Select Committee on Environment, Food and Rural Affairs Written Evidence

Memorandum submitted by Dr Helen Fullerton



  Evidence suggests that trace element deficiencies induce a susceptibility to M.bovis, which can be corrected by restoring the nutrients to depleted soils, particularly in the hot spot areas that occur on soil types intrinsically deficient. Furthermore, inadequate trace element intakes are a risk factor for false negatives—cattle that do not respond to the TB skin test because their circulating lymphocytes are suppressed, a condition known as anergy. These are silent carriers, healthy in themselves, but whose undetectable infectivity could explain the persistence of the hot spots. Suppressive factors include zinc, selenium and cobalt deficiency. Adequate trace element intakes would lift the suppression and allow the silent carrier to be identified by the skin test.


  1.1  I propose that susceptibility to infection, and not exposure to it, is the critical factor that makes cattle, and also badgers, go down with TB. If the animals can be made resistant to infection, they will overcome the challenge of the M.bovis bacilli. Resistance is primarily undermined by trace element deficiencies and its loss is precipitated by stress: uncomfortable cubicles, lack of bedding, standing in slurried yards, bullying at the feeders, transport, markets etc.

  1.2  The animal immune system depends on optimum blood levels of five trace elements, zinc, selenium, cobalt, copper and iodine. In UK cattle these are likely to be deficient due to their relentless extraction from the soil by intensive cropping, with total disregard for the need to put them back. In addition, the "hot spots" in SW England where TB has resisted eradication, and the areas to which it is spreading due to cattle mobility, are located on rock types intrinsically low in trace elements: limestone/chalk, red sandstone and granite.

  1.3  There is abundant evidence that trace elements confer health protection on farm animals. Increasing their intake eliminates respiratory diseases, mastitis, foot infections, infertility and failure of calves to thrive. This has been the experience of Danny Goodwin-Jones, Trace Element Services, whose protocol for soil micro-nutrient restoration has rescued farmers up and down UK from problems that vets could not solve. There is also anecdotal evidence that trace element treated farms are free of TB, while their neighbours are going down with it.


  2.1  Under pressure from pharmaceutical interests, the role of trace elements is dismissed. This is very damaging, because the scientific basis for their activation of immune resistance is well established. Zinc and cobalt. Numerous enzymes depend on zinc for their function. Every cell requires it for cell division and differentiation, including the white blood cells of the immune system. Together with cobalt, zinc is needed by the rumen microflora for the synthesis of vitamin B12. Without adequate B12, the cow's liver cannot convert the acids produced by rumen bacteria into glucose for her metabolic and physical energy. Nor can she defend herself against intestinal parasites. Animals—and thus both cattle and badgers—are made susceptible to TB if they carry a parasite burden. Examination of TB-infected and uninfected badgers showed that only those harbouring parasites were TB-infected[1]

  2.2  Zinc and cobalt become unavailable at the raised pH of limestone/chalk soils, particularly where ancient grassland has been ploughed for arable and the limestone brought to the surface. Over-limed soils or those heavily dressed with nitrochalk are also at risk from Zn/Co unavailability.

  2.3  Selenium as an anti-oxidant and co-factor of the enzyme glutathione peroxidase, activates the "innate" immune system, the first stage in the battle against the pathogen. It also activates the second stage, the "cell-mediated immune response", by stimulating the proliferation of T-helper 1 (Th1) lymphocytes that fight intracellular pathogens such as the TB mycobacteria.

  2.4  Selenium is desperately low in virtually all UK soils, and as admitted by MAFF, its intake is half what it should be in the human population, due both to removal by cropping and to leaching by the sulphate in acid rain and ammonium sulphate fertilisers.

  2.5  Copper. One of its important roles is as an activator of the enzyme Cu, Zn-superoxide dismutase. A TB-challenged immune system produces nitric oxide for its defence, but if due to copper or zinc deficiency, the enzyme does not work properly, nitric oxide is produced in excess, giving rise to an uncontrolled release of its free radical derivatives. These induce an over reactive immune response that not only destroys the pathogen, but also host tissue, and is responsible for the lesions that devastate the lungs of TB-infected cows.

