Badger, seen at the British Wildlife Centre, Newchapel, Surrey. Photo: Peter Trimming via Flickr (CC BY).
Alas poor Brock! The insanity of the badger cull
27th May 2016
The lives of all the thousands of badgers slaughtered in the name of TB eradication have been lost in vain, writes Martin Hancox. The cryptic reservoir of bovine TB is the cattle themselves, and no amount of badger killing will make the slightest difference to the problem. Once we have grasped this reality the solution is astonishingly simple: improved TB testing that picks up all infected cattle.
The three pilot culls in Glos., Somerset, Dorset since 2013 have cost towards £30 million. With at most two dozen infectious badgers which might have posed a risk to other badgers or cows, there will have been no effect on cattle TB.
Since the first 'official' 3 TB badgers in Gloucestershire and Glamorgan in 1971, the "highly complex and emotive" badgers and bovine TB debate has now rumbled back and forth some 45 years, without resolution (Hancox 2016).
Although there was in fact a TB badger in London Zoo in 1938, and the first wild badgers caught TB from eating infected roe deer carrion in the mid-1950s in Switzerland. This confusion has arisen for three main reasons:
1. While there is undoubtedly a link in a shared infectious TB disease between cattle and badgers, no-one has properly explained the direction of transmission between the two species (Krebs 1997, Biek 2012).
2. Since bovines, that is, cattle are the natural self-sustaining 'maintenance host' of bovine TB, it was rather unwise to effectively rule out cattle as this self-sustaining hidden reservoir of TB in the last two dozen intractable pockets of southwest TB in the 1970s. However MAFF vet John Gallagher wrongly assumed that only 'Open Visible [lung] Lesion' cattle could spread TB, and since these were so rare (20 in 1,000 reactors), cattle-to-cattle, and cattle-to-badger spread was unimportant, so the hidden reservoir must be badgers (Zuckerman 1980, p. 86, 94, Dunnet 1986 para. 60).
3. no-one has realistically explained how badgers might give cattle an entirely respiratory lung infection, a bronchopneumonia. So Godfray 2013 reviewing the science base reached the same conclusion as the earlier Krebs review (1997) "it is not known if, how, or to what extent badgers might contribute to cattle TB".
The false assumption - 'if it's not a confirmed cattle source, it must be badgers'
So, all guestimates of the contribution of badgers to cattle TB are actually based on assuming they must be the TB source where it cannot be traced back to a confirmed cattle source : bought-in, contiguous, residual, eg. 15% 'due to badgers', or 39% for Eire (Ulster 2015, More 2015).
McIlroy (1986) in fact solved this transmission problem. All his confirmed TB cattle reactors had lesions in the lymph nodes draining the lungs (bronchials and mediastinals), so cattle TB is an aerogenous bronchopneumonia, caught by prolonged close aerosol droplet 'contact' with other cattle in enclosed spaces such as barns and milking parlours.
Strikingly 20% of reactors were sputum positive / infectious, despite lacking visible lung lesions. So surprisingly cattle do still catch TB from other cattle ('The guilty secret of kissing cows', Wright 1985).
In an experiment of elegant simplicity a century ago, Svensson found that 13 calves caught TB from a group of older TB cows in a barn, a six foot gap between them so purely airborne aerosol droplet spread, five were reactors after six months, the other eight after a year. Cattle did not usually catch TB until they entered the cowshed as part of the breeding herd (Francis 1947).
So we can safely conclude that cattle cannot be catching respiratory TB from badgers after all - all the more so as badgers avoid cattle both at pasture and in farmyards and barns (Mullen 2015). Indeed - stonishingly - there has only been one proven case in 50 years where badgers gave calves TB in a very artificial yard experiment (Little 1982).
Even in the supposedly 'high risk', high badger density population with 'endemic' TB at Woodchester Park, there has not been even a single herd breakdown attributable to badgers since 1975.
That's unsurprising since amongst some 300 badgers in 11 sq.km, over 24 years there have only been 315 infectious badgers amongst 1,803 known individuals. The TB occurring in micro-pockets of one or two TB badgers per social group, in a few clans at the epicentre of spillover from cattle, is not after all self-sustaining within and between clans in the badger population - but actually dies out quite rapidly (Delahay 2013, Krebs 1997 p. 48).
