Tuberculosis Alert

TUBERCULOSIS ALERT - by Mark Purdey
Dispatches from behind the iron curtain of a British "biohazard" zone.

European livestock farmers dread the day when their cattle succumb to a tuberculosis breakdown. The implications are severe; a ruthless cull of infected cattle and badgers, with all remaining healthy cattle impounded behind an iron curtain of government mandated movement restrictions and red tape. The knock on effects have virtually paralysed small farming businesses into a state of financial melt down.

But the official procedures of TB control are archaic and outmoded. They are founded upon the age old hypothesis that humans develop TB as a sole result of exposure to TB infected animals, whilst failing to accommodate the more recent front line revelations in the multifactorial science surrounding mycobacterial disease. In this respect, we need to be questioning whether such cruel and costly strategies that are currently involved in TB control programmes are actually fulfilling their desired effect - to protect the human population against the TB agent.

Earlier this summer, I was forced to come to terms with my own cattle joining the ever increasing ranks of TB infected herds that are currently blighting the UK.

TB Breakdown; a testing time.

At dawnbreak, I scaled the hill to collect the cattle from the furthest fields. The earth still held the heat of the previous day, and I was forced to coerce the cows a little, for they seemed more reluctant to rise and amble the few feet to the green lane than usual. Perhaps the cows were more perceptive than me; their sixth sense receptive to the fate that was about to befall them in a few hours time

As we hit the steeper gradients of the shillet track, the cattle accelerated a little, rutting up the dust with their hooves. The tail swish of a cow disturbed an early morning bee, that droned off beyond the bank of bluebells and into the obscurity of the dazzling sun. Gradually, the entire caravan of cattle had snaked its way down the track to the valley bottom below. On the last stretch to the farm, a patch of giant foxgloves towered over us like a myriad of mauve lanterns on stalks, their luminescence still resonating the brilliance of first light. But I failed to heed their red alert, and just drove the cows on without a second thought.

Back at the yard, the vet was ready and waiting; so we lead the cows straight down to the inspection pens. The procedure was simple - to measure the size of any lumps that had erupted on the cows' necks which served as a yardstick for gauging the extent of allergic response to the TB skin test - an intradermal injection of tubercle bacillus that had been administered by the vet three days earlier.

Hardly a few minutes passed , when I saw the vet stand back abruptly. "Oh" he said in a despondent, drawn out tone, popping on his spectacles slightly askew. "We could have a problem here, Mark". I watched him fumbling through his pockets for the callipers, and now knew that he had to take a more precise measurement of what obviously looked like a colossal reaction lump on the cow's neck. I became anxious, and my mouth was beginning to parch up in anticipation of what was coming next.

The air seemed to hang heavy, much like the prolonged period of suspense before an encroaching thunderstorm. Even the robins who had been busy in the yard a minute earlier rustling up the brittle leafs, seemed to have stopped dead in their tracks for the duration of that eternal moment. The vet raised his glasses and wiped the sweat off his forehead. "You have a reactor, I'm afraid Mark".

A few minutes later there was another reactor, and then a bit later several more. My mouth parched up completely and my stomach nauseated as if twisted. I became angry at the thought of these fine young pedigree animals just entering high summertime in their prime, now doomed for slaughter under the government's animal health diktat.

Furthermore, like many other cattle farmers in the UK, I was confused by the perfect condition of the TB reactor cows, since I had always assumed that TB was a debilitating disease. Although these cows had reacted to the skin test and were therefore deemed to carry TB, I began to wonder whether they had successfully adapted to the infection by knocking out the greater majority of the invasive mycobacteria. In this respect, The TB slaughter programme could actually be annihilating the resistant animals - culling the genetically robust individuals that we really needed to be keeping as breeding stock for future generations.

Badgering the true evidence.

The next stage of the so called 'crisis' procedure was to retire to the farmhouse for a tree's worth of form filling, where I was presented with several sheets of TB questionnaire. I was amazed by the reductionist contents of the questions that followed, where each one had been designed upon the hypothetical assumption that the transmission of the TB agent from infected badgers to cattle was the sole cause of bovine TB. In this respect, baddie the badger had been daubed as the guilty culprit before the necessary detective work had even begun. The exact same 'back to front' investigation was applicable to the questionnaire which the government presented to farms that had experienced a case of mad cow disease; where every question was based upon the mindset assumption of a meat and bone meal feed cause - despite the diversity of evidence which indicated that this theory was totally flawed.

