Mechanisms of resistance of staphylococci grown in plasma to polymorph bactericidins

Abstract

SUMMARYThe mechanisms whereby staphylococcal strains grown in plasma assume increased resistance to polymorph bactericidins were investigated. Observations reported here showed that cultural conditions could determine the path of conversion to resistance. Staphylococcal strains and mutants lacking either free coagulase or clumping factor or both all showed enhanced resistance after 10 h incubation in plasma proteins, thus giving no clear indication that these factors were involved in the interactions. In fact, prolonged incubation in bovine serum albumin (22 h) and ordinary broth medium (24 h) also resulted in increased resistance. A distinction between staphylococcal factors interacting specifically with plasma proteins and such non-specific conversions was obtained in two different ways. Stripping of a hypothetical surface protein by treatment with trypsin or 2 M potassium bromide rendered plasma-but not 24 h-broth organisms susceptible, indicating protein coating of plasma-grown organisms. Also free coagulase-positive strains and mutants incubated in plasma for 30 min were converted while those lacking both or possessing clumping factor alone were not. It therefore appears that one of the mechanisms of acquiring resistance involves a rapid interaction between staphylococcal-free coagulase and fibrinogen, resulting in the deposition of fibrin or fibrin derivatives on the bacterial surface.

Resistance mechanisms of mucoid-grown Staphylococcus aureus to the antibacterial action of some disinfectants and antiseptics

“…The ease with which the slime layer was lost, especially by washing in saline broth, suggested that its acquisition was different from the mechanism of deposition of fibrin layer during growth in vivo in rabbits [7] or in vitro in plasma [8], since the only procedures that removed the surfacecovering in these cases were trypsin digestion or physical dissociation using 2 M potassium bromide [8]. Also, the similarity in the antibiotic sensitivity patterns of mucoid and non-mucoid organisms of the same strain showed that mucoid growth did not confer any additional resistance to antibiotics and hence that the resistance due to the mucoid layer was achieved by a mechanism which is different from the build-up of lipid in organisms grown in glycerol-broth [2,3].…”