Both ante- and post-natal infection have been linked to the development of CLD. A study of 119 ventilated preterm infants with a birth weight less than 1000 g, reported systemic sepsis to be a risk factor for CLD (Rojas et al., 1995). Of the 64 infants who had a positive blood culture with clinical or laboratory signs of sepsis, 35 (55%) developed CLD, compared to 9 (16%) without sepsis (odds ratio 4.4). This study also reported that a patent ductus arteriosus was a significant risk factor for CLD (odds ratio 6.2). If both these risk factors were combined the odds ratio markedly increased to 48.4.
Other studies have suggested an association between nosocomial infections such as Staphylococcus epidermidis and the development of CLD with 64% of infants with Staphylococcus epidermidis sepsis developing CLD compared to 24% of controls (Liljedahl et al., 2004). Ventilated preterm neonates frequently have endotracheal secretions colonised with Gram positive bacteria, particularly Staphylococcus epidermidis. In some cases Gram negative bacilli, such as Klebsiella pneumoniae, Enterobacter cloacae and Escherichia coli can also colonise endo-tracheal secretions. Such colonisation has been reported to significantly increase the incidence of CLD (Cordero et al., 1997).
Viral infections, particularly with adenovirus or cytomegalovirus (CMV) have been associated with the development of CLD. Sawyer et al. (1978) identified 32 infants born with a birth weight less than 2000 g as being infected with CMV over a five year period. Of these 24 (75%) went on to develop CLD compared to 12 of
32 (38%) matched controls. It was believed that the CMV infection was acquired postnatally. Other studies have found an association between adenovirus and the development of CLD with 27% of preterm infants who developed CLD having adenovirus detected by PCR in tracheal aspirates in the first week of life compared to 3% in the tracheal fluid from infants who did not develop CLD (Couroucli et al., 2000).
Neither the CMV nor the adenovirus finding have been widely replicated (Prosch et al., 2002) and it seems likely that for the majority of children viral infection is not the key factor in the development of CLD.
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