The smr and qacA/B genes in Staphylococcus aureus confer tolerance to antiseptics and are associated with nosocomial acquisition of infection and underlying medical conditions. Such antiseptic tolerance (AT) genes have also been reported in coagulase-negative staphylococci (CoNS) and enterococci, however, few data are available regarding their prevalence. We sought to describe the frequency of AT genes among bloodstream isolates of S. aureus, CoNS and enterococci at Texas Children’s Hospital (TCH).

Banked CoNS, S. aureus and enterococci isolated from blood cultures collected bewteen October 1, 2016, and October 1, 2017, were obtained from the TCH clinical microbiology laboratory. All isolates underwent polymerase chain reaction (PCR) assay for the qacA/B and smr genes. Medical records were reviewed for all cases.

In total, 103 CoNS, 19 Enterococcus spp, and 119 S. aureus isolates were included in the study, and 80.6% of the CoNS possessed at least 1 AT gene compared to 37% of S. aureus and 43.8% of E. faecalis isolates (P < .001). Among CoNS bloodstream isolates, the presence of either AT gene was strongly associated with nosocomial infection (P < .001). The AT genes in S. aureus were associated with nosocomial infection (P = .025) as well as the diagnosis of central-line–associated bloodstream infection (CLABSI; P = .04) and recent hospitalizations (P < .001). We found no correlation with genotypic AT in E. faecalis and any clinical variable we examined.

Antiseptic tolerance is common among bloodstream staphylococci and E. faecalis isolates at TCH. Among CoNS, the presence of AT genes is strongly correlated with nosocomial acquisition of infection, consistent with previous studies in S. aureus. These data suggest that the healthcare environment contributes to AT among staphylococci.

To document the introduction of the methicillin-resistant Staphylococcus aureus (MRSA) USA300 clone into a children's hospital. Current molecular epidemiology of infections due to the USA300 strain of MRSA in the pediatric healthcare setting remains obscure.

Retrospective study of patients with hospital-acquired S. aureus infection during the period from August 1, 2001, through July 31, 2007, at Texas Children's Hospital in Houston.

Patients with hospital-acquired S. aureus infection from whom an isolate was available for molecular analysis were included. Clinical information was obtained from patient medical records and the electronic hospital information system. S. aureus isolates underwent antimicrobial susceptibility testing, pulsed-field gel electrophoresis, and polymerase chain reaction testing for staphylococcal cassette chromosome (SCC) mec, agr, the diamine N-acetyltransferase gene, and the Panton-Valentine leukocidin genes (pvl).

Of 242 patients with hospital-acquired S. aureus infection, 147 (61%) had methicillin-susceptible S. aureus infection. Of the 95 MRSA isolates causing hospital-acquired infection, 69 (73%) were USA300 isolates, and that rate did not increase over time. Skin and soft tissue infection (P < .001), onset of infection less than 10 days after admission (P = .007), and lack of comorbidities (P < .001) were associated with hospital-acquired MRSA infection caused by the USA300 strain, compared with other isolates (hereafter referred to as non-USA300 isolates). Nine of 10 patients with a S. aureus infection at the time of death were infected with a non-USA300 strain. USA300 carried SCCmec IV, agr I, the diamine N-acetyl transferase gene, and pvl. USA300 isolates were more susceptible to clindamycin, gentamicin, and trimethoprim-sulfamethoxazole than were other non-USA300 isolates (P < .01).

In our patient population, the annual numbers of observed cases of hospital-acquired S. aureus infection have remained constant. USA300 was the most common clone and, compared with other non-USA300 MRSA isolates, was associated with skin and soft tissue infection, early onset of infection after admission, and greater susceptibility to antimicrobial agents.