as BSE. Inevitably, in practice, this can mean including in the exclusion measures a proportion of animals showing clinical signs that overlap with those of BSE. In the British epidemic overall this proportion has been in the region of 16%.

With knowledge of the structure of the British cattle industry, it is possible to estimate for any years birth cohort the ratio between animals surviving to 5 years and those that are killed before that age. For instance, a half of any cohort can be presumed male, most of which are killed before three years of age. For the females, the proportion killed for beef at a young age and the yearly culling rates from adult herds can be estimated from female replacement rates in dairy and beef cattle herds. In Britain, the survivors at five years of age seem to represent around 13% of a birth cohort, which suggests that the numbers of cattle slaughtered that were in the pre-clinical stages of BSE were in the region of seven times greater than the clinical cases detected. It was obviously deemed necessary to take measures to deal with the potential danger of transmissibility to man from the tissues of these incubating animals.

BSE has not been reported in commercial pigs. If it did occur it might be difficult to recognise under many commercial husbandry conditions, especially if the attack rate in a herd is low, as has been in cattle herds in which it was mostly < 3% and so was usually seen as isolated, individual cases. The early clinical stages in experimental BSE in pigs were insidious changes in behaviour and temperament. In commercial herds of pigs this might be manifest as withdrawal from interaction with other pigs and attendants, or could result in increased agonistic interactions, which would be difficult to discriminate from incidental changes often experienced in pig husbandry. Even the later clinical stages involving ataxia and more profound temperament change need expertise if they are to be distinguished from other porcine disorders. Accordingly it is feasible that BSE could exist in pig herds and remain undetected in clinical or sub-clinical forms if they are fed contaminated meat and bone meal.

Experimental exposures have not produced TSE in chicken, so there is no reason to suppose from current knowledge that any clinical form of BSE exists in this species.

If BSE occurs in commercial sheep the main problem in recognising it will be to discriminate it from scrapie and possibly from other disease conditions that affect sheep. In Britain scrapie is now a Notifiable Disease and sheep suspected of having it are not allowed into food.

Prohibition of Specific Tissues
Unavoidably, when BSE is prevalent, some cattle that are incubating BSE and possibly some clinical cases that are not detected are presented as carcasses for human consumption. Information on the spatial distribution of transmissibility can be applied in order to remove tissues from the carcass that are considered unsafe. Initially, in the absence of direct information on BSE in cattle, a list of cattle tissues and organs to be banned from human food was compiled mainly from what was known about the spatial distribution of transmissibility in sheep scrapie. The banned tissues were brain, spinal cord, spleen, thymus, tonsils, and intestines of bovines aged over six months. This list, now termed the Specified Risk Material, has been modified over the course of the epidemic as more information has emerged. In Britain it now is comprised of the entire head excluding the tongue but including the brain, eyes, trigeminal ganglion and tonsils, the thymus, the spleen and spinal cord of animals aged over six months. Also prohibited is the spinal cord in animals aged over twelve months and the alimentary tract from the duodenum to the rectum in bovines of all ages. The vertebral column including the dorsal root ganglia is included in the list for animals aged over thirty months,

The need to ban the tissues of the central nervous system and its closely-associated ganglia because they contain BSE transmissibility has been confirmed unambiguously from cattle studies, and this applies also to the ileum (Wells et al., 1998). For other tissues that are prohibited, no direct evidential basis for their ban has emerged except for the eyes.

If BSE became recognised in commercial pigs, this species would seem to pose much the same considerations regarding banning specific tissues as cattle, as there is evidence from experimental studies of transmissibility only in the CNS tissues and the alimentary tract.

For chicken, so little data is available on the potential transmissibility of their tissues following exposure to TSE-affected materials that informed judgements are difficult.

In sheep the position differs greatly from the other food species. The spatial distribution of PrP accumulation and, presumably, transmissibility is so wide, being in the alimentary tract, lymphoid and central nervous systems that it would seem to be very difficult, impractical or unconvincing to separate tissues that have shown BSE transmissibility, or might be suspected of it, from those tissues considered safer. In this species therefore a ban on specific tissues might not effectively or convincingly protect human food from BSE transmissibility.

Age at Slaughter
Information on the temporal development of transmissibility through the long incubation of BSE has allowed the application of precautions based on the age of cattle, either to ban them from human food or to apply tests on animals above a particular age. These precautions recognise that transmissibility develops and progresses as cattle age. The problem is in the selection of the most appropriate threshold age at which to apply these measures.

When meat and bone meals were prohibited from cattle rations in Britain in August 1988, the incidence of BSE in animals born in that month declined markedly. This indicates that BSE can be acquired under commercial conditions when calves are very young, in which case for practical purposes in considering food safety the age of an animal can be taken as the same as the duration of its potential exposure or incubation.

Accordingly, as transmissibility in the distal ileum was demonstrated to occur by six months after exposure in the Pathogenesis Experiment it would seem necessary to ensure that this tissue is not available for human consumption from cattle of any age. This can be achieved, as is practiced, by extracting this particular tissue from the carcass.

