Skip to content
The Kids Research Institute Australia logo
Donate

No results yet

Whole genome sequencing and molecular epidemiology of paediatric Staphylococcus aureus bacteraemia

The role Staphylococcus aureus antimicrobial resistance genes and toxins play in disease severity, management and outcome in childhood is an emerging field requiring further exploration.

Citation:
Campbell AJ, Mowlaboccus S, Coombs GW, Daley DA, ……… Carapetis JR, Ching NS, Francis J, Hung TY, …..…. Bowen AC, Blyth CC, Australian, New Zealand Pediatric Infectious Diseases clinical research network of the Australasian Society of Infectious D, the Australian Group on Antimicrobial R. Whole genome sequencing and molecular epidemiology of paediatric Staphylococcus aureus bacteraemia. J Global Antimicrob Resist. 2022;29:197-206.

Keywords:
Bacteraemia; Molecular; Outcomes; Paediatrics; Staphylococcus aureus; Whole genome sequencing

Abstract:
Objectives
The role Staphylococcus aureus antimicrobial resistance genes and toxins play in disease severity, management and outcome in childhood is an emerging field requiring further exploration.

Methods
A prospective multisite study of Australian and New Zealand children hospitalised with S. aureus bacteraemia (SAB) occurred over 24 months (2017–2018). Whole genome sequencing (WGS) data were paired with clinical information from the ISAIAH cohort.

Results
353 SAB isolates were sequenced; 85% methicillin-susceptible S. aureus ([MSSA], 301/353) and 15% methicillin-resistant S. aureus ([MRSA], 52/353). There were 92 sequence types (STs), most commonly ST5 (18%) and ST30 (8%), grouped into 23 clonal complexes (CCs), most frequently CC5 (21%) and CC30 (12%). MSSA comprised the majority of healthcare-associated SAB (87%, 109/125), with principal clones CC15 (48%, 11/21) and CC8 (33%, 7/21). Panton-Valentine leukocidin (PVL)-positive SAB occurred in 22% (76/353); predominantly MSSA (59%, 45/76), community-onset (92%, 70/76) infections. For community-onset SAB, the only microbiological independent predictor of poor outcomes was PVL positivity (aOR 2.6 [CI 1.0–6.2]).

Conclusion
From this WGS paediatric SAB data, we demonstrate the previously under-recognized role MSSA has in harbouring genetic virulence and causing healthcare-associated infections. PVL positivity was the only molecular independent predictor of poor outcomes in children. These findings underscore the need for further research to define the potential implications PVL-producing strains may have on approaches to S. aureus clinical management.