Necrotizing Fasciitis Caused by <scp> <i>Achromobacter xylosoxidans</i> </scp> in an Immunocompromised Patient With Chronic Venous Ulcers

Achromobacter xylosoxidans is a nonfermenting, environmental Gram-negative rod considered a low-virulence organism; skin or soft-tissue infections are rare even in immunocompromised individuals [1]. A few cases of cellulitis and wound infection have been reported, including a scalp infection with biofilm formation and bacteremia with cellulitis [1-3]. Necrotizing fasciitis (NF) caused by A. xylosoxidans has not been described to our knowledge. We report such a case. A 77-year-old man with peripheral T-cell lymphoma (PTCL) achieved stable disease after CHOP chemotherapy (completed 11 months before infection) and was subsequently treated with valemetostat, an EZH1/2 inhibitor (initiated 10 months before infection). He had refractory venous stasis ulcers on both lower legs and engaged in daily vegetable farming with routine water exposure. He developed sudden left lower leg pain one day before admission. On admission, he presented with decreased consciousness, hypotension, and cytopenia (WBC 7400/μL, neutrophils 6860/μL, ALC 300/μL, Hb 10.0 g/dL) consistent with septic shock. Key laboratory values included CRP 39.57 mg/dL, CK 47 U/L, sodium 141 mEq/L, creatinine 3.86 mg/dL, and blood glucose 57 mg/dL; the LRINEC score was 8, indicating high NF risk. The normal CK likely reflects early-stage infection prior to significant muscle involvement. Physical examination revealed extensive erythema, swelling, and purpura of the left lower leg (Figure 1a). CT demonstrated subcutaneous oedema and fascial fluid tracking (Figure 1b). NF was diagnosed and emergent debridement performed, confirming fascial necrosis (Figure 1c). Empirical meropenem, clindamycin, and vancomycin were initiated. The patient developed sepsis-associated acute kidney injury requiring continuous hemodiafiltration on hospital Day 1. Both wound and blood cultures yielded A. xylosoxidans. Susceptibility testing showed sensitivity to piperacillin-tazobactam, ceftazidime, cefepime, carbapenems, and minocycline, and resistance to aztreonam, amikacin, and levofloxacin; therapy was de-escalated to meropenem monotherapy. Dialysis was discontinued on Day 5, and repeat debridement with split-thickness skin grafting on Day 14 resulted in favorable recovery (Figure 1d). NF likely developed through three converging factors: (1) chronic venous ulcers as a portal of entry via impaired lymphatic drainage, microangiopathy, and persistent bacterial colonisation [4]—no cutaneous lymphoma lesions were present at the infection site; (2) daily agricultural water contact introducing the organism [1]; and (3) multifactorial immunocompromise including T-cell dysfunction from PTCL, residual CHOP-induced myelosuppression, and potential valemetostat-associated hematological toxicity. Although phase 2 trials of valemetostat have not universally reported severe neutropenia [5], the marked lymphopenia (ALC 300/μL) reflected profound cellular immune dysfunction inherent to PTCL, representing the predominant immunological vulnerability. A. xylosoxidans exhibits intrinsic resistance to aztreonam, aminoglycosides, and often fluoroquinolones; carbapenems and piperacillin–tazobactam are generally first-line agents [1]. Although considered low-virulence, prior reports—including bacteremia-associated cases—document rapid progression in vulnerable hosts [1-3], as illustrated by septic shock within 24 h in this case. Clinicians should recognize that even low-virulence environmental organisms can cause life-threatening NF in immunocompromised patients with chronic ulcers and environmental exposure. Early recognition, prompt surgical debridement, and susceptibility-guided antimicrobial therapy are essential. The authors have nothing to report. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.