ena-STUDY-UPPSALA UNIVERISTY-08-03-2018-09:45:15:012-118
Pseudomonas aeruginosa outbreak Karlskrona, Sweden
Pseudomonas aeruginosa with acquired Metallo-ß-lactamase (MBL) production is an increasing clinical problem world-wide. VIM-2 is the predominant gene, which has been linked to high-risk strains causing outbreaks. Remarkable in Sweden, eight patients were colonized by VIM-2 producing P. aeruginosa, during a period of 15 months, at two neighbouring hospitals. To find the source and halt this clustering an epidemiological investigation was initiated. The isolates had similar antibiograms and identical PFGE patterns, indicating a nosocomial spread. Screening of co-patients and staff yielded no additional cases. The case patients had been in the same rooms and wards, but long separated in time. Environmental screening showed growth of P. aeruginosa with identical PFGE-pattern in two sinks from rooms where the patients had been staying, whereof one in the intensive care unit.  The outbreak strain was analysed with whole genome sequencing and belonged to the high-risk strain ST111. The blaVIM-2 gene was not within the class 1 integron and the OprD-porin was mutated. The colonized hospital sinks were a probable reservoir, which contributed to the first and prolonged nosocomial outbreak of MBL-producing P. auruginosa in Sweden. As the sinks were replace the outbreak ended.
Pseudomonas aeruginosa with acquired Metallo-ß-lactamase (MBL) production is an increasing clinical problem world-wide. VIM-2 is the predominant gene, which has been linked to high-risk strains causing outbreaks. Remarkable in Sweden, eight patients were colonized by VIM-2 producing P. aeruginosa, during a period of 15 months, at two neighbouring hospitals. To find the source and halt this clustering an epidemiological investigation was initiated. The isolates had similar antibiograms and identical PFGE patterns, indicating a nosocomial spread. Screening of co-patients and staff yielded no additional cases. The case patients had been in the same rooms and wards, but long separated in time. Environmental screening showed growth of P. aeruginosa with identical PFGE-pattern in two sinks from rooms where the patients had been staying, whereof one in the intensive care unit.  The outbreak strain was analysed with whole genome sequencing and belonged to the high-risk strain ST111. The blaVIM-2 gene was not within the class 1 integron and the OprD-porin was mutated. The colonized hospital sinks were a probable reservoir, which contributed to the first and prolonged nosocomial outbreak of MBL-producing P. auruginosa in Sweden. As the sinks were replace the outbreak ended.