The tissues of the central nervous system and associated ganglia have been the next to show transmissibility but, on available information, this does not occur until 24 months or more after exposure so on an evidential basis animals less than two years old should be safe to eat, provided the distal ileum is removed. After that age, most of any other transmissibility that may be present can be removed by taking away the head and dissecting out the spinal cord. It is not practical, however, to remove the dorsal root ganglia from their sites within the vertebrae of the spinal column and so meat attached to the column or prepared from it may contain transmissibility if the animal ages beyond some point over 24 months. Judgements on the critical age at which transmissibility arises in the central nervous system and the ganglia appear to have varied in different countries.

In Britain, food safety measures for beef have included its prohibition from the food chain if derived from animals aged over 30 months, the Over Thirty Months Scheme (OTMS). The notional basis for the adoption of this 30 month threshold is that very few, if any, animals that are incubating the disease will develop the property of transmissibility in their nervous tissues before this age. Such biological evidence as there is suggests that this notion may not be valid and that, contrarily, a large proportion of animals that have acquired the disease are likely to develop transmissibility in these tissues before 30 months.

The justification for the OTMS seems to have evolved partly from a risk analysis (3) that considered the implications for food safety of the findings of the Pathogenesis Experiment (4,5). This analysis assumed that there was a regular temporal relationship between the development of transmissibility in specific nervous tissues and the onset of clinical signs, with this latter event coming around three months after the former. This may not be a valid interpretation of the experiments findings and is not consistent with earlier studies on the pathogenesis of scrapie in mice (6).

In the Pathogenesis Experiment, as already outlined, the earliest transmissibility in the tissues of the central nervous system and the closely associated dorsal root ganglia (DVG) was at 32 months after oral exposure. In eight animals kept alive for longer than 32 months, definite clinical signs were first detected at 35 months in one animal and 37 months in another. Equivocal clinical changes were present in five others at the time of killing between 36 and 40 months (5). It was from these findings that the risk analysis assumed the generality that transmissibility in nervous tissues preceded clinical signs by three months. Almost no BSE cases younger than 39 months were being reported at that time, so by subtracting 3 months plus a six-month safety margin the safety threshold of 30 months was devised.

There must be serious doubts that there is any fixed relationship between the onsets of clinical signs and transmissibility in the central nervous system that allows the onset of transmissibility to be estimated from the subtraction of a finite period from the time of clinical onset. If there is such a relationship it would likely be much longer than 3 months. The main reasons for these doubts are threefold.

First, over the period 24 to 30 months, mild changes in the emotionality of most of the animals in the cattle pathogenesis study were noted (4). Insufficient surviving, un-exposed animals were left in the study at this time to be sure that this observation was disease-specific and not of an incidental, developmental nature. However, there is analogy with several murine studies on scrapie in which subtle behavioural signs were found long before overt clinical signs appeared. In mice exposed by intracerebral inoculation, beginning approximately after one third to a halfway through the total incubation period (IP), recorded changes have been a progressive reduction in emotional responsiveness (7), increasing emergence times into an open field test (8) and a progressive reduction in spontaneous motor activity (9).

Altered drinking responses, evident from progressively reducing responses to induced polydipsia as incubation advanced, and altered feeding and body weight changes also have been observed around a third to a half way through IP after either intracerebral or intraperitoneal inoculations (10).

The nature of these early signs suggests that they are the result of functional changes in the central nervous system, presumably associated with the activity and presence of the transmissible agent, at around 40% through the incubation period.

Secondly, the cattle in the pathogenesis study were exposed to 100g of brain material from BSE affected cows. In a companion experiment (11) ten cattle were similarly exposed but were kept alive to a stage when their clinical signs were well developed. The onset of these definite clinical signs, equivalent to the stage at which the disease can be confidently diagnosed on farms, ranged from 33 to 61 months (mean 44.6) post exposure, but the onset of equivocal signs was observed substantially earlier, between 24 and 37 months (mean 31.8).

Thirdly, in six models of murine scrapie (intraperitoneal inoculation) with greatly differing incubation periods, the onset of transmissibility in the CNS varied from 41 to 55% into the IP (6).

We do not have the necessary information to construct a population distribution curve for the onset of BSE transmissibility in the CNS, but it seems probable that this begins substantially before 30 months and extends to overlap with that for the onset of clinical signs.

The mean age-specific incidence of BSE in the British epidemic has been approximately 5 years (12). Therefore the incubation period mean is something less than around 60 months, depending on the age the disease is acquired naturally. In this case, the mean age for onset of CNS infectivity, at around 45-50% of the IP, would be less than 30 months. This raises concern that it is not just a few of the animals that are incubating BSE that have transmissibility by the age of 30 months in their CNS/ganglia, but that instead it is a substantial proportion perhaps more than a half.

The annual figures for British BSE cases born in 1992/3/4 and 5, respectively, are 3173, 2400, 1283 and 331 as reported up to January 2001. The multiplier of seven to estimate the numbers incubating BSE in these birth cohorts, gives totals of 22,211; 16,800; 8,981 and 2317. Only a proportion of these would have entered the food chain between the ages of 24 and 30 months of age, of course, because a proportion of animals killed for beef are aged younger than 24 months.

