Background: We describe the incidence, risk factors and outcomes of invasive candidiasis in infants >1500 g birth weight.
Methods: We conducted a retrospective cohort study of infants >1500 g birth weight discharged from 305 neonatal intensive care units in the Pediatrix Medical Group from 2001 to 2010. Using multivariable logistic regression, we identified risk factors for invasive candidiasis.
Results: Invasive candidiasis occurred in 330 of the 530,162 (0.06%) infants. These were documented from positive cultures from ≥1 of these sources: blood (n = 323), cerebrospinal fluid (n = 6) or urine from catheterization (n = 19). Risk factors included day of life >7 (odds ratio [OR]: 25.2; 95% confidence interval: 14.6–43.3), vaginal birth (OR: 1.6 [1.2–2.3]), exposure to broad-spectrum antibiotics (OR: 1.6 [1.1–2.4]), central venous line (OR: 1.8 [1.3–2.6]) and platelet count <50,000/mm3 (OR: 3.7 [2.1–6.7]). All risk factors had poor sensitivities, low positive likelihood ratios and low positive predictive values. The combination of broad-spectrum antibiotics and low platelet count had the highest positive likelihood ratio (46.2), but the sensitivity of this combination was only 4%. Infants with invasive candidiasis had increased mortality (OR: 2.2 [1.3–3.6]).
Conclusions: Invasive candidiasis is uncommon in infants >1500 g birth weight. Infants at greatest risk are those exposed to broad-spectrum antibiotics and with platelet counts of <50,000/mm3.
From the *Department of Pediatrics, Duke University Medical Center; †Duke Clinical Research Institute, Duke University Medical Center, Durham, NC; ‡Department of Pediatric Subspecialties, KK Women’s and Children’s Hospital, Singapore; §Department of Biostatistics, University of North Carolina, Chapel Hill, NC; and ¶Pediatrix Medical Group, Sunrise, FL.
Accepted for publication September 27, 2012.
D.K.B. receives support from the US government for his work in pediatric neonatal clinical pharmacology (1R01HD057956-02, 1R01FD003519-01, 1U10-HD45962-06, 1K24HD058735-01) and is principal investigator of the Pediatric Trials Network (government contract HHSN275201000002I); from the nonprofit organization Thrasher Research Foundation for his work in neonatal candidiasis (http://www.thrasherresearch.org) and from industry for neonatal pediatric drug development (http://www.dcri.duke.edu/research/coi.jsp). P.B.S. receives support from NICHD-1K23HD060040-01, DHHS-1R18AE000028-01 and from industry for neonatal and pediatric drug development (http://www.dcri.duke.edu/research/coi.jsp). M.C.-W. receives support from the US government for his work in pediatric clinical pharmacology (government contract HHSN267200700051C, PI: D.K.B.); from the National Institute of Child Health and Human Development (1K23HD064814-01) and from the nonprofit organization Thrasher Research Foundation. He is also a consultant for Pfizer and Janssen Pharmaceuticals. The authors have no other funding or conflicts of interest to disclose.
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Address for correspondence: Daniel K. Benjamin Jr., MD, MPH, PhD, Duke Clinical Research Institute, Box 17969, Durham, NC 27715. E-mail: firstname.lastname@example.org.