Experimental mycotic encephalitis.

Abstract

Oidiodendron kalrai infection in mice is presented as a suitable model for the study of the pathogenesis of mycotic encephalitis. Intravenous inoculation of cortisone-treated and non-treated mice with the yeast-phase ofO. kalrai resulted in a neurologic syndrome characterized by head tilt, circling, hyperexcitability and ataxia. Signs of neurologic disease appeared earlier and were more severe in cortisone-treated animals. Grossly detectable areas of hemorrhage, necrosis and edema were apparent in over 80 percent of the cortisone-treated mice killed 4–6 days after infection. Lesions were demonstrated microscopically in the CNS of all mice infected withO. kalrai from the second to the 35th day following inoculation. Mice not treated with cortisone developed an immediate histiocytic response leading to the arrest of fungal proliferation by the 3rd day and to regression and scarring by the 7th day following infection. In cortisone-treated mice the cellular response was delayed and primarily neutrophilic and fungal growth continued through the 6th day after infection. The distribution of lesions was similar in both groups, although the lesions were more extensive in mice treated with cortisone. The mycelial-phase was the invasive form ofO. kalrai, while the arthrospore represented the form most resistant to the hosts' inflammatory response. The possible mechanisms of cellular penetration by the fungus and the role of cortisone in the altered course of the disease are discussed.