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S Iyobe

Publications and source records attributed to S Iyobe.

At least 37 records · Page 2Linked to original sources
PubMed1994

Mechanisms of high-level resistance to quinolones in urinary tract isolates of Pseudomonas aeruginosa.

Twenty-eight strains of Pseudomonas aeruginosa with various degrees of norfloxacin resistance were isolated from patients with urinary tract infections. P. aeruginosa strains (norfloxacin MICs, 3.13 to 200 micrograms/ml) were transformed by either pPAW207 or pNF111 plasmid DNA, which included either the gyrA or nfxB gene, respectively. For transformants with pPAW207, norfloxacin MICs decreased 8- to 128-fold. It was suggested that moderate and high degrees of resistance to norfloxacin were expressed as a result of alterations in gyrA. No strain manifesting only an alteration in nfxB permeability was observed. The MICs of norfloxacin (200 micrograms/ml) for two P. aeruginosa strains, GN17605 and GN17434-2, were decreased following transformation not only by pPAW207 but also by pNF111. Analysis of outer membrane proteins disclosed the presence of a 54,000-Da protein in these parent strains that was not expressed in the pNF111 transformants. The level of accumulation of norfloxacin by the pNF111 transformant of GN17605 was higher than that by the parent strain. The norfloxacin susceptibility of DNA gyrase subunit A purified from GN17605 was only 1/35th that of the gyrase containing a subunit A from P. aeruginosa PAO1. These findings suggest that GN17605 is a gyrA-nfxB double mutant and that strain GN17434-2 possesses double mutations in both nfxB and some unknown gene.

Anti-Infective Agents↗
PubMed1994

[Gram-negative rods: antibacterial agents effective on gram-negative rods].

Some kinds of gram-negative rods cause serious infections in the compromised hosts. The species most frequently isolated in big hospitals are P. aeruginosa, E. coli, K. pneumoniae, E. cloacae, S. marcescens, and H. influenzae. Among these species. P. aeruginosa, E. cloacae and S. marcescens show resistance to many antibacterial agents. The aminoglycoside, such as gentamicin, is effective against these strains but resistant strains are detected at a high frequency for P. aeruginosa. Resistant strains to new quinolones are isolated for both S. marcescens and P. aeruginosa. The third generation cephems are effective against these species but they easily acquire resistance to these drugs. Imipenem and cefclidin are effective and a few resistant strains to the drugs are already detectable in gram-negative rods.

Anti-Bacterial Agents↗
PubMed1994

[Drug resistance and phage typing of clinical isolates of Staphylococcus aureus].

Activities of antimicrobial agents were examined against Staphylococcus aureus strains isolated in 1990. Strains resistant to benzylpenicillin were isolated at the highest frequency (93.6%), and followed by those resistant to kanamycin (51.5%), erythromycin (49.0%), gentamicin (45.1%), fluoroquinolone (33.4%) and minocycline (12.3%). Most of these drug resistant strains of S. aureus were also resistant to methicillin. It should be noted that the MRSA strains were also resistant to other multiple drugs. Annual changes of MRSA in clinical isolates have been increasing since 1981. The isolation frequencies of MRSA strains were 18.9%, 44.8% in 1981 and 1990, respectively. Among methicillin susceptible S. aureus (MSSA), however, drug resistance to other antibiotics have been decreasing year by year. Many strains among both MRSA (73%) and MSSA (86%) were sensitive to typing phages of 100 x RTD. 76% of the MRSA strains were phage typed into groups III or mixed, and 60% of the MSSA strains were typed into these two groups, also.

Anti-Bacterial Agents↗
PubMed1993

Characterization of newly isolated plasmids from Actinobacillus pleuropneumoniae.