Fortunately the specified bovine tissues ban was in operation and this would have prevented the CNS tissues, besides other potentially dangerous tissues, from entering the food chain. This ban did not encompass the DVG, because these are physically associated with the bones of the vertebral column and, therefore, are present in joints containing these bones.

In 1997, because of the finding in the cattle pathogenesis study that the DRG contained transmissibility, a ban was also placed on selling beef joints with bone in, including the bones from the spinal column which contain the DRG. This Beef on the Bone Ban was greatly criticised, even derided, on the basis that the risk was negligible because very few, if any, animals harboured the transmissibility at the time of slaughter. In fact, as discussed above, possibly tens of thousands of carcasses may have had transmissibility in the DRG and the measure had been very appropriate. This ban was reversed in December 1999, creating a rather incongruous position in which a range of specified tissues for which there was no evidence of transmissibility continued to be banned, whilst another tissue for which there was such evidence was not controlled.

If food safety is to be based on the age when transmissibility first becomes established, it would seem that this age needs to be appreciably less than 30 months. Some countries have adopted 24 months as the age beyond which all carcasses should be tested for evidence of BSE by immunological tests for PrP.

If BSE should become recognized as a problem in pigs, too little is known about the temporal development of transmissibility in this species to apply an age related exclusion from human food, other than one based largely on indirect evidence from other species.

In chicken, similarly, there is insufficient information to judge whether or not Marshs findings might have any relationship to age.

Disease specific PrP accumulation and presumed transmissibility was present in the retropharyngeal lymph nodes of a sheep killed 4 months after exposue to BSE. Although not present in all sheep tested, this would suggest that any age related exclusion of sheep from human food would have to be at such a young age that it could not be applied practically to most sheep production systems.

Animal Production Systems
Because TSEs develop slowly, as a generalization, the younger an animal is at slaughter the less likelihood there is of transmissibility being present in its tissues. In younger cattle the distal ileum is the only tissue of proven concern and this can be reliably removed from the carcass. On grounds of food safety policy, therefore, there is an argument for encouraging beef production from younger animals. This may be especially pertinent to calves from dairy herds, because the prevalence of BSE has been higher in dairy than in beef suckler herds. Dairy-bred calves can be suitable for rapid rearing systems and slaughter at ages much younger than those at which transmissibility has been demonstrated in tissues other than the ileum.

Ante and post-mortem recognition at slaughter plants
When animals arrive at a slaughter plant, the ante mortem examination is intended to recognise and exclude clinically affected animals. However, those that are sub-clinical might be expected to escape detection. Research to date has not shown any reliable method for detection of a sub-clinical status in live animals. In the absence of a reliable method in the lairage, measures such as OTMS and post mortem detection methods are important.

Diagnostic tests on samples taken from the brain stem (obex) are now routinely used in Europe (Moynagh and Schimmel, 1999). The available tests include:

- A two-site non-competitive immunometric, using 2 monoclonal antibodies. Source: A.G. and G. Wallac

- Immunobloting test - western blot detection of protease resistant PrPSC with MAB. Source: Prionics

- Chemiluminescent ELISA using polyclonal anti-PrP antibody. Source: Enfer

- Sandwich immunoassay for PrPSC with 2 MABs, following denaturation and concentration. Source: CEA/BioRad

Current stunning and slaughter methods
Current stunning methods in ruminants include captive bolt stunning and electrical stunning. Captive bolt stunning induces a stun by the impact on the skull of a bolt at high velocity fired from a gun. The high kinetic energy of the bolt causes the concussion. Stunning can be achieved by either a penetrating or a non-penetrating gun. Either way, the stunning needs be followed by a procedure, for example exsanguinations, that results in the death of the animal (Daly, 2000).Penetrative captive bolt devices provides secondary damage to brain tissue that ensures non-recovery.

Captive bolt guns can be activated by either a blank cartridge or high air pressure to fire the bolt. Most cattle and a substantial proportion of sheep (38 % in the UK, MHS, 1997) are stunned with a penetrating captive bolt gun (CBG) prior to slaughter. Electrical stunning, however, is also used to stun most sheep by passing a current across the head to induce a state of unconsciousness. Electrical stunning has also been introduced in New Zealand and Australia for stunning cattle in special devices and are beginning to be used in the UK (Wotton et al., 2000).

Contamination of carcasses by stunning methods
There is concern that the current stunning and slaughter methods used in ruminants could, if applied to an animal with bovine spongiform encephalopathy (BSE), contaminate the edible parts of the carcass with brain tissues that contained transmissibility. Investigations have been carried out to assess the potential risk. There are two ways in which potential contamination could occur: 1) Dissemination of brain tissue during the stunning procedure; 2) Dispersal of spinal cord material during the splitting of beef carcasses.

