Low rate of Candida parapsilosis-related colonization and infection in hospitalized preterm infants: a one-year prospective study.

We determined the rate of Candida parapsilosis colonization in preterm neonates (NN) and the relationship between colonization and systemic infection through a prospective study in the Neonatal Intensive Care Unit of a university hospital. All NN born at a gestational age of 32 weeks or less were included. Specimens from rectum, mouth and retro-auricular skin were obtained at admission and weekly thereafter. All samples were inoculated on to Sabouraud agar, CHROMagar and Dixon media. Candida species were identified using API Candida and API 20C. DNA analysis was performed using pulse field gel electrophoresis.Fifty-four patients were included (mean age: 30 +/- 1.5 weeks; mean birthweight: 1347 +/- 301 g; male: 40%). Fungal colonization was detected in 43 (79.6%). Causative agents were C. parapsilosis (N= 7);Malassezia furfur (N= 30);C. albicans (N= 21), C. guillermondii (N= 1). No sample was positive for two different yeasts at the same time. C. parapsilosis colonization included anal (N= 6), buccal (N= 1), and skin (N= 2). The average age at time of colonization was 17.8+/-9.8 days. Neither fungal septicaemia nor death were observed in colonized infants. Two central venous catheters were found to be colonized, one with C. parapsilosis and one with M. furfur. Logistic regression showed a link between colonization and gestational age alone. Three different DNA profiles were observed. This study suggests that in our units, the occurrence of C. parapsilosis colonization is low and bears no relation to systemic infection. The systematic identification of C. parapsilosis carriers for the purposes of isolation and preventive treatment does not appear to be warranted.

[Transitory hyperinsulinism with hypoglycemia in asphyxia neonatorum]. / Hyperinsulinisme transitoire avec hypoglycémie par asphyxie néonatale.

BACKGROUND: Hypoglycemia is a well-known complication in neonates small for gestational age and in those with diabetic mothers. Birth asphyxiated infants can develop severe hypoglycemia due to reduced glycogen stores. CASE REPORTS: The first patient was born at 41 weeks, weighing 3,780 g by emergency cesarean section because of fetal distress. He developed a pneumothorax and hypoglycemia. He was given glucose infusion (at day 4: 20 mg/kg/d). Hyperinsulinism was confirmed: blood levels at 18.3 mU/L on day 1 and 11.7 mU/L on day 2. The infusion rate was gradually decreased. The second patient was born at 39 weeks, weighing 2,780 g by emergency cesarean section because of fetal distress. She needed glucose infusion (24 g/kg/d) because of hypoglycemia with hyperinsulinism (12.8 mU/L on day 2 and 11.7 mU/L on day 3). After 5 days, the infusion of glucose was replaced by oral feeding only. CONCLUSION: Transient hypoglycemia in asphyxiated newborn infants with hyperinsulinism must be considered even when hypoglycemia may be difficult to prove.