Experiments on white mice were undertaken to determine the reaction of bone to the intramedullary introduction of the virus of tick-borne encephalitis. The following conclusions were drawn. 1. The tick-borne encephalitis virus S47, when introduced intraosteally in white mice, provokes osteitis. 2. Inflammation may lead to acute necrosis of bone, preceded by marked medullary oedema and subsequent proliferation, or it may take a milder form with haemorrhagic effusion into the marrow tissue and subsequent hyperplasia of connective tissue. 3. Damage to the epiphysial and articular cartilage may ensue in the course of acute necrotic osteitis. 4. Skeletal and extra-skeletal osteogenesis is a characteristic feature of viral osteitis. 5. In radiographs in acute viral osteitis with extensive necrosis the expanded bone appears to be thickened. 6. Viruses of the S47 strain introduced intraosteally preserve their affinity for brain tissue after three passages through bone. 7. Viruses introduced into the bony tissue preserve their toxicity and are found in the bony tissue after ten days in quantities lethal for young mice when inoculated intracerebrally. 8. The tick-borne encephalitis virus S47 is pathogenic when inoculated into the marrow in white mice. 9. In osteitis of non-bacterial origin in man the possibility of viral infection should be considered.
1. A child is described in whom an acute osteitis was produced by some organism which could neither be identified nor cultured 2. This organism survived in a cavity in the femur for four months; it preserved its pathogenic properties, and could only be cultured in living tissue. 3. A twice repeated passage through animals increased the toxicity of this organism and proved its affinity for the central nervous system. 4. This organism may have been a virus similar to those producing encephalitis. A final answer may be obtained by further attempts to provoke experimental osteitis with live cultures of viruses in animals.
