Epidemiology and Infection

Original Papers

The prevalence, distribution and severity of detectable pathological lesions in badgers naturally infected with Mycobacterium bovis

H. E. JENKINSa1 c1, W. I. MORRISONa2a3, D. R. COXa3a4, C. A. DONNELLYa1a3, W. T. JOHNSTONa1, F. J. BOURNEa3, R. S. CLIFTON-HADLEYa5, G. GETTINBYa3a6, J. P. McINERNEYa3, G. H. WATKINSa7 and R. WOODROFFEa3a8

a1 Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College London, London, UK

a2 Division of Veterinary Clinical Sciences, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Midlothian, UK

a3 Independent Scientific Group on Cattle TB, c/o Department for Environment, Food & Rural Affairs, London, UK

a4 Nuffield College, Oxford, UK

a5 Veterinary Laboratories Agency, Addlestone, Surrey, UK

a6 Department of Statistics and Modelling Science, University of Strathclyde, Glasgow, UK

a7 Veterinary Laboratories Agency Carmarthen, Johnstown, Carmarthen, UK

a8 Department of Wildlife, Fish & Conservation Biology, University of California, Davis, CA, USA

SUMMARY

The Randomized Badger Culling Trial (RBCT) began in 1998 to determine the impact of badger culling in controlling bovine tuberculosis in cattle. A total of 1166 badgers (14% of total) proactively culled during the RBCT were found to be tuberculous, offering a unique opportunity to study the pathology caused by Mycobacterium bovis in a large sample of badgers. Of these, 39% of adults (~6% of all adults culled) had visible lesions (detectable at necropsy) of bovine tuberculosis; cubs had a lower prevalence of infection (9%) but a higher percentage of tuberculous cubs (55·5%) had visible lesions. Only ~1% of adult badgers had extensive, severe pathology. Tuberculous badgers with recorded bite wounds (~5%) had a higher prevalence of visible lesions and a different distribution of lesions, suggesting transmission via bite wounds. However, the predominance of lesions in the respiratory tract indicates that most transmission occurs by the respiratory route.

(Accepted October 17 2007)

(Online publication November 30 2007)

Correspondence:

c1 Author for correspondence: Miss H. E. Jenkins, Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK. (Email: h.jenkins@imperial.ac.uk)

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