Garland et al. (1996) found brain tissue in the lungs of slaughtered cattle and this led to concern that these fragments could result in haematogenous dissemination of transmissible material from the brain, with the risk of variant Creutzfeldt-Jakob disease to those consuming edible parts of the carcass. The validity of these findings was, however, questioned (Taylor, 1996) and similar studies carried out on 210 cattle in UK abattoirs failed to confirm the occurrence of pulmonary embolism of brain tissue (Munro, 1997). In view of the relatively crude and insensitive procedures that were used for detecting brain tissue in those studies, further research was commissioned by the Ministry of Agriculture, Food and Fisheries in the United Kingdom, to assess the risk that current methods for the stunning and slaughter of cattle and sheep may cause embolic dissemination of central nervous system (CNS) material.

To follow up the previous studies commissioned by the UK Ministry of Agriculture, Fisheries and Food, projects supported by the Food Standard Agency to determine whether CNS material could be detected in edible parts of the carcasses are still in progress in the UK. In addition, possible contamination by pathogen bacteria through the use of captive bolt stunning has been studied in an EU project.

Contamination of beef carcasses by spinal cord material during splitting
The UK legislation has required, since1989, the removal of Spinal cord from beef carcasses post splitting. A similar ban was introduced by the European Commission on 1st October 2000, requiring the removal of Central Nervous System (CNS) material from sheep carcasses over 12 months of age and all cattle carcasses in all EU states. However, in the majority of abattoirs, carcasses are split using a band saw; this often cuts the spinal cord in half along much of its length. This can obviously lead to potential dissemination of CNS material over the carcass and surrounding area resulting in possible contamination with the BSE infective agent.

Studies conducted by Helps et al (2002) have shown the presence of CNS material on carcasses after splitting with a conventional band saw. This contamination was still present after the carcass had been washed or steam-vacuum cleaned. However, significantly less CNS contamination was observed on carcasses following the removal of the spinal column by an experimental oval saw prior to splitting. With further engineering development, this new technique should be capable of removing spinal cord with minimal contamination risk.

Implications for public safety and animal welfare
The use of captive bolt guns may damage intra-cranial blood vessels and dislodge brain tissue. The heart continues pumping for several minutes following the use of a CBG, during which time any central nervous system (CNS) material that enters the jugular venous blood could be disseminated throughout the body. This possibility and the concern have been investigated in studies conducted in cattle and sheep. Blood samples from Foley catheters ,introduced into both jugular veins and inflated after stunning the animals with one of several captive bolt guns, were taken for analysis. The stunning methods tested were:

Pneumatically-activated penetrating CBG (no pithing required due to air injection into spinal canal; cartridge-operated conventional penetrating CBG, known as Cow followed by pithing ; non-penetrating cartridge-operated (therefore no pithing) CBG, known as Cash Knocker; electrical stunning (only in sheep);

These projects used two previously validated methods to look for CNS tissue in blood: immunocytochemistry on sections of buffy-coat Cytoblocks for S-100b protein, and capture ELISA for syntaxin 1-B. Neither of these CNS proteins is normally found in the blood (Anil et al. 1999, 2001a and b; Love et al. 2000). Multiple fragments of brain tissue were detected in the jugular venous blood of cattle slaughtered after use of a pneumatically operated penetrating CBG and after the use of a conventional cartridge-operated CBG followed by pithing. CNS tissue was also detected in the jugular venous blood of sheep that had been stunned with a conventional penetrating CBG or in those stunned with a pneumatically-activated penetrating CBG. Electrical stunning did not result in any detectable neural tissue. The emboli are detectable in jugular venous blood within 30s of stunning and will already have passed into and, possibly, through the lungs before exsanguination is carried out . It is noteworthy that the showers of embolic brain tissue include many fragments of small size CNS tissue, in principle, to be capable of passing through the pulmonary capillary bed. Further studies are planned to detect emboli in arterial blood and visceral organs.

These results confirm that there is a risk of embolic dissemination of brain tissue with the use of the pneumatically-operated air injection gun and show, in addition, that neuroembolism can also occur with use of a conventional penetrating CBG followed by pithing in cattle. Penetrative captive bolt devices, if applied correctly, can provide an effective stunning method that needs be followed by a procedure that results in the death of the animal (Daly, Gregory and Wotton, 1987), for example exsanguination or pithing. Pithing, a common practice in 70% of UK abattoirs (Meat Hygiene Service 1997) has been used by the industry to protect operative safety by greatly reducing the reflex kicking that takes place following captive bolt stunning. It is also commonly claimed that pithing has welfare benefits as it prevents recovery in effectively stunned animals. As a result of the BSE contamination fears, pithing is now banned in the whole of the European Union. However, this new ban has implications for abattoir operators handling carcasses as well as for animal welfare.

When penetrating captive bolt stunning is used, the bolt trajectory causes considerable damage. We have, in a preliminary investigation, examined brains of several cattle stunned with a penetrating captive bolt. We estimate that an average of 10g of brain tissue (out of a total of 450g) can be dislodged (unpublished results). On the basis of these criteria, we have calculated that between 50g and 500mg of brain tissue should be sufficient for transmission of infection by the oral route. Therefore, 10g of dislodged brain tissue may represent between 20 and 20,000 units of infectivity (Anil et al., 2001b).