The search for susceptibility factors - the seeds of TB?

But the real question that was revolving around my brain at that time had focused on the fact that my farm had always boasted a TB-free status, despite being surrounded by TB affected cattle / badgers for many years. I began to wonder what changes had been integrated into our farming practises over recent years; changes that could be responsible for switching on the susceptibility of our cattle to the TB agent ? I felt that this was the relevant question that I should be asking right now.

Afterall TB is virtually endemic in the soils, waters and atmospheres of the majority of ecosystems, where mycobacteria have co-existed hand in hand with mammalian life for centuries. Despite their widespread prevalence, the TB agent has produced relatively few major outbreaks across the world. It seems that an epidemic of clinical TB can only erupt once some anti-TB component of our immune defence has been disrupted. In this respect, the primary event is a disruption of immunity which enables the TB agent to breach the body's defences and opportunistically take a hold.

A historical study of the epidemiology of TB demonstrates that epidemics of TB have occurred since the iron age, and that this disease has always been rife amongst specific population groups who are nutritionally impoverished in some way. For example, TB was rife amongst city slum dwellers who had no choice but to breath the industrially polluted air 24 hours a day, as well as the half starved Scottish / Irish crofters who were evicted and forced onto boats bound for North America. Another more recent example involves AIDS victims whose immune systems are so severely compromised that they invariably develop TB as a secondary complication.

A Limey's view of TB cause.

So what is the key factor that has suddenly unleashed TB susceptibility amongst my cattle following so many years of TB-free status ? After much thought about the specific changes that I had integrated into my farming system over recent years, I began to wonder whether the TB breakdown in my herd could be connected to the drastic cost-cutting measures which I have been forced to adopt in order to survive the current agri-economic crisis.

Along with most other hard pressed livestock farmers across the UK, we had foolishly cut back on the use of the so called 'non essential' lime / calcified seaweed based fertilisers. Furthermore, the trend in reduced usage of lime based fertilisers has been exacerbated by recent conservation measures that have debarred the harvesting of Cornish calcified seaweed altogether - thereby preventing future usage of this material on the farm.

It is the general reduction in use of lime fertilisers, combined with the recent increases in winter rainfall across the western UK, that has acidified the top soil as a result; whilst other eco-influences such as acid rain and the continued use of so called 'essential' artificial fertilisers will undoubtably be playing their contributory roles in the acidification of Agricultural ecosystems.

The pH alkaline/acidic value of the soils on our farm has dropped from an acceptable neutral pH 6 to an acidic pH 5 over the last three years - evidenced by the invasion of buttercups into our pastures where clover used to flourish.

Research has shown that there is a correlation between areas of high mycobacteria incidence and regions where the soils are acid. This association is strengthened by the results of studies where lime was spread on farms in Michigan that were suffering from high rates of mycobacterium infection ( albeit the paratuberculosis strain of mycobacterium ). The study concluded that the lime treatment had produced a ten fold reduction in the infection of cattle after a three year period had passed. [ Johnson-Ifearulundu and Kaneene 1997 ].

Branding the Iron on TB cause.

The relevant issue in respect of TB infection and soil acidity hinges on the fact that acidification of the topsoil leads to an excessive accumulation of available iron [ Pais and Benton Jones 1997] - particularly in the regions where soil iron is naturally elevated and rainfall is high. The iron is taken up by the pasture herbage ( especially ryegrass, plantain [ McDonald and others 1973 ], bluebell tubers, etc) as well as percolating into the local water supplies as a result; which, in turn, is taken up by any animals who thrive upon the local iron rich ecosystem - particularly those individuals who are genetically predisposed to an increased uptake/retention of iron within their biosystems.

Interestingly, the key hotspot zones of bovine TB across the UK are the Forest of Dean, Exmoor, Cornwall, Devon and the Mendip hills. These regions all correlate with the areas where iron has been mined in abundance [ Flett 1935 ] and rainfall is high.

