EFFECTS OF HORMONES ON THE ADRENAL NECROSIS PRODUCED BY BESNOITIA JELLISONI IN GOLDEN HAMSTERS

Abstract

Adrenal necrosis was described in golden hamsters (Mesocricetus auratus) where it occurs during the course of infection with Besnoitia jellisoni. The 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-desoxycortico-sterone (DOCA). Besnoitia organisms proliferate in otherwise "immune" hamsters around the subcutaneous deposits of the acetates of E, F, A; a marked depression of general immunity follows the administration of pharmacologic doses of the former 2 hormones. Organisms do not proliferate around the sites of B and DOCA injection, nor next to deposits of testerone propionate, ll-desoxy-17-hydroxycorticosterone acetate and epinephrine in oil. It is postulated that certain gluco-corticoids can so modify immunity mechanism 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. 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.