Bovine TB has been misunderstood for 50 years. All because new interpretations by MAFF in 1980 sent industry and scientists in the wrong direction. A new short report here now tells the story of how this came about.
Studies of bovine TB in cattle carried out in the early twentieth century and reviewed by veterinarian John Francis in 1947 described the disease as largely respiratory. That is, beyond infected milk, bTB is transmitted mostly through exhalation and inhalation of bacteria on fine aerosol droplets and by exchange of saliva. This understanding remained dominant until the 1970’s, and the policy to get on top of the disease was based on this science – and was effective in Britain especially during the 1960s.
As bTB dissipated, it was partly the discovery of bTB in a dead badger in 1971 that led to a review of the science in 1979. A transmission experiment had suggested that when kept together in close confinement, badgers could pass bTB to calves. The review by Lord Zuckerman in 1980 was informed by reports written by a local MAFF veterinary inspector who was sure he had found the important new source of transmission, and claimed that badgers were entirely to blame for the slowing decline of the disease in the west of England.
The new view was that early-stage bTB lesions in cattle (non-visible and small) did not shed sufficient bacilli to be a risk. This was contrary to the generally accepted view that prior to slaughter, un-lesioned (nonvisible lesion) SICCT reactors can have active TB infection, and are very capable of infecting. The John Gallagher (MAFF vet) 1980 view was that TB cattle were only infectious where ‘open’, well developed lesions were found at postmortem, and that this was a rare occurrence.
Thus, the prevailing MAFF rule of thumb that came to dominate in the 1980s appears to have been that even relatively young adult cattle had a kind of ‘safe’ latency, similar to that found in TB in adult humans, via walled-off lesions or granulomas. Only around 10% of cattle infections were considered to come from other cattle, and that was via the oral ingestion route he thought. This was a huge change from the previous view that 90% of infections were respiratory and cattle-to-cattle in origin, with 10% from ingestion of faeces / infected milk.
Where did the new theory believe that the other 90% of bTB was coming from? Figure 1 below is a diagram from the 1980 Government Review of what was then labelled ‘Badger TB’. MAFFs’ position became that badgers were responsible for 90%+ of cattle herd breakdowns.
TB testing in cattle was subsequently relaxed in the 1980s, whereupon the decline of bTB in cattle stabilized, then began to slowly increase again, mid-decade. As it increased in the 1990s, concern about the growing disease problem resulted in a new review in 1997, led by Prof John Krebs at Oxford University. And the Randomised Badger Culling Trial (RBCT) followed from 1998 – 2005 to confirm the MAFF thinking that badgers were causing the new bTB epidemic.
The prevailing MAFF view, right up to the point after 2000 when it merged into DEFRA, was that badgers were;
“well adapted as the primary host of bovine tuberculosis in parts of Britain and much of Ireland”.
The attribution of infection to an external vector, principally badger, was based upon an association of high badger density with remaining breakdown areas. It is illustrated in the 1980 review (Figure 1 above), where cattle to cattle infection was regarded as a ‘remote’ possibility’. It’s hard to believe that this is what people thought back then.
Older MAFF vets maintained this position until as recently as 2019:
“Cattle are simply sentinels for the ever-increasing and widespread infection in badgers. They [cattle] are not the problem per se since the disease does not readily transmit horizontally in cattle until it becomes advanced and the animals are in close confinement.”
“Of those [cattle] reactors to the tuberculin test showing visible lesions, the great majority are in the early stages of infection and thus likely to be non infectious.”
The Government-funded ‘TB hub’ launched in 2015, promoted as the ‘go-to’ place for British beef and dairy farmers to find practical advice on dealing with bovine TB on their farm states on its microbiology page:
“Mycobacteria are unusual amongst bacteria in their robustness, resilience and slow growth characteristics, and the chronic and insidious nature of the diseases that they cause. M. bovis is a facultative intracellular ‘parasite’, meaning that it can survive and thrive inside the host’s macrophages (cells of the immune system that are meant to engulf and destroy the invading bacteria). It has many adaptations to intracellular life and may become quiescent (dormant) or divide very slowly, which enhances its survival. It has a tendency to become walled off in granulomas (small nodules of chronic inflammation) in the tissues.”
