Surgical Site Infections following Spine Surgery for Non-idiopathic Scoliosis.

BACKGROUND: Surgical site infections (SSIs) following spine surgery in children and adolescents with nonidiopathic scoliosis are associated with increased morbidity and health care costs. Potentially modifiable risk factors for SSIs merit additional study in this population. METHODS: A single-center, retrospective cohort study was performed from August 2008 through December 2013 in children and adolescents undergoing surgery for nonidiopathic scoliosis to determine the trends in SSI rate and causative microorganisms. A standardized perioperative antimicrobial prophylaxis regimen was developed from September-October 2008. Potential risk factors for SSIs were assessed by multivariable analysis using Poisson regression models. Fusion procedures and growing construct procedures were analyzed separately. RESULTS: In all, 268 patients underwent 536 surgical procedures of whom 192 underwent 228 fusion procedures, 89 underwent 308 growing construct procedures, and 13 underwent both procedures during the study period. Twenty-one SSIs (3.9% of surgical procedures and 7.8% of patients) occurred within 90 days of surgery, 17 SSIs occurred after fusion procedures (4.5% of procedures and 8.9% of patients), and 4 SSIs occurred after growing construct procedures (1.3% of procedures and 4.5% of patients). There were 9 polymicrobial SSIs (42.9%). Of the 31 bacterial pathogens isolated, 48% were Gram-negative organisms. Among patients undergoing fusion procedures, SSIs were associated with underdosing of preoperative cefazolin [relative risk (RR)=4.99; 95% confidence interval (CI), 1.89-17.43; P=0.012] and tobramycin (RR=5.86; 95% CI, 1.90-18.06; P=0.002), underdosing of intraoperative (RR=5.65; 95% CI, 2.13-14.97; P=0.001) and postoperative (RR=3.86; 95% CI, 1.20-12.40; P=0.023) tobramycin, and any preoperative or intraoperative underdosing (RR=4.89; 95% CI, 1.70-14.12; P=0.003), after adjustment for duration of surgery. No factors were associated with SSIs in those undergoing growing construct procedures. During the study period, the SSIs rate declined (P<0.0001). CONCLUSIONS: Underdosing of tobramycin and preoperative cefazolin were associated with an increased SSI risk among patients undergoing fusion procedures. Future multicenter studies should further investigate the generalizability of these findings. LEVEL OF EVIDENCE: Level II-retrospective study.

Cigarette smoke increases Staphylococcus aureus biofilm formation via oxidative stress.

The strong epidemiological association between cigarette smoke (CS) exposure and respiratory tract infections is conventionally attributed to immunosuppressive and irritant effects of CS on human cells. Since pathogenic bacteria such as Staphylococcus aureus are members of the normal microbiota and reside in close proximity to human nasopharyngeal cells, we hypothesized that bioactive components of CS might affect these organisms and potentiate their virulence. Using Staphylococcus aureus as a model organism, we observed that the presence of CS increased both biofilm formation and host cell adherence. Analysis of putative molecular pathways revealed that CS exposure decreased expression of the quorum-sensing agr system, which is involved in biofilm dispersal, and increased transcription of biofilm inducers such as sarA and rbf. CS contains bioactive compounds, including free radicals and reactive oxygen species, and we observed transcriptional induction of bacterial oxidoreductases, including superoxide dismutase, following exposure. Moreover, pretreatment of CS with an antioxidant abrogated CS-mediated enhancement of biofilms. Exposure of bacteria to hydrogen peroxide alone increased biofilm formation. These observations are consistent with the hypothesis that CS induces staphylococcal biofilm formation in an oxidant-dependent manner. CS treatment induced transcription of fnbA (encoding fibronectin binding protein A), leading to increased binding of CS-treated staphylococci to immobilized fibronectin and increased adherence to human cells. These observations indicate that the bioactive effects of CS may extend to the resident microbiota of the nasopharynx, with implications for the pathogenesis of respiratory infection in CS-exposed humans.

Emergence of the epidemic methicillin-resistant Staphylococcus aureus strain USA300 coincides with horizontal transfer of the arginine catabolic mobile element and speG-mediated adaptations for survival on skin.

UNLABELLED: The arginine catabolic mobile element (ACME) is the largest genomic region distinguishing epidemic USA300 strains of methicillin-resistant Staphylococcus aureus (MRSA) from other S. aureus strains. However, the functional relevance of ACME to infection and disease has remained unclear. Using phylogenetic analysis, we have shown that the modular segments of ACME were assembled into a single genetic locus in Staphylococcus epidermidis and then horizontally transferred to the common ancestor of USA300 strains in an extremely recent event. Acquisition of one ACME gene, speG, allowed USA300 strains to withstand levels of polyamines (e.g., spermidine) produced in skin that are toxic to other closely related S. aureus strains. speG-mediated polyamine tolerance also enhanced biofilm formation, adherence to fibrinogen/fibronectin, and resistance to antibiotic and keratinocyte-mediated killing. We suggest that these properties gave USA300 a major selective advantage during skin infection and colonization, contributing to the extraordinary evolutionary success of this clone. IMPORTANCE: Over the past 15 years, methicillin-resistant Staphylococcus aureus (MRSA) has become a major public health problem. It is likely that adaptations in specific MRSA lineages (e.g., USA300) drove the spread of MRSA across the United States and allowed it to replace other, less-virulent S. aureus strains. We suggest that one major factor in the evolutionary success of MRSA may have been the acquisition of a gene (speG) that allows S. aureus to evade the toxicity of polyamines (e.g., spermidine and spermine) that are produced in human skin. Polyamine tolerance likely gave MRSA multiple fitness advantages, including the formation of more-robust biofilms, increased adherence to host tissues, and resistance to antibiotics and killing by human skin cells.