Beta-lactamase plasmids and chromosomally mediated antibiotic resistance in pathogenic Neisseria species

Dillon, J A; Yeung, Kwok-Him

doi:10.1128/cmr.2.suppl.s125

Cited by 61 publications

(34 citation statements)

References 71 publications

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“…The study revealed the occurrence of 23.1 kb plasmid DNAs in Citrobacter and Klebsiella (Table 5; Figures 5 and 6). This occurrence of 23.1 kb plasmid in these organisms is in agreement with the research reports of Dillon and Yeung (1989) (35), Fortin et al (1993) (36), Van den Bogaard and Stobberingh (2000) (37), Sharif and Astal (2004) (38), as well as Eze (2012) (16). This 23.1 kb plasmid has been reported to be perhaps, one of the most frequently occurring plasmids in microbes known for mediating ESBL occurrence and multiple drug resistance (38).…”

Section: Discussionsupporting

confidence: 82%

Studies on Drug Resistance among Klebsiella and Citrobacter spp Isolated from two Human Groups and Wild Animals

Eze

Mustapha

Ndubuisi

et al. 2017

Jundishapur J Microbiol

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Background: The global threat of antimicrobial resistance is undoubtedly on the increase and most researches in this area have concentrated on effects of drug exposure and usage on resistance. Little attention has been given to natural environments apparently devoid of direct anthropogenic impact as possible reservoirs of drug resistance traits. Objectives: This research was undertaken to determine possible similarities between drug resistance traits in species of Klebsiella and Citrobacter obtained from wild animals and 2 human groups. Methods: Human samples were collected from Humans free from antibiotics (HN) and Human on antibiotics (HA) while samples from wildlife (WL) were taken from rats (Rattus spp), grasscutters (Thryonomys swinderianus), squirrels (Xerus erythropus), antelopes (Tragelephus scriptus), rabbits (Oryctolagus cuniculus), and farm lizards (Agama spp). Samples were analyzed using basic microbiological methods. The Disc diffusion technique was used for drug sensitivity testing while plasmid analysis was based on gel electrophoresis. Results: Members of the genus Klebsiella isolated from HA exhibited more resistance to ampicillin (AMP) and augmentin (AUG) than those isolated from HN. However, Klebsiella isolated from HN displayed higher resistance to ceftriaxone (CTN), clarithromycin (CMN), ofloxacin (OFL), and pefloxacin (PEF) than those from HA. WL isolates were mostly resistant to AMP, CMN, and AUG, and less

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Section: Discussionsupporting

confidence: 82%

Studies on Drug Resistance among Klebsiella and Citrobacter spp Isolated from two Human Groups and Wild Animals

Eze

Mustapha

Ndubuisi

et al. 2017

Jundishapur J Microbiol

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“…It is highly related to a series of small 3-lactamase-specifying plasmids found in N. gonorrhoeae, Haemophilus influenzae, Haemophilus parainfluenzae, and Haemophilus ducreyi (3,4,9,11). A similar plasmid has been reported in a clinical isolate of Neisseria meningitidis (10).…”

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confidence: 90%

“…Figure 1 depicts the relationships of two representative plasmids of this group. pJB1 carries a full and functional TnA sequence, while pFA3 contains an insertion of about 1.8 kilobase pairs (kbp) which carries a HindIII site (4,9,11,20,34). Relative to pJBl, 60% of the TnA sequence and 270 bp of the core plasmid sequences adjacent to the left-hand inverted repeat of TnA are deleted in pFA3 (3-5, 7, 20).…”

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confidence: 99%

Identification and characterization of a new replication region in the Neisseria gonorrhoeae beta-lactamase plasmid pFA3

Gilbride

Brunton

1990

J Bacteriol

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The 7.1-kilobase-pair (kbp) plasmid pFA3 specifies TEM lB-lactamase production in Neisseria gonorrhoeae. We studied the minimal region required for replication of this plasmid in Escherichia coli by constructing a set of nested deletions of the 3.4-kbp PstI-HindH fragment. The smallest fragment capable of maintenance in E. coli when ligated to a streptomycin-spectinomycin resistance cassette was 2.0 kbp in size and was different from another autonomously replicating fragment of pFA3 reported by K. H. Yeung and J. Dillon (Plasmid 20:232-240, 1988). The fragment contained single BamHI and XbaI sites and specified a 39-K protein. Fragments subcloned from the minimal region or constructed by deletion from the 3' or 5' ends were not capable of autonomous replication. Mutants constructed by end filling and religating DNA cleaved at the BamHI or XbaI sites were not capable of autonomous replication and no longer produced the 39K protein. These results suggest that replication is dependent on the 39K protein. DNA sequence analysis of the region showed an A-T-rich region followed by four 22-bp direct repeats followed by an open reading frame encoding a 39K basic protein.

