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Mechanisms of resistance of staphylococci grown in plasma to polymorph bactericidins
Abstract:
The 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.
Insights
Staphylococcal strains gain resistance to bactericidins via plasma protein interactions. Free coagulase binding to fibrinogen rapidly deposits fibrin on the bacterial surface, enhancing resistance.
Area of Science:
- Microbiology
- Immunology
Background:
- Staphylococcal infections pose a significant threat.
- Understanding bacterial resistance mechanisms is crucial for treatment.
- Polymorph bactericidins are key immune components against bacteria.
Purpose of the Study:
- Investigate how staphylococcal strains develop resistance to polymorph bactericidins when grown in plasma.
- Identify specific staphylococcal factors and mechanisms involved in acquiring this resistance.
Main Methods:
- Incubation of staphylococcal strains and mutants in plasma proteins, bovine serum albumin, and broth medium.
- Treatment with trypsin and potassium bromide to strip surface proteins.
- Short-term incubation (30 min) of specific strains in plasma.
Main Results:
- Strains showed increased resistance after incubation in plasma, but also in other media, suggesting both specific and non-specific mechanisms.
- Surface protein stripping indicated a protein coating on plasma-grown organisms.
- Free coagulase-positive strains rapidly acquired resistance in plasma, unlike mutants lacking this factor.
Conclusions:
- Staphylococcal resistance to bactericidins is influenced by cultural conditions.
- A key mechanism involves the rapid interaction of staphylococcal free coagulase with fibrinogen.
- This interaction leads to fibrin deposition on the bacterial surface, contributing to resistance.