# Case Report: Fulminant shock due to PVL-positive Staphylococcus aureus in an adolescent—superantigen-negative sepsis with toxic shock-like features

## TL;DR

A 16-year-old healthy boy died rapidly from a severe Staphylococcus aureus infection with toxic shock-like symptoms despite aggressive treatment.

## Contribution

This case report highlights the rare but severe clinical presentation of PVL-positive S. aureus sepsis without classical toxin genes.

## Key findings

- PVL-positive S. aureus can cause fulminant shock with toxic shock-like features even when superantigen genes are absent.
- The patient's condition deteriorated rapidly despite VA-ECMO and broad-spectrum antibiotics.
- Atypical presentations of S. aureus infections pose diagnostic and management challenges.

## Abstract

Panton-Valentine leukocidin (PVL)-positive Staphylococcus aureus strains are associated with severe necrotising infections and may be linked to fulminant systemic inflammatory presentations. We report an exceptionally fulminant and rapidly fatal case of PVL-positive S. aureus sepsis with toxic shock-like features and early deterioration despite escalation to veno-arterial extracorporeal membrane oxygenation (VA-ECMO).

A previously healthy 16-year-old boy presented with chest pain, dyspnoea and circulatory collapse. Initial evaluation demonstrated massive bilateral pulmonary embolism, severe biventricular systolic dysfunction, acute kidney injury and marked systemic inflammation. He received prompt haemodynamic support, systemic thrombolysis for high-risk pulmonary embolism and empirical broad-spectrum antibiotics. Echocardiography confirmed profound myocardial dysfunction and VA-ECMO was instituted as salvage support. S. aureus grew from respiratory samples and blood cultures, with susceptibility consistent with meticillin-susceptible S. aureus. Virulence gene profiling by multiplex PCR detected lukS-PV and LukF-PV, while tst, eta and etb were not detected. Antimicrobial therapy was shifted to include antitoxin agents (clindamycin and linezolid). Intravenous immunoglobulin was not administered. Despite maximal supportive care, he developed refractory multi-organ failure and died within 24 h of ICU admission.

PVL-positive S. aureus can, albeit rarely, be associated with an extreme toxic shock-like phenotype even when classical toxin genes are not detected. This case highlights the diagnostic and management challenges posed by atypical presentations and mixed shock physiology, and underscores the need for early recognition and rapid escalation of supportive care.