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Chapter 8 : Mechanisms of Microbial Resistance

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Abstract:

This chapter discusses the various mechanisms of biocide resistance described in microorganisms. Resistance can be either a natural property of an organism (intrinsic) or acquired by mutation or by the acquisition of plasmids (self-replicating extrachromosomal DNA) or transposons (chromosomal or plasmid-integrating transmissible DNA cassettes). The biocide concentration is an important variable and must at least be at the MIC or, preferably, at the minimum biocidal concentration to have a significant effect. Mechanisms of intrinsic resistance are described with further consideration of the various types of bacteria. The first acquired resistance mechanisms reported were against mercury compounds and other metallic salts. In recent years, acquired mechanisms of resistance to other types of biocides have been observed, notably in gram-positive staphylococci. The proposed mechanisms of prion resistance are summarized. In comparison with bacteria, very little is known about the ways in which fungi can circumvent the actions of biocides and biocidal processes. As with bacteria, two general mechanisms of resistance can be identified: intrinsic resistance, a natural property or development of the organism during normal growth, and acquired resistance, with examples of both identified or proposed.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8

Key Concept Ranking

Bacteria and Archaea
0.6594754
Bacterial Proteins
0.5238402
Type II Fatty Acid Synthase
0.469254
0.6594754
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Figures

Image of FIGURE 8.1
FIGURE 8.1

General microbial resistance to biocides and biocidal processes.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.2
FIGURE 8.2

The initial sequence of events in biocide-microorganism interaction.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.3
FIGURE 8.3

A typical bacterial growth curve, showing the four phases of growth.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.4
FIGURE 8.4

The activation and deactivation of the OxyR protein, as an activator in the peroxide-induced oxidative-stress response.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.5
FIGURE 8.5

The functions of various enzymes induced during oxidative stress.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.6
FIGURE 8.6

Transport systems in bacteria across a typical cell membrane.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.7
FIGURE 8.7

Establishment of the PMF.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.8
FIGURE 8.8

Summary of the various types of efflux pumps associated with antimicrobial resistance identified in bacteria. A typical gramnegative bacterial cell wall is shown with associated cytoplasmic and outer membranes (see section 1.3.4.1). Note that similar cytoplasmic-membrane-associated efflux pumps (MFS and ABC) have been identified in grampositive bacteria (which do not have an outer membrane [see section 1.3.4.1]). Efflux is energy dependent, with energy derived from the PMF (antiporter efflux with H) or ATP hydrolysis (to ADP plus inorganic phosphate).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.9
FIGURE 8.9

Intrinsic mechanisms of microbial resistance to heavy metals. The heavy-metal ions can pass through the cell wall and membrane with a subsequent intracellular increase in concentration and inhibitory or biocidal effects (shown on the far left). Mechanisms of resistance are exclusion, due to the presence of various surface structures or more subtle changes in the porin or pump specificity to allow the uptake of essential but not biocidal ions (1); active efflux out of the cell, against a concentration gradient (2); enzymatic conversion of the ion to a different form, which can be released from the cell (3); sequestration, in which macromolecules can absorb the biocide, reducing the available concentration (4); and changes in the structure of the target molecule, reducing its susceptibility to biocidal action (5).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.10
FIGURE 8.10

A biofilm on a surface. Individual rod-shaped bacteria can be seen developed in a polysaccharide matrix. © William Fett and Peter Cooke (USDA Agricultural Research Service). Courtesy of Peter Cooke and Paul Pierlott (USDA Agricultural Research Service).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.11
FIGURE 8.11

The development of a biofilm. Initial attachment (adsorption) of a microorganism may be reversible or permanent, leading to profileration and extracellular-polysaccharide production. This matrix develops over time, allowing the entrapment of nutrients and other microorganisms, which can also proliferate to produce a mature biofilm. Sections of the biofilm can slough off over time, bind to other surfaces, and subsequently develop further biofilms.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.12
FIGURE 8.12

An example of survival of radiation. The survival of (solid line) is compared to that of a typical radiation-sensitive bacterial strain (dotted line) when exposed to increasing doses of γ-irradiation (measured in kilograys) (see section 5.4).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.13
FIGURE 8.13

Micrograph of cells in a typical tetrad formation.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.14
FIGURE 8.14

Microbial growth and optimum temperature conditions. Examples of various vegetative microorganisms are shown, although the sensitivities of specific species to heat vary. spores may be considered hyperthermophilic but are dormant (see section 8.3.11 ).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.15
FIGURE 8.15

Microbial growth and optimum pH conditions. Examples of various microorganisms are shown, although the sensitivities of specific species to pH vary.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.16
FIGURE 8.16

