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Biomedical subjects

S G Amyes

Publications and source records attributed to S G Amyes.

At least 109 records · Page 6Linked to original sources
PubMed1990

Antibacterial activity of fluoroquinolones in combination with zidovudine.

Since patients with AIDS may receive fluoroquinolones concurrently with zidovudine, the antibacterial interaction of these drugs was investigated. No evidence was found of antagonism between zidovudine and ciprofloxacin, DR-3355, enoxacin, lomefloxacin or ofloxacin against enterobacteria, staphylococci or Pseudomonas aeruginosa. Furthermore, the bactericidal activity of the fluoroquinolones against selected enterobacteria in nutrient broth was not affected by a clinically achievable concentration of zidovudine. It seems unlikely that zidovudine will have an adverse effect on the antibacterial activity of the fluoroquinolones in patients with AIDS.

Anti-Infective Agents↗
PubMed1990

Mechanisms of zidovudine resistance in bacteria.

Unlike their parent strains, zidovudine-resistant derivatives of Escherichia coli KL16 and Salmonella typhimurium NCTC 5710 were found to be incapable of incorporating radiolabelled thymidine into their chromosomal DNA. Since incorporation was still prevented in the presence of EDTA, resistance to zidovudine was not associated with a permeability barrier, but appeared to result from the loss of thymidine kinase activity, required for the phosphorylation of zidovudine. Pseudomonas aeruginosa, which is intrinsically zidovudine-resistant, was also shown to be incapable of incorporating thymidine into its DNA, but Staphylococcus epidermidis SK360 and Staph. aureus E3T, which are also intrinsically zidovudine-resistant, possessed thymidine kinase activity. This suggests that two distinct mechanisms of resistance to zidovudine exist in bacteria. Zidovudine resistance did not appear to confer resistance to other antibacterial agents.

DNA, Bacterial↗
PubMed1990

Isolation of zidovudine resistant Escherichia coli from AIDS patients.

Zidovudine-resistant Escherichia coli were isolated from faecal samples from 6 out of 11 AIDS patients receiving zidovudine. Resistance appeared to be due to the loss of thymidine kinase activity which is required for the phosphorylation of zidovudine to its active form. No zidovudine resistant enterobacteria were isolated from 30 control faecal samples. Hence, clinically, there appeared to be a high correlation between the development of zidovudine-resistance in E. coli and exposure to zidovudine (chi 2: 11.77, P less than 0.001). However the development of zidovudine resistance does not appear to be associated with cross-resistance to other antimicrobial agents as the zidovudine-resistant E. coli did not display a high degree of resistance to other antibacterials.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Susceptibility of bacterial isolates from AIDS patients to six fluoroquinolones.

The susceptibilities to ciprofloxacin, DR-3355 (S-(-)-ofloxacin), enoxacin, lomefloxacin, ofloxacin and PD127,391 of 69 significant bacterial isolates from HIV-positive patients at the City Hospital, Edinburgh have been determined. With the exception of the enterococci, most of the strains tested (including staphylococci, Escherichia coli and Pseudomonas aeruginosa) were susceptible to the fluoroquinolones. Ciprofloxacin was the most active of the clinically available drugs followed by ofloxacin, lomefloxacin and enoxacin. PD127,391 and DR-3355, the new fluoroquinolones tested, were at least as active as ciprofloxacin. Hence bacterial infections in AIDS patients should respond to fluoroquinolone therapy.

4-Quinolones↗
PubMed1990

In vitro activities of 4-quinolones against the fish pathogen Aeromonas salmonicida.

The activities of five fluorinated 4-quinolones, namely, sarafloxacin, enrofloxacin, PD127391, PD117596, and CI934, against the fish pathogen Aeromonas salmonicida were investigated and compared with that of oxolinic acid. The results indicated that with the exception of CI934, these drugs are more active than oxolinic acid in terms of MIC. No inoculum effect was observed, but the drugs were less active at 10 degrees C than at 22 degrees C. The presence of 3% of NaCl caused an increase in drug activity. Resistance to the drugs appeared to be fairly stable, with only a small decrease in activity after 10 successive passages of the test strains on drug-free tryptone soya agar.

Aeromonas↗
PubMed1989

SAR-2: identification of a novel plasmid-encoded beta-lactamase from India.

A novel beta-lactamase has been identified in an Escherichia coli strain isolated in South India. The beta-lactamase gene was carried on a plasmid (pUK734) along with resistance determinants to sulphonamides and tetracycline. The novel enzyme has a pI of 8.3 and an Mr of 36,000. The enzyme has a broad-spectrum of activity against both penicillins and cephalosporins. It is also active against oxacillin and methicillin.

Conjugation, Genetic↗
PubMed1989

Bactericidal activity of enoxacin and lomefloxacin against Escherichia coli KL16.

Enoxacin and lomefloxacin were found to display a biphasic response when their bactericidal activities were investigated against Escherichia coli KL16 in nutrient broth. Although enoxacin required bacterial protein and RNA synthesis to exert bactericidal activity, it was able to kill non-dividing bacteria. On the other hand, the protein synthesis inhibitor chloramphenicol and the RNA synthesis inhibitor rifampicin did not abolish enoxacin's killing activity against Escherichia coli KL16 in nutrient broth. Lomefloxacin was also shown to be active against non-dividing Escherichia coli KL16.

Anti-Infective Agents↗
PubMed1989

Conditions required for the antibacterial activity of zidovudine.

In a study to determine the conditions required for its antibacterial activity, zidovudine was found to be bactericidal against Escherichia coli and Salmonella typhimurium in nutrient broth over 6 h. Zidovudine was also found to be active against ten clinical isolates of Salmonella and Escherichia coli at 1 mg/l, which is a clinically achievable concentration of the drug. Bacterial protein synthesis was required for the bactericidal activity of zidovudine against both Escherichia coli and Salmonella typhimurium. Zidovudine was found to be inactive against non-dividing bacteria, as it was unable to kill bacteria of either species when they were suspended in PBS.

