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Ways to Protect ourselves and the animals in our care from BSE-like diseases

by Helen Fullerton(more info)

listed in environmental, originally published in issue 12 - May 1996

1. Types of Transmissible Spongiform Encephalopathies

Transmissible spongiform encephalopathic (TSE) diseases, sometimes loosely called prion diseases, include Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträusler syndrome and Kuru in humans, scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle and scrapie-like diseases found in some 20 cats and a number of captive wild animals, notably mink. Sheep scrapie is probably very ancient. First described in Britain in 1772, it is now distributed in Europe, Asia and America. It is a wasting disease with symptoms of nervousness, weakness and un-coordination, and like all TSE diseases, lesions are confined to the central nervous system (CNS), where microscopic examination shows a non-inflammatory degeneration of brain and spinal cord. Characteristic and always present are neuron death, proliferation of the supportive glial cells and a spongiform appearance that gives the disease its name. There are intracellular vacuoles, the deposition of fibrils and tubulo-filamentous particles and sometimes of plaques[1]. The most diagnostic feature however is now thought to be the presence of an abnormal form of the prion protein which can be identified by an immuno-staining test in which antibodies raised in antiserum recognise the aggregated deposits of the abnormal prion[2,3,4,5].

2. CJD

CJD is extremely rare, affecting about 1 per million or 30-40 cases a year in the UK and a similar order elsewhere. It may be of genetic, sporadic or acquired origin[2]. About 15% are inherited, due to mutations in the single gene that codes for prion protein, and needs both parents to carry the gene for its expression. 85% are sporadic cases of unknown aetiology. Kuru is an acquired CJD and was endemic in a tribe of New Guinea aboriginals. Ritualistic practices involving deceased relatives recycled what must have been a genetic carrier and the disease declined once the rituals were stopped. A number of acquired iatrogenic cases have arisen following peripheral inoculation with growth hormone or gonadotrophin and neurosurgical grafts of cornea or dura matter taken inadvertently from corpses infected with CJD; or from cross-contamination of surgical instruments[6].

The distribution, severity and character of the lesions differ between types of CJD, as do their clinical symptoms. Classical CJD is a rapidly progressing dementia with average onset 61 years[7]. Myoclonus (shock-like muscle contractions) is usually accompanied by un-coordination, withdrawal, depression, memory and sleep disturbance, producing a characteristic electroencephalogram (EEG), and with death in 3-6 months. However, there are other forms. A retrospective survey of the Corsellis collection brain bank revealed that out of 1,000 that died with dementia, 19 had the characteristic lesions of CJD, but 6 or 1/3 of these were non-typical cases, in that they had prolonged illness of 3-6 years, macroscopic cerebral atrophy, psychiatric disturbance, few recorded motor symptoms, and 2 of the 3 available EEGs were normal. These had been diagnosed as Alzeimers or some other dementia[3]. Bruton remarks that “our understanding of CJD may be less robust than we originally thought and could represent an unidentified source of future iatrogenic infection (ie, via donor transplants) particularly in view of a massive national decline in hospital post-mortem examinations needed to confirm clinical diagnosis”[8], reflecting expenditure cuts in recent years both in the NHS and in basic research.

Kuru-CJD is a third type, characterised by much cerebellar damage and histopathological plaques. A fourth has now emerged in the 10 new cases that have rung the alarm bells by suggesting a possible link with BSE. These were a young age group (eldest 39, youngest 16) diagnosed since 1994. All had psychiatric disturbance and their illness lasted longer than usual, 1 to 2 years. None had the EEGs, characteristic of CJD and none would have been diagnosed as CJD on clinical grounds, but microscopically all had the spongiform lesions and immuno-reaction. Most worrying was the extensive distribution of Kuru-type plaques that are almost never found in younger patients, except in those who had growth hormone and were otherwise neuropathologically different[9].