Microbial growth and optimum salt conditions. Examples of various microorganisms are given, although the sensitivities of specific species to salt concentrations vary.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.17
FIGURE 8.17

The basic life cycle of grampositive endospore-forming rods. The vegetative growth of the bacteria is limited due to the reduction of essential nutrients (for example, carbon or nitrogen sources) or other environmental factors, causing the initiation of the sporulation cascade, death of the mother cell, and release of the dormant spore. Under the right environmental conditions, conducive to bacterial growth, the spore becomes activated, germinates, and grows out to produce a viable vegetative bacterial cell, which resumes metabolism and multiplication.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.18
FIGURE 8.18

Typical bacterial-endospore structure. An actual micrograph of endospores on a surface is shown, with a representation of the various spore layers shown below (not to scale). The shapes of the spores vary, depending on the bacterial genus and species.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.19
FIGURE 8.19

A representation of a typical sporulation process, with the key stages identified.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.20
FIGURE 8.20

The development of resistance of bacterial endospores to biocides and biocidal processes. The various defined stages of sporulation are given from stage III (engulfment of the forespore) to stage VII (release of the mature spore), as shown in Fig. 8.19 . The point at which the developing spore demonstrates resistance to each biocide or biocidal process is indicated.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.21
FIGURE 8.21

Loss of resistance to various biocides and heat during bacterial-endospore germination and outgrowth. Various biocides inhibit the activation of endospores (sporistatic) and are bactericidal to vegetative cells. Others (marked by asterisks) are also sporicidal at higher concentrations and temperatures and longer exposure times. Biocides at low concentrations and temperatures have also been shown to specifically inhibit germination or outgrowth following activation of the spore.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.22
FIGURE 8.22

Typical life cycle of . A desiccated spore, under the right environmental conditions, will germinate and initiate hyphal growth. Under conditions of environmental stress and/or nutrient limitation, aerial hyphae develop in parallel with the production of secondary metabolites, including antibiotics and hydrolytic enzymes, to assist in survival. The aerial filaments separate by simple cross-wall division to form prespore compartments and to develop desiccated spores, which are released into the environment.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.23
FIGURE 8.23

The revival of microorganisms after biocidal treatment. On exposure, microorganisms may survive due to lack of contact or intrinsic resistance to the biocide. In other cases, the damaged microorganisms can be revived by active repair mechanisms and undergo subsequent growth or infectivity. Damaged microorganisms may therefore be initially uncultivable by normal laboratory methods but remain viable. Biocidal effects may also be sufficient to render the microorganism nonviable (cell death or loss of infectivity).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.24
FIGURE 8.24

A representation of the mycobacterial cell wall structure.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.25
FIGURE 8.25

A representation of a typical grampositive bacterial cell wall structure.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.26
FIGURE 8.26

A representation of a typical gramnegative bacterial cell wall structure.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.27
FIGURE 8.27

The primary mechanisms of action of penicillin and of bacterial resistance to it. The antibiotic penetrates through the cell wall to the cytoplasmic-membrane-associated PBPs and disrupts their role in the synthesis of the cell wall peptidoglycan (shown on the left). The first mechanism of resistance (1) is exclusion from the cell, which can be intrinsic or acquired. In the second (2), the target PBPs have mutated to become less sensitive to penicillin binding. The third (3) is the presence (naturally induced or otherwise acquired) of β-lactamases, which hydrolyze the antibiotic.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.28
FIGURE 8.28

The modes of bacterial tolerance of triclosan due to acquired mutations. Exclusion (1) may be due to loss of outer membrane porin proteins (reduced influx) or changes in the outer or inner membrane lipid structure. Efflux mechanisms (2) include overproduction of cell membrane- or wall-associated efflux pumps due to the mutation of regulator proteins. Enoyl reductases have been shown to be specific targets for triclosan in the inhibition of fatty acid biosynthesis, with mutations identified with less affinity for these enzymes (3). Finally, the overproduction of enoyl reductases or other proteins provides greater tolerance of the biocide (4).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.29
FIGURE 8.29

Demonstration of the resistance of glutaraldehyde-resistant strains. The aldehyde antimicrobial activity of a wild-type glutaraldehyde-sensitive strain of was compared to that of a glutaraldehyde-resistant strain. Glutaraldehyde (2%) demonstrated little or no effect against the resistant strain; another aldehyde (0.55% OPA) demonstrated efficacy but required a longer exposure time than for the wild-type strain.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.30
FIGURE 8.30

