BackgroundCommunity acquired (CA) methicillin-resistant Staphylococcus aureus (MRSA) increasingly causes disease worldwide. USA300 has emerged as the predominant clone causing superficial and invasive infections in children and adults in the USA. Epidemiological studies suggest that USA300 is more virulent than other CA-MRSA. The genetic determinants that render virulence and dominance to USA300 remain unclear.ResultsWe sequenced the genomes of two pediatric USA300 isolates: one CA-MRSA and one CA-methicillin susceptible (MSSA), isolated at Texas Children's Hospital in Houston. DNA sequencing was performed by Sanger dideoxy whole genome shotgun (WGS) and 454 Life Sciences pyrosequencing strategies. The sequence of the USA300 MRSA strain was rigorously annotated. In USA300-MRSA 2658 chromosomal open reading frames were predicted and 3.1 and 27 kilobase (kb) plasmids were identified. USA300-MSSA contained a 20 kb plasmid with some homology to the 27 kb plasmid found in USA300-MRSA. Two regions found in US300-MRSA were absent in USA300-MSSA. One of these carried the arginine deiminase operon that appears to have been acquired from S. epidermidis. The USA300 sequence was aligned with other sequenced S. aureus genomes and regions unique to USA300 MRSA were identified.ConclusionUSA300-MRSA is highly similar to other MRSA strains based on whole genome alignments and gene content, indicating that the differences in pathogenesis are due to subtle changes rather than to large-scale acquisition of virulence factor genes. The USA300 Houston isolate differs from another sequenced USA300 strain isolate, derived from a patient in San Francisco, in plasmid content and a number of sequence polymorphisms. Such differences will provide new insights into the evolution of pathogens.

Community-acquired methicillin-resistant S aureus is a substantial and increasing proportion of S aureus infections in previously healthy neonates. Male infants 7 to 12 days of age are affected most often. Neonatal community-acquired S aureus infection may be associated with concurrent maternal infection. USA300 is the predominant clone among these neonatal isolates in our region.

Evaluation and treatment strategies for neonatal community-acquired S. aureus disease are varied at our hospital. Prospective studies are needed to determine optimal management strategies.

The objective of this study was to implement a strategy for critical congenital heart disease (CCHD) newborn screening in the neonatal intensive care unit (NICU). A NICU-specific curriculum, screening algorithm, slide presentations, and templates of orders, policies, and procedures were developed into a toolkit for training NICU personnel. Screening was conducted on first and second screen pre- and postductal oxygen saturations (SpO) on newborns admitted or transferred to the NICU. We trained 347 NICU personnel in 13 Texas hospitals, representing rural, suburban, and metropolitan settings. Key hospital staff submitted deidentified, case-based screening data. Of 4,621 NICU admissions, 80% received a first screen. Second screening rates were substantially lower in all gestational age groups. Screening rates on first and second screens were lowest among infants born< 28 weeks. For the first screen, SpO was lowest among the youngest gestational ages. The false positive rate was 2.3%. CCHD screening in the NICU is challenging, given the complexities of the NICU population. A modified screening protocol that recognizes special circumstances of neonatal intensive care could facilitate a more efficient system.