In regard to sheep, although there are no naturally occurring cases, the possible infection of sheep with BSE is a cause for concern. Therefore, the use of electrical stunning seems to be the safer option at present (Anil et al., 2001a).

Contamination by microorganisms during captive bolt stunning
To determine whether penetrating captive bolt stunning of animals can result in internal and/or external microbial contamination of meat, slaughter sheep were inoculated with a marker organisms (E. coli K12 or Ps. fluorescens) into the brain through the stun wound immediately after stunning by a cartridge-operated, penetrative captive bolt gun. The marker organisms were detected in blood, liver, lungs, spleen, lymph nodes, in deep muscle and on carcass. When the gun which had been used to stun a brain-inoculated animal was used to stun consecutive, intact sheep, the marker organisms were found in blood of 30% and on the carcass surface of 40% consecutively stunned animals. Overall, the results from this study indicate that penetrative stunning of food animals can carry risks of internal and/or external microbial contamination of edible tissues and organ. Similar results have been obtained using the same markers in cattle (Daly et al., personal communication).

These recent developments summarized above could undoubtedly have implications for public health measures and animal welfare at slaughter. It is clear that there is a risk of contamination of carcasses with CNS tissue if pneumatically operated CBG or a cartridge operated CBG followed by pithing are used. The ban on pithing shopuld reduce the risk considerably. However, it is also possible that penetrating CBGs alone could cause problems. As with the USA, pneumatically operated guns for stunning cattle are likely to be banned in the EU. In addition, penetrating CBGs in sheep and, depending on the results of current research, these guns may also be prohibited in cattle. Therefore, there is need to consider the options left and improvements to be made:

Firstly, non-penetrating guns offer a good alternative. However, the potential problems associated with this type of gun should be resolved, such as the infrequent recovery before exsanguination. Secondly, the removal of pithing is causing operative safety problems in some plants, especially, where space is limited. An alternative solution to this problem is required. Thirdly, electrical stunning should be considered for stunning cattle. This system is used in 3 plants in the UK. However, the high cost and some doubts about animal welfare associated with sometimes ineffective use of this method need looking into.

Anderson, R.M., Donnelly, C.A., Ferguson, N.M., Woolhouse, M.E.J., Watt, C.J., Udy, H.J., Mawhinney, S., Dunstan, S.P., Southwood, T.R.E., Wilesmith, J.W., Ryan J.B.M., Hoinville, L.J., Hillerton, J.E., Austin, A.R. and Wells, G.A.H. 1996. Nature, 382: 779-788.

Anil M. H. , Love S., Helps C.R. and Harbour D.A. 2002. Potential for carcass contamination with brain tissue following stunning and slaughter in cattle and sheep, Food Control (in press)

Anil M.H., Love, S., Helps, C.R., McKinstry, J.L., Brown, S.N., Philips, A., Williams, S., Shand, A., Bakirel, T. and Harbour, D.A. 2001. Jugular venous emboli of brain tissue induced in sheep by use of captive bolt guns. Veterinary Record, 148, 619-620

Anil M.H. and Harbour, D.A. 2001. Current stunning and slaughter methods in cattle and sheep: Potential for carcass contamination with central nervous tissue and microorganisms. Fleichwirtschaft, 11, 123-124.

Anil, M.H., Love, S., Williams, S., Shand, A., McKinstry, J.L., Helps, C.R., Waterman-Pearson, A., Seghatchian, J. and Harbour, D.A. 1999. Potential contamination of beef carcasses with brain tissue at slaughter. Veterinary Record, 145, 460-462

Baker, H.F., Ridley, R.M. and Wells, G.A.H. 1993. Experimental transmission of BSE and scrapie to the common marmoset. Veterinary Record 132, 403-406.

Barlow, R.M. and Middleton, D. 1990. Dietary transmission of bovine spongiforrn encephalopathy to mice. Veterinary Record 126, 111-112.

Bone, J. (2000). BSE alert over sheep imported to US The Times Newspaper July 18: http://www.the-times.co.uk/news/pages/Times/timfgnusa01003.htm

Bons, N., Mestre-Frances, N., Belli, P., Cathala, F., Gajdusek, C. & Brown, P. (1999). Natural and experimental oral infection of nonhuman primates by bovine spongiform encephalopathy agents. Proceedings of the National Academy of Sciences of the United States of America 96, 4046-4051.

Bruce, M. E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994). Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and the species barrier. Philosophical Transactions of the Royal Society of London B 343, 405-411.

Bruce, M.E., Will, R.G., Ironside, J.W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. & Bostock, C.J. (1997). Transmissions to mice indicate that new variant CJD is caused by the BSE agent. Nature 389, 498-501.

Buncic S., McKinstry J., Reid C.-A. and Anil M.H. (2002). Spread of microbial contamination associated with penetrative captive bolt stunning of food animals. Food Control (in press)

Daly C, Gregory N.G. and Wotton S.B., (1987). Captive bolt stunning of cattle: Effects on brain function and role of bolt velocity. Br Vet J., 143, 574

Dawson, M., Wells, G.A.H. & Parker, B.N.J. (1990a). Preliminary evidence of the experimental transmissibility of bovine spongiform encephalopathy to cattle. Veterinary Record 126, 112-113.

