Effects of hormones on the adrenal necrosis produced by Besnoitia jellisoni in golden hamsters.

Adrenal necrosis has been described in golden hamsters where it occurs during the course of infection with Besnoilia jellisoni. This necrosis results directly from the active intracellular proliferation by this obligate intracellular protozoan organism. After infection, adrenal necrosis is rarely observed in hypophysectomized hamsters. In unoperated animals adrenal necrosis is suppressed to varying degrees by cortisone (E), hydrocortisone (F), corticosterone (B), 11-dehydrocorticosterone (A), and possibly by 11-desoxycorticosterone (DOCA). Besnoitia organisms proliferate in otherwise "immune" hamsters around the subcutaneous deposits of the acetates of cortisone (E), hydrocortisone (F), and 11-dehydrocorticosterone (A); a marked depression of general immunity follows the administration of pharmacologic doses of the former two hormones. Organisms do not proliferate around the sites of corticosterone acetate (B) and 11desoxycorticosterone acetate (DOCA) injection, nor next to deposits of testosterone propionate, 11-desoxy-17-hydroxycorticosterone acetate (Reichstein's compound S) and epinephrine in oil. It is postulated that certain glucocorticoids can so modify immunity mechanisms locally, that general immunity becomes ineffective; this occurs in the adrenal glands owing to endogenous corticoid production, at the sites of exogenous corticoid injection, and proximal to that in the lungs. A comparison is made with the pathogenesis of tuberculosis and histoplasmosis of the adrenal gland which results in Addison's disease in man, and it is concluded that a similar pathogenetic mechanism is operative. The use of glucocorticoids for replacement therapy is discussed in reference to their relative resistance-depressing activities in pharmacologic doses. These undesirable side effects would appear to be less pronounced, if not absent, if corticosterone (B) rather than cortisone (E) and hydrocortisone (F) therapy were used. Porcine adrenocorticotrophic hormone (ACTH) appearsto depress the incidence of adrenal necrosis in unoperated hamsters, and supports proliferation of organisms in the adrenal cortex with subsequent necrosis in only a small proportion of hypophysectomized hamsters. The possibility is discussed that ACTH from a different species (hog) might lead to a change in the secretory activity of the hamster adrenal gland.