The problem with this statement is that it is vague about the timing and stability of ‘walling-off’ in cattle, whether it actually happens in stock slaughtered at a young age or older and how this may contribute to the spread of disease. In reality, the understanding of the infectiousness of lesions at different stages has not changed significantly within the science community. The veterinary research publications, and in particular advances in histopathology and immunology, widely confirm that early-stage micro and small lesions in cattle release bacilli and are infectious. Those with infected lymph glands almost always have small lung lesions that may be impossible or hard to see during standard meat inspection or even post mortem.
This dichotomy of views has had an enormous impact on disease policy making, because it is the old MAFF view (that informed the RBCT), that is still underpinning the current DEFRA / APHA view that Officially TB Free Suspended (OTF-S) herds present less infection risk than Officially TB Free Withdrawn herds (OTF-W). In reality, they are likely to have similar disease risk status, even if the number of cases recorded with visible lesions has fallen.
As the number of necropsy (post mortem / meat inspection) cases with visible lesions diminishes even further, the fact that the bTB epidemic can be heavily driven by cows with non-visible and small lesions becomes clearer to the epidemiologist. Evidence is now indicating that cattle-to-cattle infection is caused by the non-visible microlesions, and small and often hard or impossible to detect stage I and II lesions.
This is why, for example, in the Republic of Ireland the rate of bTB decline slows (after decades of testing and inadequate control) and stops at the point where visible lesions become rarer, yet new infection keep developing. This is what is now happening in England. Its all down to 50 years of misunderstanding.
Progress on the control of bTB has been limited by misdescription of the epidemiology and pathology of bovine TB. This has caused confusion to non-specialists including Government administrators. It is important to note that bTB tests that can now identify live bacteria in blood, milk (and potentially faeces) offer a paradigm shift in clinical management of TB both in cattle and humans. Within years, not decades. The skin (SICCT) test, even at severe interpretation, is inconsistent in its ability to detect inactive infection that may begin or continue within days. Other tests used between SICCT tests may do this, and would lead to an advantage in detection and control opportunity.
This summary is based upon an independent report “Fifty years (1975-2025) of changing perspectives on bovine tuberculosis infection in cattle and badgers”, February 2025, (here) that has been sent to Defra in the hope of gaining recognition of this major historic issue.
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An animal that is a ‘reactor’ is slaughtered and examined for signs of bTB. It must have either a ‘post-mortem examination’ (PME) undertaken either by an APHA veterinary pathologist, or in the vast majority of cases, an examination at an abattoir where meat inspectors undertake a ‘simple post-mortem meat inspection’ (PMMI). Both processes (PME & PMMI) are looking for ‘visible lesions’. These are physiological changes to organs, glands and other areas caused by the disease. Tissue samples from selected ‘positive’ animals are taken for further testing (bacteriological culture) in one of APHA’s designated diagnostic laboratories to try and grow M. bovis (the bovine TB bacilli) and then identify the specific strain of the bacterium through DNA typing or sequencing. Alternatively, M. bovis may be confirmed via PCR (Polymerase Chain Reaction) analysis. PCR is a laboratory technique for rapidly producing copies of a specific segment of DNA, which can then be studied in greater detail. Evidence of bTB infection by one of these methods results in the ‘confirmed’ status.