Dawson, M., Wells, G.A.H., Parker, B.N.J. & Scott, A.C. (1990). Primary parenteral transmission of bovine spongiform encephalopathy to the pig. Veterinary Record 127, 338-339.

Dawson, M., Wells, G.A.H., Parker, B.N.J. & Scott, A.C. (1991). Transmission studies of BSE in cattle, hamsters, pigs and domestic fowl. In Subacute Spongiform Encephalopathies, pp. 25-32. Edited by R. Bradley, M. Savey and B. Marchant. Commission of the European Communities, Dordrecht: Kluwer Academic Publishers.

Dawson, M., Wells, G.A.H., Parker, B.N.J., Francis, M.E., Scott, A.C., Hawkins, S.A.C., Martin, T.C., Simmons, M.M. & Austin, A.R. (1994). Transmission studies of BSE in cattle, pigs and domestic fowl. In Transmissible Spongiform Encephalopathies, pp. 161-167. Edited by R. Bradley & B. Marchant. A Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities held in Brussels, 14-15 September 1993. Document VI/4131/94-EN. European Commission, Agriculture, Brussels.

Department of Agriculture and Fisheries (1983). Results of June 1983 Annual Agricultural and Horticultural Census, Scotland. DAFS, Edinburgh

Department of Health, Ministry of Agriculture, Fisheries & Food (1989). Report of the Working Party on Bovine Spongiform Encephalopathy. Department of Health, London.

Det Norske Veritas Assessment of Risk from Possible BSE Infectivity in Dorsal Root Ganglia. A report prepared for MAFF and SEAC. (1997)

Dickinson, A.G., Meikle, M.H., Fraser, H. (1968) Identification of a gene which controls the incubation period of some strains of scrapie agent in mice. Journal of Comparative Pathology 78: 293-299.

Donnelly, C.A. Nature 408, 787 788 (2000)

Electrical stunning of cattle (2000).Vet Rec. Dec 9;147(24):681-4.

Foster, J.D., Hope, J. & Fraser, H. (1993). Transmission of bovine spongiform encephalopathy in sheep and goats. Veterinary Record 133, 339-341.

Fraser, H, Bruce, M.E., Chree, A., McConnell, I. & Wells, G.A.H. (1992). Transmission of bovine spongiform encephalopathy and scrapie to mice. Journal of General Virology 73, 1891-1897.

Fraser, H. & Foster, J. (1994). Transmission to mice, sheep and goats and bioassay of bovine tissues. . In Transmissible Spongiform Encephalopathies, pp. 145-159.

Edited by R. Bradley, M Savey & B. Marchant. A Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities held in Brussels, 14-15 September 1993. Document VI/4131/94-EN. European Commission, Agriculture, Brussels.

Fraser, H., McConnell, I., Wells, G.A.H. & Dawson, M. (1988).. Transmission of bovine spongiform encephalopathy to mice. Veterinary Record, 123, 472.

Garland, T., Bauer, N. & Bailey, M. (1996) Brain emboli in the lungs of cattle after stunning. The Lancet 348, 610

Gibbs, C.J. Jr., Gajdusek, D.C. & Amyx, H. (1979). Strain Variation in the Viruses of Creutzfeldt-Jakob Disease and Kuru. In Slow Transmissible Disease of the Nervous System, vol. 2, pp. 87-110. Edited by S. B. Prusiner and W.J. Hadlow. New York: Academic Press.

Hatfield, S. & Challa, V.R. (1980) Embolism of cerebral tissue to lungs following gunshot wound to head Journal of Trauma 20, 353-355.

Hawkins, S.A.C., Ryder, S.J., Wells, G.A.H., Austin, A.R. & Dawson, M. (1998). Studies of experimental transmissibility of BSE and scrapie to pigs. In Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, 5-9 July 1998.

Heitzman, R.J. & Carp, C.R. (1968) Behaviour in emergence and open-field tests of normal and scrapie mice. Res. Vet. Sci. 9, 600-601.

Helps C.R., Hindell P., Hillman T.J., Fisher A.V., Anil H. , Knight A. C., Whyte R.T , O'Niell D.H. , Knowles T.G. and Harbour D.A. (2002). Contamination of beef carcasses by spinal cord tissue during splitting, Food Control (in press).

Hill, A.F., Desbrusliers, M., Joiner, S., Sidle, K.C., Gowland, I., Collinge, J., Doey, L.J. & Lantos, P.L. (1997). The same prion strain causes vCJD and BSE. Nature 389, 448-451.

Hornabrook, R.W. (1979). Kuru and Clinical Neurology. In Slow Transmissible Disease of the Nervous System, vol. 1, pp. 37-66. Edited by S. B. Prusiner and W.J. Hadlow. New York: Academic Press.

Kimberlin, R.C. and Walker, C.A. J. gen. Virol. 69, 2933-2960 (1988)

Kirkwood, J.K. & Cunningham, A.A. (1994). Spongiform encephalopathy in captive wild animals in Britain: epidemiological observations. In: Transmissible Spongiform Encephalopathies, pp. 29-47. Edited by. R. Bradley & B. Marchant. A Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities held in Brussels, 14-15 September 1993. Document VI/4131/94-EN. European Commission, Agriculture, Brussels.

