xiv List of Figures
Fig. 9.14. Multifocal granulomas at different stage of development in a badger infected with M. bovis.
Some of the lesions are small and solid, while other show a central area of necrosis surrounded
by a rim of epithelioid cells, no multinucleated giant cells and lymphocytes at the outer layers of
the lesion. No evident capsule can be identified. (H&E, 40×)
Fig. 9.15. Large coalescent caseous granulomas in the lung of a fallow deer infected with M. bovis.
Yellowish creamy material can observed within the lesion. Courtesy of ‘Red de Recursos
Faunisticos’ group, University of Extremadura, Spain.
Fig. 9.16. Solid well-encapsulated lesion in the mandibular lymph node from a wild boar infected
with M. bovis. The lesion is also heavy mineralized and ‘gritty’ on sectioning. Courtesy of ‘Red
de Recursos Faunisticos’ group, University of Extremadura, Spain.
Fig. 12.1. Hierarchy of T-cell responses to 626 M. bovis/M. tuberculosis proteins. Results are shown
as responder frequencies (proportion of tested animals responding to a given protein). Responses
were established using whole blood cultures from M. bovis-infected cattle to measure antigen-
specific IFN-γ responses.
Fig. 15.1. Direct and indirect pathways for spread of bovine tuberculosis between and within species
in New Zealand. Bold arrows indicate a main source or route of infection; brown depicts direct
transmission, green depicts indirect transmission via scavenging or investigation of tuberculous
carcasses and offal, red indicates that the source of infection is unknown but is likely to be by
direct means. This figure is reproduced with permission of the Editor, New Zealand Veterinary
Journal, where it was first published as Figure 2 in the following paper: P.G. Livingstone,
N. Hancox, G. Nugent, G.W. de Lisle (2015) Toward eradication: the effect of Mycobacterium
bovis infection in wildlife on the evolution and future direction of bovine tuberculosis
management in New Zealand. New Zealand Veterinary Journal 63 (S1), p7.