2020 Pediatric Research Forum Poster Session

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Osteoarticular infections (OAI), most commonly caused by S. aureus, cause extreme morbidity in children and may result in permanent sequelae (e.g. limb-length discrepancies). However, S. aureus is also a common colonizing bacteria of skin and a cause of soft tissue abscesses. Virulence determinants for S. aureus are likely complex, and may include the genetic composition of the isolate, the host immune response and the transcriptomic profile of the organism. A necessary first-step in characterizing these virulence factors includes assessing virulence gene carriage between S. aureus isolates from children with OAIs and from less virulent isolates.


S. aureus isolates from children with OAIs (septic arthritis, acute or chronic osteomyelitis) were prospectively collected over 2 years and underwent metagenomic next generation sequencing on the Illumina MiSeq. S. aureus isolates were also prospectively collected from children with soft tissue abscesses and children with asymptomatic skin colonization.


Forty-eight children (61 isolates) were enrolled (7 with chronic osteomyelitis, 4 with septic arthritis, 9 with acute osteomyelitis, 16 with soft tissue abscesses without systemic invasion and 12 uninfected children with skin colonization). Each isolate underwent mNGS. Our literature search identified approximately 300 putative S. aureus virulence genes, which were organized by function (e.g. toxins, adhesins, immune evasion). This spring, comparisons of virulence gene carriage for these genes will be performed for each group of isolates (those taken from OAIs, soft tissue abscesses and skin colonization).


Using this data, we hope to expand our study to include transcriptomic profiles of S. aureus, as well as concurrent analysis of the host immune response during OAIs. Knowledge of specific genes involved in the pathogenesis of OAIs may serve a diagnostic role (e.g. screening of colonizing isolates for virulence genes) or a therapeutic function (e.g. use of agents which antagonize gene products involved in pathogenesis).


Presented at the Annual Pediatric Research Forum Poster session. Contact Walter Dehority WDehority@salud.unm.edu for questions.

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