Krebs, J. Nature 408, 767 (2000)

Lasmzas, C. I., Deslys, J.-P., Demalmay, R., Adjou, K. T., Lamoury, F., Dormont, D., Robain, O., Ironside, J., Hauw, J.- J. (1996). BSE transmission to macaques. Nature 381, 743-744.

Love, S., Helps, C.R., Williams, S., Shand, A., Mckinstry, J.L. , Brown, S.N., Harbour, D.A. & Anil, M.H. (2000) Assessing the risk of haematogenous dissemination of brain tissue after stunning of cattle with captive bolt guns Journal of Neuroscience Methods 9, 53.

Martin, T., Hughes, S., Hughes, K. & Dawson, M. (1995). Direct sequencing of PCR amplified pig PrP genes. Biochimica et Biophysica Acta 1270, 211-214.

McMillan, J.B. (1956) Embolism of cerebral tissue in lungs following severe head injury. American Journal of Pathology 32, 405.

Meat and Livestock Commission (1999). MLC Pig Yearbook 1999,. p.59 MLC, Milton Keynes.

Meat Hygiene Service (1997). Abattoir Welfare Survey, November.

Ministry of Agriculture, Fisheries and Food (1983). Annual Agricultural and Horticultural Census, England and Wales, MAFF, London.

Ministry of Agriculture, Fisheries and Food (1992) The Report of the Expert Group on Animal Feedingstuffs. London, HMSO.

Ministry of Agriculture, Fisheries and Food (1995). Annual Agricultural and Horticultural Census, England and Wales, MAFF, York.

Moynagh J. & Schimmel H. (1999) Nature, 400, 105.

Order (1996). The Bovine Spongiform Encephalopathy (Amendment) Order 1996. Statutory Instrument No. 962. HMSO, London.

Outram, G.W. (1972) Changes in drinking and feeding habits of mice with experimental scrapie. Journal Comparative Pathology 82, 415-427.

Robinson, M.M., Hadlow, W.J., Huff, T.P., Wells, G.A.H., Dawson, M., Marsh, R.F. & Gorham, J.R. (1994). Experimental infection of mink with bovine spongiform encephalopathy. Journal of General Virology, 75, 2151-2155.

Ryder, S.J., Hawkins, S.A.C., Dawson, M. & Wells, G.A.H. (2000). The neuropathology of experimental bovine spongiform encephalopathy in the pig. Journal of Comparative Pathology 122, 131-143.

Savage, R.D. & Field, E.J. (1965) Brain damage and emotional behaviour: the effects of scrapie on the emotional responses of mice 13, 443-446.

Scott, P.R. (1990). Detailed neurological examination of suspected cases of BSE. The University of Edinburgh. Fellowship thesis for RCVS.

Scottish Office, Agriculture, Environment and Fisheries Department (1995). Results of June 1995 Annual Agricultural and Horticultural Census, Scotland. SOAEFD, Edinburgh

Shmakov, A.N., McLennan, N.F., McBride, P., Farquhar, C.F., Bode, J., Rennison,K.A. and Ghosh, S. (2000) Cellular prion protein is expressed in the human enteric nervous system. Nature Medicine, 6, 840-841.

Suckling, A.J., Bateman, S., Waldron, C.B., Webb, H.E. & Kimberlin, R.H. (1976) Motor activity changes in scrapie-affected mice. Br. J. Exp. Path. 57, 742-746.

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

Wells, G.A.H., Dawson, M., Hawkins, S.A.C., Austin, A.R., Green, R.B., Dexter, I., Horigan, M.W. and Simmon,M.M. Bovine Spongiform Encephalopathy The BSE Dilemma: Preliminary Observations on the Pathogenesis of Experimental Bovine Spongiform Encephalopathy (C.J.Gibbs/Springer-Verlag, New York, 1996)

Wells, G.A.H., Dawson, M., Hawkins, S.A.C., Austin, A.R., Green. R.B., Dexter, I., Horigan, M.W. & Simmons, M.M. (1996). Preliminary observations on the pathogenesis of experimental bovine spongiforrn encephalopathy. In Bovine Spongiform Encephalopathy. The BSE Dilemma, pp. 28-44 .Edited by C.J. Gibbs, Jr. New York: Springer-Verlag.

Wells, G.A.H., Dawson, M., Hawkins, S.A.C., Green, R.B., Francis, M.E., Simmons, M.M., Austin, A.R. & Horigan, M.W. (1994). Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Veterinary Record 135, 40-41.

Wells, G.A.H., Hawkins, S.A.C., Green, R.B., Austin, A.R., Dexter, I., Spencer, Y.I., Chaplin, M.J., Stack, M.J. & Dawson, M. (1998). Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Veterinary Record 142, 103-106.

