Transposon-mediated multiple antibiotic resistance in Acinetobacter strains

Area of Science:

• Microbiology
• Molecular Biology
• Epidemiology

Background:

• An epidemic of respiratory tract infections in an intensive care unit was caused by Acinetobacter calcoaceticus subsp. anitratus.
• The epidemic strain exhibited unusual resistance to multiple antibiotics, including aminoglycosides, penicillins, cephalosporins, chloramphenicol, tetracycline, and sulfonamides.
• The resistance patterns resembled those commonly found in hospital flora, suggesting potential plasmid transfer.

Purpose of the Study:

• To investigate the genetic basis of the multi-drug resistance in the epidemic strain of Acinetobacter calcoaceticus subsp. anitratus.
• To determine the mechanism by which antibiotic resistance was acquired and maintained in this bacterial isolate.
• To understand the epidemiological implications of multi-drug resistant Acinetobacter strains in healthcare settings.

Main Methods:

• Characterization of antibiotic resistance mechanisms, including the identification of specific modifying enzymes (e.g., 3-N-acetyltransferase, TEM-2 beta-lactamase).
• Attempted transfer of antibiotic resistance via bacterial mating procedures.
• Plasmid transfer experiments using plasmid RP4 and a susceptible derivative of the epidemic strain, followed by analysis of resistance mobilization.

Main Results:

• The epidemic strain possessed multiple aminoglycoside-modifying enzymes and a TEM-2 beta-lactamase, conferring resistance to gentamicin, kanamycin, streptomycin, and penicillins.
• While direct plasmid transfer was unsuccessful, mobilization of resistance markers (chloramphenicol, gentamicin, streptomycin, sulfonamides, tetracycline) occurred after introducing plasmid RP4.
• This mobilization was attributed to the transposition of a 16-megadalton DNA sequence from the Acinetobacter chromosome into plasmid RP4, near specific restriction sites.

Conclusions:

• A multi-drug resistant plasmid likely transferred into Acinetobacter sp. from hospital flora but was not stably maintained.
• Instead, a multiply resistant DNA sequence (transposon) integrated into the Acinetobacter chromosome, conferring stable resistance.
• The integration of such transposons contributes to bacterial genetic variability and can have significant epidemiological and therapeutic consequences.