Action of Disinfectant Quaternary Ammonium Compounds against<i>Staphylococcus aureus</i>

<jats:title>ABSTRACT</jats:title><jats:p>Mode-of-action studies concluded that alkyldimethylbenzylammonium chloride (ADBAC) (a blend of C<jats:sub>12</jats:sub>, C<jats:sub>14</jats:sub>and C<jats:sub>16</jats:sub>alkyl homologues) and didecyldimethylammonium chloride (DDAC) are both membrane-active agents, possessing subtly different modes of action reflecting early cell interactions against<jats:italic>Staphylococcus aureus</jats:italic>. ADBAC and DDAC exhibited similar MIC behaviors from 0.4 ppm to 1.8 ppm over an inoculum range of 1 × 10<jats:sup>5</jats:sup>to 1 × 10<jats:sup>9</jats:sup>CFU/ml at 35°C. For ADBAC and DDAC, an increased rapidity of killing against<jats:italic>S. aureus</jats:italic>(final concentration, 2 × 10<jats:sup>9</jats:sup>CFU/ml) was observed at 35°C compared to 25°C. Concentration exponents (η) for killing were <2.5 for both agents, and temperature influenced the η value. Examination of leakage and kill data suggested that a single leakage marker was not indicative of cell death. ADBAC and DDAC possessed Langmuir (L4) and high-affinity (H3/4) uptake isotherms, respectively. ADBAC molecules formed a single monolayer of coverage of cells at the end of primary uptake, and DDAC formed a double monolayer. Rapid cell leakage occurred at bactericidal concentrations, with total depletion of the intracellular potassium and 260-nm-absorbing pools released in this strict order. Autolysis was observed for ADBAC and DDAC at concentrations of 9 μg/ml (0.0278 mM and 0.0276 mM, respectively) and above, together with the depletion of approximately 30% of the internal potassium pool. Autolysis contributed to ADBAC and DDAC lethality, although high biocide concentrations may have inhibited autolytic enzyme activity.</jats:p>