Candida is the third most common cause of late-onset neonatal sepsis in infants born at <1500 g. Candida parapsilosis infections are increasingly reported in preterm neonates in association with indwelling catheters.
We systematically reviewed neonatal literature and synthesized data pertaining to percentage of C. parapsilosis infections and mortality by meta-analyses. We also reviewed risk factors, virulence determinants, antimicrobial susceptibility patterns and outlined clinical management strategies.
C. parapsilosis infections comprised 33.47% (95% confidence interval [CI]: 30.02, 37.31) of all neonatal Candida infections. C. parapsilosis rates were similar in studies performed before the year 2000, 33.53% (95% CI: 30.06, 37.40) (28 studies), to those after 2000, 27.00% (95% CI: 8.25, 88.37) (8 studies). The mortality due to neonatal C. parapsilosis infections was 10.02% (95% CI: 7.66, 13.12). Geographical variations in C. parapsilosis infections included a low incidence in Europe and higher incidence in North America and Australia. Biofilm formation was a significant virulence determinant and predominant risk factors for C. parapsilosis infections were prematurity, prior colonization and catheterization. Amphotericin B remains the antifungal drug of choice and combination therapy with caspofungin or other echinocandins may be considered in resistant cases.
C. parapsilosis is a significant neonatal pathogen, comprises a third of all Candida infections and is associated with 10% mortality. Availability of tools for genetic manipulation of this organism will identify virulence determinants and organism characteristics that may explain predilection for preterm neonates. Strategies to prevent horizontal transmission in the neonatal unit are paramount in decreasing infection rates.
From the *Department of Pediatrics, Section of Neonatology, Texas Children’s Hospital and Baylor College of Medicine, Houston, TX; †UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Ireland; ‡Department of Microbiology, University of Szeged, Szeged, Hungary; and §Department of Pediatrics, Women & Infants Hospital of Rhode Island, Warren Alpert Medical School, Brown University, Providence, RI.
Accepted for publication 04, 2013.
G.B. is supported by Science foundation, Ireland. A.G. is supported by OTKA NF84006, NN100374 and by EMBO Installation Grant 1813. Work in Dr.Bliss’ laboratory was supported by grants from the National Center for Research Resources (5P20RR018728-10) and the National Institute of General Medical Sciences (8P20GM103537-10) from the National Institutes of Health. The authors have no other funding or conflicts of interest to disclose.
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