ABSTRACT
OBJECTIVES: The aim of this study was to characterize the different inhibitor-resistant TEM beta-lactamases, extended-spectrum beta-lactamases (ESBLs) and plasmid-mediated AmpC beta-lactamases implicated in beta-lactam resistance in Proteus mirabilis, which has increased over recent years. METHODS: From February 2000 to December 2005, 1423 clinical isolates of P. mirabilis were collected. The AmpC phenotype was checked by means of a double-disc synergy test using cloxacillin as an inhibitor of AmpC enzymes. The production of ESBL was assessed by the double-disc synergy method and by Etest ESBL. Analytical isoelectric focusing, determination of kinetic constants, conjugation, PCR and a sequencing strategy were used to characterize the enzymes. The possible relationships between isolates were analysed by PFGE. RESULTS AND CONCLUSIONS: Twenty-five of 1423 isolates were found to display intermediate or full resistance to co-amoxiclav, cefotaxime or ceftazidime. Seventeen isolates had reduced susceptibility to co-amoxiclav; of these, seven produced TEM-110, eight produced the new TEM-159, one the new TEM-160 and one TEM-1. Five isolates producing TEM-110, TEM-159 or TEM-160 enzymes shared the same PFGE profile. Three isolates produced an ESBL, CTX-M-1, CTX-M-32 and the new variant, VEB-4. Finally, five isolates with an AmpC phenotype produced CMY-2, two with the same PFGE profile. Our data emphasize the diversity of beta-lactamases found in this species.
Subject(s)
Anti-Bacterial Agents/pharmacology , Proteus mirabilis/drug effects , beta-Lactam Resistance/genetics , beta-Lactamases/metabolism , Amino Acid Substitution , Gene Expression Regulation, Bacterial , Humans , Proteus Infections/microbiology , Proteus mirabilis/metabolism , beta-Lactamase Inhibitors , beta-Lactamases/chemistry , beta-Lactamases/geneticsABSTRACT
Nocardiosis has been believed to be caused by the members of the Nocardia asteroides complex and the Nocardia brasiliensis species. However, recent advances in genotypic identification have shown that the genus exhibits considerable taxonomic complexity and the phenotypic markers used in the past for its identification can be ambiguous. The aim of this study was to assess the species distribution of Nocardia isolates and to determine whether there are differences in pathogenicity or antimicrobial susceptibility between the different species identified. Nocardia isolates obtained over a 7 year period were retrospectively reviewed. The isolates were identified genotypically, their antibiotic susceptibility was tested and the clinical data of the 27 patients were retrieved. Eight different Nocardia species were identified: Nocardia farcinica (n=9), Nocardia abscessus (n=6), Nocardia cyriacigeorgica (n=6), Nocardia otitidiscaviarum (n=2), Nocardia nova (n=1), N. nova complex (n=1), Nocardia carnea (n=1) and Nocardia transvalensis complex (n=1). All species were susceptible to co-trimoxazole but different patterns of susceptibility to other agents were observed. All patients had active comorbidities at the time of infection. A total of 19 patients were immunosuppressed, due to human immunodeficiency virus infection, chronic corticosteroid therapy, immunosuppressive therapy or haematological malignancies. Six patients displayed a Charlson comorbidity index score above 4. Global mortality was 50 % while attributable mortality was 34.6 %. Patients infected with N. farcinica--the most resistant species--had the highest Charlson index score and the highest mortality rate. Accurate identification of the species and susceptibility testing of Nocardia isolates may play an important role in diagnosis and treatment.