Bacteria↗
PubMed1989

TEM-E1: a novel beta-lactamase conferring resistance to ceftazidime.

A novel beta-lactamase, conferring resistance to ceftazidime, has been identified to be encoded by a 31 kb plasmid (pUK720) in a clinical E. coli strain isolated in Belgium. The beta-lactamase, new designated TEM-E1, has a pI of approximately 5.4 and lies in between the iso-electric focused bands of the beta-lactamases TEM-1 and TEM-7. The TEM-E1 beta-lactamase has a similar molecular weight of 22,000 to the TEM-1 and it is also inhibited by clavulanic acid. However, the TEM-E1 enzyme differs from TEM-1 by its low rates and efficiency of hydrolysis for ceftazidime and cefotaxime, TEM-E1 has similar efficiency of hydrolysis values for ceftazidime and cefotaxime, but only confers resistance to ceftazidime.

Ceftazidime↗
PubMed1989

Mutants of the TEM-1 beta-lactamase conferring resistance to ceftazidime.

Spontaneous ceftazidime resistant mutants were obtained from an Escherichia coli K12 J62-2 expressing the TEM-1 beta-lactamase (mutation frequency = 10(-9). These mutants produced beta-lactamases with similar molecular weights, kinetic parameters and isoelectric points (pI) to the beta-lactamases produced by ceftazidime resistant clinical isolates which have recently been identified in this laboratory. Mutant enzyme A focused as a doublet band at pI 5.3 with an additional weak pI 5.4 band. The doublet co-focused with the TEM-E2 beta-lactamase, produced by a ceftazidime resistant Klebsiella oxytoca isolate, which was originally obtained in a Liverpool hospital. Mutant enzyme B had a pI identical to the TEM-E1 beta-lactamase produced by a ceftazidime resistant clinical isolate of E. coli found in Belgium. These results suggest that the two beta-lactamases in the clinical strains may have come from simple mutations of the TEM-1 beta-lactamase gene.

Ceftazidime↗
PubMed1989

The type VII dihydrofolate reductase: a novel plasmid-encoded trimethoprim-resistant enzyme from gram-negative bacteria isolated in Britain.

Plasmid pUN835 was identified in an Escherichia coli strain isolated from an outbreak of porcine diarrhoea on a farm near Nottingham, UK. The trimethoprim resistance gene did not hybridize with any of the gene probes derived from known plasmid-encoded trimethoprim resistance genes. The trimethoprim resistance gene of pUN835 was shown to encode the production of a dihydrofolate reductase which confers high-level resistance on its host. This enzyme was smaller than most plasmid-encoded dihydrofolate reductases (molecular mass = 11,500) and was labile to heat. It had relatively low affinity for the substrate dihydrofolate (Km = 20 microM) and it was resistant to competitive inhibition by trimethoprim (Ki = 7.0 microM). We classify this novel enzyme as type VII.

Animals↗
PubMed1989

The bactericidal activity of DR-3355, an optically active isomer of ofloxacin.

The bactericidal activity of compound DR-3355, an optically active isomer of ofloxacin, was measured against Escherichia coli, Staphylococcus aureus and S. epidermidis, in nutrient broth and in phosphate-buffered saline. DR-3355 was found to be approximately twice as active as ofloxacin in terms of the concentration at which maximum bacterial kill was achieved. Hence it appears that DR-3355 is twice as active as ofloxacin not only in terms of its ability to inhibit bacterial multiplication but also in its ability to kill bacteria. DR-3355 was found to be active against non-dividing bacteria and did not require either active RNA or protein biosynthesis in order to kill bacteria.

Bacterial Proteins↗
PubMed1989

A novel method for the identification and distinction of the beta-lactamases of the genus Acinetobacter.

The characterization of the chromosomal beta-lactamases of Acinetobacter has proved difficult because of the poor focusing of these enzymes in conventional isoelectric focusing on polyacrylamide gels. We describe a novel isoelectric focusing method, which employs an agarose gel incorporating a detergent with sorbitol and urea, to examine the beta-lactamases produced by eight clinical strains of Acinetobacter calcoaceticus; we have identified four different beta-lactamases. The molecular masses of each of the beta-lactamases was estimated and most of them ranged from 600,000 to greater than 1,000,000. These are the largest beta-lactamases so far described and their size is likely to be one reason for their poor solubility in conventional polyacrylamide systems.

Acinetobacter↗
PubMed1988

The differential expression of genes for the PSE-4 beta-lactamase in Pseudomonas aeruginosa and the Enterobacteriaceae.

The PSE-4 beta-lactamase has been identified, for the first time, in two non-pseudomonal strains. The gene in Klebsiella pneumoniae 241 (dal1) was located on a plasmid (pUK700) and was freely transferable to other enterobacterial strains and Pseudomonas aeruginosa. On the other hand, the gene in Enterobacter cloacae A113 (dal2) could only be transferred in the presence of a mobilizing plasmid. When both these genes were transferred within the Enterobacteriaceae, the beta-lactamase produced was slightly different from the prototype 'Dalgleish' PSE-4 enzyme. However, when dal1 and dal2 were transferred to P. aeruginosa the enzyme expressed was identical to this prototype enzyme. In addition, both these genes expressed higher levels of PSE-4 beta-lactamase production in P. aeruginosa than found in the Enterobacteriaceae. Thus it appears that the biochemical properties of the PSE-4 gene products from dal1 and dal2 are host-modified.

Enterobacteriaceae↗