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Ampicillin induced septum formation in Bacillus cereus

W G Salt, R J Stretton, M E Wall

    Microbios
    |January 1, 1983
    PubMed

    Insights

    Subinhibitory ampicillin concentrations altered Bacillus cereus septum formation and cell length. Escherichia coli showed filamentation, with B. cereus cell length increasing at higher temperatures.

    Area of Science:

    • Microbiology
    • Cell Biology
    • Bacterial Physiology

    Background:

    • Subinhibitory antibiotic concentrations can induce morphological changes in bacteria.
    • Understanding these changes is crucial for predicting antibiotic resistance and treatment outcomes.
    • Bacillus cereus and Escherichia coli are important model organisms for studying bacterial cell division.

    Purpose of the Study:

    • To investigate the effects of subinhibitory ampicillin concentrations on the cell division and morphology of Bacillus cereus and Escherichia coli.
    • To compare the responses of these two bacterial species to temperature variations and antibiotic stress.
    • To explore the roles of penicillin-binding proteins and autolysins in observed cellular changes.

    Main Methods:

    • Culturing Bacillus cereus and Escherichia coli in the presence of subinhibitory ampicillin concentrations.
    • Incubating cultures at different temperatures (30°C and 45°C).
    • Microscopic examination to quantify septum formation and cell length.

    Main Results:

    • Bacillus cereus exhibited increased septum formation centers per unit cell length under subinhibitory ampicillin.
    • Escherichia coli grew as aseptate filaments under identical conditions.
    • Untreated Bacillus cereus cells were longer at 45°C compared to 30°C, while E. coli filamentation was not affected by temperature.

    Conclusions:

    • Subinhibitory ampicillin significantly impacts Bacillus cereus cell division and morphology.
    • Temperature influences Bacillus cereus cell elongation but not Escherichia coli filamentation.
    • Penicillin-binding proteins and autolysins are likely key mediators of these antibiotic- and temperature-induced cellular responses.

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