Objective To assess the utility of clinical predictors of persistent respiratory morbidity in extremely low gestational age newborns (ELGAN). Study Design We enrolled ELGAN (<29 weeks’ gestation) at ≤7 postnatal days and collected antenatal and neonatal clinical data through 36 weeks’ post-menstrual age. We surveyed caregivers at 3, 6, 9 and 12 months corrected age to identify post-discharge respiratory morbidity, defined as hospitalization, home support (oxygen, tracheotomy, ventilation), medications, or symptoms (cough/wheeze). Infants were classified as post-prematurity respiratory disease (PRD, the primary study outcome), if respiratory morbidity persisted over ≥2 questionnaires. Infants were classified with severe respiratory morbidity if there were multiple hospitalizations, exposure to systemic steroids or pulmonary vasodilators, home oxygen after 3 months or mechanical ventilation, or symptoms despite inhaled corticosteroids. Mixed effects models generated with data available at one day (perinatal) and 36 weeks’ postmenstrual age were assessed for predictive accuracy. Results Of 724 infants (918±234g, 26.7±1.4 weeks’ gestational age) classified for the primary outcome, 68.6% had PRD; 245/704 (34.8%) were classified as severe. Male sex, intrauterine growth restriction, maternal smoking, race/ethnicity, intubation at birth, and public insurance were retained in perinatal and 36-week models for both PRD and respiratory morbidity severity. The perinatal model accurately predicted PRD (c-statistic 0.858). Neither the 36-week model nor the addition of bronchopulmonary dysplasia (BPD) to the perinatal model improved accuracy (0.856, 0.860); c-statistic for BPD-alone was 0.907. Conclusion Both BPD and perinatal clinical data accurately identify ELGAN at risk for persistent and severe respiratory morbidity at one year. Trial registration ClinicalTrials.gov: NCT01435187

Eliciting a migration history is important at every encounter; migrant patients may have acute illness or chronic conditions related to exposure in their country of origin. Early detection and treatment, particularly for diagnoses related to tuberculosis, HBV, Strongyloides, and schistosomiasis, may improve outcomes. Policy makers should consider expansion of refugee screening programs to include all migrants.

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Objective: To determine patterns of respiratory medications used in neonatal intensive care unit (NICU) graduates. Study design: The Prematurity Respiratory Outcomes Program enrolled 835 babies <29 weeks gestation in the first week. Of 751 survivors, 738 (98%) completed at least 1, and 85% completed

Network (CDN) launched a research and learning collaborative project with six community health centers in the New York City metropolitan area to determine the nature (clonal type) of community-acquired Staphylococcus aureus strains causing skin and soft tissue infections (SSTIs). Between November 2011 and March 2013, wound and nasal samples from 129 patients with active SSTIs suspicious for S. aureus were collected and characterized by molecular typing techniques. In 63 of 129 patients, the skin wounds were infected by S. aureus: methicillinresistant S. aureus (MRSA) was recovered from 39 wounds and methicillin-sensitive S. aureus (MSSA) was recovered from 24. Most-46 of the 63-wound isolates belonged to the CC8/Panton-Valentine leukocidin-positive (PVL ؉ ) group of S. aureus clone USA300: 34 of these strains were MRSA and 12 were MSSA. Of the 63 patients with S. aureus infections, 30 were also colonized by S. aureus in the nares: 16 of the colonizing isolates were MRSA, and 14 were MSSA, and the majority of the colonizing isolates belonged to the USA300 clonal group. In most cases (70%), the colonizing isolate belonged to the same clonal type as the strain involved with the infection. In three of the patients, the identity of invasive and colonizing MRSA isolates was further documented by whole-genome sequencing. Staphylococcus aureus is the most common cause of bacterial infections in humans worldwide (1), and methicillin-resistant Staphylococcus aureus (MRSA) is the main cause of skin and soft tissue infections (SSTIs) in North America, with a single clone, USA300, accounting for 98% of these infections (2, 3).The first human case of MRSA infection in the United States was reported in Boston, MA, in 1968 (4). MRSA was first detected in hospitals, and over the following decades, it became the main nosocomial pathogen around the world (5). In 1998, the prevalence of MRSA in 12 hospitals throughout the city of New York was assessed (6), and a single MRSA clone was found to be responsible for an overwhelming majority of MRSA infections. The same MRSA clone was subsequently identified as dominant in MRSA infections in 29 hospitals in the tristate area (7), and it was also identified in MRSA infections in Japan (8). This MRSA clone (multilocus sequence typing [MLST] clonal complex CC5, sequence type ST5, SCCmecII, and unique pulsed-field gel electrophoresis [PFGE] profile)-also known as the "New York/Japan clone" or "MRSA clone USA100"-became the most prevalent MRSA clone involved in MRSA infections in hospitals in the United States in the 1990s (9).In 1993, a new MRSA clone emerged in Kimberley, Western Australia (10), in a community of patients without previous health care contact (community-acquired MRSA [CA-MRSA]). In the late 1990s, CA-MRSA also appeared in the United States and was responsible for the death of four otherwise healthy pediatric patients in Minnesota and North Dakota (11). These new CA-MRSA strains belonged to a clone (USA400/CC1/SCCmecIV)