Chlorhexidine is rapidly adsorbed by bacterial cells and this adsorption is accompanied by other cytological changes which include changes in the permeability of the cells and in their optical properties. The amount of drug adsorption causing maximum leakage of cell constituents and changes in extinction was found to be equivalent for Escherichia coli and for Staphylococcus aureus. Higher doses of chlorhexidine causing a higher level of drug adsorption caused correspondingly less leakage and change in extinction although such higher doses were more rapidly bactericidal.

Chlorhexidine does not cause lysis of isolated cell walls, nor does it prevent the synthesis of the mucopeptide component of the cell wall. Low concentrations of the drug stimulate dehydrogenase activity but higher concentrations inhibit the activity. Chlorhexidine reacts with and precipitates proteinaceous and pentosecontaining components of a solution of cell-free cytoplasmic constituents in concentrations greater than those causing their maximum leakage. The effect of chlorhexidine concentration on the electrophoretic mobility of bacterial cells is consistent with the hypothesis that the drug accumulates in aggregates at the cell surface rather than in the form of a monolayer or multilayers of drug.T has been shown that chlorhexidine causes the release of cytoplasmic

Chlorhexidine prevents the transformation of Bacillus megaterium cells to protoplasts by lysozyme, of E. coli cells to spheroplasts by penicillin and causes lysis of “protoplasts” and spheroplasts of E. coli stabilised in hypertonic sucrose solution. Transformation of Staphylococcus aureus cells to the Gram‐negative condition occurred in contact with 10 to 800 μg/ml of chlorhexidine and 10, 50 and 100 μg/ml of cetyltrimethylammonium bromide but higher concentrations of the latter prevented this change. Results indicate that chlorhexidine damages the permeability barrier of bacterial cells.

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