The genetic basis of drug-resistant strains of Actinobacillus pleuropneumoniae in Japan was studied. The A pleuropneumoniae strains AV277 and AV281 that belong to serotype 2 were resistant to streptomycin (SM) and sulfonamide (SA). Both strains had an 8.1-kilobase (kb) SM-SA plasmid that was previously classified in the H1 group. The AV177 (serotype 1) strain was resistant to SM, SA, ampicillin, and kanamycin (KM), but did not have any plasmids. The AV319 and AV324 (serotype 1) strains were resistant to SM, SA, tetracycline (TC), and chloramphenicol (CP). The AV318 (serotype 12) strain was resistant to SM, SA, TC, minocycline, and CP. These 3 strains (AV319, AV324, and AV318) had a 4.3-kb SM-SA plasmid and a 5.2-kb CP plasmid. The 4.3-kb plasmid was classified in the H2 group. The AV263 (serotype 1) strain was resistant to SM, SA, KM, TC, and CP. It had a 5.2-kb CP plasmid and a 6.6-kb SM-SA-KM plasmid. Both plasmids did not replicate stably in Escherichia coli strains. The former 5.2-kb plasmid was mobilized in E coli strains by plasmid RP4, which belonged to incompatibility P with broad host range, but the latter 6.6-kb plasmid was not so mobilized. Three 5.2-kb CP plasmids isolated from strains AV319, AV324, and AV318, had the same restriction endonuclease pattern after digestion with Ava I and EcoRI. They coexisted with H1 group plasmids in the incompatibility test, and coexisted also with H2 group plasmids of the original A pleuropneumoniae strains. Results indicated that the 5.2-kb CP plasmids could be classified in a new incompatibility group, H3. In this study, 4 types of plasmids were isolated, but no plasmids encoded TC and minocycline resistance.

Actinobacillus Infections↗
PubMed1992

Occurrence of the nfxB type mutation in clinical isolates of Pseudomonas aeruginosa.

Seven spontaneous norfloxacin (NFLX)-resistant mutants obtained in vitro from 20 NFLX-susceptible clinical isolates and 3 NFLX-resistant clinical isolates of Pseudomonas aeruginosa were transformed with the pNF111 plasmid, whose BamHI fragment is responsible for conferring susceptibility to NFLX, by complementing the nfxB mutation. The resulting patterns of MICs of NFLX, beta-lactams, aminoglycosides, and chloramphenicol and the observed increased accumulation of NFLX were consistent with the occurrence of the nfxB type mutation in these clinical isolates.

Carbenicillin↗
PubMed1992

In vitro activity of E1040 against imipenem-resistant Pseudomonas aeruginosa strains.

E1040 showed the most potent activity (MIC for 90% of strains, 6.25 micrograms/ml) among beta-lactams tested against 70 strains of imipenem-resistant Pseudomonas aeruginosa. Two strains showed high-level resistance to E1040; one strain produced a type II oxyiminocephalosporin-hydrolyzing beta-lactamase (group 3), and the other produced an enzyme similar to a type II penicillinase (OXA-1). Both beta-lactamases contributed to resistance to E1040.

Anti-Bacterial Agents↗
PubMed1991

Cloning and characterization of a DNA fragment that complements the nfxB mutation in Pseudomonas aeruginosa PAO.

The 2.2-kilobase DNA fragment that can complement the nfxB mutation in Pseudomonas aeruginosa PAO was cloned from chromosomal DNA of P. aeruginosa PAO1. The nfxB mutants show an increase in resistance to quinolones and hypersusceptibility to beta-lactam and aminoglycoside antibiotics. In the mutants, a 54 kDa outer membrane protein newly appeared. The phenotype was restored to the wild-type by transformation with plasmid carrying the 2.2-kb DNA fragment.

Chromosomes, Bacterial↗
PubMed1991

Transferable imipenem resistance in Pseudomonas aeruginosa.

We isolated an imipenem-resistant strain, GN17203, of Pseudomonas aeruginosa. The strain produced a beta-lactamase that hydrolyzed imipenem. The beta-lactamase was encoded by a 31-MDa plasmid, pMS350, which belongs to incompatibility group P-9. The plasmic conferred resistance to beta-lactams, gentamicin, and sulfonamide and was transferable by conjugation to P. aeruginosa but not to Escherichia coli. The molecular weight of the purified enzyme was estimated to be 28,000, and the isoelectric point was 9.0. The enzyme showed a broad substrate profile, hydrolyzing imipenem, oxyiminocephalosporins, 7-methoxycephalosporins, and penicillins. The enzyme activity was inhibited by EDTA, iodine, p-chloromercuribenzoate, CuSO4, and HgCl2 but not by clavulanic acid or sulbactam.

Conjugation, Genetic↗
PubMed1991

Characterization and classification of Actinobacillus (Haemophilus) pleuropneumoniae plasmids.

