Frontiers in cellular and infection microbiology · 2026
Fatal Panton-Valentine leukocidin-positive MSSA toxic shock syndrome: a call for rapid virulence detection and optimized antimicrobial therapy.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Zhao Congcong, Ren Rongrong, Wu Wei, Liu Jingxian, Chen Chun, Yin Na, Li Lixia
Аннотация
BACKGROUND: Toxic shock syndrome (TSS) is a rare but potentially life-threatening toxin-mediated infection. Cases associated with Panton-Valentine leukocidin (PVL)-producing Staphylococcus aureus are particularly uncommon in clinical settings and remain insufficiently documented in the literature.
OBJECTIVES: This report aims to strengthen clinical understanding of TSS caused by methicillin-sensitive Staphylococcus aureus (MSSA) harboring PVL, assess optimal antimicrobial strategies for treating MSSA infections, minimize the risk of therapeutic failure, and offer insights that may inform timely diagnosis and effective clinical management.
METHODS: We present a case involving a 26-year-old female patient with MSSA isolated from multiple anatomical sites who initially received vancomycin before being diagnosed with PVL-positive MSSA-induced TSS. Therapeutic efficacy was evaluated by integrating her clinical course with contemporary evidence on the management of severe MSSA infections. In addition, treatment considerations for highly virulent MSSA infections with distinct clinical characteristics were examined.
RESULTS: The patient's clinical course enabled a comparative assessment of β-lactam antibiotics, such as cefazolin, versus glycopeptide agents, such as vancomycin, in the management of MSSA infections. Upon confirmation of MSSA, early transition to targeted therapy with cefazolin or anti-staphylococcal penicillins may be considered. In critically ill patients, early virulence gene testing is important for rapid identification of PVL-positive strains.
CONCLUSIONS: PVL-positive MSSA may be associated with a fulminant, atypical toxic shock syndrome-like phenotype characterized by disseminated pustulosis and pancytopenia, which should raise immediate suspicion of a toxin-driven process. This case suggests that de-escalation from vancomycin to a β-lactam antibiotic upon MSSA confirmation may be a key therapeutic strategy. Increased vigilance, rapid virulence factor testing, and early aggressive management are important to improving outcomes.
OBJECTIVES: This report aims to strengthen clinical understanding of TSS caused by methicillin-sensitive Staphylococcus aureus (MSSA) harboring PVL, assess optimal antimicrobial strategies for treating MSSA infections, minimize the risk of therapeutic failure, and offer insights that may inform timely diagnosis and effective clinical management.
METHODS: We present a case involving a 26-year-old female patient with MSSA isolated from multiple anatomical sites who initially received vancomycin before being diagnosed with PVL-positive MSSA-induced TSS. Therapeutic efficacy was evaluated by integrating her clinical course with contemporary evidence on the management of severe MSSA infections. In addition, treatment considerations for highly virulent MSSA infections with distinct clinical characteristics were examined.
RESULTS: The patient's clinical course enabled a comparative assessment of β-lactam antibiotics, such as cefazolin, versus glycopeptide agents, such as vancomycin, in the management of MSSA infections. Upon confirmation of MSSA, early transition to targeted therapy with cefazolin or anti-staphylococcal penicillins may be considered. In critically ill patients, early virulence gene testing is important for rapid identification of PVL-positive strains.
CONCLUSIONS: PVL-positive MSSA may be associated with a fulminant, atypical toxic shock syndrome-like phenotype characterized by disseminated pustulosis and pancytopenia, which should raise immediate suspicion of a toxin-driven process. This case suggests that de-escalation from vancomycin to a β-lactam antibiotic upon MSSA confirmation may be a key therapeutic strategy. Increased vigilance, rapid virulence factor testing, and early aggressive management are important to improving outcomes.