The objective of this study was to determine the distribution of staphylococcal cassette chromosome mec (SCCmec) elements in meticillin-resistant coagulase-negative staphylococci (MR-CoNS) isolated from a tertiary-care hospital in Mexico and to examine the relationship to drug resistance. Fifty selected MR-CoNS isolates collected from catheters (n515), blood (n515), bone (n59), bronchial lavage (n52) and urine (n52) and one isolate each from an abscess, cerebrospinal fluid, eye, pleural effusion, synovial fluid, tracheal aspirate and wound secretion were examined. Susceptibility testing was performed by the broth microdilution method. SCCmec types were determined by multiplex PCR and PFGE was carried out as described previously for Staphylococcus aureus. Among the MR-CoNS strains studied, the most frequently isolated species were Staphylococcus epidermidis (n526) and Staphylococcus haemolyticus (n513). Staphylococcus cohnii (n55), Staphylococcus hominis (n53), Staphylococcus sciuri (n51), Staphylococcus pasteuri (n51) and the recently described species Staphylococcus pettenkoferi (n51) were also identified. The most frequent MR-CoNS genotype identified was SCCmec type IVa in S. epidermidis isolates, which also showed a high diversity in their PFGE patterns. A clone was found that amplified both SCCmec III and V elements in five isolates examined. The single MR S. pettenkoferi isolate harboured SCCmec type IVd and the single MR S. pasteuri isolate harboured SCCmec type I. The carriage of SCCmec type III was associated with resistance or intermediate resistance to meropenem (P ,0.05). These results confirm the high prevalence of S. epidermidis SCCmec IVa and the high genetic diversity among MR-CoNS strains. As far as is known, this is the first report describing the newly identified S. pettenkoferi possessing SCCmec IVd and S. pasteuri harbouring SCCmec type I. MR-CoNS harbouring SCCmec type III were found to be more resistant to meropenem.
Background Antenatal detection and management of small for gestational age (SGA) is a strategy to reduce stillbirth. Large observational studies provide conflicting results on the effect of the Growth Assessment Protocol (GAP) in relation to detection of SGA and reduction of stillbirth; to the best of our knowledge, there are no reported randomised control trials. Our aim was to determine if GAP improves antenatal detection of SGA compared to standard care. Methods and findings This was a pragmatic, superiority, 2-arm, parallel group, open, cluster randomised control trial. Maternity units in England were eligible to participate in the study, except if they had already implemented GAP. All women who gave birth in participating clusters (maternity units) during the year prior to randomisation and during the trial (November 2016 to February 2019) were included. Multiple pregnancies, fetal abnormalities or births before 24+1 weeks were excluded. Clusters were randomised to immediate implementation of GAP, an antenatal care package aimed at improving detection of SGA as a means to reduce the rate of stillbirth, or to standard care. Randomisation by random permutation was stratified by time of study inclusion and cluster size. Data were obtained from hospital electronic records for 12 months prerandomisation, the washout period (interval between randomisation and data collection of outcomes), and the outcome period (last 6 months of the study). The primary outcome was ultrasound detection of SGA (estimated fetal weight <10th centile using customised centiles (intervention) or Hadlock centiles (standard care)) confirmed at birth (birthweight <10th centile by both customised and population centiles). Secondary outcomes were maternal and neonatal outcomes, including induction of labour, gestational age at delivery, mode of birth, neonatal morbidity, and stillbirth/perinatal mortality. A 2-stage cluster–summary statistical approach calculated the absolute difference (intervention minus standard care arm) adjusted using the prerandomisation estimate, maternal age, ethnicity, parity, and randomisation strata. Intervention arm clusters that made no attempt to implement GAP were excluded in modified intention to treat (mITT) analysis; full ITT was also reported. Process evaluation assessed implementation fidelity, reach, dose, acceptability, and feasibility. Seven clusters were randomised to GAP and 6 to standard care. Following exclusions, there were 11,096 births exposed to the intervention (5 clusters) and 13,810 exposed to standard care (6 clusters) during the outcome period (mITT analysis). Age, height, and weight were broadly similar between arms, but there were fewer women: of white ethnicity (56.2% versus 62.7%), and in the least deprived quintile of the Index of Multiple Deprivation (7.5% versus 16.5%) in the intervention arm during the outcome period. Antenatal detection of SGA was 25.9% in the intervention and 27.7% in the standard care arm (adjusted difference 2.2%, 95% confidence interval (CI) −6.4% to 10.7%; p = 0.62). Findings were consistent in full ITT analysis. Fidelity and dose of GAP implementation were variable, while a high proportion (88.7%) of women were reached. Use of routinely collected data is both a strength (cost-efficient) and a limitation (occurrence of missing data); the modest number of clusters limits our ability to study small effect sizes. Conclusions In this study, we observed no effect of GAP on antenatal detection of SGA compared to standard care. Given variable implementation observed, future studies should incorporate standardised implementation outcomes such as those reported here to determine generalisability of our findings. Trial registration This trial is registered with the ISRCTN registry, ISRCTN67698474.
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