Effect of homogenates of organs from immunized guinea pigs on the respiration of Mycobacterium tuberculosis.

An outstanding feature of the phenomenon of acquired immunity in tuberculosis is the lack of multiplication of virulent mycobacteria in the tissues of the immunized host. As the result, viable, virulent, tubercle bacilli may remain dormant in vivo for long periods of time. The nature of the acquired specific mechanism responsible for this bacteriostasis in vivo has never been determined although there are reports which suggest that growth inhibitory substances may be present in the blood, body fluids, or tissues of immunized or infected animals (Pagel, 1935, 1940; Lurie, 1936, 1939; Myrvik and Weiser, 1951; Soltys, 1952, 1953; Tsuji, Ito, and Oshima, 1957). The role, if any, of most of these growth inhibitory substances in the production of the state of "physiological imprisonment" (McDermott, 1958) of virulent mycobacteria in the tissues of immunized animals has never been defined. Lysozyme, the only one which has been identified, does not increase the resistance of normal mice to tuberculous infection when administered in large quantities (Weiser et al., 1958). Regardless of the role of growth inhibitory substances in immunity to tuberculosis, it is possible that certain cells of the immunized animals might acquire the ability to reduce the physiological activity of viable virulent mycobacteria to a level incompatible with reproduction, and thereby account for a significant portion of the acquired immunity. If such a mechanism is involved, it would be reasonable to expect that cells, or homogenates of organs obtained from immunized animals, might interfere with some essential metabolic function of virulent mycobacteria.