Metallo-β-lactamase and genetic diversity of Pseudomonas aeruginosa in intensive care units in Campo Grande, MS, Brazil

Infection by Pseudomonas aeruginosa has spread worldwide, with limited options for treatment. The purpose of this study was to investigate metallo-β-lactamase-producing P. aeruginosa strains and compare their genetic profile using samples collected from patients in intensive care units. Forty P. aeruginosa strains were isolated from two public hospitals in Campo Grande, Mato Grosso do Sul State, from January 1st, 2007 to June 31st, 2008. Profiles of antimicrobial susceptibility were determined using the agar diffusion method. Metallo-β-lactamase was investigated using the double-disk diffusion test and PCR. Molecular typing was performed by pulsed-field gel electrophoresis (PFGE). Respiratory and urinary tracts were the most common isolation sites. Of the 40 samples tested, 72.5 percent (29/40) were resistant to ceftazidime and 92.5 percent (37/40) to imipenem, whereas 65 percent (26/40) were resistant to both antimicrobials. Fifteen pan-resistant samples were found. Five percent (2/40) of samples were positive for metallo-β-lactamase on the phenotype test. No metallo-β-lactamase subtype was detected by PCR. Macrorestriction analysis revealed 14 distinct genetic patterns. Based on the superior accuracy of PCR, it can be inferred that P. aeruginosa isolates from the investigated hospitals have alternative mechanisms of carbapenem resistance. The results also suggest clonal spread of P. aeruginosa between the studied hospitals.

Occurrence of blaOXA-23 gene in imipenem-susceptible Acinetobacter baumannii

The aim of the current study was to describe the occurrence of the blaOXA-23 gene and the ISAba1 element in imipenem-susceptible Acinetobacter baumannii strains. By performing the polymerase chain reaction mapping using combinations of ISAba1 forward primers and the blaOXA-23-like gene reverse primers, we demonstrated that the ISAba1 element did not occur upstream of the blaOXA-23 gene in five of 31 isolates, which explained the lack of resistance to imipenem despite the presence of the blaOXA-23 gene. All of the blaOXA-23-positive isolates were susceptible to imipenem and meropenem with minimal inhibitory concentration < 4 µg/mL. Pulsed-field gel electrophoresis analysis revealed four genotypes among the five blaOXA-23-positive isolates. The current report of the blaOXA-23 gene in imipenem-susceptible isolates provided evidence that this gene may be silently spread in a hospital environment and highlighted the threat of undetected reservoirs of carbapenemase genes.