Actinobacillus (Haemophilus) pleuropneumoniae plasmids were characterized and classified. They were isolated from A pleuropneumoniae strains different in serotype, year isolated, or location from which isolated. Six of 8 plasmids encoded streptomycin (Sm) and sulfonamide (Su) resistance (SmSu). One of the other plasmids, pVM105, encoded ampicillin (Ap) resistance and another, pHM0, encoded no drug resistance. All SmSu plasmids were transferred to Escherichia coli strains by transformation. Among them, pABO and pMS260 were 8.1 kb and incompatible with each other; they were stable in E coli. The other SmSu plasmids, pHM1, pVM104, pVM106, and pKD25, were 4.3 kb and did not replicate stably in E coli. The former SmSu plasmids were mobilized in E coli strains by a plasmid RP4, which belonged to incompatibility (Inc) group P, but the latter plasmids were not. Further, each 8.1-kb SmSu plasmid and each 4.3-kb plasmid had the same respective restriction pattern. These results indicated that there were at least 2 types of SmSu plasmids in A pleuropneumoniae. The 2 types were classified in 2 groups: H1(pMS260 and pABO) and H2(pHM1, pVM104, pVM106, and pKD25). The H1 and H2 plasmids belonged to different Inc groups, and H2 plasmids belonged to a different Inc group from that of pHMO and pVM105.

Actinobacillus pleuropneumoniae↗
PubMed1990

New norfloxacin resistance gene in Pseudomonas aeruginosa PAO.

A new type of norfloxacin-resistant mutant of Pseudomonas aeruginosa PAO was isolated. This mutant showed cross resistance to imipenem and chloramphenicol and hypersusceptibility to beta-lactam and aminoglycoside antibiotics. The new norfloxacin resistance gene nfxC was mapped near catA (46 min) on the PAO chromosome. Norfloxacin accumulation was decreased in the nfxC mutant; furthermore, the rate of imipenem diffusion through the outer membrane of the nfxC mutant was lower than that of the parent strain. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of outer membrane proteins showed a decrease of a 46-kilodalton protein and an increase of a 50-kilodalton protein in the nfxC mutant. We conclude the nfxC is a new norfloxacin resistance gene that affects outer membrane permeability to quinolones and other antimicrobial agents.

Bacterial Outer Membrane Proteins↗
PubMed1990

Drug-susceptibility and isolation of a plasmid in Haemophilus (Actinobacillus) pleuropneumoniae.

We isolated 56 Haemophilus (Actinobacillus) pleuropneumoniae strains from the pneumonic porcine lung tissues and tested them for antimicrobial susceptibility. Two drug-resistant strains were obtained. One, named KH-265, was resistant to streptomycin (SM) and sulfonamide (SA), and the other, named KH-195, was resistant to tetracycline (TC). The minimum inhibitory concentrations (MICs) of drugs for resistant strains were 100 micrograms/mliters for SM, 3200 micrograms/mliters for SA, and 12.5 micrograms/mliters for TC. KH-265 possessed a 8.3Kb nonconjugative plasmid, pMS260, encoding SM and SA resistance, which was transformable to E. coli strains. pMS260 belonged to none of 14 incompatibility groups including Inc. P and Inc. Q, so far tested. It was mobilizable to various causative strains for respiratory infections, Pseudomonas aeruginosa, Bordetella bronchiseptica, Pasteurella multocida and Haemophilus pleuropneumoniae, by RP4 (Inc. P) plasmid.

Animals↗
PubMed1987

Mutations producing resistance to norfloxacin in Pseudomonas aeruginosa.

Two genetically distinct classes of norfloxacin-resistant Pseudomonas aeruginosa PAO4009 mutants were isolated spontaneously. Two norfloxacin resistance genes, nfxA and nfxB, were mapped hex-9001 and leu-9005 and between pro-9031 and ilv-9023, respectively, on the P. aeruginosa PAO chromosome. The nfxA gene was shown to be an allele of nalA by transductional analysis with bacteriophage F116L. The nfxB mutant showed a 16-fold increase in resistance to norfloxacin and a slight increase in resistance to nalidixic acid. The nfxB mutant was unique in that it showed hypersusceptibility to beta-lactam and aminoglycoside antibiotics. This mutant had about a threefold-lower rate of norfloxacin uptake than that of the wild-type strain or nfxA mutant. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of outer membrane proteins demonstrated the appearance of a 54,000-dalton protein in the nfxB mutant. These findings suggested that the norfloxacin resistance mechanism in the nfxB mutant might be an alteration in outer membrane permeability to norfloxacin.

Aminoglycosides↗