A healthy 70-year-old woman was admitted with a 3-day history of a pus-emitting wound on her left shin, in the absence of trauma. She was afebrile, and examination was normal excepting a warm, erythematous and tender area over her left distal tibia with a central swollen area discharging pus.
Hemoglobin was 11.7 g/dL, white blood cell count 17.2 × 109/L, platelets 480 × 109/L. Erythrocyte sedimentation rate and C-reactive protein were only mildly elevated (31 mm/h and 37 mg/L, respectively). Results of other blood tests were normal. Gram stain of the pus revealed Gram-positive cocci. Leg x-ray and computed tomography showed chronic tibial osteomyelitis with cortical perforation and sinus tract formation (Figures 1 and 2). When asked, she remembered having leg osteomyelitis when she was a 5-year-old child in Russia.
Pus cultures demonstrated penicillin-sensitive Staphylococcus aureus. Blood cultures were negative. At operation, debridement of subcutaneous granulation tissue and pus was done, followed by drilling of the anterior tibial wall. Pus under pressure came out of the bone marrow, and extensive debridement and washings were performed. Deep surgical biopsies grew penicillin-sensitive S. aureus. A peripherally inserted central catheter (PICC line) was placed, and she was discharged home for prolonged treatment with intravenous cloxacillin (8 g daily).
Our immunocompetent patient’s only risk factor was a remote history of osteomyelitis that apparently healed 65 years earlier. Her current infection developed in the same location and involved the same organism; although no records of her 1951 hospitalization were available, the isolated S. aureus was sensitive to penicillin G, whereas the vast majority of strains became resistant to the drug in the 1950s and 1960s owing to its widespread use and production of β-lactamases.1, 2
Staphylococcus aureus is the most common cause of osteomyelitis and very probably caused the patient’s acute illness when she was a child by hematogenous spread, typically involving the metaphysis of a long bone.3 The associated intense inflammatory response often compromises medullary and periosteal blood supply, leading to dead bone (sequestrum) formation, the hallmark of chronic osteomyelitis. Within this necrotic ischemic tissue bacteriae can be hard to eradicate, and intracellular S. aureus persistence in osteoblasts has been well documented in vitro, in vivo, and in chronic osteomyelitis.4 Reactivation can occur after many years as in our patient, whose presenting feature was extension through cortical bone and sinus tract formation (Figures 1 and 2). Blood tests may appear misleadingly innocent, but thrombocytosis may be a diagnostic clue.5 Sinus tract cultures may not indicate the pathogenetic organism, and deep surgical specimen isolates are necessary. In our patient they were identical, demonstrating that a 65-year-old S. aureus can still matter.
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-Moshe Gelber, MD, Frida Babushkin, MD, Ami Schattner, MD
This article originally appeared in the March 2017 issue of The American Journal of Medicine.
