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Ureaplasmacolonisation and chronic lung disease in neonates
  1. VINEET BHANDARI
  1. Department of Paediatrics
  2. Albert Einstein Medical Center
  3. Philadelphia, PA 19141, USA
  4. Department of Paediatrics
  5. University of Connecticut Health Center
  6. Mailcode 2203, Farmington, CT 06030–2203, USA
    1. NAVEED HUSSAIN
    1. Department of Paediatrics
    2. Albert Einstein Medical Center
    3. Philadelphia, PA 19141, USA
    4. Department of Paediatrics
    5. University of Connecticut Health Center
    6. Mailcode 2203, Farmington, CT 06030–2203, USA
      1. GL GILBERT
      1. Centre for Infectious Diseases and Microbiology
      2. Institute of Clinical Pathology and Medical Research
      3. Westmead Hospital, Westmead
      4. NSW Australia 2145

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        Editor—We read the article by Hannaford et al 1 with interest. We would like to point out that in our recent retrospective analysis,2 our findings of the colonisation rate of genital mycoplasmas (Ureaplasma urealyticumand Mycoplasma hominis) in the respiratory tract of premature infants of 27% were similar to their study. We also found a higher incidence of chronic lung disease (CLD) in our cohort colonised with genital mycoplasmas.2

        We are, however, intrigued by the implication of a “protective effect” of Ureaplasma urealyticum (Uu) colonisation on respiratory distress syndrome (RDS) in this study. The hypothesis that this may be related to the “stimulatory effect of subacute intrauterine infection on lung maturation . . .” is interesting but unsubstantiated. Current evidence suggests that the sicker infant with RDS has an increased early inflammatory response and a higher rate of CLD.3 4 In the present study,1 the incidence of RDS in Uu colonised infants was lower—but their incidence of CLD at 36 weeks was higher. Were there other factors—for example, increased incidence of PDA, more IV fluid use, that predisposed these infants to develop CLD? Another issue is that in the multivariate analyses, Uu colonisation was a significant risk factor for CLD only in singleton infants, but the relationship did not hold true when all infants were analysed. Based on these observations, we wonder if the “protective effect” is real or a statistical aberration? More research needs to be done to study this “protective effect” of Uu colonisation on RDS before any conclusions can be drawn.

        The treatment of Uu colonisation was not discussed in this paper. In our experience, erythromycin alone was not effective in clearing the organism from the respiratory tract. We found a short course of postnatal steroids alone or in combination with erythromycin more effective.2 We wonder if infants receiving postnatal steroids were confounders in the discrepancy between the incidence of RDS and CLD.

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        Dr Gilbert et al respond:

        Editor—We thank Drs Bhanadri and Hussain for their interest in our paper. We too were intrigued by the apparently contradictory effects of ureaplasma colonisation on the lungs of affected infants and acknowledge that our hypothesis is unsubstantiated. The possibility that a subacute intrauterine infection could stimulate endogenous surfactant production is a plausible explanation for the significantly lower incidence of respiratory distress syndrome (RDS) in these infants. The fact that intrauterine infection is low grade, may also mean that delivery is delayed for long enough for exogenous steroids to take effect.

        The development of chronic lung disease (CLD) is dependent on many factors, and, in our study, it correlated less closely with ureaplasma infection than did RDS. We assumed that other effects of multiple gestation outweighed those of ureaplasma infection on the development of CLD in twins. Presumably, the lower rate of RDS in ureaplasma infected singleton infants reduced their risk of CLD, directly or indirectly. If so, there must be other respiratory insults severe enough to offset this effect. We were unable to identify factors associated with CLD apart from RDS and ureaplasma infection. In particular, the incidence of PDA did not differ between infants with and without CLD.

        We postulate that the low grade inflammatory effect of intrauterine ureaplasma infection could cause significant irreversible lung damage and predispose to CLD, as well as stimulating the production of surfactant. The outcome is unlikely to be affected by erythromycin therapy after birth, except in the minority of infants in whom there is frank pneumonitis, with progression after birth.

        We have not studied the effects of postnatal steroids, but this is unlikely to be a significant confounding factor in these infants since, at the time the study was done, steroid therapy was not given until about four weeks of age, when CLD was already established.

        Although we agree that further research is needed to confirm our findings, we believe that the inverse relationship between ureaplasma colonisation and RDS was too strong to be dismissed as a statistical aberration.

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