Preliminary pasture sampling from the specific fields on my own farm ( June 2005) where the TB reactors had been pastured has consistently demonstrated an excessive elevation of iron ( average 378 mg/kg), in relation to the levels of 143 mg/kg recorded three years previously. This research is being expanded to cover TB-free and TB farms across the key TB cluster areas of the UK .

What is the relationship between elevated iron and increased susceptibility to TB?

Much research is published in the scientific literature which demonstrates that Iron represents an essential prerequisite in the pathogenesis of TB , enabling TB and other strains of mycobacterium to proliferate, metabolise and survive within the mammalian biosystem [ Ratledge 2004 ]. In this respect, it is the supply of 'free' iron within the host which provides the TB agent with its 'fire power' capacity to unleash its deleterious pathogenicity; thereby invoking the often fatal, devastating consequences that result from TB infection.

Although TB victims adapt to their parasitic attacks by stashing away their iron supplies in tissues that are inaccessible to the mycobacteria, the grand finale of the TB disease process usually culminates in the parasite getting the upper hand; whereby the host develops the classic iron deficient anaemic state that is a central clinical feature of TB.

Mycobacteria acquire their iron from the host's own transferrin / ferritin molecules - the iron binding transport / storage proteins that are integral to the healthy metabolism of iron within the mammalian biosystem. The mycobacteria rob their host's iron by releasing a type of iron-capturing siderophore called an exochelin; which, in turn, transfers and donates the iron back to the mycobactins which exist in the cell walls of the mycobacteria themselves [ Gobin and Horwitz1996 ].

This hijaking of the host's iron supply is beneficial for the survival of the TB mycobacteria in more ways than one. Not only does the TB agent utilise the host's iron for its own proliferation and survival, but it also utilises this metal to indemnify its own long term security within the host; by disabling the host's immune defence against itself. The parasite achieves this means of self protection by curtailing the viable synthesis of the iron binding beta-2-microglobulin molecules whose role is to activate the killer T lymphocytes [ Schaible and others 2002 ] - the host's main line of immune defence against mycobacteria infection.

This could explain why individual humans whose T immune systems have become compromised through nutritional deprivation or AIDS toxicity are at a significantly greater risk of developing TB as a secondary complication.

But TB is not the only pathogen that depends upon the host's iron for its maintenance and growth within the body. The infamous Clostridium Botulinum ( implicated in grass sickness of horses ), Leprosy, HIV, Candida , Listeria, Salmonella, Malaria etc, are all members of this insidious family of ironmonger pathogens to which TB belongs [Weinberg 1999]

Only last week, champion horsebreeder Gail Dunsbee had been in touch with me over the sudden death of one of her horses as a result of grass sickness - a devastating paralysis of the autonomic nerve endings in the horse's gut due to infection with clostridium botulinum. But much like TB, Botulinum is virtually endemic in the gastro tract of horses where it rarely produces any adverse health effects at all. So what environmental factor had suddenly switched on the susceptibility of her horse's gut to the infection ?

Dissatisfied with the professional ignorance surrounding the root causes of grass sickness, Gail had taken matters into her own hands in order to safeguard the future of her surviving horses. And once again, it looks like the results of her preliminary soil analyses have provided the causal clues that might address this catastrophic problem for horse breeders.

Apart from the low potassium readings, the extremely excessive readings for Iron ( at 1344 ppm ) was the only other element of the twelve elements tested which had deviated from its respective reference range. This result could explain why grass sickness, like TB, has invariably remained confined to acid soil districts where iron levels are generally elevated.

Ironing out the TB pathogen.

Since elevated iron increases TB risk , it is easy to understand how the management of dietary iron can influence the outcome of TB [ Ratledge 2004, Cronje and Bornman 2005 ]. For example. when TB infected mice were treated with the iron chelating lactoferrin protein ( a natural ingredient of colostrum milk ) , there was a one hundred fold reduction in the number of pathogens present in the mice. [ Schaible and others 2002 ].

