Nosocomial infection by VIM-2 metallo-β-lactamase-producing Pseudomonas putida

• Published in: Journal of medical microbiology Vol. 59; no. 7; pp. 853 - 855
• Main Authors: TREVINO, M, MOLDES, L, HERNANDEZ, M, MARTINEZ-LAMAS, L, GARCIA-RIESTRA, C, REGUEIRO, B. J
• Format: Journal Article
• Language: English
• Published: Reading Society for General Microbiology 01.07.2010
• Subjects: Aged; Anti-Bacterial Agents - pharmacology; Bacteremia - microbiology; Bacteriology; beta-Lactamases - metabolism; Biological and medical sciences; Cross Infection - microbiology; Drug Resistance, Bacterial; Female; Fundamental and applied biological sciences. Psychology; Genes, Bacterial; Humans; Infectious diseases; Male; Medical sciences; Microbiology; Miscellaneous; Pseudomonas Infections - microbiology; Pseudomonas putida - drug effects; Pseudomonas putida - enzymology; Pseudomonas putida - genetics; Pseudomonadales; Nosocomial infection; Enzyme; Bacteria; Hydrolases; Pseudomonadaceae; β-Lactamase; Pseudomonas putida
• ISSN: 0022-2615; 1473-5644
• DOI: 10.1099/jmm.0.018036-0

Nosocomial infections caused by multidrug-resistant and carbapenem-resistant Pseudomonas putida isolates have been reported occasionally in severely ill or immunocompromised patients. Here we report the microbiological characteristics of what are believed to be the two first carbapenem-resistant VIM metallo-beta-lactamase (MBL)-producing P. putida strains in Spain, which were isolated from patients at the University Hospital Complex of Santiago de Compostela. Both patients were immunocompromised with severe underlying diseases and had been hospitalized for more than 15 days. One of them had previously been treated with a broad-spectrum therapy. Antimicrobial susceptibility testing showed that both strains were resistant to piperacillin/tazobactam, ceftazidime, cefepime, imipenem, meropenem, gentamicin, tobramycin, aztreonam, trimethoprim/sulfamethoxazole and ciprofloxacin, but sensitive to amikacin and colistin. For both isolates PCR and sequencing was positive for the bla(VIM-2) gene. Fingerprinting analysis revealed these were two different strains. One patient recovered clinically and one died; no direct link could be established between the isolation of P. putida and death. Our data expose the emergence of multidrug-resistant P. putida VIM-2 MBL, probably arising by independent horizontal transfer of resistance genes. So, although P. putida is not frequently isolated, it may survive easily in the hospital setting and occasionally cause difficult-to-treat nosocomial infections in severely ill patients.