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.