The Randomized Badger Culling Trial began in 1998 to determine the impact of badger culling on bovine tuberculosis (bTB) incidence in cattle. 1166 proactively culled badgers (14% of total) were tuberculous. Of these, 39% of adults (∼6% of culled adults) had visible lesions (at necropsy) of bTB; cubs had a lower prevalence of infection (9%) but a higher percentage of tuberculous cubs (55·5%) had visible lesions. Only ∼1% of adults had extensive, severe pathology. Tuberculous badgers with recorded bite wounds (∼5%) had a higher prevalence of and different distribution of visible lesions, suggesting transmission via bite wounds. However, the predominance of respiratory tract lesions indicates that the respiratory transmission route dominates.
Although there were positive associations between recorded bite wounds and infection with the causative agent Mycobacterium bovis, the sequence of these events is unclear. To investigate this, data were collected from badgers at Woodchester Park routinely examined from 1998 to 2005, with bite wounds and infection status recorded. Many badgers had multiple observations. At each observation, the badger was assigned a “state” depending on presence of bite wounds and/or infection. Hence each badger had a “transition” from the previous state to the current. Across all badgers, the numbers of each transition and the time spent in each state were calculated. Rates were calculated for each transition category, dividing the number of such transitions by the total time at risk. The following were compared: the rate of bite wounds in infected badgers with that for uninfected badgers (rate ratio=1.55; 95% CI: 1.02-2.36) and the rate of infection in bitten badgers with that in unbitten badgers (rate ratio=1.31; 95% CI: 0.73-2.36).
Further methodological development is required to allow for adjustment for potential confounding factors. Results could improve our understanding of M. bovis transmission dynamics in badgers and inform disease control policies.
Keywords: Bovine TB; Badgers; Transmission routes; Disease control
Biography: Helen Jenkins received an MSc in Medical Statistics from the London School of Hygiene and Tropical Medicine and a PhD in Infectious Disease Epidemiology from Imperial College London. During her doctoral work she collaborated with the World Health Organisation studying poliomyelitis in Nigeria. Since 2005, she has been involved in analysis of data from the Randomised Badger Culling Trial, co-authoring several important publications. She is currently undertaking post-doctoral research at Harvard Medical School on human tuberculosis and drug resistance.