Severe co-infection with influenza A virus H3N2 and community-acquired methicillin-susceptible Staphylococcus aureus in a child presenting with septic shock, acute respiratory distress syndrome, and necrotizing pneumonia: a rare case report.
Influenza co-infection with Staphylococcus aureus (S. aureus) can cause rapidly fatal necrotizing pneumonia, septic shock, and acute respiratory distress syndrome (ARDS) in children. Although methicillin-resistant S. aureus is often highlighted, community-acquired methicillin-susceptible S. aureus (CA-MSSA) can also produce equally severe disease.
We report an 8-year-4-month-old male with influenza A (H3N2) who developed septic shock and refractory hypoxemia, requiring immediate intubation. Due to persisting respiratory failure despite maximal ventilation, veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated on day 1. Metagenomic next-generation sequencing identified S. aureus as the dominant pathogen, and bronchoalveolar lavage fluid culture later confirmed MSSA. After vancomycin failed clinically, the regimen was switched to linezolid. However, on day 15 of linezolid therapy, the patient developed severe linezolid-induced lactic acidosis (LILA), which resolved within 3 days of stopping the drug. The clinical course was further complicated by pneumothorax and multidrug-resistant organism superinfections. After 54 days of intensive care, the patient was discharged in good condition.
This case underscores that during influenza seasons, early empirical anti-staphylococcal therapy should be considered in children with rapidly progressive pneumonia and shock, even when CA-MSSA is suspected. Additionally, routine lactate monitoring is critical during linezolid therapy to enable prompt recognition and management of life-threatening LILA.
We report an 8-year-4-month-old male with influenza A (H3N2) who developed septic shock and refractory hypoxemia, requiring immediate intubation. Due to persisting respiratory failure despite maximal ventilation, veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated on day 1. Metagenomic next-generation sequencing identified S. aureus as the dominant pathogen, and bronchoalveolar lavage fluid culture later confirmed MSSA. After vancomycin failed clinically, the regimen was switched to linezolid. However, on day 15 of linezolid therapy, the patient developed severe linezolid-induced lactic acidosis (LILA), which resolved within 3 days of stopping the drug. The clinical course was further complicated by pneumothorax and multidrug-resistant organism superinfections. After 54 days of intensive care, the patient was discharged in good condition.
This case underscores that during influenza seasons, early empirical anti-staphylococcal therapy should be considered in children with rapidly progressive pneumonia and shock, even when CA-MSSA is suspected. Additionally, routine lactate monitoring is critical during linezolid therapy to enable prompt recognition and management of life-threatening LILA.