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Experimental infection of immunodeficient NIH-3 (N:NIH-bg-nu-xid) mice with Borrelia burgdorferi was found to result in multisystem histopathologic lesions. In addition to T-cell deficiency due to the nude mutation, these mice have an x-linked defect affecting the B-cell maturation and the beige mutation resulting in the absence of NK cells. NIH-3 mice were susceptible to progressive infection with B. burgdorferi resulting in pancarditis, synovitis, and skeletal interstitial myositis whereas controls remained normal. Cardiomyopathy was characterized by inflammatory mononuclear infiltration and fibrillar necrosis. Synovial hyperplasia and inflammation were seen in the tibiotarsal and ulna-carpal joints. Advanced myositis was observed in peripheral skeletal muscle. Gastrointestinal submucosa, heart, and skeletal muscle were heavily colonized with B. burgdorferi. This mouse is proposed as a model for
Lyme borreliosis carditis, synovitis, and myositis.