The emergence of a new type of CJD, and studies of the lesion profile of BSE transmitted to mice suggested that many of the newly recognised animal prion diseases in cats and captive animals resulted from the transmission of BSE, rather than of scrapie. Although none of them were farmers or abattoir workers who might be thought more at risk; and although four dairy farmers whose death from CJD had raised earlier concern, but shown only the clinical and histopathological symptoms of sporadic CJD, nevertheless researchers worked on the basis of it being a new variant, the possibility that BSE might be transmitted to humans was no longer “remote”. There was no direct evidence of a link, but the most plausible interpretation was that BSE might have been transmitted before the Specified Offal Ban in November 1989 prohibited incorporation of nervous and lymphatic offal from cattle more than 6 months old into burgers, sausages and pies. It was extended to include calves and others under 6 months in November 1994.

3. BSE

The first case appeared in 1985 and was identified as BSE with the diagnosis of 10 cases in 1986. Scientists at the Central Veterinary Laboratory hypothesised it was introduced by the feeding of scrapie-infected sheep offal to cattle, together with a relaxation in the early 1980s of regulations governing the heat treatment of such “meat and bonemeal” in the rendering process. It was thought that the lower temperatures and the abandonment of fat extraction with organic solvents meant the scrapie agent was no longer destroyed[10]. Unknown to farmers, the offal from slaughtered animals was incorporated into cattle cake by the feed companies as a cheap source of protein to boost milk production and calf growth rates. Attempts by farmers to find out what went into the 16% or 18% “protein” labelled on the bag was thwarted by the Government who thought it more important that the feed companies’ right to commercial secrecy was protected.

In July 1988 the feeding of ruminant protein to ruminants was banned, although it was still fed to pigs and chickens right up to the end of March 1996, when all mammalian meat and bonemeal was prohibited as feed for farm animals. Even now, chicken bone, meat and droppings can continue to be incorporated in cattle feed, and the feed companies, represented by UKASTA, persist in their refusal to declare the contents[11]. More and more of the smaller companies, however, practice “open declaration”.

It was confidently predicted that with the ban the disease would peak at about 2,000 cases and then decline. It did not happen. Reported cases soared to 44,846 in 1992 and then slowly fell to about 7,000 in 1995. 59.2% of dairy herds have had at least one case, and 15.2% of beef herds one case, mostly of suckler cows bought in from the dairy herd. “Closed” beef herds of our national breeds, and organic herds have been virtually free. Most puzzling have been the 35,000 suspected cases “born after the ban” (BABs) in 1988 and contracting BSE at 2-5 years, when they would supposedly have never been fed the contaminated feed[12]. Either there was maternal transmission, a possibility under investigation in a 7-year trial, or as thought more likely, contaminated feed was still being given to cattle and calves via cross-contamination at feedmills and the using up of old stocks by the unscrupulous. The last BAB was in 1993.

BSE is expressed in changed behaviour: extreme nervousness, hyperesthesia (increased sensitivity to touch and noise) and aggression; with tremor, un-coordination and sometimes culminating in convulsions. Or there may be only a generalised paresis, with failure to rise. The clinical condition may last from 2 weeks to 6 months, but the incubation time is unknown. Early symptoms may be confused with hypomagnesaemia, nervous ketosis, viral or bacterial meningo-encephalitis, lead poisoning and “downer-cow” syndrome[5]. All diagnoses thus require brain autopsies to confirm. The correlation between suspected and confirmed cases turns out to be 88%. A number of the younger cattle did not have lesions, but only an immuno-positive reaction to the abnormal prion[5].

