ABSTRACT
The molecular analysis of 130 multidrug-resistant nosocomial Acinetobacter baumannii strains was performed. The strains were obtained from patients admitted to different Russian hospitals (Chelyabinsk, Moscow, Nizhni Novgorod, and St. Petersburg) in 2005-2010. Species identification was performed using the amplified 16S rRNA gene restriction analysis and by determining intrinsic for A. baumannii blaQXA-51-like genes using PCR. The genetic typing of the strains was performed by RAPD-PCR. All strains fell into two clusters: A and B with dominant RAPD-groups A1 and B1, respectively, including 82% (107 of 130) of all studied strains. The susceptibility to the bacteriophage AP22 of the strains was determined. The phage was found to infect specifically and to constitute 69% of 130 strains and 82% (88 of 107) of the A. baumannii strains from the dominant RAPD groups. The ability of the bacteriophage AP22 to constitute a broad range of the clinically relevant A. baumannii strains makes it an attractive candidate for designing the phage cocktails intended to control the A. baumannii-associated nosocomial infections. Moreover, the phage can be used for the identification of A. baumannii in bacteriological analysis of clinical materials.
Subject(s)
Acinetobacter baumannii , Bacteriophages/pathogenicity , Cross Infection/microbiology , RNA, Ribosomal, 16S/genetics , Acinetobacter baumannii/classification , Acinetobacter baumannii/genetics , Acinetobacter baumannii/pathogenicity , Bacteriophages/genetics , Cross Infection/genetics , Drug Resistance, Multiple/genetics , Genotype , HumansABSTRACT
In Pseudomonas mallei, spontaneous mutants (Tra- mutants) of the plasmids RP4 and R68.45, losing the ability to transfer at conjugation are formed. The plasmids RP4 and R68.45 with Tra(+)-phenotype caused a decrease in P. mallei virulence for laboratory animals. At the same time, Tra- mutants of these plasmids do not affect P. mallei virulence. The insertion of DNA fragment of about 1900 bp into the plasmid transfer gene regions (tra-2-tra-3) gave rise to RP4 and R68.45 tra mutations detectable on examination.
