Abstract 1759 Poster Session I, Saturday, 5/1 (poster 81)

Bronchopulmonary dysplasia (BPD) is an important cause of morbidity and mortality in preterm infants. Many factors contribute to the development of BPD and the role of congenital infections has been debated. The purpose of this study was to test the hypothesis that the early detection of infectious agents in tracheal aspirate samples was associated with the development of BPD. Tracheal aspirate samples were obtained within the first week of life and, after isolation of nucleic acids, screened by polymerase chain reaction (PCR) or reverse transcription-PCR for adenovirus, enterovirus, CMV, parvovirus, U. urealyticum, M. hominis, M. pneumoniae and Chlamydia species. BPD was defined as persistent supplemental oxygen dependence at 28 days of age or 36 weeks postconceptional age (PCA). Infants that expired prior to these time points were excluded from statistical analysis. Out of 89 infants studied, at 28 days of life, 13 had expired, 45 had BPD and 31 had no BPD (controls). At 36 weeks PCA, 15 infants expired, 39 still had BPD and 35 did not. A significant increase in the frequency of adenovirus DNA was identified in BPD patients compared with controls, both at 28 days of life (12/45 = 27% versus 1/31 = 3%: p≤0.01) and at 36 weeks PCA (10/39 = 29% versus 2/35 = 6%: p=0.01). One patient who had a supplemental oxygen requirement both at 28 days of life and 36 weeks of PCA age was PCR-positive for CMV DNA. Among the infants not requiring supplemental oxygen, 1 patient was positive for CMV and one for enterovirus. Only one sample was positive for M. hominis (an infant not requiring supplemental oxygen) while no cases were positive for M. pneumoniae, or any Chlamydia species. U. urealyticum was detected in the tracheal aspirates of 18 (24%) of the 76 infants. However, there was not a statistically significant difference between the frequency of detection between the BPD and no BPD groups, either at 28 days of life (p=0.72) or 36 weeks of PCA (p=0.56). Of note was that there was a significant difference (p≤0.01) between the mean gestational age of BPD patients that were adenovirus positive (27.0±1.1 weeks) and adenovirus negative (25.7±1.5 weeks). These data suggest that the major factor in the development of BPD could be immaturity unless the patient is exposed to adenovirus, in which case BPD develops even in the more mature preterm infant. All adenovirus-specific amplification products were characterised by DNA sequencing: in each case adenovirus type 5 was identified. This is the first study reporting the frequency of detection of adenovirus DNA in tracheal aspirate samples from infants with BPD and suggests that prenatal acquisition may be important in the development of BPD.