What question did this study set out to answer?

This case highlights an unusual instance of rapidly fatal necrotizing fasciitis caused by Serratia marcescens in an immunosuppressed patient.

March 26, 2026

859: Case Report of Rapidly Fatal Serratia Marcescens Necrotizing Fasciitis

Key Points

This case highlights an unusual instance of rapidly fatal necrotizing fasciitis caused by Serratia marcescens in an immunosuppressed patient.
Detailed patient history and physical examination.
Imaging studies including CT to assess soft tissue involvement.
Laboratory analysis for inflammatory markers and infection indicators.
Emergent surgical interventions, including excisional debridement.
Administration of broad-spectrum antibiotics.
The patient presented with severe symptoms and rapid deterioration despite treatment.
Serratia marcescens was identified as a rare cause of necrotizing fasciitis.
She required multiple surgical interventions but ultimately succumbed to multi-organ failure.
Initial imaging and scoring did not accurately reflect her clinical severity.

Abstract

Introduction: Necrotizing soft tissue infections (NSTIs) are aggressive infections involving skin, fascia, and muscle, with mortality rates of 25–30%. Pathogenesis includes infection, toxin production, cytokine release, and tissue ischemia. NSTIs may occur without trauma, particularly in immunosuppressed hosts. Serratia marcescens, a gram-negative opportunistic pathogen, is rarely implicated in monomicrobial NSTIs. Description: A 67-year-old woman with rheumatoid arthritis on golimumab, CKD-4, type 2 diabetes, and transfusion-dependent anemia presented with fever, hypotension, and left calf pain. She had a history of recurrent urinary tract infections. Labs revealed neutropenia (WBC 0.5 K/μL), creatinine 6.66 mg/dL, and lactate 3.8 mmol/L. CT showed nonspecific subcutaneous edema without gas or fluid collection. LRINEC score was 4. She was transferred to a tertiary ICU and rapidly progressed to vasoplegic shock requiring triple vasopressors/inotropes and stress-dose steroids. Her left leg was erythematous, tender, and showed progression beyond marked borders. Emergent exploration revealed extensive necrosis with “dishwater fluid” and thrombosed fascia, confirming NSTI. Aggressive excisional debridement of skin, fascia, and muscle was performed. Postoperatively, her multi-organ failure worsened, requiring continuous renal replacement despite broad antimicrobial therapy (meropenem, vancomycin, clindamycin, tobramycin). A second excisional debridement was performed at 12-hours, but her refractory acidosis worsened and she died following transition to comfort measures. Discussion: Monomicrobial S. marcescens NSTI is exceedingly rare, with only 17 cases reported. This patient’s profound immunosuppression from golimumab likely predisposed her to this pathogen and blunted classic inflammatory signs. TNF-α plays a central role in immune response; its blockade impairs pathogen clearance and immune activation. Imaging and LRINEC were falsely reassuring in this case—emphasizing the limitations of these tools in immunocompromised patients. Serratia’s ability to produce beta-lactamase and cause severe infection highlights the need for rapid surgical intervention and broad antimicrobial coverage. This case underscores the potential for atypical, fulminant infections in TNF-α-inhibited hosts.

Mark Helpful

Bookmark

Relay