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Penicillin-resistant and penicillin-tolerant mutants of group A Streptococci
Abstract:
Penicillin-resistant and penicillin-tolerant mutants have been isolated from group A streptococci mutagenized by ethyl methane sulfonate. The resistant mutants had an elevated minimal growth inhibitory concentration for benzylpenicillin (minimal inhibitory concentration, 0.2 microgram/ml, as compared with the minimal inhibitory concentration of 0.006 microgram/ml in the penicillin-susceptible parent strain); they also had an abnormal cellular morphology and showed altered penicillin-binding proteins. Penicillin-tolerant mutants were killed more slowly than were the parental cells during treatment with penicillin; they had virtually unchanged minimal inhibitory concentration values for penicillin and normal cellular morphology and penicillin-binding proteins.
Insights
Researchers isolated penicillin-resistant and penicillin-tolerant mutants of group A streptococci. Resistant strains showed altered cell structure and penicillin-binding proteins, while tolerant strains exhibited slower killing rates with normal morphology.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Group A Streptococcus (GAS) is a significant human pathogen.
- Penicillin is a primary antibiotic for treating GAS infections.
- Understanding antibiotic resistance mechanisms in GAS is crucial for effective treatment.
Purpose of the Study:
- To isolate and characterize penicillin-resistant and penicillin-tolerant mutants of group A Streptococcus.
- To investigate the phenotypic and genotypic changes associated with these resistance and tolerance mechanisms.
Main Methods:
- Group A Streptococcus strains were mutagenized using ethyl methane sulfonate.
- Isolation of mutants based on resistance or tolerance to benzylpenicillin.
- Determination of minimal inhibitory concentration (MIC) for benzylpenicillin.
- Analysis of cellular morphology using microscopy.
- Assessment of penicillin-binding proteins (PBPs).
Main Results:
- Penicillin-resistant mutants exhibited a significantly elevated MIC for benzylpenicillin (0.2 µg/ml vs. 0.006 µg/ml in the parent strain).
- Resistant mutants displayed abnormal cellular morphology and altered penicillin-binding proteins.
- Penicillin-tolerant mutants showed virtually unchanged MIC values but were killed more slowly by penicillin.
- Tolerant mutants maintained normal cellular morphology and penicillin-binding proteins.
Conclusions:
- Mutations conferring penicillin resistance in GAS can lead to changes in cell morphology and penicillin-binding proteins.
- Penicillin tolerance in GAS is distinct from resistance, characterized by slower killing rates without significant changes in MIC, morphology, or PBPs.
- These findings highlight diverse mechanisms of penicillin interaction in GAS, impacting therapeutic strategies.