Likewise, TB diseased individuals used to be regularly treated with the iron-chelating compound p-aminosalicylate with some success [ Ratledge 2004 ]. In this respect, it could prove beneficial from a preventative as well as a curative perspective to introduce copper or zinc bicarbonate supplements into the diet of TB affected populations [ Pais and Benton Jones 1997 ]. Whilst these anionic compounds do not act as iron chelators as such, they will impair the absorption of iron across the gastrotract by competing for its uptake system of transport proteins. Furthermore, any foodstuffs containing phytic acids, such as legumes ( alfalfa, clover, etc ) and grains [ McDonald and others 1973 ] will produce the same anti-iron effects.

Use of inorganic phosphorus as an inclusion in fertilisers or mineral feed supplements would also assist in reducing the amount of free iron that is rendered 'available' in the soil or taken up into the animal respectively [ Underwood 1977 ]. The phosphorus competes for the iron binding site on the transport proteins that normally convey iron across the gut wall; thereby arresting the uptake of iron at its initial point of entry into the body.

It is also important to consider the knock-out effects that iron chelators might impact upon the horror chamber of other pathogens which need to bite the iron bullet before they can trigger disease. For instance, it has already been demonstrated that the iron chelating compounds, deferoxamine and 8-hydroxyquinoline-5-sulfonic acid have produced beneficial effects in the treatment of leprosy and clostridium botulinum respectively .[Weinberg 1999][ Bhattacharyya and Sugiyama 1989]

Iron in the Ecosystem.

It is proposed that badgers and cattle that co-exist within the same environments will both develop TB due to their separate co-exposure to the same iron-rich foodchain, and not necessarily due to a cross-infection from one animal to the other.

Bluebell and other iron-rich tubers constitute a large part of the badger's diet and these will gradually load up the badger's biosystem with a concentrated source of iron until threshold levels are exceeded - thereby providing any mycobacterial pathogens that are present with the sustenance to proliferate to pathogenic levels. Likewise, the high incidence rates of human TB that have been recorded amongst steelworkers and slum dwellers ( who lived beside their workplaces during the industrial revolution ) could have been induced by the high levels of iron in the atmospheres of their local environment.

The politics of TB.

I believe that government ministers in the UK have been correct in resisting pressures to re-enact wholesale slaughter of badgers as a means of controlling TB in the bovine / human populations. For the badger culls of bygone years have achieved nothing in terms of eradicating TB. The disease has kept on re-occurring irrespective of the various slaughter measures that have been put in place. In this respect, we need to consider what is actually achieved each time that we re-enact this final farcical solution for TB control -eg; badger gassing and blanket cattle culls ?

Furthermore, it is scientifically naïve to think that we will ever be able to eradicate a pathogen that is endemic in the environment at large. As long as optimum eco-conditions for the survival of TB mycobacterium are allowed to exist ( eg; high iron / soil acidity ), then TB epidemics will continue to rear their ugly head, as and when alterations in weather conditions and husbandry methods permit.

In respect of consumers who are anxious about exposure to TB pathogens in their foods, they need to be aware that modern methods of food processing safeguard consumers from exposure to the TB agent - methods that did not exist half a century ago. For example, any milk that is taken from a TB affected animal today is automatically pasteurised in the modern dairy set up. Although pasteurisation produces some negative health effects - by switching our immune response to TB and other pathogens into 'sleep mode' - this ultra efficient sterilisation process provides a guarantee of biosecurity for those who are concerned about TB exposure.

Whilst it is high time that governments should say farewell to their archaic strategy for TB control, some viable alternative will be needed to replace it. In this respect, governments should begin to examine the considerably cheaper / animal welfare friendly option of encouraging farmers ( via subsidies) to adopt husbandry practices which prevent cattle from succumbing to TB infection in the first instance. Eg; by subsidising the spreading of lime fertilisers across the TB endemic/high iron regions, as well as promoting feeding / fertilising with iron-chelating/ anti-iron compounds on farms in the TB risk areas. This would reduce the amount of iron that is flowing up the farm foodchain, which, in turn, would reduce the levels of TB mycobacteria.

Such a radical approach which curtails the susceptibility of cattle to the TB agent could produce some major advantages over the existing system which slaughters out the end results of TB infection. This would achieve a considerable reduction in the overall incidence rates of TB, thereby reaping major savings for both human and animal life, farmers' livelihoods and the tax payer.