  2.6  Iodine as is well known, is essential to thyroid function.

  2.7  The thyroid plays a unique role in TB resistance, activating macrophages to mediate the innate immune response. This was researched over 50 years ago by Max Lurie, Professor of experimental pathology at the University of Pennsylvania. In those days there was extensive research into TB resistance, and Lurie discovered that intramuscular injections of the thyroid hormone T3 into rabbits prevented TB onset and could partially reverse an existing disease, whereas the induction of hypothyroidism accelerated the disease[2]However, Lurie's work was forgotten. Scientists lost interest in stimulating resistance with the advent of antibiotics. Now as we struggle with the consequences of their over-use, it should be remembered that all five elements are needed for a properly working thyroid, and here we have another pathway conferring resistance to TB.


  3.1  Soil trace elements are restored following soil analysis and stock health appraisal. Optimum levels for total selenium should be 0.8-1.2 ppm. Goodwin-Jones finds they are seldom more than 0.3, and frequently undetectable. Available zinc should be 12-15 ppm, and is often as low as 3.0. Available cobalt should be 1-3.0 ppm, copper 10-12 ppm and total iodine 6-8 ppm[3]The trace elements are mixed in the hopper with fertiliser or seaweed and spread evenly by the farmer. Soil restoration means the cattle take up the nutrients in their most available form. The widely used mineral licks, boluses and injections are only band-aids.

  3.2  It can be anticipated that badgers also will become TB-resistant through the raised trace element content in the worms and beetles of their diet.


  4.1  MAFF followed by Defra have long taken the stance that trace element deficiencies are irrelevant. They were supported in this view by the Independent Husbandry Panel (IHP). The IHP was set up to consider the husbandry factors that might influence TB susceptibility. Unfortunately their careful assessment relied heavily on the results of an epidemiological survey commissioned by the Dublin Veterinary College TB Investigation Unit. This covered 1,985 Irish herds and its object was to ascertain whether the blood levels of copper, selenium and iodine influenced the incidence of TB reactors. Zinc and cobalt levels, crucial to TB resistance were not monitored. The two researchers found no apparent correlation between Se, Cu and I blood levels and the tuberculin test results[4]

  4.2  However, when I scrutinised the data it was obvious that all the 1,985 herds were either deficient, low or marginal in selenium, thereby contributing to the TB breakdowns[5]This was not surprising since the incidence of TB in the Irish Republic is comparable to that of the SW England hot spots, and Irish soils are even more depleted in selenium than UK soils. What is inexplicable is the failure of the researchers to understand their own results, and the role of stress in an individual cow, triggering infection from susceptibility.

  4.3  The units and corresponding scales used by Irish vets (iu/g Hb), are different to those used in UK (iu/ml PCV). An unfamiliarity with the Irish units may explain why the IHP failed to spot the selenium deficiencies, and why they advised the Government that differences in TB resistance could only be genetic[6]giving Defra every excuse to dismiss the role of trace elements in immune protection. My letters to the IHP Chairman and to the two researchers went unanswered.


  5.1  Studies have shown it is difficult for an infected animal to transmit to others. In one trial when groups of two reactor steers were confined with one attested steer in 10 loose houses for 12 months, only four of the challenged animals were found at slaughter to be infected[7]The other six had presumably acquired immunity. Yet Defra deny that cattle can develop TB immunity. The Independent Scientific Group (ISG) did indeed raise the question, commenting: "it is unclear whether or not cattle can resolve infection with M.bovis, and if so, whether such animals are detected by TB testing procedures"[8]The answer may lie in the high level of false positives diagnosed by the TB skin test. Some 8-12% of UK reactors are shown at post mortem not to have been infected.[9] In the Anglesey outbreak September 2003, 20 reactors were diagnosed in a herd of 160 sucklers, of which five heifers and a bullock were confirmed, and 13 sucklers and a bull were false positives, unnecessarily slaughtered. The much-touted interferon- (IFN) test is at present unacceptable because it diagnoses even more false positives than the skin test

  5.2  False positives are mainly ascribed to environmental mycobacteria. Huge numbers of these inhabit soil, water, herbage and the digestive tracts of herbivores, and occasionally a species has been found to sensitise cattle to tuberculin. But I suggest that false positives are identifying animals that have mounted a cell mediated immune response, conferring an immunity which neither the skin test nor the IFN test can distinguish from infection.


