Prevalence of AmpC and other beta-lactamases in enterobacteria at a large urban university hospital in Brazil.

Production of extended-spectrum beta-lactamases (ESBLs) has been reported in virtually all species of Enterobacteriaceae, which greatly complicates the therapy for infections caused by these organisms. However, the frequency of isolates producing AmpC beta-lactamases, especially plasmid-mediated AmpC (pAmpC), is largely unknown. These beta-lactamases confer resistance to extended-spectrum cephalosporins and aztreonam, a multidrug-resistant (MDR) profile. The aim of the present study was to determine the occurrence of ESBL and pAmpC beta-lactamases in a hospital where MDR enterobacterial isolates recently emerged. A total of 123 consecutive enterobacterial isolates obtained from 112 patients at a university hospital in Rio de Janeiro, Brazil, during March to June 2001 were included in the study. ESBL was detected by the addition of clavulanate to cephalosporin containing disks and by double diffusion. AmpC production was evaluated by a modified tridimensional test and a modified Hodge test. The presence of plasmid-mediated ampC beta-lactamase genes was evaluated by multiplex polymerase chain reaction. Sixty-five (53%) of 123 enterobacterial isolates were MDR obtained from 56 patients. ESBL production was detected in 35 isolates; 5 clonal Escherichia coli isolates exhibited high levels of chromosomal AmpC and ESBL production. However, no isolates contained pAmpC genes. Infection or colonization by MDR enterobacteria was not associated with any predominant resistant clones. A large proportion of hospital infections caused by ESBL-producing enterobacteria identified during the study period were due to sporadic infections rather than undetected outbreaks. This observation emphasizes the need to improve our detection methods for ESBL- and AmpC-producing organisms in hospitals where extended-spectrum cephalosporins are in wide use.

Mupirocin for controlling methicillin-resistant Staphylococcus aureus: lessons from a decade of use at a university hospital.

BACKGROUND: From 1990 to 1995 at Hospital Universitário Clementino Fraga Filho, patients colonized or infected with methicillin-resistant Staphylococcus aureus (MRSA) were treated with mupirocin to eliminate MRSA carriage. In 1995, 65% of MRSA patients at this hospital had mupirocin-resistant isolates. Starting in 1996, mupirocin use was restricted to patients colonized, but not infected, with MRSA. OBJECTIVES: To describe the use of mupirocin for controlling MRSA over a decade and to analyze the molecular epidemiology of mupirocin-resistant MRSA infections at this hospital. SETTING: A 490-bed, tertiary-care university hospital. METHODS: The incidence densities of patients with MRSA and acquisition of mupirocin by the hospital were calculated for the period 1992-2001. S. aureus isolates from 1999-2000 were analyzed by pulsed-field gel electrophoresis. Mupirocin-resistant MRSA isolates from 1994-1995 and 1999-2000 were analyzed for ileS-2 gene background polymorphisms. RESULTS: The incidence density of MRSA patients increased slightly over time, whereas the purchase of mupirocin decreased dramatically. Mupirocin-resistant MRSA infections decreased from 65% in 1994-1995 to 15% in 1999-2000. The MRSA Brazilian clone, detected in 1992, was still highly prevalent. The same ileS-2 encoding plasmid found in 1994-1995 persisted in three identical MRSA isolates from 1999-2000 belonging to the Brazilian clone. CONCLUSIONS: After mupirocin use decreased, the ileS-2 encoding plasmid persisted in only a few Brazilian clone isolates. Our data on mupirocin-resistant MRSA incidence and mupirocin use strongly suggested that restricted use was related to decreased rates of mupirocin resistance at our hospital.

Risk factors for acquisition of multidrug-resistant Pseudomonas aeruginosa producing SPM metallo-beta-lactamase.

To evaluate risk factors for colonization or infection due to multidrug-resistant Pseudomonas aeruginosa (MDRPa) carrying the bla(SPM) gene (SPM-MRDPa) among hospitalized patients, we undertook a case control study at a 480-bed, tertiary-care university hospital. Two different case definitions were used. In the first definition, a case patient (SPM case patient) was defined as a patient who had at least one isolate of SPM-MDRPa (14 patients). In the second, a case patient (non-SPM case patient) was defined as a patient who had at least one isolate of non-SPM-MDRPa (18 patients). For each case patient, we selected two controls, defined as a patient colonized and/or infected by a non-MDRPa isolate during the same study period and with the closest duration of hospitalization until the isolation of P. aeruginosa as cases. The use of quinolones was the single independent predictor of colonization and/or infection by bla(SPM) MDRPa (odds ratio [OR] = 14.70, 95% confidence interval [95% CI] = 1.70 to 127.34, P = 0.01), whereas the use of cefepime was the single predictor of colonization and/or infection by non-bla(SPM) MDRPa (OR = 8.50, 95% CI = 1.51 to 47.96, P = 0.01). The main risk factor for MDRPa was a history of antibiotics usage. Stratification of risk factor analysis by a precise mechanism of resistance led us to identify a specific antibiotic, a quinolone, as a predictor for SPM-MDRPa.