be detectable by visual examination (gross postmortem) of the carcass (Corner et al., 1990), and samples collected from infected animals for microscopic examination or culture may not always include the infected tissue.
Small numbers of M. bovis remain viable for years within macrophages at the center of encapsulated, inactive tubercles in some cattle. The lesions sometimes become active again later in life, perhaps caused by a number of factors including stress, concurrent disease, or old age (Griffin, 1989).
Mycobacterium bovis contains an extensive array of complex lipids that enable the bacteria to survive in macrophages (Thoen and Himes, 1986). These lipids are thought to inhibit fusion of lysosomes (macrophage organelles that contain enzymes that kill and digest bacteria) with phagosomes (macrophage organelles that contain bacteria). The lipids also protect M. bovis against the effects of lysosomal enzymes and the array of other antimicrobial substances produced by macrophages. Mycobacterium bovis also produces an array of proteins (called stress or heat-shock proteins) that further protect the bacteria from destruction by phagocytes and enable them to compete with host cells for the limited nutrients available within phagosomes (Munk and Kaufmann, 1991; Young et al., 1988).
Although production of specific endotoxins by M. bovis has not been established, the metabolic products of the bacteria are assumed to be toxic for neutrophils and macrophages. Tissue necrosis is mediated in part by the direct effects of bacterial products and in part by the immune response of the host (Rook, 1988). Once immunity has been established, cytotoxic T-lymphocytes kill macrophages bearing M. bovis antigens. The enzymes, cytokines (for example, tumor necrosis factor, and interleukin 1), and other products released by lymphocytes and activated or necrotic macrophages are toxic to some host cells and may result in expansion of the necrotic core of the granuloma. They can also cause systemic manifestations of disease (fever, emaciation, and changes in the concentration of some blood proteins such as fibrinogen and haptoglobin). Histologically, giant cells, epithelioid cells, and acid-fast organisms characterize tuberculous abscesses. Culture and identification of M. bovis confirms the diagnosis (Beatson, 1985).
Mycobacterium bovis can be shed from virtually any body orifice. The respiratory route is consistently described as the major route of infection although oral infection is also common. This inference is largely based on location of lesions, although early experimental work indicated that it was more difficult to infect via the oral route than via the aerosol route. Respiratory shedders also tend to shed organisms in their feces subsequent to swallowing bronchial exudate. Shedding, particularly by the respiratory route, can precede the development of grossly identifiable lesions.
Introduction and maintenance of bovine tuberculosis in a herd is greatly influenced by herd or population factors such as size (number of animals), confinement density, and exposure to individuals from the outside. The risk of introduction is lowest in populations that do not introduce new animals from the outside and have no contact with other herds or populations of susceptible animals. Large herds provide the greatest number of opportunities for contact of an infected individual with individuals that are susceptible to the disease. High density and confinement enhance the efficiency