Such micro-pockets of transient TB are seen elsewhere in population studies in Avon, Cornwall, Dorset, Glos., Staffs, Sussex, and in Ireland with up to three M.bovis spillover DNA 'types' per clan! (Krebs 1997 p. 48, Delahay 2013, Tuyttens 2000, Biek 2012).
The simple truth: culling badgers has zero impact on TB in cattle
Badger culling policy as determined by at least three DEFRA Consultations (2006, 2010, 2015), is based on the results of the Randomised Badger Culling Trial (RBCT, ISG 2007). And even now further badger culls or vaccination schemes are still based on the claim that badgers cause 50% of herd breakdowns, although positive and negative effects of culls are balanced out. For example, Wales (2016), and TVR, Test, Vaccinate, Remove Ulster badger trial (Bielby 2014), or England (Karolomeas 2012).
Godfray (2013) rightly questioned the 50% badger element, so Donnelly (2013) downgraded this to a mere 5.7%, but rather bizarrely and illogically uses the cattle-to-badger TB spillover rate to predict badger-to-cattle spread.
No-one seems to have noticed, but in the ISG 2007 Report, Lefevre (2005) found that reactive culls had nil effect on cattle TB, as evidenced by figures of accumulated breakdowns as compared to no cull areas: 356 vs 358 confirmed herd breakdowns, 175 vs 172 unconfirmeds, 56 vs 59 repeat breakdowns.
In fact out of 2,046 badgers culled reactively, only 311 actually had TB, and at 1.65% infectious (super-excretors) that amounted to fewer than 10 from 900 sq.km - so no wonder there was no effect on cattle TB!
Also, the ISG 2007 (10 Tables in Chapter 5) the final accumulated total breakdowns were almost identical between cull versus no cull areas, 1,737 vs 1,840, so just 103 breakdowns after seven years, or ten per triplet area. So it is bizarre that many subsequent studies are still claiming a reactive cull badger perturbation effect (Beilby 2014, Karolomeas 2012, Vial 2011).
And the cull of 11,000 badgers had no effect on unconfirmed breakdowns either, because they are caused by unconfirmed cattle reactors, not badgers at all! (ISG 2007, p. 96, 101; see bovine TB 2016).
The false premise of 'badger perturbation'
So, several recent studies have rightly questioned whether culls work, and indeed the whole concept of badger perturbation via culls increasing the spread of TB.
On the one hand culls do reduce badger numbers, hence a loss of territoriality and wider ranging animals. But the doubled prevalence in badgers - which was a foot and mouth spillover effect to badgers - does not logically make them twice as likely to spread TB to cows, since that is improbable even from unperturbed badgers.
The mechanism for this badger perturbation increased transmission is hence that mystery of mysteries! (Macdonald 2006, Riordan 2011, Karolomeas 2012, Bielby 2014). Born Free vet Mark Jones (2016) rightly claims culls are "unscientific, inefficient, inhumane, and unnecessary". The whole perturbation hypothesis is based on very "Dodgy data and bad science" (Langton 2016, bovine TB 2016).
The three pilot culls in Glos., Somerset, Dorset since 2013 have cost towards £30 million, including c. £7 million in extra policing, and removed a mere 3,943 badgers from c. 450 sq.km. With perhaps at most two dozen infectious badgers which might have posed a risk to other badgers or cows, there will have been no effect on cattle TB.
More (2015, 2007 ), had previously raised doubts as to the biological plausibility of any effect on cattle TB: the rise in reactive areas actually happened before the cull, and in fact was via bought-in cattle with a new spoligotype in both the cull and no cull areas in the Wilts reactive 'TEE' study (Riordan 2011).
And although this gaffe slipped past peer reviewers, the supposed increases and decreases in the two kilometre wide buffer ring outside the proactive cull areas cannot have been due to the cull, because there was no cull out there! There was even an unexplained drop in the first 500 metres which would supposedly be the key 'edge' effect area (ISG 2007).
