Some people will insist that the badger cull is completely political. Yet in some senses, everything in society that is large-scale, expensive, complex and at the heart of a national industry, is bound to be political to some extent. Priorities, such as who gets the money and decisions on what success or failure may look like are political decisions. It is easy to ‘blame’ hidden agendas and dark forces, and they may to some extent exist. But quite often the answers are simpler and routed in the frailties and fallibility of humans – the human factor. And science with all its inner secrets and complexities is not immune from all that.

There is no shortage of science in badger culling. Whether it is the molecular biology of bTB strains, intricacies of bTB testing, badger, or cattle vaccination, the hands-on anatomy and pathology of disease investigation, population size estimation and trend analysis or modelling of hypothetical disease pathways. The list seems endless and a boggling arena for the non-biologist. Understanding the inter-relationships of these disciplines may require simultaneous insight into such areas of expertise and uncertainty. So, before we blame politicians too quickly, there is a need to look through the microscope at the science that is involved. After all, get two experts on any issue in front of you, any politician will say, and they are bound to disagree.

From 2013 onwards, the rallying cry of the ‘anti-badger cull’ movement was that badger culling could offer “no meaningful contribution to cattle bTB control in Britain”. This is a direct quote from the final (ISG 2007) report on the Randomised Badger Culling Trials (RBCT) that took place between 1998 and 2005. And that was also my understanding at the time, based on generalised reports of the published findings. The main conclusion from culling 70%+ of badgers over a six week period was that any reduced bTB transmission from badgers to cattle is offset by a ‘perturbation effect’, whereby increased movement of badgers due to culling, causes an increased transmission of bTB to cattle around a culling zone. By 2015, having attended a few protest rallies and with culling spreading to Dorset, it was clear that the animal conservation and welfare charities had completely failed to convince government that their policy was both wrong and not based on scientific advice. Checking the scientific detail became the last remaining option.

The RBCT had two types of culling (Reactive and Proactive), each planned in ten areas of around 100 square km in size. Reactive culling is where badgers are killed only on land within a few km of a new bTB herd breakdown and not widely over a large area as in proactive culling. But from 1998, RBCT badger culling had a faltering start, further hampered by the Foot and Mouth crisis in 2001 restricting access to farms. The result was a depleted data-set due to these unforeseen circumstances. The ISG report nevertheless had come up with its hypothesis that badgers were giving bTB to cows rapidly by catching and passing it on via the ‘perturbation effect’. But for many, the speed of bTB transmissions involved looks unrealistically rapid for it to be a real phenomenon.

The sequence of events following disruption of badgers would need to be: increased transmission of TB amongst surviving badgers, newly infected badgers becoming infectious (a process taking months or longer), then infective badgers making contact with cattle somehow in a mechanism that is unknown, cows becoming exposed to bTB from the unknown pathway and establishing new bTB infection in vulnerable individuals, sufficiently to trigger responsiveness to the tuberculin test and detection at slaughter/post mortem culture/microscoopy ,breakdowns might need to wait six months on average (and up to a year for the next testing period) to be detected, during which time there was a 20-50% chance per cow of it being missed and possibly picked up in a further year’s time or longer.

Reviewing the literature on BTB and badgers, I found a group of six academics including Professor Simon More from the Centre for Veterinary Epidemiology and Risk Analysis in Dublin who had studied the ISG and published an immediate critique of several aspects. In addition, the record showed Sir David King (Chief Scientist at the time) had set up his own expert group that effectively dismissed the strength of the statistics concerning reactive badger culling and the bTB spread via the perturbation effect. More recently, the Chief Veterinary Officer for Wales has drawn the same conclusions as those before her. So now we have three separate expert appraisals saying independently that reactive culling and perturbation effect are not safe science.All in all, the suggested increase in bTB transmission would have been likely to take years, if indeed it was real at all. The cold fact is that the duration of the reactive culling periods was too short to prove the increased bTB herd breakdowns had resulted from them.

Slightly taken aback, I turned to the aspect of the RBCT that had been suggested was more robust; the proactive badger cull ‘benefit’ of reducing bTB from mass badger culling across a wide area. This involved looking at the methods and analysis of proactive culling. The first, and rather shocking thing to notice is that the raw data shows that in four of the ten proactive culling zones, bTB actually went up and not down when compared with its control area, either as paired comparisons or as percentages. There was no ‘benefit’ nearly half of the time in terms of what the farmer and veterinarian might see ‘on the ground’. How could that be?

Next came tackling mathematical modelling and the assumptions and adjustments made to the raw data that had turned this into a ‘significant’ result. After a lot of hard work by a statistician who had volunteered to retrace the analysis, there was nothing per-se in the analysis that actually looked ‘wrong’ in terms of the mechanics of what had been done. However a number of serious problems began gradually to emerge. Using an alternative but equally valid model on the RBCT produced no significance from the data. This was simply using, for each comparison between cull and control area, the years over which proactive culling was actually carried out, rather than the average number of years, as used in the ISG analysis. A very simple adjustment using the time that each set of herds had been exposed to change rather than the average. This is an equally valid approach to the one that was used.

