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J A Reguera

Publications and source records attributed to J A Reguera.

7 recordsLinked to original sources
PubMed1994

vanA-mediated vancomycin-resistant Enterococcus spp. in sewage.

Three high-level vancomycin-resistant Enterococcus strains (two Enterococcus faecium and one Enterococcus durans) were recovered from three of eight sewage samples taken from the general sewage collector at Logroño (Northern Spain). The strains were present in the sewage samples at estimated concentrations of ten resistant bacteria/mL, corresponding to about 0.4% of the enterococcal population. The VanA protein was detected in each strain by immunoblotting of membrane extracts of the vancomycin-induced cells, and the vanA gene was demonstrated in the wild strains and their transconjugants by DNA-DNA hybridization. This is the first, confirmed report of vanA mediated vancomycin resistance in E. durans.

Bacterial Proteins↗
PubMed1992

[1st Spanish epidemic of plasmid resistance to 3d generation cephalosporins: the implication of SHV-2].

BACKGROUND: The first spanish outbreak of bacterial strains showing resistance to third generation cephalosporins and due to the presence of the extended spectrum beta-lactamase SHV-2 is reported. This outbreak was observed in Madrid during the years 1988-1990 and involved the San Carlos University Hospital with the same type of isolates at the Ramón y Cajal University Hospital. METHODS: The screening for extended-spectrum beta-lactamases was performed by the double-disk synergy test. Analytical isoelectric focusing and susceptibility tests were performed in all the strains showing a presumptive extended-spectrum beta-lactamase. RESULTS: Fifty-nine strains belonging to four bacterial species (Klebsiella pneumoniae, 61%; Serratia marcescens, 31%; Klebsiella oxytoca, 5%, and Escherichia coli, 3%) showed a beta-lactamase of point isoelectric 7.6; the susceptibility tests demonstrated more resistance to cefotaxime and ceftriaxone than to ceftazidime and aztreonam. CONCLUSIONS: The biochemical, kinetic and isoelectrofocusing parameters demonstrated the presence of a SHV-2 enzyme. The blind application of NCCLS breakpoints would lead to false "susceptibility" results in over 40% of the cases.

Bacterial Proteins↗
PubMed1991

Factors determining resistance to beta-lactam combined with beta-lactamase inhibitors in Escherichia coli.

The influence of inoculum size, beta-lactamase hyperproduction (multicopy plasmid) and modifications in the outer membrane protein profile on the susceptibility of Escherichia coli to combinations of amoxycillin/clavulanate, amoxycillin/sulbactam, amoxycillin/tazobactam and piperacillin/tazobactam were studied. For all combinations the bacterial susceptibility was affected by factors determining an increase in beta-lactamase (inoculum size or hyperproduction). Clavulanic acid was the most efficient beta-lactamase inhibitor. The absence of the outer membrane proteins, OmpF and OmpC, did not significantly affect susceptibility to the combinations per se but when combined with the presence of beta-lactamase high MICs were observed. Seven out of eight amoxycillin/clavulanate resistant clinical isolates of E. coli had beta-lactamase hyperproduction and a decrease or absence of OmpF.

Amoxicillin↗
PubMed1990

Beta-lactam-fosfomycin antagonism involving modification of penicillin-binding protein 3 in Pseudomonas aeruginosa.

Antagonism between fosfomycin and antipseudomonal penicillins, cefotaxime, and ceftriaxone was observed in Pseudomonas aeruginosa RYC212. Fosfomycin, a non-beta-lactam antibiotic that acts on bacterial cell wall synthesis, decreased the expression of penicillin-binding protein 3 and induced beta-lactamase. The antagonistic effect was reduced in the presence of high concentrations of the beta-lactamase inhibitor tazobactam or in fosfomycin-resistant mutants. We suggest that products resulting from fosfomycin cell wall damage could interact with a system that regulates penicillin-binding protein and beta-lactamase production.

Anti-Bacterial Agents↗
PubMed1988

Synergistic effect of dosage and bacterial inoculum in TEM-1 mediated antibiotic resistance.

The effect of inoculum size and gene dosage on the level of antibiotic resistance mediated by TEM-1 beta-lactamase was measured. From the results it seemed that gene dosage is a more efficient mechanism than inoculum size for increasing TEM-1 mediated resistance to beta-lactam antibiotics. It also seemed that the two mechanisms for enhancing antibiotic resistance are synergistic. The clinical implications of these results are discussed.

Anti-Bacterial Agents↗
PubMedDate not supplied

Capnophilic and anaerobic bacteremia in neutropenic patients: an oral source.

The currently accepted empiric antibiotic therapy for bacterial infections in neutropenic patients may not cover the possibility of capnophilic and anaerobic bacteremia. Many of these infections develop in patients with severe mucositis or periodontitis, and the type of organisms recovered also suggests an oral source of infection. We present two cases of bacteremia in neutropenic patients who had been empirically treated with ceftazidime and piperacillin plus amikacin. In the first case a beta-lactamase-producing strain of Capnocytophaga ochracea was isolated; in the second case bacteremia was due to a mixture of Leptotrichia buccalis and Fusobacterium nucleatum. These observations emphasize the necessity for a reevaluation of the possible use of antimicrobial agents active against beta-lactamase-producing capnophilic organisms and anaerobic bacteria during empiric therapy in neutropenic patients with an oral source of infection.

Adult↗