An ampC gene was cloned from a clinical isolate of Acinetobacter baumannii (strain RAN). DNA sequencing and primer extension studies showed that ampC is transcribed from a promoter contained within a putative insertion sequence element which has been found to abut several different genes in Acinetobacter spp

BackgroundExtended spectrum beta-lactamase producing bacteria (ESBL) are common causes of neonatal sepsis worldwide. Neonatal sepsis due to ESBL is associated with increased morbidity and mortality at Bugando Medical Centre (BMC). Due to limited information on the sources of these ESBL strains at BMC, this study was conducted to evaluate the existence, magnitude and transmission of ESBL from post-delivery women to neonates at BMC, Mwanza-Tanzania.ResultsA cross-sectional study was conducted at obstetrics and neonatal wards from May to July 2013, involving post-delivery women and their neonates. Rectal swabs were collected and processed to identify the ESBL strains and their antimicrobial susceptibility patterns. Patients’ data were obtained using a standardized data collection tool. We enrolled 113 women and 126 neonates with mean age of 26.5 ± 5.5 years and median gestation age [IQR] of 39 [35–40] weeks respectively. The prevalence of ESBL carriage among women and neonates were 15% (17/113) and 25.4% (32/126) respectively. The acquisition of ESBL isolates among neonates on day 1, day 3 and day 7 were 60.0% (21/35), 25.7% (9/35) and 14.3% (5/35) respectively. There was no phenotypic similarity between ESBL strains from women and their respective neonates, suggesting other sources of transmission. Neonates given antibiotics were more likely to carry ESBL than those not given [100% (32/32) versus 86% (81/94), p = 0.018].ConclusionThe carriage rate of ESBL strains among post-delivery women and neonates at BMC is high. Our findings suggest that neonates acquire these strains from sources other than post-delivery women and more than half acquire them on the first day of life. More studies are recommended to further explore the sources of ESBL strains among neonates.

DNA sequencing data showed that five clinical isolates of Escherichia coli with reduced susceptibility to ceftazidime, ceftriaxone, and cefotaxime contain an ampC gene that is preceded by a strong promoter. Transcription from the strong promoter was 8-to 18-fold higher than that from the promoter from a susceptible isolate. RNA studies showed that mRNA stability does not play a role in the control of AmpC synthesis.

Resistance to selected beta-lactams in two clinical isolates of K. pneumoniae was due to interplay between the expression of OMPs and TEM-1.

Clinical isolates of Klebsiella pneumoniae and Serratia marcescens at a hospital that had used amikacin as its principal aminoglycoside for the preceding 42 months demonstrated high-level resistance to amikacin (greater than or equal to 256 micrograms/ml), kanamycin (greater than or equal to 256 micrograms/ml), gentamicin (greater than or equal to 64 micrograms/ml), netilmicin (64 micrograms/ml), and tobramycin (greater than or equal to 16 micrograms/ml). The resistant strains contained an identical 6.8-kilobase plasmid, pRPG101. Transformation of pRPG101 into Escherichia coli produced high-level resistance to amikacin (greater than or equal to 256 micrograms/ml) and kanamycin (greater than or equal to 256 micrograms/ml) but unchanged susceptibilities to gentamicin, netilmicin, and tobramycin. The clinical isolates and transformants produced a novel 3'-phosphotransferase, APH(3'), that modified amikacin and kanamycin in vitro. The location and orientation of the amk gene encoding this APH(3') were determined by analysis of insertions in pRPG101 of the defective gene fusion phage Mu dII1681 (mini-Mulac). Cells containing plasmids with insertions into amk that had the lac operon fused to the amk promoter were selected as Lac+ and amikacin susceptible. A collection of these mini-Mulac insertions was mapped by restriction enzyme analysis. This characterization of amk facilitated its cloning as a 1.8-kilobase EcoRI-Bg/I fragment of pRPG101 into the pUC19 vector. E. coli strains containing this recombinant plasmid had APH(3') activity and demonstrated high-level resistance to amikacin and kanamycin (greater than or equal to 256 micrograms/ml) but were as susceptible to gentamicin, tobramycin, and netilmicin (less than or equal to 1.0 microgram/ml) as the strains harboring the original pRPG101 plasmid.