The Influence of Cortisone

A basic feature of the host-parasite relationship in brucellosis is the intracellular localization of Brucella in the tissues of animals and man (1-6). This intracellular parasitism is a contributing factor in the tendency of the disease to become chronic. Experimental studies have shown that intracellular Brucella organisms are afforded protection against antibiotics, and also against the lethal action of serum (7, 8). Brucella organisms in an extracellular position are readily destroyed by antibiotics, and by fresh serum. Prompt elimination of Brucella from the tissues of the host appears to depend, in part at least, upon dislodging the bacteria from their intracellular localization. The report on experimental tuberculosis by Hart and Rees (9) suggested that the host-parasite relationship in brucellosis could be disrupted by cortisone, and Brucella organisms would then be liberated from the cells of the host. The pathogenesis of brucellosis simulates that of tuberculosis in many respects. Of primary importance is the tendency of both tubercle bacilli and Brucella to localize in macrophages. Hart and Rees (9) demonstrated that cortisone enhanced both acute and chronic tuberculosis in mice. There was more dissemination of the infection in the cortisonetreated animals; the individual lesions showed more necrosis and caseation, and contained many more tubercle bacilli than were found in the non-treated control animals. Contrary to expectations, preliminary observations revealed that cortisone caused a marked proliferation and dissemination of Brucella organisms in animals with acute brucellosis, but the steroid did not provoke any demonstrable changes in the animals with chronic infections (10). The present studies also provided information for investigations on the influence of adrenocorticotropic hormone in human subjects having acute or chronic Brucella infections. METHODS OF STUDY