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cluded from the study; 65 bacteremic patients were included (table 1). Of those 65 patients, 29 (44.6%) presented with Streptococcus pneutmoniae bacteremia. Thirteen (65%) of 20 patients with CK levels of >500 IU/L had pneumococcal bacteremia. CK levels peaked on the first or second day after admission to the hospital, and levels normalized within 5 days. The presence of rhabdomyolysis did not correlate with age or the presence of fever, a state of hypoperfusion, renal failure, respiratory failure, alcohol intoxication, hypophosphoremia, or disseminated intravascular coagulation. Outcome was not affected by the severity of rhabdomyolysis, and no patients suffered renal failure related to muscular injury. No patient had leptospirosis. Our patients were not phosphoremic; thus, the development of rhabdomyolysis can not be explained by the presence of hypophosphoremia, as it was by Spataro and Marone in their study [1]. We do not know what the mechanism of muscular injury was; others have assumed that direct toxicity of bacterial products [2] or cytokin-mediated interleukin 1 and injury are the causes of rhabdomyolysis [3]. Rhabdomyolysis, as demonstrated by a rise in serum levels of