You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
Effects of Corticosteroids on Antibody and Immunity in "Besnoitia" Infection of Hamsters
J. K. Frenkel and Milford N. Lunde
The Journal of Infectious Diseases
Vol. 116, No. 4 (Oct., 1966), pp. 414-424
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30103711
Page Count: 11
Preview not available
Infection with the obligate intracellular protozoan Besnoitia jellisoni can pass from an acute into a chronic latent phase, especially when aided by sulfadiazine therapy. Chronically infected hamsters are immune to challenge by the intraperitoneal or subcutaneous route. The acquisition of immunity is also accompanied by sharply decreasing parasite numbers. Small numbers of organisms persist in many organs, however. No cross immunity or nonspecific resistance to the related Toxoplasma is acquired. The administration of pharmacologic doses of potent corticoids brings about relapse in 7 to 14 days, with a 4 to 5 log lo increase in parasites. Cortisol was effective subcutaneously but not intraperitoneally or perorally. Corticoids do not significantly accelerate death from primary infection and show their activity only in the presence of some immunity. The longer the period of immunogenesis the longer do hamsters survive after starting corticoid administration. Antibody measured by dye test and indirect hemagglutinationtest during chronic infection is stable over a 20-day period during which all animals died from corticoid-induced relapse. Antibody confers a measure of passive immunity. However, even with high titers persisting for over 2 weeks and with antibody being actively elaborated, the resulting immunity is less than that acquired during sulfadiazine prophylaxis for 1 week. Cortisone diminishes the partial immunity of passively protected hamsters due to interference with the development of active immunity which is completely suppressed when corticoids are administered from the time of infection. Besnoitia immunity appears to be dependent on intracellular processes (possibly intracellular digestion) with which corticoids can interfere. Viral and other intracellular bacterial and fungal infections which give rise to clinical disease in patients with hypercorticism are discusred in the light of the present model.
The Journal of Infectious Diseases © 1966 Oxford University Press