Brucellosis in mice results in a distinct immunosuppression which may be abrogated by immunomodulators, such as levamisole, bestatin, interleukin-2 (IL-2) and Polyporus umbellatus. The data presented here provide evidence that immunosuppression in addition to infection of target tissues and allergic reactions (including types 3 and 4) contributes to the pathogenesis of brucellosis. The present study also provides some basic data regarding the value of this animal model, and criteria for observing the effect of therapy on chronic brucellosis.