In order to determine the risk factors and outcomes of ventilator-associated pneumonia (VAP) in the neonatal intensive care unit (NICU), a retrospective cohort study was conducted on 259 patients who were ventilated >48 h. Clinical characteristics and risk factors were compared and non-conditional logistic regression analysis was performed to determine independent predictors for VAP. There were 52 episodes of VAP (20.1%). The main pathogens were G(-) bacterium (82.1%, 23/28). Hospital stay in the VAP group was 19.9+/-5.9 vs. 16.7+/-7.2 days in controls (P<0.01). The mortality rate of the VAP group was 13.5% (7/52) vs. 12.1% in controls (P>0.05). By logistic regression analysis the following independently predicted VAP: re-intubation (OR 5.3, 95% CI 2.0, 14.0), duration of mechanical ventilation (OR 4.8, 95% CI 2.2, 10.4), treatment with opiates (OR 3.8, 95% CI 1.8, 8.5) and endotracheal suctioning (OR 3.5, 95% CI 1.6, 7.4). VAP occurred at significant rates among mechanically ventilated NICU patients and is associated with care procedures. The risk factors of neonatal VAP were re-intubation, duration of mechanical ventilation, treatment with opiates and endotracheal suctioning. Additional studies are necessary to develop interventions to prevent neonatal VAP.

The predominant factors identified with IFI were third-generation cephalosporin use, peripherally inserted central venous catheter use, intubation > 6 days, any prior abdominal surgery, and neutropenia during first week of life < 1.5 · 109/L.

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BackgroundIntrauterine infection/inflammation plays an important role in the development of lung injury and bronchopulmonary dysplasia (BPD) in preterm infants, While a multifactorial genesis is likely, mechanisms involved in BPD after intrauterine infection/inflammation are largely unknown. Recent studies have suggested microRNAs (miRNAs) are likely to play a role. Therefore, this study aimed to study the effects and mechanisms of intrauterine infection/inflammation on lung development, and to identify miRNAs related to lung injury and BPD.MethodsAn animal model of intrauterine infection/inflammation was established with pregnant SD rats endocervically inoculated with E.coli. The fetal and neonatal rats were observed at embryonic day (E) 17, 19, 21 and postnatal day (P) 1, 3, 7, 14, respectively. Body weight, lung weight, the expression levels of NLRP3, TNF-α, IL-lβ, IL-6, VEGF, Collagen I, SP-A, SP-B and SP-C in the lung tissues of fetal and neonatal rats were measured. Expression profiles of 1218 kinds of miRNAs in the lungs of neonatal rats were detected by miRNA microarray technique. Target genes of the identified miRNAs were predicted through online software.ResultsIntrauterine infection/inflammation compromised not only weight development but also lung development of the fetal and neonatal rats. The results showed significantly increased expression of NLRP3, TNF-α, IL-1β, IL-6, Collagen I, and significantly decreased expression of VEGF, SP-A, SP-B and SP-C in the fetal and neonatal rat lung tissues in intrauterine infection group compared to the control group at different observation time point (P < 0.05). Forty-three miRNAs with significant differential expression were identified. Possible target genes regulated by the identified miRNAs are very rich.ConclusionsIntrauterine infection/inflammation results in lung histological changes which are very similar to those observed in BPD. Possible mechanisms may include NLRP3 inflammasome activation followed by inflammatory cytokines expression up-regulated, inhibiting the expression of pulmonary surfactant proteins, interfering with lung interstitial development. There are many identified miRNAs which target a wide range of genes and may play an important role in the processes of lung injury and BPD.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0787-y) contains supplementary material, which is available to authorized users.

In order to investigate the neuropathological effects on the developing rat brain after intrauterine infection, identification of GFAP was observed. Escherichia coli (E. coli) was inoculated into uterine horn of pregnant rats when gestation was 70% complete (15 days) and the control group was inoculated with normal saline. Immunohistochemistry was used for evaluation of GFAP expression in pup brains at postnatal day 1 (P1), P3, P7, P14 and P21, and RT-PCR was used to analyze GFAP mRNA, interleukin-1beta, mRNA (IL-1beta mRNA) and tumor necrosis factor-alpha mRNA (TNF-alpha mRNA) expression in pup brains at P1, P3 and P7. At P1 and P3, GFAP was expressed very scarcely in periventricular white matter but not in other brain regions between the two groups. Compared with the control group, at P7 GFAP expression of the E. coli-treated pups was remarkably increased in periventricular white matter and hippocampus. The E. coli-treated pups at P14 showed a marked increase of GFAP expression in periventricular white matter, corpus callosum and cortex. However, no significant difference in levels of GFAP expression in any brain regions were found at P21 between the two groups. GFAP mRNA expression of the E. coli-treated pups was higher than the control at P1 and P3, but there was no significant difference between the two groups at P7. IL-1beta mRNA and TNF-alpha mRNA expressions of the E. coli-treated pups were higher than the control at P1 but there was no significant difference between the two groups at P3 and P7. These present results suggest that intrauterine infection could increase GFAP expression in the pup brain and indicate that intrauterine infection might damage the developing white matter and IL-1beta, TNF-alpha might be a mechanism mediating between the two events.