Iain McGill and Mark Jones argue that recent data released by the APHA show that it is the prevalence or ‘infectivity’ of cattle that is sustaining bTB infection and driving transmission of Mycobacterium bovis to new herds.
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Iain McGill is director of the Prion Group.
Mark Jones is head of policy at Born Free.
There has been much debate over the efficacy of badger culling as a means of controlling bovine TB (bTB) in cattle. Culling is now licenced across 43 zones of England and a recent paper by Downs and colleagues1 is widely cited by supporters as evidence that badger culling is working.
Buried in the detail of the APHA’s data lie route maps towards the epidemic’s true cause
However, more recent data released by the Animal and Plant Health Agency (APHA)2,3 paint an entirely different picture – and buried in the detail of the data lie route maps towards the epidemic’s true cause and resolution.
The Downs paper1 compared bTB herd incidence data from the first three licenced badger culling zones (Gloucestershire, Somerset and Dorset) with data from areas in which no culling had taken place. The study covered the first four years of culling (2013 to 2017) in the original pilot zones of Gloucestershire 01 and Somerset 02 and the first two years of culling (2015 to 2017) in Dorset 03. The authors concluded that ‘Industry-led culling was associated with reductions in cattle TB incidence rates after four years but there were variations in effects between areas’,1 and set particular store by a claimed 66 per cent fall in the incidence in Gloucestershire 01 when compared to control areas.
The recently released information from APHA2 includes data from an additional year of badger culling in the three cull zones – up until September 2018 – for both cohort herds (ie, herds present through all the years of badger culling) and ‘herds in existence’ (HIE) (ie, what APHA calls the combination of cohort herds plus those herds formed since culling started) (Fig 1).
The APHA data also reveal information on the prevalence, or proportion of herds affected by bTB at a given point in time, in the three cull zones (Fig 2). The agency equates prevalence to the ‘burden of disease’2, and a paper in Appendix Q of the Independent Scientific Group on Cattle TB’s final report4 (pp 271-284 of the report) equates the prevalence of bTB to ‘infectivity’,4 which sustains infection in the herd and drives transmission of Mycobacterium bovis to new herds. The paper argues that, in the absence of sufficient movement controls, it is prevalence which drives epidemic spread of bTB.
While epidemiological analyses of bTB focus on the government’s preferred headline indicator of incidence, an analysis of prevalence is therefore equally important. Figs 1 and 2 show the incidence and prevalence data, respectively, and reveal the following:
In the two years before culling started there was a rapid decrease in prevalence in Gloucestershire 01 and Somerset 02 (2011 to 2013), but relative stability in Dorset 03 (2013 to 2015).
In Gloucestershire 01 the incidence increased over five years of culling (2013 to 2018), while prevalence increased by approximately 20 per cent.
In Somerset 02, despite a halving of the incidence, prevalence decreased slightly at the start of culling but has remained broadly stable over the five years.
In Dorset 03, despite an initial increase in incidence, overall it fell over the three years of culling. However, the prevalence increased by approximately 20 per cent over these three years (2015 to 2018).
In all three zones, cohort herds fare worse than HIE, and by September 2018 HIE have a lower prevalence and incidence (dashed lines on the graphs) than cohort herds across all three zones. While there may be confounding factors, if culling was working then the cohort herds, exposed to the full impacts of badger culling for five years, should have a lower prevalence and incidence than the HIE, which have had less exposure to badger culling.
Further data released by APHA3, shows that there was a 130 per cent increase in the number of bTB incidents in Gloucestershire 01 during the calender year of 2018 when compared to 2017 (Fig 3). The data2,3 are in stark contrast to predictions arising from the Randomised Badger Culling Trial (RBCT),4 which suggested that an overall benefit in terms of a reduction in bTB cases should be seen from the third year of culling and for each subsequent cull. The increased prevalence in Gloucestershire and Dorset means after five years and three years of culling, respectively, herds had a higher probability of being under bTB restrictions than when culling started.2
APHA data2 show that by September 2018, although an increased incidence has translated into an increased prevalence in Gloucestershire 01, the falls in incidence in Somerset 02 and Dorset 03 have not similarly translated into falls in prevalence. As a decreased incidence has not lowered the percentage of affected herds in these areas, it follows that individual breakdowns must, on average, last longer.
So what is resulting in such herds suffering from chronic infection or successive breakdowns?
In some confirmed breakdowns, interferon gamma (IFNγ) testing is used in addition to the traditional skin test (SICCT or single intradermal comparative cervical tuberculin test). In such herds in cull zones, many cattle that are negative on skin testing are subsequently identified as positive with gamma testing and slaughtered, although a proportion of these are expected to be false positives. Given that the skin test has a sensitivity of around 50 per cent5 for detecting individual infected cattle, and that in the high risk area (HRA) around 20,000 cattle are detected annually by skin testing alone, these figures suggest that across the HRA, tens of thousands of genuinely infected cattle are being missed by skin testing.
It follows that if the skin test is missing half of the infected animals in the herd, this high undetected in-herd prevalence is the most likely cause of ‘recurrent’ breakdowns, many of which are currently being incorrectly attributed to badgers, even by experienced vets. As the skin test alone is used for pre- and post-movement testing, a failure to identify 50 per cent of infected animals involved in the 2.8 million annual cattle movements would have serious ramifications for the geographical spread of bTB, and this warrants a detailed and urgent clarification from Defra.
It is our contention that the main factor contributing to the ongoing bTB epidemic is the high number of infected cattle not detected by the SICCT skin test. It is this hidden burden of disease and its geographical spread which needs to be addressed and dramatically reduced.
We fully support the British Cattle Veterinary Association’s urgent call for a cattle vaccine to reduce the prevalence of bTB.
Movement controls and better testing will also clearly be required, but with caution – for under a test and slaughter policy, better testing equates to more slaughter.
Given the sheer scale of hitherto hidden infection in the HRA, neither farmers, vets or the public would be likely to countenance the mass slaughter of tens of thousands of additional cattle.
We urge the veterinary profession to move away from a failing policy based on the test-and-slaughter of cattle and the culling of wildlife. We should collectively explore ways to fast-track licencing and use of a cattle vaccine, and elucidate progressive measures such as risk-based trading, molecular testing protocols and slurry controls, which have the capacity to markedly reduce disease prevalence.
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