Carriage and within-host diversity of harbouring from pregnant mothers: inter- and intra-mother transmission dynamics of .

Exchange of antimicrobial resistance genes via mobile genetic elements occur in the gut which can be transferred from mother to neonate during birth. This study is the first to analyse transmissible colistin resistance gene, , in pregnant mothers and neonates. Samples were collected from pregnant mothers (rectal) and septicaemic neonates (rectal and blood) and analysed for the presence of , its transmissibility, genome diversity, and exchange of between isolates within an individual and across different individuals (not necessarily mother-baby pairs).

A Decade-Long Evaluation of Neonatal Septicaemic Escherichia coli: Clonal Lineages, Genomes, and New Delhi Metallo-Beta-Lactamase Variants.

Longitudinal studies of extraintestinal pathogenic Escherichia coli (ExPEC) and epidemic clones of E. coli in association with New Delhi metallo-β-lactamase () in septicaemic neonates are rare. This study captured the diversity of 80 E.

Hypervirulent Klebsiella pneumoniae Causing Neonatal Bloodstream Infections: Emergence of NDM-1-Producing Hypervirulent ST11-K2 and ST15-K54 Strains Possessing pLVPK-Associated Markers.

Klebsiella pneumoniae is a major cause of neonatal sepsis. Hypervirulent Klebsiella pneumoniae (hvKP) that cause invasive infections and/or carbapenem-resistant hvKP (CR-hvKP) limit therapeutic options. Such strains causing neonatal sepsis have rarely been studied.

Neonatal Sepsis: The Impact of Carbapenem-Resistant and Hypervirulent .

The convergence of a vulnerable population and a notorious pathogen is devastating, as seen in the case of sepsis occurring during the first 28 days of life (neonatal period). Sepsis leads to mortality, particularly in low-income countries (LICs) and lower-middle-income countries (LMICs). , an opportunistic pathogen is a leading cause of neonatal sepsis.

Evaluation of co-transfer of plasmid-mediated fluoroquinolone resistance genes and gene in causing neonatal septicaemia.

Background: The (New Delhi Metallo-β-lactamase-1) gene has disseminated around the globe. NDM-1 producers are found to co-harbour resistance genes against many antimicrobials, including fluoroquinolones. The spread of large plasmids, carrying both and plasmid-mediated fluoroquinolone resistance (PMQR) markers, is one of the main reasons for the failure of these essential antimicrobials.

Acinetobacter baumannii transfers the blaNDM-1 gene via outer membrane vesicles.

Objectives: To investigate the transmission of the gene encoding New Delhi metallo-β-lactamase-1 ( bla NDM-1 ) through outer membrane vesicles (OMVs) released from an Acinetobacter baumannii strain (A_115).

Methods: Isolation and purification of OMVs by density gradient from a carbapenem-resistant clinical strain of A. baumannii harbouring plasmid-mediated bla NDM-1 and aac(6')-Ib-cr genes was performed.

A reliable phenotypic assay for detection of ESBLs and AmpCs in MBL-producing gram-negative bacteria with the use of aminophenylboronic acid, dipicolinic acid and cloxacillin.

ESBLs and AmpCs may escape detection when they coexist with metallo-β-lactamases such as New Delhi Metallo-β-lactamases-1. In this study a combination disk assay was established using cefotaxime, cefotaxime/clavulanic acid, cefotaxime/clavulanic acid/cloxacillin, cefoxitin and cefoxitin/phenylboronic acid/cloxacillin on Mueller Hinton agar supplemented with dipicolinic acid for determination of β-lactamases in the presence of NDM-1.

Characterization of novel plasmid-mediated β-lactamases (SHV-167 and ACT-16) associated with New Delhi metallo-β-lactamase-1 harbouring isolates from neonates in India.

Neonatal sepsis due to carbapenem-resistant bacteria is difficult to treat due to limited therapeutic options. The detection of the new carbapenemase New Delhi metallo-β-lactamase-1 (NDM-1) from neonates has further complicated the situation (Roy et al., 2011a).