Encephalitozoon cuniculi infection in MRL/MPJ-LPR (lymphoproliferation) mice.

Experiments were conducted to determine (a) whether mice bearing the single autosomal recessive gene lpr (lymphoproliferation) are more susceptible to encephalitozoonosis than syngeneic mice without the lpr gene and (b) whether infection with Encephalitozoon cuniculi in autoimmune MRL/MPJ mice accelerates and/or exacerbates the development of hypergammaglobulinemia, a manifestation of encephalitozoonosis in dogs and foxes. The results suggested that the lpr gene does not influence susceptibility to murine encephalitozoonosis. Infection with E. cuniculi changed neither the onset nor the severity of the spontaneous, age-related hypergammaglobulinemia in MRL/MPJ mice. Hypergammaglobulinemic lpr mice with encephalitozoonosis did not develop more severe lesions than lpr mice without encephalitozoonosis nor was their death accelerated.