  6.1  False negatives are cattle that do not respond to the skin test, but are identified by lung lesions as carriers of infections when they eventually come to be slaughtered. They are "silent carriers" who, although healthy themselves, can infect the susceptible or pass it on by maternal transmission. It is thought that about 10% of those tested are false negatives, but this is probably an underestimate. The cause of the non-responsiveness is a suppression of the circulating Th1 lymphocytes and hence of the inflammatory reaction at the injection site, a condition known as anergy. There is also a reduction in the interferon- which these cells produce, so that the IFN- test in this respect is no better than the skin test. Finally the defensive nitric oxide produced by macrophages is reduced. This means (a) that the TB bacillus persists, protected from nitric oxide's lethal free radical derivatives, and (b) since there is no immune over-reaction that destroys host tissue, the cow can live for years in good health, a long term and undetectable reservoir of infection.

  6.2  Suppressive agents giving rise to chronic—as opposed to temporary—anergy, include malnutrition, secondary infections, intestinal parasites, zinc deficiency, corticosteroids and stress[10]Recent research explains the suppressive role of zinc deficiency. Adequate levels of serum zinc activate a molecular cascade that propagates to the nucleus, stimulating DNA sequences specific for lymphocyte proliferation[11]Hence where zinc is deficient, the Th1 lymphocytes do not multiply to induce an immune reaction.

  6.3  MAFF have argued that silent carriers are a minute fraction of the cattle population as evidenced by the small number diagnosed at the abattoir. This assertion was disproved by McIlroy et al. who carefully dissected the lungs of reactors which had tested negative the year before and found that the lesions were often minute, and would have been missed in routine inspection[12]

  6.4  I propose that irrespective of any contribution by infected badgers, silent carriers are the prime cause for the persistence of the hot spots in SW England, as also in Ireland, and contribute to the spread to other areas. Since there are no badgers on Anglesey, is there a silent carrier, imported from the mainland? Although soils are nutrient deficient, the farmer's husbandry avoids stress. But note it was only the young stock, five heifers and a bullock that were confirmed positives. Was susceptibility triggered by stress eg at weaning?

  6.5  It is obviously urgent to remove the silent carriers. I suggest that if trace element deficiencies in the cattle are corrected, the suppressive effects of zinc and selenium deficiencies on lymphocyte proliferation, and of cobalt (B12) deficiency on parasite overload would be lifted and the silent carrier identified by the skin test. We should be warned that unless this is done, a reservoir of infection will persist in the old and in new hot spots, far more potent than any from the badger. Carriers eat from the same mangers, dropping saliva and mucous, breathe out aerosols in the same cubicle house air as their companions, putting at risk the susceptible. And despite the proposed mandatory pre- and post movement testing, the silent carrier will escape detection and carry the disease to other herds.


  7.1  Recently the Thornbury badger clearance has been quoted as irrefutable evidence for-badger to-cattle transmission. 1975-1981 badgers were totally cleared from 104 sq kilometres centred on Thornbury, Avon. Setts were gassed with hydrocyanic acid and recolonisation prevented by further gassing until 1981, after which it was allowed to proceed. The 104 herds in the area were thereafter free of TB until 1992. The decline of the disease, in step with badger clearance was studied by Clifton-Hadley et al.[13] from detailed records of reactor numbers, false positives and false negatives. The authors concluded that "eradication of tuberculous badgers resolves the cattle problem for at least 10 years."