Since the incidence of TB is increasing amongst the human population, it is high time that we adopted a more intelligent, civilised and updated strategy for dealing with the prevention of TB. In this respect, we need to be taking a closer look at the underlying causes of 'iron overload' in the human foodchain and ecosystem at large. This would entail looking at the impacts of acid rain and how it brings about a rise in the levels of available iron within the soil and water supplies. Issues surrounding the industrial emission of iron particulates into the atmosphere, as well as the supplementation of our foods with iron additives represent important areas that warrant investigation and the development of controls.

Likewise, the indirect impact of various toxic or mutagenic environmental agents upon the metabolic processes that regulate iron homeostasis is an area that also needs to be considered. For a whole range of environmental chemicals /metals are recognised to disrupt or mutate the body's capacity to regulate the balanced uptake, storage and/or excretion of iron; thereby representing an alternative means through which iron levels could become elevated in the biosystem; which, in turn, switches on an increased susceptibility to TB infection.

Meanwhile back on the farm, the knacker man had arrived to collect the TB reactors at nightfall. I lead the unsuspecting cows to the loading pen, feeling guilty that I had betrayed them by failing to mount any kind of resistance against the government's strategy of senseless slaughter. The cows waited, absorbing their final moments of life in the half light. Their backs were steaming and heads held low.

The monster lorry rattled in like an aluminium alien, and then backed up to the loading pen. The ramps came down, and after a rapid fire of whelpings and whip lashings, the cattle reluctantly surrendered themselves to their fate; hooves sliding and clattering up the steely ramp into the dark hold of the lorry.

As the truck turned the top corner, I caught my last glimpse of the cows, their noses frantically pressing through the six inch slats - a last ditch attempt to escape their premature and pointless execution. Tonight they will be sectioned to the post mortem bench, abattoired into oblivion..

As I walked back to the farmhouse in the half light, I caught a glimpse of the foxglove patch on the hill - their petals glowing like red hot irons, still resonating the last light of the evening sun. It was a timely reminder that our TB problem had not been extinguished by the removal of our reactor cows from the farm, but was still very much alive and well , and rooted in the acidity of our soils. As I returned to the farmhouse, I remembered that the presence of foxgloves indicates high iron and high manganese levels in the soil.

References -

Bhattacharyya SD, Sugiyama H. (1989) Inactivation of botulinum
and tetanus toxins by chelators. Infect Immun; 57(10): 3053-3057

Cronje L, Bornman L (2005). Iron Overload and tuberculosis; a case for iron chelation therapy. Int J Tuberculosis and lung disease.
2005 9; (1) 2-9.

Flett, Sir JS (1935). Map of Iron Ores of England and Wales. Geological Survey of Great Britain; Ordnance Survey Office, Southhampton, UK.

Gobin J, Horwitz MA (1996). Exochelins of mycobacterium tuberculosis remove iron from human iron-binding proteins and donate iron to mycobactins in the M tuberculosis cell wall. J Experimental Med; 183, 1527-1532.

Johnson-Ifearulundu YJ, Kaneene JB (1997) relationship between soil type and mycobacterium paratuberculosis. Am Vet Med Ass; 210 1735-1740.

McDonald P, Edwards RA, Greenhalgh JFD (1973). Animal Nutrition . 2rd Edition. Longman , London.

Pais I, Benton Jones J. (1997) The Handbook of Trace elements. Saint Lucie Press, Florida.

Ratledge C (2004). Iron , mycobacteria and tuberculosis. Tuberculosis ( Edin ); 84 (1- 2): 110-130.

Schaible UE, Collins HL, Priem F, Kaufmann SH (2002). Correction of the iron overload defect in beta-2-microglobulin knockout mice by lactoferrin abolishes their increased susceptibility to tuberculosis. J Experimental Med; 196 (11); 1507-1513.

Underwood EJ.(1977) Trace Elements in Human and Animal Nutrition 4th Edition London . Academic Press.

Weinberg E (1999). Iron loading and disease surveillance.
Emerging Infectious Diseases; 5 (3) 346-352.


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