The answer: a lack of TB testing under FMD restrictions
Astonishingly - and few have fully appreciated the fact and its implications - the lack of testing during the foot and mouth disease (FMD) outbreak meant a build-up in TB amongst cattle. Breakdowns with over six reactors shot up from 23% in 2000, to 42% in 2002. Numbers then fell to 17% by 2005 as strict testing brought the FMD upsurge under control - a jump from 7,000 to 23,000 reactors.
A similar upsurge resulted from catching up with the backlogs in testing with 30,000 reactors in 2005, then 40,000 in 2008 (Wales 2015). The ISG in fact recorded this rise in all 30 trial areas, and their 30 two km wide outside buffer rings, the latter plus the 10 no cull areas had no culls so it is a bit daft to claim any badger perturbation effect in the first place.
And the 50% drop after five years in the core areas and outside ring was not due to the cull either. Five to seven years of strict cattle testing will halve cattle TB, regardless of any alleged badger effect. Since 2008 TB has halved in Wales, from 12,000 to 6,000 reactors, with a similar effect observed in Ulster, and Eire 30,000 to 15,000 reactors (Wales 2015, Abernethy 2011, Ulster 2015, CVERA 2016).
So, in further questioning the scientific basis of 'perturbation' and the true effect on confirmed cattle TB More (2015) concluded strangely that the SICTT Skin Test used alone produces a greater than 50% false positive rate, but nearly all negatives are true negative - even though the specificity of the SICTT is 99.96-100%, ie. only 1 in 5,000 are truly false positive and do not have TB.
However, if the SICTT is accompanied by abattoir checks and histopathology and bacteriology, then we find that all positive herds are true positives, and most negatives are also true negatives. So this confused verdict is muddling false positives with early TB reactors which have yet to show visible lesions or detectable M. bovis: 'No Visible Lesion', 'Unconfirmed reactors'.
The Godfray 2013 review also found that the skin test was effectively only 49% accurate, ie. it misses 51% truly infected animals. So, obviously - according to the ISG, and More as regards Eire DAFM (Department of Agriculture, Food and the Marine) policy on TB - the supposed 'false positive' 50% must be 'due to badgers'!
He found that "there is little doubt that badgers are a maintenance host, with a spillback to cattle ... essentially an upstream driver of infection" - in effect still the engine driving the ongoing TB situation (More 2015 a, b; CVERA 2016).
Chief Vet Dr. Gibbens has had a lot of bad press from farmers and auctioneers ever since the 6th April introduction of tighter movement and testing conditions, but he does not really seem to understand the outcome of last years DEFRA Consultation on post-movement testing (DEFRA 28th August 2015).
It is absurd to require a 60-120 day post-movement restriction after attending agricultural shows. It takes at least six months for new TB cases to progress to the reactor stage, which is why routine surveillance does not include cattle under six months old.
'A more robust approach to dealing with TB'
There have always been two types of skin test reactors: early TB cases with 'No Visible Lesions', so 'Unconfirmed reactors', and later TB ones with 'Confirmatory Visible Lesions'. Up to 90% of breakdowns are caused by these Unconfirmed cases, which since they are not traced back to confirmed TB cattle, have been assumed to not have TB, so 90% of the breakdown by default blamed on badgers.
But the Consultation (DEFRA 2015 b) at last clearly 'discovered' that all these 'No Visible Lesion' reactors do have TB so the 90% of breakdowns allegedly 'due to badgers' are merely caused by early 'No Visible Lesion' / 'Unconfirmed' bought-in cattle after all ... and have absolutely nothing to do with badgers.
Government believes that the current approach for these OTFS (Officially TB Free Suspended ('No Visible Lesion' / 'Unconfirmed')) herds in the High Risk Area increases the risk of lifting restrictions before all infected animals have been identified, allowing potentially high risk animals to be moved to other holdings and increasing the already high risk of recurrence of infection in the same herd.
The current approach also perpetuates the view that the test reactors without visible lesions of TB at post-mortem examination are false positives, whereas the testing odds suggest that they are true positive results.
To simplify the terminology and counter the perception that lesion- and culture-negative breakdowns represent false positive test results we also propose that APHA no longer distinguish between OTFS and OTFW (Withdrawn) breakdowns. Pre- and post-movement tests are the simple way to stop exporting TB from the HRA 'hotspot', as has been used successfully for Scotland for years.
