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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

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1,2‐benzisothiazolin‐3‐one (BIT), at growth inhibitory concentrations, has little effect on membrane integrity but significantly inhibits the active transport and oxidation of glucose by washed Staphylococcus aureus cells. The dependancy of these metabolic processes on thiol‐containing enzymes and the observed interaction of BIT with glutathione and isolated enzyme preparations suggests that cellular thiol groups are a major target for BIT.

Fentichlor is adsorbed in fairly large amounts by Staphylococcus aureus and Escherichia coli and, according to the quantity adsorbed, is either bacteriostatic or bactericidal. The observed pattern of uptake, measured under various conditions, indicates that uptake involves reversible adsorption of the neutral molecule on to the cell. The drug is taken up by the cell wall and cell membrane, the latter probably being the main site of adsorption and main site of action. Although both whole cells and cell walls of E. coli have a higher affinity for Fentichlor than those of Staph. aureus, the former is less susceptible to its antibacterial action. Results indicate that this may be due to the lipid‐rich nature of the cell walls of E. coli which act as an adsorbing barrier preventing the access of the drug to its site of action.