Candida is an important cause of infections in premature infants. Gastrointestinal colonization with Candida is a common site of entry for disseminated disease. The objective of this study was to determine whether a dietary supplement of medium-chain triglycerides (MCTs) reduces Candida colonization in preterm infants.
Preterm infants with Candida colonization (n = 12) receiving enteral feedings of either infant formula (n = 5) or breast milk (n = 7) were randomized to MCT supplementation (n = 8) or no supplementation (n = 4). Daily stool samples were collected to determine fungal burden during a 3-week study period. Infants in the MCT group received supplementation during 1 week of the study period. The primary outcome was fungal burden during the supplementation period as compared with the periods before and after supplementation.
Supplementation of MCT led to a marked increase in MCT intake relative to unsupplemented breast milk or formula as measured by capric acid content. In the treatment group, there was a significant reduction in fungal burden during the supplementation period as compared with the period before supplementation (rate ratio, 0.15; P = 0.02), with a significant increase after supplementation was stopped (rate ratio, 61; P < 0.001). Fungal burden in the control group did not show similar changes.
Dietary supplementation with MCT may be an effective method to reduce Candida colonization in preterm infants.
From the *Department of Pediatrics, Women & Infants Hospital of Rhode Island
†Warren Alpert Medical School of Brown University, Providence, Rhode Island
‡Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts
§Department of Biology, Siena College, Loudonville, New York
¶Cardiovascular Nutrition Laboratory, JM USDA Human Nutrition Research Center, Tufts University, Boston, Massachusetts.
Accepted for publication November 29, 2017.
K.T.W.G. (K12GM074869) and J.M.B. (P20GM103537 and P20GM104317) were supported by the National Institute of General Medical Sciences of the National Institutes of Health (NIH). E.S.V. was supported by the Alpert Medical School Summer Assistantship program. C.A.K. was partially supported by grant R01AI081794 and C.A.K. and J.M.B by grant R21HD089278 from the NIH. Work in the Bliss laboratory was also supported by funds from the William and Mary Oh—William and Elsa Zopfi Professorship for Pediatrics and Perinatal Research from Brown University and Women & Infants Hospital. The other authors have no conflicts of interest to disclose.
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Address for correspondence: Department of Pediatrics, Women & Infants Hospital of Rhode Island, 101 Dudley St, Providence, RI 02905. E-mail: firstname.lastname@example.org.