Abstract:

Hypertonic sucrose inhibited the bactericidal activity of lysozyme-free serum against a rough strain of Escherichia coli. The duration of the inhibition correlated with the duration of plasmolysis caused by the sucrose. Although the lethal action of the serum was delayed, the prompt release of alkaline phosphatase by the cells suggested that nonlethal damage to the cell wall had taken place under these conditions. In contrast, the crypticity of the cells for beta-galactosidase did not deteriorate until the viability of the bacteria began to decrease. It is concluded that the primary site of action of serum is at the bacterial cell wall; however, in the absence of lysozyme, the lethal event was subsequent damage to the bacterial cell membrane.

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Locus of the Lethal Event in the Serum Bactericidal Reaction<sup><a href="#fn1" rid="fn1" class=" fn">1</a></sup>

D Feingold

J Goldman

H Kuritz

Abstract

Hypertonic sucrose inhibited the bactericidal activity of lysozyme-free serum against a rough strain of Escherichia coli. The duration of the inhibition correlated with the duration of plasmolysis caused by the sucrose. Although the lethal action of the serum was delayed, the prompt release of alkaline phosphatase by the cells suggested that nonlethal damage to the cell wall had taken place under these conditions. In contrast, the crypticity of the cells for β-galactosidase did not deteriorate until the viability of the bacteria began to decrease. It is concluded that the primary site of action of serum is at the bacterial cell wall; however, in the absence of lysozyme, the lethal event was subsequent damage to the bacterial cell membrane.

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Selected References

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^{Departments of Medicine, Harvard Medical School and Beth Israel Hospital, Boston, Massachusetts 02215}

^{Presented in part at the 7th Interscience Conference on Antimicrobial Agents and Chemotherapy, Chicago, Ill., 25–27 October 1967.}

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Abstract

Hypertonic sucrose inhibited the bactericidal activity of lysozyme-free serum against a rough strain of Escherichia coli. The duration of the inhibition correlated with the duration of plasmolysis caused by the sucrose. Although the lethal action of the serum was delayed, the prompt release of alkaline phosphatase by the cells suggested that nonlethal damage to the cell wall had taken place under these conditions. In contrast, the crypticity of the cells for β-galactosidase did not deteriorate until the viability of the bacteria began to decrease. It is concluded that the primary site of action of serum is at the bacterial cell wall; however, in the absence of lysozyme, the lethal event was subsequent damage to the bacterial cell membrane.

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