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Montserrat Sabaté

Publications and source records attributed to Montserrat Sabaté.

6 recordsLinked to original sources
PubMed2006

Quinolone, fluoroquinolone and trimethoprim/sulfamethoxazole resistance in relation to virulence determinants and phylogenetic background among uropathogenic Escherichia coli.

INTRODUCTION: The goal of this study was to assess how resistance to quinolones, fluoroquinolones and trimethoprim/sulfamethoxazole relates to the virulence potential and phylogenetic background of clinical Escherichia coli isolates. METHODS: Among 150 uropathogens (21% resistant to quinolones, 12% resistant to fluoroquinolones and 29.3% resistant to trimethoprim/sulfamethoxazole), E. coli phylogenetic group, 15 virulence-associated genes and 7 O antigens were analysed. Clonal group A (CGA) and genomic PCR profiles were studied among trimethoprim/sulfamethoxazole-resistant isolates. RESULTS: Isolates susceptible to the three antimicrobial agents were significantly associated with phylogenetic group B2, whereas resistant isolates exhibited shifts to non-B2 groups (quinolone and fluoroquinolone-resistant isolates to group A; trimethoprim/sulfamethoxazole-resistant isolates to group D). Diverse virulence traits, including UTI-associated O antigens, were significantly less frequent among resistant isolates, particularly those resistant to fluoroquinolones (median score, 3.9 virulence factors/strain) and also to quinolones (5.2) or trimethoprim/sulfamethoxazole (6.4), as compared with the corresponding drug-susceptible isolates (median scores of 7.9, 8.6 and 7.9, respectively). Among 44 trimethoprim/sulfamethoxazole-resistant isolates, 3 (6.8%) belonged to CGA. All these 3 CGA strains caused pyelonephritis (P=0.02) and exhibited the consensus virulence profile of previously described CGA strains from abroad. CONCLUSIONS: E. coli isolates resistant to quinolones, trimethoprim/sulfamethoxazole and especially fluoroquinolones were associated with reductions in virulence traits and shifts to non-B2 phylogenetic groups. Moreover, fluoroquinolone resistance usually occurred in low-virulence E. coli group A isolates rather than in isolates from groups B2 and D which had lost virulence traits. CGA accounted for 23% of trimethoprim/sulfamethoxazole-resistant E. coli producing pyelonephritis.

Adult↗
PubMed2002

Beta-lactamases involved in resistance to broad-spectrum cephalosporins in Escherichia coli and Klebsiella spp. clinical isolates collected between 1994 and 1996, in Barcelona (Spain).

The aim of this study was to evaluate the incidence of decreased susceptibility to broad-spectrum cephalosporins in Enterobacteriaceae that lack inducible chromosomal bla genes, and to determine the enzymes responsible for resistance. From all clinically relevant Enterobacteriaceae strains isolated between 1994 and 1996, 88 of 7054 Escherichia coli, seven of 581 Klebsiella pneumoniae and 23 of 166 Klebsiella oxytoca strains were studied because of their decreased susceptibilities to broad-spectrum cephalosporins (as reflected in intermediate susceptibilities and/or positive synergy tests and/or irregular crenellated inhibition zones). The most frequent mechanism implicated in decreased susceptibility to broad-spectrum cephalosporins displayed by E. coli and K. oxytoca was hyperproduction of chromosomal beta-lactamase, followed by plasmid-mediated SHV-1 hyperproduction in E. coli. In our hospital, the incidence of plasmid-mediated extended-spectrum beta-lactamases (ESBLs) between 1994 and 1996 was low. ESBLs were found in only 10 (0.14%) E. coli strains (six CTX-M-9, two TEM-12 and two SHV-2), in one (0.17%) K. pneumoniae strain (SHV-2) and in no K. oxytoca strains. The relatively wide variety of beta-lactamases that were detected among these common bacteria isolated from a single medical centre, including non-TEM- and non-SHV-derived ESBLs, appears epidemiologically remarkable.

Cephalosporin Resistance↗
PubMed2002

Prevalence of clinical isolates of Escherichia coli producing inhibitor-resistant beta-lactamases at a University Hospital in Barcelona, Spain, over a 3-year period.

About 7% of 7,252 nonduplicated clinical Escherichia coli strains from a Spanish hospital showed reduced susceptibility to amoxicillin-clavulanate. Of these, 0.37% produced the IRTs TEM-30, TEM-31, TEM-33, TEM-34, TEM-37, TEM-40, TEM-51, and TEM-54; 5.3% were probable class C beta-lactamase overproducers; 0.8% were probable TEM-1 hyperproducers; 0.18% produced OXA-30; 0.15% overexpressed SHV-1; and 0.03% produced a PSE-1 enzyme.

Amoxicillin-Potassium Clavulanate Combination↗
PubMed2002

Novel complex sul1-type integron in Escherichia coli carrying bla(CTX-M-9).

For the present report, a novel complex class 1 integron, In60, was characterized. Part of this integron includes the bla(CTX-M-9) gene and its downstream nucleotide sequence, which shares 81% and 78% nucleotide identity with those of kluA-1 beta-lactamase and orf3 of K. ascorbata, respectively. Furthermore, a new insertion sequence, IS3000, has been found in In60. PCR analysis indicates that integron In60 is present in 33 of 34 nonclonal enterobacterial isolates carrying the putative beta-lactamase CTX-M-9.

Base Sequence↗
PubMedDate not supplied

[Structure and function of integrons].

Integrons are genetic elements known for their role in the acquisition and expression of genes conferring antibiotic resistance. Integrons have an integrase gene (intI), an attachment site (attI), into which individual resistance genes are inserted and a promotor sequence (Pant), allowing expression of resistance genes (cassette-associated genes), which do not have promotors. Integrase recognizes 59-be, a specific sequence in certain resistance genes, which is captured by recombination at the attI attachment site. The fragment intI - attI is highly conserved in all integrons and is called 59 -CS. Integrons have been classified according to the sequence of their integrase and the ones most frequently detected in isolated clinical strains belong to Class I. Class I integrons contain the 59 -CS region followed by gene cassettes in a variable region and finally, a conserved region known as 39 -CS containing two genes, the quaternary ammonium resistance gene (qacEDI) and the sulphonamide resistance gene (sul1); both genes are fixed in this structure. Accordingly, the structure of a Class 1 integron would be IntI - attI [R11 R21.] - qacED1 - sul1. Integrons are probably not mobile, but they are often found in transposons within conjunctive plasmids, which assures their mobility, as can be seen by their wide diffusion among bacteria.

Drug Resistance, Microbial↗