Sequential Folliculitis, Paraspinal Myositis, and Septic Arthritis Due to Hematogenous Staphylococcus aureus Infection in a Patient Receiving Adalimumab Therapy

Skin infections are a well-recognized source of bacteremia and can serve as foci for hematogenous spread leading to sepsis, septic arthritis, or osteomyelitis. Immunosuppressive therapies, particularly tumor necrosis factor alpha (TNF-α) inhibitors such as adalimumab, predispose patients to severe infections and are associated with increased infectious morbidity and mortality. These agents impair innate immune signaling and may attenuate the clinical manifestations of infection. Specifically, TNF-α blockade disrupts downstream interleukin-1β (IL-1β) and interleukin-6 (IL-6) pathways that mediate leukocyte recruitment and the febrile response. Consequently, patients receiving TNF-α inhibitors may present with bacteremia or early sepsis in the absence of typical findings such as fever or leukocytosis, potentially delaying diagnosis and treatment. We report a middle-aged Caucasian male patient receiving adalimumab therapy who initially presented to the emergency department with presumed paraspinal muscle strain and degenerative spondylosis. Magnetic resonance imaging (MRI) was interpreted as consistent with muscular strain and degenerative spondylosis. Subsequent orthopedic evaluation revealed a septic-appearing left knee, with synovial and blood cultures positive for methicillin-sensitive <i>Staphylococcus aureus </i>(MSSA). Further review of his history revealed that he had been treated for folliculitis over the occipital scalp one week prior to presentation, suggesting hematogenous dissemination from a cutaneous source. Given the patient's immunosuppressed state and atypical presentation, we conclude that bacteremia secondary to folliculitis resulted in occult paraspinal myositis mimicking a muscle strain, and ultimately progressed to septic arthritis. This case highlights the need for high clinical suspicion for hematogenous infection in patients receiving TNF-α inhibitors who present with musculoskeletal pain and minimal systemic findings.