Wells, G.A.H., Hawkins, S.A.C., Green, R.B., Austin, A.R., Dexter, I., Spencer, Y.I., Chaplin, M.J., Stack, M.J. and Dawson, M. Vet. Rec. 142, 103 106 (1998)

Wilesmith, J.W. Bovine Spongiform Encephalopathy The BSE Dilemma: Recent Observations on the Epidemiology of Bovine Spongiform Encephalopathy (C.J.Gibbs/Springer-Verlag, New York, 1996)

Wilesmith, J.W., Ryan, J.B.M. & Atkinson, M.J. (1991). Bovine spongiform encephalopathy: epidemiological studies on the origin. Veterinary Record 128, 199-203.

Wilesmith, J.W., Wells, G.A.H., Cranwell, M.P. & Ryan, J.B.M. (1988). Bovine spongiform encephalopathy: epidemiological studies. Veterinary Record 123, 638-644.

Wotton SB, Gregory NG, Whittington PE, Parkman ID.
Could you find a larger report?

I'll have to look at it later. But I immediately note that tranmission studies continue to use homogenised brain tissue. This is not a practice found in food preparation, by the way.

Then it quotes the Wells study. I have it here, and I find it is extremely flawed, besides using homogenised brain. I one case they pooled mice-brain samples (1 was positive and 2 were originally negative). After pooling the samples, guess what, all were positive.

Wilesmith is quoted as well. His epidemiology is biased and selective. Too bad this is all they can throw out there as evidence. It is a shame that they refuse to acknowledge that if it isn't infectious, then something (metals - my opinion) in the tissue causes disease when injected into other animals; then isn't this poisoning; which by the way, would be dose dependent.

It is her opinion that prions are transmissible, not poisonous, in essence. Except, it isn't the protein that is causing new malformed proteins - it is the "energized" possibly radioactive, metal that the proteins have globbed onto, that is perpetuating the misfolding of more proteins. Certain metals would likely have the affinity to misfold different proteins, depending on their molecular charge. This could explain the various forms of TSEs. Or maybe, it is host/metal specific? AS in the Auburn University patent application, without the filtrate (metals - void of proteins) there can be no amplification of new prions.

It is a shame they couldn't find enough cattle/calves to do their test on. Yes, there is such a shortage of cattle in the world.

I'll read you posting more thoroughly later on. We have work to do and company coming for supper. We will be having roast beef.
SH, I learned that BSE has not been found in commercial pigs or chickens.

Kathy, This report is used by both the OIE and FAO as a determining document on risk of food safety. Heck, I don't know who's studies are flawed. Are everyone's but Purdey's flawed?
:roll: Baffle with Bull ****. Amazing how people are impressed by articles with length even though substance is lacking.

It could be simply said that this article along with thousands like it are based on supposition and not proven facts.

I would suspect that if Mark Purdey and others studying metal contamination had 1/1000th the budget of those following the OTHER THEORY, that questions could also be raised. However, the metal contamination theory moves ahead without money, without government approval, and without thousands of scientists hanging on to the theory of the day to keep their own family's in groceries with grant money etc.
rkaiser said:
:roll: Baffle with BS. Amazing how people are impressed by articles with length even though substance is lacking.

It could be simply said that this article along with thousands like it are based on supposition and not proven facts.

I would suspect that if Mark Purdey and others studying metal contamination had 1/1000th the budget of those following the OTHER THEORY, that questions could also be raised. However, the metal contamination theory moves ahead without money, without government approval, and without thousands of scientists hanging on to the theory of the day to keep their own family's in groceries with grant money etc.

I have a sneaking suspicion that if the prion theories of today's "sound" or "best available science" were reversed in position with Purdey's or the "Virino" theories there would be a whole lot of head shaking going on.
Have a good friend who believes that Purdey is right on the money with his ideas in origination of BSE and also believes the status quo in today's prion transmission evidence that perputuates the disease.
It is a shame that most professors are always having to apply for grants to keep their department functioning.
By the way, there are few proven facts in BSE, but Prusiner got there first.
:shock: I dismiss you blythely Reader(the second), and I don't even know what blythely means.

Show me some proof of transmission or infection, and I will eat my words blythely, or with passion and zeal.

Yours truely
I noted that the Well's transmission experiment used homogenate, it pooled samples and then stated that all these samples were positive (even though they independently tested 1 positive / 2 negative). I have read of this tactic used before, to discredit, work. In this case it is being used to validate work.

I am open to read the studies, as provided here. If you believe my mind is so closed, Reader, then why the h*** do you continue to debate the issue with me.

Show me a tranmission study that uses controls and does not include homogenised brain tissue. I will give it a look.

Even Terry Church's Alberta Agri. Research Institute's (flawed) paper, states that the "prion only theory" is the "umbrella most scientists are comfortable working under."

If there was nothing to fear from investigating the metals and uses of Organophosphates (at the UK levels applied, which were not the manufacturer's recommended levels, nor the levels used in America), then boat loads of money would be flowing to researchers to investigate this. Somebody must fear the outcome; the "prion only supporters" are scared to fund these other areas, even if it would help prove their "prion only" theory. I think they should buck-up or shut-up!

Do you have proof that metals are NOT involved, do you?

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