Please note: this key conclusion nullifies and overturns decades of EC policy on controlling cattle TB EC Directive 64/432. All OTFS Now are OTFW (EFSA 2014).
Actually it's all embarrassingly simple
The solution to the 45-year old Great Badger Debate is so spectacularly simple, that no one can believe its all down to such an embarrassingly very simple very silly mistake.
Badgers have been traditionally blamed as the 'main cause' of all these new herd breakdowns, where the reactor has not yet reached the Visible Lesion in lung stage, so is unconfirmed. But these new cases are the result of respiratory cattle-to-cattle aerosol spread within the herd.
Then these new 'NVL' / 'Unconfirmed' early TB reactor cases get dispersed to a random scatter of new NVL / Unconfirmed herd breakdowns ... up to 60% within hotspots. And 90-100% of Unconfirmed new incidents simply spread via local cattle movements outwards through Edge to 'low risk areas' where there is no background TB in either badgers or cattle.
Wales had some 700 such brief herd breakdowns 1972-1996, which were according to MAFF mostly "due to badgers", but there were a mere 46 TB badgers out of 2,363 sampled during that period. What was overlooked was a staggering amount of re-stocking and routine 'stock management' movements within the cattle population, approaching 20 million movements of cattle each year, 40% of which were local dispersals of under 20 km.
Since the FMD (Foot and Mouth) 2001 upsurge in TB-infected cattle TB due to the lack of testing then, out of some 450,000 cattle removed, some 260,000 were these unconfirmed reactors swirling about within the cattle population. Thus cattle have been the main cause of the spread of cattle TB all along.
The expansion of cattle TB hotspots has merely been via the widening clonal expansion of Cattle TB DNA 'Spoligotype Home Ranges' by local cattle movements (DEFRA 2015 a). After all, bovines / cattle are the natural 'normal' host of bovine TB, and it is not only self-maintaining within the cattle population but gently expansionist!
Note: out of some 53,000 badgers sampled in 1972-2005, a mere 6,000 had TB ... so they were not the major hidden reservoir of TB.
A tragic and costly mistake
Oh what a tangled web we weave when first we practice to deceive. MAFF vet John Gallagher got it wrong in Zuckerman 1980 (p. 86, 94) in assuming that only 'Open Visible Lesion' cattle could spread TB, so badgers came to be blamed as the "main cause of the spread of TB".
It was a very costly tragic mistake. If pre- and post-movement testing from the last southwest cattle TB hotspots had been in place in the 1970s, TB would not have spread to an area now of half of Britain. And depopulating the small number of problem herds within these residual southwest islands of TB would have fully eradicated TB. Even the intractable Lands End / West Penwith area went clear in 1985 (Richards 1972).
As Francis's classic review (1947) had pointed out previously, it has been clear from the outset, that "in practice all tuberculin positive cattle are regarded as infectious to other cattle ... and if any reactor to the tuberculin test, even with very slight lesions is left in a herd, spread will be more or less rapid within the herd."
It has been known for a century that the skin test misses early and late TB cases. So these are - as Blood's 1989 Veterinary Medicine points out - the usual cause of recrudescence in herds which have supposedly tested clear of TB. Francis had also noted that "it is known that the primary focus in cattle may remain latent for many years or progress only very slowly" (Bang 892, 1899, M'Fadyean 1899).
And "problem herds in which infection continues to show on retests indicates the need for identifying skin test non-reactor (anergic) spreader cows" (Francis 1958). So the simple answer to such herds with chronic TB is a late TB fast blood antibody test ENFER, ENFERPLEX, IDEXX Ab test (OIE approved), or even more simply PCR (DNA testing) for M.bovis in faecal swabs (both solutions in NFU 2014).
Badger culling or vaccination has been a wonderfully insane solution to a non-existent problem. And as vet David Coffey pointed out back in New Scentist in 1977, continuing with badger culling is political expediency pursued way beyond the point of absurdity. Alas poor Brock !
Martin Hancox is a badger biologist and a former member of the UK Government's Consulative Panel on TB.
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