Other issues cropped up, such as the wide range of confounding variables that were likely to have been uneven within and between study areas and controls. However without proof of these being skewed, it was hard to conclusively prove the relevance without tracking down new data from the RBCT period. There was no time to do that - something for the future perhaps? It also became clearer that the RBCT had actually been a study of bTB very rapidly increasing, not declining. Many of the study areas were heavily infected before the study had started. What was being looked at was not an actual decline but a slower rate of increase.

Slightly taken aback, I turned to the aspect of the RBCT that had been suggested was more robust; the proactive badger cull ‘benefit’ of reducing bTB from mass badger culling across a wide area. This involved looking at the methods and analysis of proactive culling. The first, and rather shocking thing to notice is that the raw data shows that in four of the ten proactive culling zones, bTB actually went up and not down when compared with its control area, either as paired comparisons or as percentages. There was no ‘benefit’ nearly half of the time in terms of what the farmer and veterinarian might see ‘on the ground’. How could that be?

Next came tackling mathematical modelling and the assumptions and adjustments made to the raw data that had turned this into a ‘significant’ result. After a lot of hard work by a statistician who had volunteered to retrace the analysis, there was nothing per-se in the analysis that actually looked ‘wrong’ in terms of the mechanics of what had been done. However a number of serious problems began gradually to emerge. Using an alternative but equally valid model on the RBCT produced no significance from the data. This was simply using, for each comparison between cull and control area, the years over which proactive culling was actually carried out, rather than the average number of years, as used in the ISG analysis. A very simple adjustment using the time that each set of herds had been exposed to change rather than the average. This is an equally valid approach to the one that was used.

Other issues cropped up, such as the wide range of confounding variables that were likely to have been uneven within and between study areas and controls. However without proof of these being skewed, it was hard to conclusively prove the relevance without tracking down new data from the RBCT period. There was no time to do that - something for the future perhaps? It also became clearer that the RBCT had actually been a study of bTB very rapidly increasing, not declining. Many of the study areas were heavily infected before the study had started. What was being looked at was not an actual decline but a slower rate of increase.

This dilemma comes up in the 2007 ISG report (see pages 93-96). In fairness, it points towards difficulties with post-mortem culturing of bTB as the reason that the disease would be overlooked in unconfirmed reactors. In hindsight, and what may be seen now as a disastrous move, the ISG analysis decided just to use ‘confirmed’ breakdown-only data as opposed to ‘all’ breakdowns (confirmed and unconfirmed). What happens when we add all the unconfirmed test results back into the model (as being correctly identified as having bTB) is that there is no significant effect of proactive culling of badgers on new herd bTB breakdown.

Here was a lethal blow to the ISG proactive cull analysis and conclusions. The ISG should have concluded that the RBCT had failed to find a link between proactive badger culling and a reduction in bTB herd breakdowns, the exact opposite of the ISG finding. Instead it concluded that badgers do pass bTB to cattle at a significant rate. It also said badger culling was not worth doing because of a balancing effect resulting from perturbation. A story that the public and government of the day embraced, but one that extended way beyond the limit of what actually constituted a safe scientific conclusion.

The strength of the RCBT had slowly crumbled in front of me. Several scientists I had spoken too along the way had not considered the RBCT to be good science but, busy with their own issues, they had tended to see the ‘pro-badger’ conclusion i.e. that the advice not to cull badgers was possibly ‘right for the wrong reasons’ and so fairly harmless, not realising what a change of government might then do. Others had felt doubt but no need to comment over the bTB ‘hot potato’, especially as much of their funding was provided by government.

By August 2016, as more badger killing was announced, I began to realise the awful truth. The badger protection movement, with the exception of a handful of informed people had joined with the ISG scientists to uphold ‘the ISG science’, unreliably based upon badgers giving bTB to cattle with significant frequency. They were supported by a number of Oxford University academics although I noted this was on more general terms than the ISG specifics. Speaking out were some who were behind the scenes in setting up the 1997 Krebs review and the RBCT in the first place. On checking and double checking, many closest to the issue either did not want to accept my analysis or even to talk about it, which just seemed suspicious. Some wanted it covered up for tactical reasons. The phrase ’reputational damage’ was used more than once.

Looking back to the RBCT design, it does seem odd that John Krebs and Roy Anderson at Oxford concluded the need for a trial of the kind undertaken, given the uncertainties over the disease and the role of wildlife. Robert May (Oxford and Imperial) who was Chief Scientific Adviser (1995–2000) has acknowledged that the use of mathematical models during the 2001 Foot and Mouth Disease epidemic had created controversy based on a “lack of mutual understanding between veterinarians and modellers.” It looks perhaps as if the RBCT may have been a prelude to such problems, but also involving zoologists.

Krebs was recently quoted as saying, "We must acknowledge as scientists that we don't always get it right. Models make assumptions, labels slip in freezers”. Was this perhaps a message regarding the trials that bear his name? Now is the time to find out.

Tom Langton

Ecologist, Badger Trust Supporter

April 2017

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