4. The prion protein

The normal prion is a glycoprotein, designated PrPc (c=cell) occurring in lowly as well as mammalian species, and genetically expressed in a range of tissues[13]. It is primarily located on the surface of neural membranes of cells in the lympho-reticular system, notably the dendritic cells of the spleen. It is also on the membranes of lymphocytes. Its function is unknown and may differ between cell types. Recent evidence indicates that it plays a part in cell signalling and synaptic transmission, and in particular in the activity of aminobutyric acid (GABA), a major inhibitory transmitter of the CNS[14]. The aberrant prion, designated PrPsc (sc=scrapie) is a mis-folded version where the helical conformation is partially replaced by ß-sheets, induced either by mutation or a chemical interference in the cell’s environment. It is “protease resistant”, ie it is not degraded in the lab by a range of enzymes that destroy the normal form. Its half-life is thought to be between 3 and 30 times longer, thus it accumulates during metabolic turnover and inhibits the synthesis of normal prion[1]. This presents two problems: a) a loss of PrPc function and b) a toxic choking of the nerve axon transport pathways. If the neural inhibitory system which is largely mediated by GABA is under-functioning there is over-stimulation of neural activity, giving rise to the motor disturbance and excessive sensory transmission that produce the muscular and nervous symptoms. If there is choking of axon tracts, this induces disruption of the cytoskeleton neurofilaments responsible for transport to the synapse, and is followed by neuron death[15], which it can be speculated, gives rise to the wasting in sheep and cattle, accompanied in humans by the dementia of CJD.

There are two schools of thought as to how PrPsc is infective, ie replicates itself, in neural tissue. (i) That the malformed protein acts as a template inducing a conformational change in the normal protein[16]. (ii) That an informational molecule, ie a virino or viral fragment must be associated with the protein in order to account for the post-translational strains or phenotypes of scrapie[17]. Narang[18] has identified it as a piece of DNA sandwiched between a prion core and protein coat in the tubulo-filament deposits; in which case it is this which induces the prion to change to its toxic, infective shape.

5. Transmission

Scrapie’s transmission in sheep has both a hereditary and what appears to be a slow infectious component[4]. Sheep uninfected with scrapie can be infected if put on pasture that has carried infected sheep. The mystery may have been solved by the discovery of a pasture mite carrying PrPsc[19]. It is not clear whether it infects via oral digestion or skin parasitism. But the mite must be an intermediate host, or even the long-sought causal host of scrapie.

Twenty strains of scrapie have been identified, all of which can be transmitted to a range of species by massive inoculation or ingestion in experimental animals, but they show the “species barrier” by the slowness with which they infect. The one strain of BSE is more virulent. Many researchers now believe that BSE was induced either by mutation and selection of a scrapie strain in serial/passage through cattle, or accumulated from a low level incidence in cattle – scrapie was noted in ox in 1912. In either case, it was built to epidemic proportions by the cannibalistic recycling of cattle remains to cattle.

Crossing of the species barrier has been investigated in experimental animals by injecting their brains or peritoneal cavity with infective homogenated material, or by feeding high concentrations of infected meat and bonemeal. Transgenic mice mutated to express normal human prion are similarly being challenged in lengthy trials to see if BSE can be passed to humans. So far it appears it is not[20].

6. Predisposing factors

Such routes of transmission are unrealistic and, in my view, involve unacceptable animal experiments. One object should surely be to discover what makes a few of us, animal or human, susceptible while most of us appear resistant? What are the broken defences in the digestive, immune and neurophagocytic systems that allow the toxic prion to pass unrecognised or unchallenged from the gut to the central nervous system? And once there, what potentiating factors enhance its toxicity and power to disorganise the neural circuitry?

Let us start with scrapie. Why has scrapie, aside from the genetic susceptibility of some breeds, been endemic in sheep for centuries, while cattle and wild ruminants have escaped?

An outstanding characteristic of sheep is that they are extremely sensitive to cobalt deficiency. Cattle are far less so, and horses can thrive on very little. Cobalt is necessary for the synthesis of B12. Evidence suggests that the critical importance of cobalt to sheep might be that they are totally dependent on the B12 pathway to recycle their methione for the synthesis of S-adenosyl methionine (SAM), while cattle most probably and horses certainly can use another pathway20. Among its many functions SAM is essential for the mythylating detoxification of metabolites, self or foreign, and adequate B12 probably for that very reason, protects against worms, mites and other parasites. Since a mite is now known to carry PrPsc, it can be postulated it is cobalt deficiency that makes sheep as a species susceptible to scrapie, while the reduced dependence of cattle on cobalt gives them their resistance.

