A chemical and biological study of antibiotic resistance in bacteria

Abstract

Particulate microelectrophoresis was used to study changes in the surface properties of strains of Pseudomonas aeruginosa and Staphylococcus aureus with respect to changes of growth temperature and growth media which could be related to antibiotic resistance.

Gentamicin-sensitive and intrinsically resistant strains of P. aeruginosa exhibited characteristic, but differently shaped pH-mobility curves; the shape was correlated with surface lipid. The surface properties and MIC values of cells grown at 37°C were not significantly affected by growth at 25°C. Cells of some resistant strains grown at 43°C became gentamicin-sensitive, surface lipid was lost and the shape of the pH-mobility curve altered. Surface lipid was related to intrinsic gentamicin resistance; surface lipid variations were independent of the growth media.

Repeated subculture of P. aeruginosa in the absence of the antibiotic affected the R-factor strains only; resistance was lost after repeated subculture at 37 and 43°C. Cells of strain PL11 also lost both R-factor and intrinsic resistance mechanisms.

When cells were grown on agar containing large amounts of divalent cations the mobility values were lower and the MIC values greater. These changes are attributed to the presence of a metal ion induced resistance barrier, due to association of calcium at the cell surface and to increased polysaccharide production. This barrier prevented the initial accumulation of gentamicin at the cell surface. Intrinsic gentamicin resistance is not due to the inability of gentamicin to bind to the cell surface. The uptake of calcium or gentamicin at the cell surface appeared to be a complex growth effect. Changes in cellular calcium could not be correlated with changes in the antibiotic resistance or surface properties of Staph. aureus.

There was no correlation between the surface and biological properties of animal strains of Staph. aureus or between divalent cation content and methicillin resistance of human strains.