Observations on Quaternary Ammonium Disinfectants

323

227

Mode-of-action studies concluded that alkyldimethylbenzylammonium chloride (ADBAC) (a blend of C 12 , C 14 and C 16 alkyl homologues) and didecyldimethylammonium chloride (DDAC) are both membrane-active agents, possessing subtly different modes of action reflecting early cell interactions against Staphylococcus aureus. ADBAC and DDAC exhibited similar MIC behaviors from 0.4 ppm to 1.8 ppm over an inoculum range of 1 ؋ 10 5 to 1 ؋ 10 9 CFU/ml at 35°C. For ADBAC and DDAC, an increased rapidity of killing against S. aureus (final concentration, 2 ؋ 10 9 CFU/ml) was observed at 35°C compared to 25°C. Concentration exponents () for killing were <2.5 for both agents, and temperature influenced the 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 g/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.

Section: Fig 7 Leakage Of Potassium (}) and 260-nm-absorbing (■) Mamentioning

confidence: 99%

Action of Disinfectant Quaternary Ammonium Compounds against Staphylococcus aureus

Ioannou¹,

Hanlon

Denyer

2007

323

227

“…QACs are bacteriostatic at low concentrations and bactericidal at high concentrations (33), and thus, low concentrations of this agent may favor the development of adaptive resistance. Adaptive resistance to QACs by prolonged sublethal exposure and the cross-resistance of adapted strains to antimicrobial chemotherapeutic agents (amoxicillin, clavulanic acid, chloramphenicol, imipenem, polymyxin B, tetracycline, and trimethoprim) and other biocides (chlorhexidine and triclosan) have been documented in various bacteria, including Serratia marcescens (8), Escherichia coli (5,24,33), Pseudomonas aeruginosa (15,30), Pseudomonas fluorescens (46), and Salmonella enterica (5).…”

mentioning

confidence: 99%

Adaptive Resistance and Differential Protein Expression of Salmonella enterica Serovar Enteritidis Biofilms Exposed to Benzalkonium Chloride

Mangalappalli-Illathu

Korber

2006

The development of adaptive resistance of Salmonella enterica serovar Enteritidis ATCC 4931 biofilms following exposure to benzalkonium chloride (BC) either continuously (1 g ml ؊1 ) or intermittently (10 g ml ؊1 for 10 min daily) was examined. Biofilms adapted to BC over a 144-h period could survive a normally lethal BC challenge (500 g ml ؊1 for 10 min) and then regrow, as determined by increases in biofilm thickness, total biomass, and the ratio of the viable biomass to the nonviable biomass. Exposure of untreated control biofilms to the lethal BC challenge resulted in biofilm erosion and cell death. Proteins found to be up-regulated following BC adaptation were those involved in energy metabolism (TpiA and Eno), amino acid and protein biosynthesis (WrbA, TrxA, RplL, Tsf, Tuf, DsbA, and RpoZ), nutrient binding (FruB), adaptation (CspA), detoxification (Tpx, SodB, and a probable peroxidase), and degradation of 1,2-propanediol (PduJ and PduA). A putative universal stress protein (YnaF) was also found to be up-regulated. Proteins involved in proteolysis (DegQ), cell envelope formation (RfbH), adaptation (UspA), heat shock response (DnaK), and broad regulatory functions (Hns) were found to be down-regulated following adaptation. An overall increase in cellular protein biosynthesis was deduced from the significant up-regulation of ribosomal subunit proteins, translation elongation factors, and amino acid biosynthesis protein and down-regulation of serine endoprotease. The cold shock response, stress response, and detoxification are suggested to play roles in the adaptive resistance of Salmonella serovar Enteritidis biofilms to BC.

“…Early studies of the resistance of pigmented S. marcescens to quaternary ammonium compounds showed that resistance was lowered by action of lipase (6). In 1972 Chang et al (5) reported that a nonpigmented strain of S. marcescens, Bizio, that was antibiotic resistant differed from a pigmented, antibiotic-sensitive strain in lipid content.…”

mentioning

confidence: 99%

Relation of Cell Wall Lipid Content of Serratia marcescens to Resistance to Antimicrobial Agents

Winshell

Neu

1974

Serratia marcescens strains were divided into three groups on the basis of antimicrobial sensitivity and pigment production. Group I, nonpigmented, was resistant to most antibiotics. Group II, nonpigmented, was susceptible to many antimicrobial agents, as was group III which was pigmented. Representative organisms of each group were examined for all lipid content. There were no significant differences in total lipid, phospholipid, or fatty acid esters among the three groups. Differences in susceptibility to antibiotics in Serratia do not seem to be explained on the basis of wall lipid content.