Consider next the immunological barriers in the oral route to infection. It is known that PrPsc is taken up by the lymphoreticular system probably via the Peyer’s patches of lymphoid follicles in the mucosa of the small intestine[21], which in turn are accessed by an epithelial layer of antigen transporting M cells. The PrPsc is diverted to the dendritic cells of the spleen where it is detectable long before its detection in the CNS, but without showing lesions of any kind. From these it is thought to migrate, on the poliomyelitis model, by visceral autonomic fibres of the splanchic system to the CNS. The dendritic cells have antigen-presenting properties, but paradoxically, mutant mice deprived of their dendritic cells and inoculated intraperitoneally with scrapie tissue did not develop the disease in one case[22] or only 33% of them did so in another[23]. This indicates that the dendritic cells are a major gateway for oral transmission. Secondary pathways via fibres in the peritoneal walls might account for the partial infectivity.

It might be thought that the job of the dendritic cells was to differentiate acceptable metabolites from the unacceptable. The fact that they harbour and give safe passage to PrPsc suggests to me that these antigen-presenting cells are recognising PrPsc as “self”, and perhaps are part of the mechanism known as “oral tolerance”. Oral tolerance is the rationale behind a novel therapy for autoimmune diseases whereby proteins that lymphocytes have come to recognise as foreign – collagen in rheumatoid arthritis, or myelin sheath protein in MS – when presented as food are protected from attack by activation of suppressive lymphocytes and/or suppressive cell populations that curb the aggressive immune cells[24]. Suppressor cells are found in Peyer’s patches and in spleen after oral administration of antigens, while gut epithelial cells can prevent antigens to certain intestinal epithelial lymphocytes that mediate immune suppression.

Hence it can be postulated: 1) that the infective agents, whether self-replicating prion or its inductive virus, switch on the immuno-suppressive machinery and thereby smuggle its way to the CNS. 2) If the suppressive cells are inactivated, less discerning immune agents are called upon, and recognising PrPsc as foreign, signal the splenic macrophages to destroy it. 3) But it is only the sheer unrealistic quantity of administered infective material that allows the suppressive cells to override the normal immune response, and that most lymphatic systems when presented with minuscule amounts of infective prion can phagocytose it safely. 4) Those that cannot are likely to belong to animals either with depressed immune systems through stress or co-infection and/or through trace element deficiencies, particularly of selenium and zinc, both of which are essential to immune function. Zinc is depleted in blood plasma and from cell membranes during stress[25]. Selenium is inadequate in the diet of our cattle unless their pastures have had it restored, or they have received selenium as injections or drenches. In the UK, human intake of selenium is below the lower reference nutrient intake (LRNI) limit[26]. Hence selenium deficiency depresses both our human and animal immune systems. I have postulated elsewhere[27] that selenium is essential to the macrophage. Should this turn out to be correct, the phagocytic destruction and clearance of PrPsc is compromised. Finally, epidemiological surveys demonstrate that selenium deficiency is a contributory factor in all our neurodegenerative diseases[28].

Other key questions regarding failed defences against PrPsc are summarised by Collee[21], who asks: (i) Whether factors influencing gut permeability are important? We already know that in humans gut leakage is a widespread problem. (ii) Whether local mucosal immunity merits more study? In this regard, the ages of many of the BSE sufferers have been 2-6 years. It suggests that BSE was probably acquired in calf-hood, especially by the early weaners, who would almost certainly have been supplied with contaminated calf cake, predictably before their immune systems were properly developed to cope.

7. A chemical predisposing factor

It has been generally hypothesised that the virulence of the BSE outbreak has been solely due to the recycling and accumulating of PrPsc in cattle brains. Given that the complexity of degenerative diseases suggests that they are probably multi-factorial; given the swiftness with which the epidemic attacked the national dairy herd, and the soaring figures, albeit of sporadic cases in each one; and given the ferocity of the symptoms, earning it the title of “mad cow disease”, is it likely there was also some predisposing factor which either triggered and/or exacerbated the pathological lesions and symptoms they produce?