  7.2  However neither the researchers nor those that quote the Thornbury experience as proof of badger culpability ask the question: what was happening to the cattle after 1975? There is no record how many were culled apart from the reactors. It was presumably not thought relevant. But we know that from the mid seventies, two factors operated to increase the severity of culling. First, farmers were buying in high yielding Holsteins, and getting rid of their long lived Friesians. Second, 1975 the EU expansion programme started, with large subsidies available for bulk tanks, new cubicle houses and money for Holstein replacements. Moreover the researchers ignored the fact, pointed out in the Dunnet Report[14]that there was a similar drop in TB reactor incidence throughout the rest of England and Wales where virtually no badger gassing took place. Defra's Consultation Document gives an updated version of the Dunnet Report graph, showing a steady decline of TB reactor incidence after Foot and Mouth 1987 when Holsteins were introduced, reaching an all time low in the mid seventies and rising swiftly after 1981. The graphs for the "rest of England and Wales" and for SW England fall and rise in parallel[15]

  7.3  When TB declines, no conclusions can be drawn from the effects of badger culling, unless the effects of cattle culling are also assessed. The reason for the overall decline could, I suggest, be attributed to the removal of silent carriers. Its present resurgence is due to their return, hastened by an accelerating soil depletion of trace elements, and aggravated by cattle mobility.

  7.4  MAFF/Defra failed to ask the critical question because for thirty years it was believed that cattle-to-cattle transmission was of minimal importance. This assumption was not challenged by the scientific establishment until the ISG took it up in their 2nd Report: "We consider the issue has not been adequately addressed in the past and may be of greater practical significance than has been appreciated". In 2003 the over-riding importance of cattle-to-cattle transmission was proved via spoligotesting (DNA tracing of reactor cattle to their place of origin) and the need to restrict cattle mobility was at last recognised by Defra[16]


  8.1  Government expenditure on bovine TB has risen to £71m/yr (15), and there are fears for the demise of cattle farming in the hot spot areas. Hopes are pinned on a vaccine, but current funding is said to be insufficient. How much is spent on research into trace element nutrition? nothing. Defra refuse to do trials, arguing that health protection measures must be based on "sound science." Their own scientific credentials are not reassuring. They denied the importance of cattle-to-cattle transmission and allowed TB to spread via unrestricted marketing and inadequate testing. They believed cattle could not acquire immunity and thus neglected research into resistance. They were ignorant of the silent carrier's role in hot spot persistence, and fixated on exposure and the badger. This is not the time for intransigence and a clinging to beliefs. Science depends on exploration and the testing of hypotheses.

  8.2  Treat the ground of say 50 herds in TB areas with trace elements, according to Goodwin-Jones' protocol. Leave the ground of 50 matched herds untreated. Monitor for 12 months, but anticipate an initial increase from unmasked silent carriers. Let policy be dictated by results.

Dr Helen Fullerton

Farming and Livestock Concern UK

May 2004

1   Gallagher J et al. Vet Rec 1998;142:719-714. Back

2   Lurie M B Resistance to Tuberculosis. Harvard Univ Press 1964 pp 265-301. Back

3   Goodwin-Jones D Trace Element Services. Farm Reports. Back

4   Fallon R I and Rogers P A M Tuberculosis Investigation Unit, University College, Dublin 1993. Back

5   Fullerton H Bovine Tuberculosis: A Nutritional Solution 2003. Back

6   Independent Husbandry Panel. MAFF Pubs 2000. Back

7   Costello E et al. Vet J 1998; 155:245-250. Back

8   Independent Scientific Group. 2nd Report MAFF Pubs 1999. Back

9   Monaghan M L et al. Vet Microbiol 1994; 40:111-124. Back

10   Lagrange P H and Hurtrel B in Mycobacterium Tuberculosis Eds. M Bendinelli and H Friedman. Plenum Press 1998 pp 171-193. Back

11   Hirshfinkel M et al. PNAS 2001; 98:11749-11754. Back

12   McIlroy SG et al. Vet Rec 1986; 118:718-721. Back

13   Clifton-Hadley R et al. Epidemiol Infect 1995; 114:179-193. Back

14   Dunnet G M et al. Badgers and Bovine Tuberculosis HMSO 1986. Back

15   Consultation Document Fig 2 p 16. Defra Feb 2004. Back

16   TB Forum Feb 2003. Back

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