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Background: Metallo-ß-lactamases (MBL) confer high resistance to carbapenems in Pseudomonas aeruginosa (Psae). They are encoded in mobile elements of different genes (VIM, IMP, SMP, GIM), along with other resistance genes. Aim: To detect the presence of MBL in imipenem resistant Psae strains. Material and methods: Fifty-nine imipenem resistant Psae strains isolated from January 2004 to August 2005 in a University Clinical Hospital, were included. The presence of MBL was studied by Etest (phenotypic) and genotypic polymerase chain reaction (PCR) methods. To rule out a nosocomial outbreak, MBL positive strains, were studied by pulse field gel electrophoresis. Results: The presente of MBL was detected in eleven strains. AH were type VIM and were not clonally related. There was no concordance between phenotypic and genotypic MBL detecting methods. AH the strains were also multiresistant. Conclusions: The presence of MBL was detected in 19% of imipenem resistant Psae strains

Background: A progressive frequency of resistance to fluorquinolones is observed among Gram-negative bacilli. Aim: To investigate the mechanism of resistance to fluoroquinolones mediated by mutations affecting gyrA and gyrB genes in strains of Gram negative bacüli isolated from CMean hospitals. Material and method: Minimal inhibitory concentration of fluoroquinolones was determined in 91 randomly selected nalidixic acid-resistant strains of Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii and Pseudomonas aeruginosa, isolated from hospitals of 12 Chilean cities. Quinolone resistance determining region (QRDR) was amplified by PCR and mutations were determined by restriction fragment length polymorphism (RFLP) and DNA sequencing. Results: Strains with mutation in codon 83 of gyrA showed decreased susceptibility to ciprofloxacin with MICs ranging from 0.25 to 1024 fig/ml. The sequencing of PCR products for gyrA indicated amino acid changes in the QRDR region. One strain ofE. coli presented a double mutation, in codon 83 Ser to Leu as well as in codon 87 Asp to Asn. In strains ofK. pneumoniae, however, the change of codon 83 was Ser to Tyr, in A. baumannii was Ser to Leu and in P. aeruginosa was Thr to He. No strains with mutations affecting gyrB were found. Conclusions: Mutations in codon 83 of gyrA is a frequent genetic event involved in the mechanism leading to decreased susceptibility to fluoroquinolone in strains of Gram-negative bacilli

Background: A progressive frequency of resistance to fluorquinolones is observed among Gram-negative bacilli. Aim: To investigate the mechanism of resistance to fluoroquinolones mediated by mutations affecting gyrA and gyrB genes in strains of Gram negative bacüli isolated from CMean hospitals. Material and method: Minimal inhibitory concentration of fluoroquinolones was determined in 91 randomly selected nalidixic acid-resistant strains of Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii and Pseudomonas aeruginosa, isolated from hospitals of 12 Chilean cities. Quinolone resistance determining region (QRDR) was amplified by PCR and mutations were determined by restriction fragment length polymorphism (RFLP) and DNA sequencing. Results: Strains with mutation in codon 83 of gyrA showed decreased susceptibility to ciprofloxacin with MICs ranging from 0.25 to 1024 fig/ml. The sequencing of PCR products for gyrA indicated amino acid changes in the QRDR region. One strain ofE. coli presented a double mutation, in codon 83 Ser to Leu as well as in codon 87 Asp to Asn. In strains ofK. pneumoniae, however, the change of codon 83 was Ser to Tyr, in A. baumannii was Ser to Leu and in P. aeruginosa was Thr to He. No strains with mutations affecting gyrB were found. Conclusions: Mutations in codon 83 of gyrA is a frequent genetic event involved in the mechanism leading to decreased susceptibility to fluoroquinolone in strains of Gram-negative bacilli

Background: Klebsiella pneumoniae is a pathogenic bacterium frequently isolated from nosocomial samples, specially the subspecie pneumoniae, with extensive antibiotic resistance profiles, including third generation cephalosporins, aminoglycosides and quinolones. This is specially true for those strains producing extended spectrum beta lactamases (ESBL). Aim: To investigate the susceptibility to gentamicin, amikacin and ciprofloxacin and the presence of some aminoglycoside modifying enzyme (AMEs) among nosocomial strains of K pneumoniae subspecie pneumoniae producing ESBL. Material and methods: The antibiotic resistant patterns and the level of resistance (minimal inhibitory concentration, MIC) of 100 strains, isolated from several hospitals of different Chilean cities, were determined. The presence of some aminoglycosides modifying enzyme (AMEs) was investigated by PCR. Results: Sixty five percent of strains were resistant to gentamicin, 47% were resistant to amikacin and 29% were resistant to ciprofloxacin. The most frequent AMEs genes detected were the aac(6')-Ib gene (6'-N-Acetyltransferase type Ib enzyme) in 69% of strains, conferring resistance to amikacin, kanamycin, tobramycin, and neomycin, and the gene aac(3)-IIa (3-Acetyltransferase type 3-IIa enzyme), in 36% of strains, conferring resistance to gentamicin. Conclusions: Among nosocomial strains of K pneumoniae subspecie pneumoniae isolated from Chilean hospitals, there is an association between the production of ESBL and the resistance to others antimicrobial agents, especially aminoglycosides. Nevertheless, 71% of isolates are susceptible to ciprofloxacin (Rev Méd Chile 2004; 132: 1173-8)

Background: The resistance of Shigella flexneri to antimicrobial agents can be associated to the presence of integrons that may contain and express antimicrobial resistance gene cassettes. Aim: To study antimicrobial resistance and the presence of integrons and antimicrobial gene cassettes in Shigella flexneri strains. Material and methods: In vitro susceptibility to 27 antimicrobials was studied in twenty four Shigella flexneri strains isolated from stools. The presence of integrons class 1, 2 and 3 and antimicrobial resistance gene cassettes was investigated by polymerase chain reaction (PCR) using specific primers for each gene. Results: Most strains were resistant to one of the following antimicrobials: ampicillin, sulphonamide, trimethoprim, tetracycline, streptomycin, sulfamethoxazole-trimethoprim or chloramphenicol. Twenty nine percent were simultaneously resistant to all these antimicrobials. Integrons class 1 and 2 were found in 19 strains (79%). Class 3 integrons were not found. Gene cassettes dfrA1 and ant(3")I were associated to integrons class 2 in most strains (15/20, 75%). Genes cat, tetB and blarTEM were detected in 18/24 (75%), 7/24 (29%) and 4/24 (17%) of the strains, respectively and were not associated to any of the studied integrons. Genes that codify enzymes AAC(6')Ib and APH(3')VI were not detected in any strain. Conclusions: The high frequency of integrons found in the studied strains, could partly explain the increasing antimicrobial resistance of Shigella flexneri strains, isolated in Chile (Rev Méd Chile 2003; 131: 727-33)