Mark Purdey has put forward a theory[29] that it was the compulsory treatment of cattle with high doses of an organophosphate(OP) warblecide particularly in the mid 1980s which correlates with the timing, symptoms and histopathology of BSE. The treatment was to pour an OP preparation along the backs of the cattle once or twice a year to kill the embedded larvae of the hated warble fly. Purdey proposed that in some cases it penetrated to the CNS causing progressive chronic CP poisoning or mutagenic damage to the cow’s unborn calf, thus accounting for the surge of cases 1990-1994, and the high incidence of BSE in those “born after the ban”. In addition cattle have been subjected to low but prolonged exposure to OPs as insecticidal sprays and powders, and to their ingestion via the treatment of stored grain, citrus pulp and other components of their feed, all of which is a heavy load for an animal’s detoxification systems. He cites as evidence that BSE has occurred in animals that were never fed the contaminated feed; and that the symptoms of chronic and acute OP poisoning which have been observed in cattle, sheep and humans (un-coordinating tremors, anxiety, aggression, weight loss) are identical to those of BSE, while OP toxicity is similarly expressed as intra-axonal vacuals in many grey matter regions of the brain stem, and with the same spongiosis and astroglial proliferation[30,31].

Purdey’s hypothesis is twofold: (i) That the OP activity induced conversion of PrPc into PrPsc, either by direct binding to the prion, or via interference with a chaperone protein that ensured correct folding, or by misdirecting RNA transcription. In addition, OPs are known to inhibit the degradative function of lysosomes and proteases[32]. “Recycling of PrPsc in the contaminated feed would follow, as would transmission to the calf via the placenta.” MAFF, DoE and the Medical Research Laboratory dismissed the theory on the grounds there was no evidence of OP binding to prions, and did not consider other mechanisms[33]. (ii) That the OP acting as an anticholinesterase precipitated a train of neural malfunctions culminating in excessive intra-cellular calcium accumulation. The primary toxic effect of an anticholinesterase is to overstimulate acetylcholine activity as motor, autonomic and CNS nerve synapses. Chronic GABA, depletion of serotonin and desensitisation of acetylcholine receptors[34]. The last two present a complex picture since they might be exculpatory or inhibitory at different receptors, and thus initiate different pathways in each individual, but GABA is uniformly inhibitory.

Is it not possible that their combined effects exacerbated and precipitated the motor and sensory symptoms of BSE? In those cattle that proved susceptible, could the body’s versatile defences nevertheless have compensated for PrPsc suppression of GABA’s inhibition, if they had not also been compromised by toxic OP? Could they have cleared the PrPsc from the spleen, if the OP had not stressed the animal and suppressed its immune system? Could the lysosome enzymes have degraded the PrPsc more rapidly in the neuronal cytoplasm, had they been free of OP interference?

Purdey found a temporary remission of all symptoms in response to subcutaneous administration of magnesium sulphate. A boosted intake of Mg2+ would have promoted inhibition of cell membrane over-excitation in the peripheries and in the NMDA neurons of the CNS[35]. It should be added that adequate zinc is also required to inhibit NMDA-induced over-excitation[36] and to stimulate the Ca-efflux pumps that remove intracellular excess Ca2+ and allow relaxation. In my experience, zinc administration cures hyperesthesia in cows and the excessive nerviness of sheep responds to zinc and cobalt.

Unfortunately there is no commercial reward for funding research into trace elements and the privatisation of our publicly-owned research laboratories will ensure it continues to be ignored. This despite that open-minded clinical, epidemiological and in vitro research is urgently needed to discover the defence mechanisms against BSE, and find out whether and if so how far it is induced not only by an unforgivable cannibalism imposed on a vegetarian ruminant, but in combination with the needless use of a discredited pesticide, and correctable deficiencies.

