A.D. Russell

The effects of antiseptics, disinfectants and preservatives on smooth, rough and deep rough strains of Salmonella typhimurium

The effects of some antiseptics, disinfectants and preservatives on a smooth strain and rough mutant strains (Ra, Rd1 and Re) of Salmonella typhimurium are described. The inhibitors consisted of three phenolics, a homologous series (the parabens) of esters of p-hydroxybenzoic (4-hydroxybenzoic) acid, chlorhexidine diacetate and other cationic bactericides and two mercury compounds. The responses of the strains to these agents have been related: (a) to the nature of the bacterial outer membrane; and (b) to the physical properties of the compounds.

Aspects of the action of chlorhexidine on bacterial spores

Abstract At low concentrations, chlorhexidine diacetate (CHA) was sporostatic towards Bacillus subtilis spores. Concentrations of CHA up to 25) μg/ml had little sporicidal activity at 20, 30 or 37°C, but the effect increased when the temperature was increased to 60 or 70 °C. CHA at low concentrations inhibited spore outgrowth but not germination; this inhibitory effect could, to some extent, be reversed by Tween 80. The outgrowth-inhibiting effect was also shown by two other cationic bactericides, a quaternary ammonium compound (cetylpyridinium chloride) and a diamidine (dibromopropamidine isethionate). In contrast, phenol was an effective inhibitor of germination.

Susceptibility of porin- and lipopolysaccharide-deficient mutants of Escherichia coli to a homologous series of esters of p-hydroxybenzoic acid

Abstract The methyl (Me), ethyl (Et), propyl (Pr) and butyl (Bu) esters of p -hydroxybenzoic acid have been tested against wild type and porin- and/or lipopolysaccharide (LPS)-deficient mutants strains of Escherichia coli. The Bu ester was the most active inhibitor, the Me the least. The most sensitive strains to an individual ester were those with LPS-defective outer membranes, whilst the most resistant were the wild type (PCO479) and rough mutant (D21) strains. The results are discussed in relation to some of the physical properties of the parabens, especially their hydrophobic nature.

Surface changes in Pseudomonas aeruginosa exposed to chlorhexidine diacetate and benzalkonium chloride

Abstract Pseudomonas aeruginosa strains 799 (wild-type) and 799/61 (envelope mutant) were exposed to chlorhexidine diacetate and benzalkonium chloride, and their hydrophobicity measured in a hydrocarbon (xylene) system. Both drugs induced changes in surface hydrophobic properties at concentrations well below those that inhibited cellular growth, A comparison of these findings has been made with a wild-type and an envelope mutant of Escherichia coli, both of which strains are more sensitive than Ps. aeruginosa to these drugs.

Comparative sensitivity of smooth, rough and deep rough strains of Escherichia coli to chlorhexidine, quaternary ammonium compounds and dibromopropamidine isethionate

Abstract The effects of chlorhexidine diacetate (CHA) and some quaternary ammonium compounds (QACs) on wild-type strains of Escherichia coli and on mutants (slightly rough, moderately rough and deep rough) are described. CHA was almost equally active in low concentrations against all the strains, whereas the three QACs, cetylpyridinium chloride (CPC), domiphen bromide and benzethonium chloride were most active against the deep rough strains, and least against the wild type and slightly rough strains. Moderately rough strains were consistently found to be slightly less sensitive to the QACs than the deep rough ones. The inhibitory concentration of CPC for any strain was much less in broth than in agar. Studies with ethylenediamine tetraacetate (EDTA) demonstrated that the chelating agent had only a marginal, if any, effect on the activity of CHA, whereas in the presence of EDTA, the activity of CPC against strains with complete or almost complete lipopolysaccharide was enhanced considerably.

Activity of benzalkonium chloride and chlorhexidine diacetate against wild-type and envelope mutants of Escherichia coli and Pseudomonas aeruginosa

Abstract Whole cells of wild-type (DCO) and envelope mutant (DC2) strains of Escherichia coli took up approximately equal amounts of the cationic surfactant, benzalkonium chloride, although the mutant was considerably more sensitive to this bactericide. Lower concentrations of benzalkonium were needed to induce K+ leakage from the mutant than from the parent cells. DCO and DC2 showed the same order of sensitivity to chlorhexidine diacetate (minimum inhibitory concentrations against single cell inocula, 1.5 and 0.4 μg ml , respectively) and took up approximately equal amounts of this antiseptic. K+ leakage was much greater from DC2 exposed to benzalkonium and slightly higher from chlorhexidine-treated DC2 than from drugtreated DCO. Similar studies with wild type (799) and envelope mutant ( 799 61 ) strains of Pseudomonas aeruginosa showed that they took up similar amounts of benzalkonium or of chlorhexidine from solution. However, somewhat greater leakage of K+ occurred from 799 61 than from 799. Lysozyme-EDTA spheroplasts of a wild-type strain and its envelope mutant were equally sensitive to an antibacterial agent.

Reversal of the inhibition of bacterial spore germination and outgrowth by antibacterial agents

Abstract The effects of some antibiotics and other antibacterial agents on the germination and outgrowth of Bacillus subtilis are described. The antibiotics tested (benzylpenicillin, cephalothin, chloramphenicol, minocycline, actinomycin D and mitomycin C) had no effect on germination but inhibited outgrowth to varying degrees. Of the preservative-type compounds, phenol and cresol acted predominantly at the germination stage, whereas the quaternary ammonium compound, benzalkonium chloride (BZK), and the organomercurial, phenylmercuric nitrate, inhibited out-growth but not germination. The inhibitory effect of phenol was reversed by membrane filtration, but not by 2% polysorbate 80, whereas BZK appeared to be tightly bound to the cells and could not be removed by filtration.

Interactions between β-lactam and aminoglycoside antibiotics

Abstract Incubation of an aminoglycoside antibiotic (gentamicin or tobramycin) with a penicillin (carbenicillin or ticarcillin) at 20 or 37 °C, but not at 5 °C, resulted in considerable loss of antibacterial activity, possibly as a result of complexing, of the former as determined by plate assay against an aminoglycoside-sensitive, penicillin-resistant strain of Klebsiella edwardsii . The extent of this loss of aminoglycoside activity depended on the relative ratio of aminoglycoside:penicillin. Pretreatment of a penicillin with a broad-spectrum β-lactamase, or addition of the β-lactamase at the time of mixing an aminoglycoside with a penicillin, prevented this loss of activity. Reversal of preformed complex formation could be achieved to some extent by subsequent incubation with this β-lactamase. Incubation of other penicillins with gentamicin also resulted in loss of antibacterial activity of the latter antibiotic.