Several mechanisms conferring bacterial resistance to biocides have been described;
some are inherent to the bacterium, other to the bacterial population. In addition, some
of the resistance mechanisms are intrinsic (or innate) to the micro-organism while others
have been acquired through forced mutations or through the acquisition of mobile
genetic elements (Poole 2002a). Innate mechanisms can confer high-level bacterial
resistance to biocides. In this case, the term unsusceptibility is used (see definition;
section 3.1.1.1).
The most described intrinsic resistance mechanism is changes in the permeability of the
cell envelope, also referred to as "permeability barrier". This is not only found in spores
(Cloete, 2003, Russell 1990, Russell et al. 1997), but also in vegetative bacteria such as
mycobacteria and to some extent in Gram-negative bacteria. The permeability barrier
limits the amount of a biocide that enters the cell, thus decreasing the effective biocide
concentration (Champlin et al. 2005, Denyer and Maillard 2002, Lambert 2002). In
mycobacteria the presence of a mycoylacylarabinogalactan layer accounts for the
impermeability to many antimicrobials (Lambert 2002, McNeil and Brennan 1991, Russell
1996, Russell et al. 1997). In addition, the presence and composition of the
arabinogalactan/arabinomannan cell wall also plays a role in reducing the effective
concentration of biocide that can penetrate within mycobacteria (Broadley et al. 1995,
Hawkey 2004, Manzoor et al. 1999, Walsh et al. 2001).
The role of the lipopolysaccharides (LPS) as a permeability barrier in Gram-negative
bacteria has been well documented (Ayres et al. 1998, Denyer and Maillard 2002, Fraud
et al. 2003, McDonnell and Russell 1999, Munton and Russell 1970, Stickler 2004). There
have also been a number of reports of reduced biocide efficacy following changes in other
components of the outer membrane ultrastructure (Braoudaki and Hilton 2005,
Tattawasart et al. 2000a, Tattawasart et al. 2000b) including proteins (Brözel and Cloete
1994, Gandhi et al. 1993, Winder et al. 2000), fatty acid composition (Guérin-Méchin et
al. 1999, Guérin-Méchin et al. 2000, Jones et al. 1989, Méchin et al. 1999) and
phospholipids (Boeris et al. 2007). It must be noted that in the above mentioned
examples, an exposure to biocides was followed by changes in ultrastructure related to a
decrease in biocidal susceptibility, usually at a low concentration (under the MIC value).
The charge property of the cell surface also plays a role in bacterial resistance
mechanisms to positively charged biocides such as QACs (Bruinsma et al. 2006). It is
likely that bacterial resistance emerges from a combination of mechanisms (Braoudaki
and Hilton 2005, Tattawasart et al. 2000a, Tattawasart et al. 2000b), even though single
specific mechanisms are often investigated.
Several mechanisms conferring bacterial resistance to biocides have been described;some are inherent to the bacterium, other to the bacterial population. In addition, someof the resistance mechanisms are intrinsic (or innate) to the micro-organism while othershave been acquired through forced mutations or through the acquisition of mobilegenetic elements (Poole 2002a). Innate mechanisms can confer high-level bacterialresistance to biocides. In this case, the term unsusceptibility is used (see definition;section 3.1.1.1).The most described intrinsic resistance mechanism is changes in the permeability of thecell envelope, also referred to as "permeability barrier". This is not only found in spores(Cloete, 2003, Russell 1990, Russell et al. 1997), but also in vegetative bacteria such asmycobacteria and to some extent in Gram-negative bacteria. The permeability barrierlimits the amount of a biocide that enters the cell, thus decreasing the effective biocideconcentration (Champlin et al. 2005, Denyer and Maillard 2002, Lambert 2002). Inmycobacteria the presence of a mycoylacylarabinogalactan layer accounts for theimpermeability to many antimicrobials (Lambert 2002, McNeil and Brennan 1991, Russell1996, Russell et al. 1997). In addition, the presence and composition of thearabinogalactan/arabinomannan cell wall also plays a role in reducing the effectiveconcentration of biocide that can penetrate within mycobacteria (Broadley et al. 1995,Hawkey 2004, Manzoor et al. 1999, Walsh et al. 2001).The role of the lipopolysaccharides (LPS) as a permeability barrier in Gram-negativebacteria has been well documented (Ayres et al. 1998, Denyer and Maillard 2002, Fraudet al. 2003, McDonnell and Russell 1999, Munton and Russell 1970, Stickler 2004). Therehave also been a number of reports of reduced biocide efficacy following changes in othercomponents of the outer membrane ultrastructure (Braoudaki and Hilton 2005,Tattawasart et al. 2000a, Tattawasart et al. 2000b) including proteins (Brözel and Cloete1994, Gandhi et al. 1993, Winder et al. 2000), fatty acid composition (Guérin-Méchin etal. 1999, Guérin-Méchin et al. 2000, Jones et al. 1989, Méchin et al. 1999) andphospholipids (Boeris et al. 2007). It must be noted that in the above mentionedexamples, an exposure to biocides was followed by changes in ultrastructure related to adecrease in biocidal susceptibility, usually at a low concentration (under the MIC value).The charge property of the cell surface also plays a role in bacterial resistancemechanisms to positively charged biocides such as QACs (Bruinsma et al. 2006). It islikely that bacterial resistance emerges from a combination of mechanisms (Braoudakiand Hilton 2005, Tattawasart et al. 2000a, Tattawasart et al. 2000b), even though singlespecific mechanisms are often investigated.
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