Septic arthritis in sickle-cell thalassemia. Pathophysiology of impaired response to infection.

The knee of a boy with sickle-cell thalassemia became infected with Salmonella enteritidis, sensitive to ampicillin. Doses of ampicillin that achieved anti-bacterial titers of 32 in synovial fluid failed to eradicate the organism. The synovial fluid exhibited severe hypoxia, hypercapnia, and lactic acidosis. Methods were developed to estimate the oxygen saturation of blood in regional venous capillaries, the degree of periarticular sickling, changes in the viscosity of local blood, and the articular ratio of blood flow to oxygen utilization. The results suggest that local vascular insufficiency associated with sickling may affect host response to infection and efficacy of antibiotics. The Salmonella C1 readily transformed to an L form on hypertonic medium, thus acquiring resistance to ampicillin and other cell-wall inhibitors.