Does Ureaplasma spp. cause chronic lung disease of prematurity: Ask the audience?

Maxwell, Nicola C.; Nuttall, Diane; Kotecha, Sailesh

doi:10.1016/j.earlhumdev.2008.12.002

Cited by 17 publications

(12 citation statements)

References 40 publications

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“…Data are presented as n (%) or n. RDS: respiratory distress syndrome; CLD: chronic lung disease. decrease the rates of CLD [23,24]. Our data also suggest that late manifestation of Ureaplasma spp., whether acquired antenatally or not, will need to be considered in the causation of CLD and be accounted for in any future interventional trials investigating if eradication of pulmonary Ureaplasma spp.…”

Section: Discussionsupporting

confidence: 72%

Role of pulmonary infection in the development of chronic lung disease of prematurity

Beeton

Maxwell²,

Davies³

et al. 2010

European Respiratory Journal

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We studied the role of ante- and post-natal infection in the development of chronic lung disease (CLD) of prematurity. 192 newborn infants (61 term and 131 pre-term of <34 weeks gestation: 88 with respiratory distress syndrome, 35 developed CLD and eight died) were recruited. 16S ribosomal RNA (rRNA) genes were identified by PCR of DNA isolated from 840 gastric and lung fluid samples. Ureaplasma spp. were also cultured. Presence of 16S rRNA genes (OR 1.6, 95% CI 1.2-2.2) and Ureaplasma spp. (OR 3.6, 95% CI 1.7-7.7) was significantly associated with the development of CLD. This association remained if the 16S rRNA genes and Ureaplasma spp. were first identified within the first 3 days of life (OR 2.4 (95% CI 1.4-4.1) and 3.8 (95% CI 1.4-10.0), respectively) or if first identified after 3 days of age (OR 1.7 (95% CI 1.1-2.8) and OR 5.1 (95% CI 1.3-19.8), respectively). Peak lung fluid interleukin (IL)-6 and IL-8 were significantly associated with presence of microbes (p<0.0001 and p=0.0001, respectively) and development of CLD (p=0.003 and 0.001, respectively). Both early and late microbial presence in neonatal lung fluid samples was significantly associated with the development of CLD suggesting that both ante- and post-natal infection play a role in the development of CLD.

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Section: Discussionsupporting

confidence: 72%

Role of pulmonary infection in the development of chronic lung disease of prematurity

Beeton

Maxwell²,

Davies³

et al. 2010

European Respiratory Journal

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“…There is considerable controversy regarding the role of U. parvum in the pathogenesis of human BPD (28). While some studies have associated exposure to chorioamnionitis with BPD (47,50), other recent reports have failed to document associations between chorioamnionitis and BPD (2,23,25,40,45).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary vascular and alveolar development in preterm lambs chronically colonized with Ureaplasma parvum

Polglase

Dalton

Nitsos

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Ureaplasma species, the most commonly isolated microorganisms in women with chorioamnionitis, are associated with preterm delivery. Chorioamnionitis increases the risk and severity of bronchopulmonary dysplasia and persistent pulmonary hypertension in newborns. It is not known whether the timing of exposure to inflammation in utero is an important contributor to the pathogenesis of bronchopulmonary dysplasia. We hypothesized that chronic inflammation would alter the pulmonary air space and vascular development after 70 days of exposure to infection. Pregnant ewes were given intra-amniotic injection of Ureaplasma parvum serovars 3 or 6 at low (2 x 10(4) cfu) or high doses (2 x 10(7) cfu) or media (controls) at 55 days gestational age. Fetuses were delivered at 125 days (term = 150 days). U. parvum was grown from the lungs of all exposed fetuses, and neutrophils and monocytes were increased in the air spaces. Lung mRNA expression of IL-1beta and IL-8, but not IL-6, was modestly increased in U. parvum-exposed fetuses. U. parvum exposure increased surfactant and improved lung gas volumes. The changes in lung inflammation and maturation were independent of serovar or dose. Exposure to U. parvum did not change multiple indices of air space or vascular development. Parenchymal elastin and collagen content were similar between groups. Expression of several endothelial proteins and pulmonary resistance arteriolar media thickness were also not different between groups. We conclude that chronic exposure to U. parvum does not cause sustained effects on air space or vascular development in premature lambs.

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“…With better laboratory detection and increasing knowledge about their significance in maternal and neonatal infections, this situation is now changing (8), as high as 40 to 80% of women have been reported to be colonized with genital mycoplasmas (9). Their role in infertility, post-partum endometritis, chorioamnionitis, preterm labor, and spontaneous abortion has been extensively investigated.…”

Section: Discussionmentioning

confidence: 99%

Ureaplasma Urealyticum and Mycoplasma Hominis Colonization and Chronic Lung Disease in Preterm Neonates Under Ventilation

et al. 2013

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A B S T R A C TBackground: Ureaplasma urealyticum (U. urealyticum) and Mycoplasma hominis (M. hominis) are two important pathogens in neonatal respiratory tract infections. As low gestational age and birth weight increase the colonization rate with these pathogens, and they are also risk factors of chronic lung disease (CLD), it is difficult to establish a statistically significant relation between these two factors. Objectives: To determine the colonization rate of preterm ventilated neonates with U. urealyticum and M. hominis , and the relationship between infection and chronic lung disease in these neonates, a prospective study was performed. Patients and Methods: Determining tracheal colonization rate of preterm neonates with ureaplasma and mycoplasmsa and its relation to CLD. In a cohort prospective study in Hazrat Rasoul Akram Hospital, with 62 ventilated neonates (< 35 weeks) in the first 24 h of life, where tracheal secretions were aspirated, transported, and cultured in a specific media. CLD was diagnosed as oxygen requirement at 28 days or 36 weeks post conceptional age. Results: From 62 cultures, 7 were positive for U. urealyticum (11.3%, CI95%: 3.4-19.2%) and 3 were positive for M. hominis (4.8%, CI95%: 0-10.2%). From 53 neonates who were alive at 28 days after birth, 11 neonates needed oxygen (20.8%, CI95%: 9.8-31.7%). From 10 neonates with positive cultures, 2 (20%, CI95%: 0-44.8%) died, and from 8 alive neonates, 3 (37.5%, CI95%: 4.0-71.0%) survived without CLD. From 52 neonates with negative cultures, 7 (13.5%, CI95%: 4.2-22.7%) died, and from 45 alive neonates, 39 (86.7%, CI95%: 76.7-96.6%) survived without CLD, and there was a significant difference between neonatal groups with positive and negative tracheal culture progressing to CLD (62.5% vs. 13.3%) (P < 0.001) (Figure 1). Conclusions: Intrauterine infection with U. urealyticum and M. hominis leads to negative neonatal outcome and increased rate of chronic lung disease in preterm neonates (< 35 weeks).

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Does Ureaplasma spp. cause chronic lung disease of prematurity: Ask the audience?

Cited by 17 publications

References 40 publications

Role of pulmonary infection in the development of chronic lung disease of prematurity

Role of pulmonary infection in the development of chronic lung disease of prematurity

Pulmonary vascular and alveolar development in preterm lambs chronically colonized with Ureaplasma parvum

Ureaplasma Urealyticum and Mycoplasma Hominis Colonization and Chronic Lung Disease in Preterm Neonates Under Ventilation

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