{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T07:42:50Z","timestamp":1781595770253,"version":"3.54.5"},"reference-count":39,"publisher":"American Academy of Pediatrics (AAP)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,10,1]]},"abstract":"<jats:p>Objective. Most clinical descriptions of invasive staphylococcal disease (ISD) in neonates date from before the mid-1980s, when neonatal viability and intensive care differed substantially from current standards. We aimed to describe the contemporary incidence, clinical features, and outcome of infants with ISD in a neonatal intensive care unit.<\/jats:p><jats:p>Methods. A retrospective cohort study was conducted of infants who had ISD and were in the neonatal intensive care unit of the Woman's Hospital of Texas, Houston, from January 2000 to June 2002. Confirmed ISD was defined as clinical sepsis and Staphylococcus aureus (SA) isolated from \u22651 blood culture (BC) or a sterile body site excluding urine or coagulase-negative staphylococci (CoNS) isolated from \u22652 BC or from 1 BC and a sterile body site. Probable ISD was defined as CoNS isolated from 1 BC or a sterile body site for which clinical and laboratory data review by 3 infectious disease specialists indicated that antimicrobial treatment was appropriate. Confirmed and combined confirmed plus probable cases were analyzed.<\/jats:p><jats:p>Results. A total of 149 episodes (83 confirmed [39 SA, 44 CoNS], 66 probable) in 137 infants (mean gestational age [GA]: 27.6 weeks [22.4\u201336.4]; mean birth weight: 981 g [350\u20132995]) were reviewed. Four (3%) infants had early-onset infection (2 SA, 2 CoNS). Median age at infection onset was similar (17 days SA; 18 days CoNS). Intravascular catheters (IVC) were in situ in a minority of infants with ISD episodes (38% SA, 43% CoNS). CoNS more than SA infections were associated with very low birth weight (&amp;lt;1500 g), lower GA, a history of more IVCs and concurrent total parenteral nutrition, but IVC and parenteral nutrition days were similar. By multivariate analysis correcting for birth weight and complications of prematurity, hypoxia at the time of sepsis evaluation was significantly associated with CoNS and hypotension with SA infections; other clinical features were similar. Methicillin-resistant SA caused 8% of SA infections. Among bacteremic infants, SA more frequently than CoNS involved \u22652 sites. Overall, SA had more focal complications (primarily bone and joint) than CoNS, resulting in a 2- to 3-fold higher SA-associated morbidity rate. Mortality directly attributable to either organism was similar (5% SA; 5% confirmed, 3% confirmed\/probable CoNS).<\/jats:p><jats:p>Conclusion. CoNS ISD occurred in smaller, more premature infants than SA and was IVC associated in a minority of cases. Hypoxia and hypotension were the only presenting features that differentiated CoNS and SA. SA-associated morbidity was substantial, but SA infection carried no greater risk of death (5%) than CoNS.<\/jats:p>","DOI":"10.1542\/peds.2004-0043","type":"journal-article","created":{"date-parts":[[2004,10,13]],"date-time":"2004-10-13T18:57:26Z","timestamp":1097693846000},"page":"953-961","source":"Crossref","is-referenced-by-count":105,"title":["Features of Invasive Staphylococcal Disease in Neonates"],"prefix":"10.1542","volume":"114","author":[{"given":"C. Mary","family":"Healy","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debra L.","family":"Palazzi","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morven S.","family":"Edwards","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Baylor College of Medicine, Houston, Texas"},{"name":"The Woman's Hospital of Texas, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith R.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Baylor College of Medicine, Houston, Texas"},{"name":"The Woman's Hospital of Texas, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol J.","family":"Baker","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Baylor College of Medicine, Houston, Texas"},{"name":"The Woman's Hospital of Texas, Houston, Texas"},{"name":"Department of Molecular Virology & Microbiology, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2004,10,1]]},"reference":[{"key":"2021120906074819300_R1","unstructured":"Call EL. 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