RESUMEN
The microbial dysbiosis associated with necrotizing enterocolitis (NEC) in preterm infants suggests that early exposure to probiotics may decrease and antibiotics may increase NEC risk. However, administration of Bifidobacterium breve strain BBG-001 to preterm infants did not affect NEC incidence in a multicenter randomised controlled phase 3 trial (PiPS trial). Using a subset of these subjects we compared the fecal microbiome of probiotic and placebo groups and assessed the impact of early antibiotic treatment. Extracted DNA from 103 fecal samples collected at 36weeks post-menstrual age underwent PCR amplification of a fragment of the 16S rRNA gene. Heatmaps were constructed showing the proportions of sequences from bacterial families present at >1% of the community. Stepwise logistic regression assessed the association between early antibiotic exposure and microbiome group. There was no difference in the microbial richness and diversity of the microbiome of preterm infants following treatment with probiotic or a placebo. Conversely, early antimicrobial exposure was associated with different patterns of colonisation, specifically a relative abundance of Proteobacteria. These findings highlight that the potential influence of probiotics on the microbiome of preterm infants remains unclear whereas the modulatory effect of antibiotic exposure on microbial colonisation requires further research.
Asunto(s)
Enterocolitis Necrotizante/prevención & control , Microbiota , Probióticos/administración & dosificación , Bifidobacterium , Disbiosis , Enterocolitis Necrotizante/etiología , Microbioma Gastrointestinal , Humanos , Lactante , Recién Nacido , Recien Nacido Prematuro , Metagenoma , Metagenómica , Oportunidad Relativa , Evaluación de Resultado en la Atención de Salud , ARN Ribosómico 16S , Tiempo de TratamientoRESUMEN
OBJECTIVES: The objectives of this study were to characterize ESBL-producing Enterobacteriaceae present in 24 neonatal units (NNUs) in eight networks participating in a multicentre probiotic study and to test the hypothesis that specific strains would cluster within individual units and networks. METHODS: We performed analysis of stool samples for the presence of ESBL-producing Enterobacteriaceae at 2 weeks post-natal age and 36 weeks post-menstrual age. ESBL-producing Enterobacteriaceae were characterized and typed using molecular methods. RESULTS: ESBL-producing Enterobacteriaceae (nâ=â71) were isolated from 67/1229 (5.5%) infants from whom we received a sample at either sampling time or both sampling times, and from infants in 18 (75%) of the 24 recruiting NNUs. Thirty-three Escherichia coli, 23 Klebsiella spp. and 6 Enterobacter spp. strains were characterized. ESBL-producing E. coli were all distinguishable within individual NNUs by antibiotic resistance genotype, serogroup (O25b), phenotype, phylotype or ST. Ten of the 33 were ST131 and 9 of the 10 ST131 isolates were ciprofloxacin resistant. Seven of the 10 ST131 isolates carried genes encoding CTX-M group 1 enzymes. ST131 isolates were isolated from centres within five of the eight NNU networks. There were clusters of indistinguishable ESBL-producing Klebsiella and Enterobacter isolates associated with specific NNUs. CONCLUSIONS: Strains of E. coli ST131 were distributed across neonatal networks in the south of England. There was no evidence of clustering of clonally related ESBL-producing E. coli strains, by contrast with Klebsiella spp. and Enterobacter spp., which did cluster within units. The possibility that ESBL-producing E. coli strains are spread by vertical transmission requires further investigation.