Mutations biocide resistance

Acquired microbial resistance has been extensively investigated with various antibiotics, but similar studies with biocides are fewer and more recent. It has been confirmed that many biocides can also be rendered meffective or less effective by acquired microbial resistance. This acquired resistance to both biocides and antibiotics may be genetic and/or biochemical [16, 26]. Chromosomal gene mutation and acquisition of plasmids and transposons by the microbes are the genetic modes that have been observed. As shown in Table I, plasmid-mediated biocide resistance can occur by... 

Bacterial resistance to biocides (Table 13.2) is usually considered as being of two types (a) intrinsic (innate, natural), a natural property of an organism, or (b) acquired, either by chromosomal mutation or by the acquisition of plasmids or transposons. Intrinsic resistance to biocides is usually demonstrated by Gram-negative bacteria, mycobacteria and bacterial spores whereas acquired resistance can result by mutation or, more frequently, by the acquisition of genetic elements, e.g. plasmid- (or transposon-) mediated resistance to mercury compounds. Intrinsic resistance may also be exemplified by physiological (phenotypic) adaptation, a classical example of which is biofilm production. 

Acquired resistance to biocides results fiem genetie ehanges in a cell and arises either by mutation or by the acquisition of genetic material (plasmids, transposons) from another cell (Table 13.5). 

Few studies have determined whether or not chromosomal gene mutation is responsible for conferring resistance to biocides. However, many years ago it was demonstrated that Ser. marcescens, normally inhibited by a QAC in broth at a concentration of less than 100 g/ml, could adapt to grow in this culture medium in the presence of 100 mg/ml of the antibacterial agent... 

Antibiotics usually have a specific site or mode of action whereby they achieve a selective toxic effect against bacteria but not human host cells. In contrast, biocides frequently have multiple target sites in the bacterial cell and by their very nature are often toxic not only to bacteria and other micro-organisms but also to host cells [7,23,24], Thus, mutation at, or absence of, a normal target site (or the presence of an additional target site) may be responsible for producing resistance to antibiotics but not to biocides. 

Acquired, non-plasmid-encoded resistance to biocides can result when bacteria are exposed to gradually increasing concentrations of a biocide. Examples are provided by highly QAC-resistant Serratia marcescens, and chlorhexidine-resistant Pr. mirabilis, Ps. aeruginosa and Ser. marcescens. However, in view of the multiple target sites associated with biocide action, it is unlikely that mutation plays a key role in resistance. 

Concern has been expressed about whether microorganisms could become resistant as a result of increased usage of antimicrobials, but it has been pointed out that they are different from antibiotics, because their attack on microorganisms is carried out by multiple mechanisms, and the development of resistance would therefore need more than one mutation. Moreover if the concentration of biocidal agent used in an inanimate material is higher than the minimum inhibitory concentration by a sufficiently large factor, any small decrease in susceptibility would be of little relevance. 

Acquired resistance to biocides arises by the acquisition of extrachromoso-mal genetic elements (plasmids and transposons) or as a consequence of a chromosomal gene mutation [53, 236, 237]. Acquired resistance to chromosomal mutation can arise when bacteria are sequentially exposed to increasing concentrations of a biocide. 

From the table it may be observed that bacteria would need to alter the structure of every protein in the cell to enable it to become resistant to a biocide. This would require that the bacteria would need a large number of mutations at the same time or in a short time to become resistant to a biocide. Such patterns of mutations, however, must occur over time spans much longer than what is normally available in an industrial system. The main reasons that explain why a biocide that seemed to be working previously is not working any more can be summarised as follows [34] ... 

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