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“…Resistance to these antibiotics can be either plasmid mediated or chromosomally mediated. Plasmid-mediated resistance to penicillin or tetracycline involves expression of a TEM-1-like ␤-lactamase (8,30) or the TetM protein (25), respectively. In contrast, chromosomally mediated resistant N. gonorrhoeae (CMRNG) strains arise from cumulative mutations in endogenous genes or loci that gradually increase resistance until treatment failure occurs (3).…”

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Porin-Mediated Antibiotic Resistance in Neisseria gonorrhoeae : Ion, Solute, and Antibiotic Permeation through PIB Proteins with penB Mutations

et al. 2006

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Neisseria gonorrhoeae has two porins, PIA and PIB, whose genes (porA and porB, respectively) are alleles of a single por locus. We recently demonstrated that penB mutations at positions 120 and 121 in PIB, which are presumed to reside in loop 3 that forms the pore constriction zone, confer intermediate-level resistance to penicillin and tetracycline (M. Olesky, M. Hobbs, and R. A. Nicholas, Antimicrob. Agents Chemother. 46: 2811-2820, 2002). In the present study, we investigated the electrophysiological properties as well as solute and antibiotic permeation rates of recombinant PIB proteins containing penB mutations (G120K, G120D/A121D, G120P/A121P, and G120R/A121H). In planar lipid bilayers, the predominant conducting state of each porin variant was 30 to 40% of the wild type, even though the anion selectivity and maximum channel conductance of each PIB variant was similar to that of the wild type. Liposome-swelling experiments revealed no significant differences in the permeation of sugars or ␤-lactam antibiotics through the wild type or PIB variants. Although these results are seemingly contradictory with the ability of these variants to increase antibiotic resistance, they are consistent with MIC data showing that these porin mutations confer resistance only in strains containing an mtrR mutation, which increases expression of the MtrC-MtrD-MtrE efflux pump. Moreover, both the mtrR and penB mutations were required to decrease in vivo permeation rates below those observed in the parental strain containing either mtrR or porin mutations alone. Thus, these data demonstrate a novel mechanism of porin-mediated resistance in which mutations in PIB have no affect on antibiotic permeation alone but instead act synergistically with the MtrC-MtrD-MtrE efflux pump in the development of antibiotic resistance in gonococci.In the 1970s and early 1980s, Neisseria gonorrhoeae, the etiological agent of the sexually transmitted infection gonorrhea, gradually became more resistant to penicillin and tetracycline until these antibiotics were discontinued as a first-line therapy. Resistance to these antibiotics can be either plasmid mediated or chromosomally mediated. Plasmid-mediated resistance to penicillin or tetracycline involves expression of a TEM-1-like ␤-lactamase (8, 30) or the TetM protein (25), respectively. In contrast, chromosomally mediated resistant N. gonorrhoeae (CMRNG) strains arise from cumulative mutations in endogenous genes or loci that gradually increase resistance until treatment failure occurs (3).Four genes or loci (penA, mtrR, penB, and ponA) are known to be involved in high-level penicillin resistance (MICs, Ն2 g/ml) in CMRNG strains, while the existence of a fifth resistance gene is inferred but not yet identified (3, 9, 32). penA (38, 39) and ponA (32, 33) encode alterations in the two essential penicillin-binding proteins (PBP 2 and PBP 1, respectively) that decrease their rates of acylation by ␤-lactam antibiotics. A single-base-pair deletion in the mtrR promoter abolishes transcription of the mtrR...

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Beta-lactamase plasmids and chromosomally mediated antibiotic resistance in pathogenic Neisseria species

Cited by 61 publications

References 71 publications

Studies on Drug Resistance among Klebsiella and Citrobacter spp Isolated from two Human Groups and Wild Animals

Studies on Drug Resistance among Klebsiella and Citrobacter spp Isolated from two Human Groups and Wild Animals

Identification and characterization of a new replication region in the Neisseria gonorrhoeae beta-lactamase plasmid pFA3

Porin-Mediated Antibiotic Resistance in Neisseria gonorrhoeae : Ion, Solute, and Antibiotic Permeation through PIB Proteins with penB Mutations

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