We describe the incidence, risk factors and outcomes of invasive candidiasis in infants >1500 g birth weight.
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.
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]).
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.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com).
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.