8. The new variant of CJD

The 10 new cases of CJD differ from that of the previous sporadic cases in their age of onset, clinical course and histopathology, giving rise to the worrying possibility that PrPsc-contaminated offal incorporated into processed meat prior to the November 1989 ban, had escaped elimination in the digestive process or immuno-destruction in the lymphatic system, and had crossed the species barrier to invade the CNS.

The first thing we notice in the Lancet paper36 is that neither the symptomology nor the neuropathology are characteristic of BSE. Four had dysesthesia (impairment of any sense, especially touch) in contrast to the hyperesthesia typical of the cows. One had persistent pain in her feet. Three had choreoathetosis, not usually given as a distinctive symptom of CJD. But its most striking and consistent abnormality in all cases was that of plaques, extensively distributed in the cerebrum and cerebellum. They resembled Kuru plaques, not seen in 175 cases of sporadic CJD, noted and described in a 1979 Paper on scrapie as “florid” plaques[37], but not seen to my knowledge in BSE. Their presence indicates that an extensive PrPsc choking of the axonal transport tracts must have excessively disrupted the cytoskeleton filaments[15].

Is it possible we are here seeing a different chemical trigger to that postulated for BSE, a trigger common to all 10 patients, potentiating and hastening the infecting of PrPsc? This hypothesis does not tell us the source of the abnormal prion: whether it is from offal-derived BSE, or whether it is an accelerated sporadic CJD that was not due to be manifested for another 40 or 50 years. It does suggest, however, that such cases may be fewer than have been feared. If the hypothesis is correct, it would be urgent to identify the common trigger.

9. The need for a test

As I write thousands of healthy cattle reared traditionally on grass or in organic systems, in herds that never had BSE, are threatened with slaughter and incineration because they are in the category “over 30 months old”. Beef and dairy herds built up over the years could be decimated if the EU gets its way, with farmers facing financial ruin and the loss of cows to whom they have given years of work, care and often devotion. Only a test at the abattoir or better still a live test will establish the facts and restore public confidence. Random tests at abattoirs were recommended by the Tyrrell Committee in 1989, and called for by Labour Spokesman Ron Davis in May 1989[38], together with other essential measures belatedly introduced by the Government as each new crisis or revelation overtook them. An abattoir test has been available for 2 years from the Macclesfield firm Proteus Molecular Design, and is still resisted by MAFF. A live and an abattoir test have been offered for development by Narang and repeatedly rejected. The Government remains deaf to the now insistent demands for a test, since they would clearly be culpable of the whole catastrophe by refusing one all along.

10. What should we resolve?

Perhaps out of this tragic shambles will come a catalyst for change. Farmers know the public are their customers and even the technocrats among them will not now be easily lured into forcing up production with hormones and genetically engineered animals and plants, under pressure from chemical companies seeking an expanding market. Consumers want animals reared in welfare-friendly conditions and food that it safe for them to eat. The BSE crisis shall teach us what a Pandora’s box is opened if we try to manipulate nature instead of learning from her. The farm-assured schemes, the move into organic farming and traditional grass rearing which were slowly gaining ground are likely to accelerate. Producers must respond to consumers and replace live export with home rearing and a meat trade, and the intensive systems of agribusiness with free ranging pigs and poultry. Perhaps then we could make Britain a market to be preferred and emulated for its unpolluted food, contented animals and abundant countryside.


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About Helen Fullerton

Helen Fullerton BSc. MSc. PhD campaigns on nutritional, animal welfare issues and others such as organo-phosphate poisoning, challenging flawed and corrupted science. She Learned homeopathy and the importance of trace element nutrition from my dairy cows, calves and sucklers. She urges unresponsive bodies such as MAFF (Defra) that our farm animals could resist TB and other diseases if trace elements were restored to our depleted soils. Her academic qualifications include a BSc in chemistry, PhD in agricultural chemistry. She has lectured on Soil Science at Glasgow University for 12 years. She can be reached on Tel: 01269 831 752;

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