In February, DEFRA’s Animal and Plant Agency (APHA) published a controversial paper (Birch et al.) in Scientific Reports that the DEFRA Minister Steve Barclay trumpeted immediately as showing that badger culling since 2013 was ‘working’ (
DEFRA’s tactics appeared to be to try to justify badger culling in order to reverse the ‘phasing out’ of badger culling by the 2020 ‘Next Steps’ policy. This was perhaps also addressing the High Court’s expectation, stated 5 years previously, that policy should ‘adapt and learn’ from the results of Supplementary Badger Culling. The DEFRA plan, as revealed on 14th March, was to introduce something called ‘targeted culling‘ (
The March 2024 DEFRA plan was to allow extensive culling into the future across England at the discretion of the Chief Veterinary Officer, potentially under a general licence, further negating provisions of the Protection of Badgers Act 1992. It looked like Defra were trying to put a policy in place before a General Election, to commence in autumn 2024. The DEFRA plan looked like a normalization of widespread badger culling into the future. Likely to further stimulate illegal badger culling that is now reported to be rife in some bovine TB areas.
Ultimately, the consultation fell victim to the announcement by Prime Minister Rishi Sunak on 22nd May of a General Election on 4th July. This froze consideration of the consultation responses until after the election. The Labour Party manifesto for the 2024 General Election was published on 13th June, and stated its intention to end “ineffective” badger culling, as previously pledged during the 2019 general election. Labour had been keeping very quiet about its position on culling in the months leading up to the election. Presumably this was a tactic to placate the farming vote which was needed before Reform UK Party decided to stand. It appeared to have agreed to keep some badger culling going as a part of a back-room deal with the NFU, a fix that was later exposed by reliable sources (
An important new extensive re-evaluation of the Randomised Badger Culling Trial was published in Nature Scientific Reports by Prof Paul Torgerson with others, on 15th July, shaking the foundation stone of Government policy since 2011. It provided further and highly extensive evidence that the role of badgers in bovine TB in cattle was fatally misconstrued, and the problems had not been spotted over 20 years ago (
Throughout 2023 and 2024 the Oxfordshire Badger Group (OBG), with support from others, had tried to initiate discussion of the RBCT design and findings with Oxford University, but reported a wall of reluctance or silence. Around 7,000 badgers have been shot in Oxfordshire so far. On 18th July OBG presented a petition with over 50,000 signatures to Oxford University School of Biology in central Oxford. OBG called on Oxford University to own what it called “Your Bloody Science” and asked them to “Speak out against badger extermination”, (
There followed a tirade of rather ill-founded and rushed accusations and complaints by multiple members of the usually secretive BTB Partnership (
On 24th October APHA’s “Year End Descriptive Epidemiology Reports” for Bovine TB control were published online for the Edge Area counties of Berkshire, Buckinghamshire, Cheshire, Derbyshire, East Sussex, Hampshire, Leicestershire, Northamptonshire, Nottinghamshire, Oxfordshire and Warwickshire. Progress is no longer on target for any of these areas, apparently due to inadequate funding for disease control following Brexit cutbacks (see 
As the year wound down, the Oxfordshire Badger Group supported a scientific seminar, in Oxford, delivered by Prof. Paul Torgerson on 18th November: key RBCT academics together with Defra & APHA officials were invited to discuss the science and statistics but all declined. 
On 3rd December, Rob Pownall of Protect The Wild launched a parliamentary petition to end the English badger cull. Standing at around 30,000 signatures at the time of writing, the petition calls for “an immediate end to the cull and the implementation of cattle focused measures to control bTB, rather than what we see as scapegoating wildlife.” As the petition points out, research that has been “peer reviewed and published, shows no evidence that culling badgers reduces confirmed bTB in cattle. Over 230,000 badgers — many healthy — have been killed, disrupting ecosystems without solid scientific justification”. Please add your name to this petition 
Vetsuisse Faculty at Zurich University. This looked at the flawed assumptions made back in the 1970’s that led to badgers being wrongly labelled as a ‘self-perpetuating bTB reservoir‘, on to field trials that tried to show a ‘bTB perturbation effect’, and statistics chosen to ‘prove‘ this as a way to stop culling. And the u
The ‘Comment’ submission to the Royal Society Open Science is an extensive response to the two new Mills et al. (2024) papers which reproduced much of Torgerson et al.’s models, whilst re-interpreting the results.
