The progression of acute haematogenous osteomyelitis into a chronic infection was investigated in a group of ten dogs in which the infection was produced by injection of micropaque barium mixed with Staphylococcus aureus or Salmonella Group C-2 into the tibial nutrient artery. Antibiotics were not used. Twenty four months later the infected limb of the surviving animals exhibited clinical, histological, radiological and microbiological changes which closely resembled those found in chronic haematogenous osteomyelitis (CHO) in humans. We observed spontaneous fractures, skin fistulae, bone sequestration and active bone remodelling. The original infecting bacteria were often replaced by different microorganisms because of skin fistulae or haematogenous contamination. Although the initial mortality was high the surviving animals showed signs of local and systemic symbiosis with the infecting bacteria. In two animals the previously infected and remodelled bone failed to show histological evidence of infection. This model may be useful in the study of a variety of factors affecting the natural history of CHO, particularly those encompassing the immunological response of the host.
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