Open AccessLipopolysaccharide changes in impermeability-type aminoglycoside resistance in Pseudomonas aeruginosa
Author(s) -
L. E. Bryan,
Koji Ohara,
SuiLam Wong
Publication year - 1984
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.26.2.250
Subject(s) - pseudomonas aeruginosa , microbiology and biotechnology , aminoglycoside , plasmid , streptomycin , strain (injury) , gentamicin , lipopolysaccharide , chemistry , bacterial outer membrane , bacteria , transformation (genetics) , pseudomonadaceae , biology , escherichia coli , antibiotics , dna , biochemistry , gene , genetics , anatomy , endocrinology
Clinical isolates of Pseudomonas aeruginosa were examined for the basis of impermeability-type aminoglycoside resistance. Two apparently related burn isolate strains with high-level (strain 8803) and low-level (strain 13934) gentamicin resistance each had a plasmid. Transformation of the plasmid from either strain to P. aeruginosa PAO503 resulted in low-level gentamicin resistance. No mechanism for this resistance could be determined. Low-level gentamicin and streptomycin resistance from strain 8803 (but not 13934) was transduced with phage E79.tv2 to PAO503 without transfer of plasmid DNA. Transductants like strain 8803 showed absence or reduction of the lipopolysaccharide (LPS) "ladder" pattern of PAO503, had a change in chemical composition of LPS, and, like strain 8803, had a reduced capability to accumulate streptomycin. Comparison of the resistant clinical isolates 8803 and P10 with the apparently related but less-resistant strains 13934 and P10R, respectively, showed the latter strains had LPS ladder patterns and the former strains did not. Strain 8803 had normal outer membrane protein profiles, electron transport components, and transmembrane electrical potential relative to PAO503 and has been previously shown to have no detectable gentamicin-modifying enzymes and normal protein synthesis. We conclude that low-level impermeability-type aminoglycoside resistance in P. aeruginosa results from conversion of smooth LPS to superficial or deeper rough LPS phenotypes. High-level resistance apparently results from a plasmid-specified, but as yet unknown, mechanism combined with the preceding change in LPS structure.