The simplified structure of a typical mercury resistance operon in gramnegative bacteria. The numbers, types, and control of expression of proteins from the operon can vary from isolate to isolate. In all cases, a mercuric reductase (MerA) is expressed;however, only broad-spectrum plasmids and transposons are found to have MerB homologues (which are enzymes that hydrolyze organomercurial compounds to release the mercuric ion for subsequent reduction). The other proteins expressed are involved in mercury transport and control of the expression of the operon.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.31
FIGURE 8.31

Mechanisms of resistance to mercury.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.32
FIGURE 8.32

pSK41, an example of a multidrug resistance plasmid in staphylococci (not drawn to scale). pSK41 is a 46.4-kb plasmid carrying various genes for its transfer by conjugation (), resistance to antibiotics (gentamycin, tobramycin, and kanamycin by , neomycin by , and bleomycin by ), and a biocide efflux pump (). The plasmid contains sequences from a transposon (Tn) and an integrated plasmid (pUB110).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.33
FIGURE 8.33

Mechanisms of viral resistance to biocides. The typical structure of an enveloped virus is shown as an example (see section 1.3.5). Resistance can be due to indirect factors, like viral clumping and the presence of soils (A), or directly to the structure of the virus particles (B), such as the presence of an envelope and lack of damage to the nucleic acid.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.34
FIGURE 8.34

Mechanisms of resistance of prions to biocides and modes of action of biocides against prions. Prions (hydrophobic protein fibrils) are present in associated macromolecules (including lipids, carbohydrates, and proteins), through which the biocidal process must penetrate. Following penetration, ineffective processes are those that have no effect on proteins, that fix proteins, or that cause prion protein dispersal (potentially leading to cross-contamination). Biocidal processes that denature and/or hydrolyze (or degrade) proteins have been shown to be effective against prions; however, with denaturation alone, renaturation of the protein could occur to produce the reassociated infectious protein form. Further, protein hydrolysis may be partial or complete. In some cases, partial hydrolysis of the protein is ineffective, because smaller components of the protein retain an infectious nature.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.35
FIGURE 8.35

Scanning electron micrograph of an encapsulated strain. The capsule appears as a loose fibrillar network in encapsulated strains. Reprinted from A. Casadevall and J. R. Perfect, (ASM Press, Washington, D. C., 1998), with permission. Micrograph originally supplied by Wendy Cleare (Albert Einstein College of Medicine, Bronx, N. Y.).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.36
FIGURE 8.36

Typical growth of a fungus on a medium surface. Shown are 7-day-old colonies grown on Ueda medium at 28°C in a humid environment. Courtesy of Anna Oller (Central Missouri State University).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.37
FIGURE 8.37

Fungal life cycle (ascomycota). The life cycle shown is typical of ascomycota, such as . In the case of the yeast ascomycetes, including , the single cells reproduce asexually by binary fission or budding and sexually by two cells uniting, leading to the development of ascospores. Similar asexual and sexual spores are formed in other fungi, although in some cases, only asexual conidiospores have been described ( Table 8.33 ).

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.38
FIGURE 8.38

Examples of various types of fungal spores and spore-bearing structures. Zygomycota: a, aseptate hypha; b, zygospore; c, sporangiophore (with spores within sporangia); d, sporangiospores. Basidiomycota: e, basidiomata; f, basidium; g, naked basidiospores; h, hypha with clamp connections. Ascomycota: i, ascomata; j, ascus-containing spores; k, ascospores; l, septate hypha. Deuteromycetes: m, pycnidium; n, conidiophore; o, conidiogenous cells; p, conidia. Oomycota: q, zoospore (motile); r, gametangia; s, oospores. Reprinted from J. Guarro et al., . 454–500,1999, with permission.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.39
FIGURE 8.39

Representation of the structure of a helminth () egg.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.40
FIGURE 8.40

oocysts and sporozoites.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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Image of FIGURE 8.41
FIGURE 8.41

An cyst. Reprinted with permission of the U.S. Armed Forces Institute of Pathology.

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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26. Russell, A. D.,, W. B. Hugo, and, G. A. J. Ayliffe. 1992. Principles and Practice of Disinfection, Preservation & Sterilization, 2nd ed. Blackwell Science, Cambridge, Mass.
27. Schweizer, H. P. 2001. Triclosan: a widely used biocide and its link to antibiotics. FEMS Microbiol. Lett. 202: 17.
28. Springthorpe, V. S., and, S. A. Satter. 1990. Chemical disinfection of virus-contaminated surfaces. Crit. Rev. Environ. Contam. 20: 169229.

Tables

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TABLE 8.1

Examples of intrinsic and acquired mechanisms of resistance to biocides in bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.2

Examples of bacterial responses to environmental stress

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.3

Differences observed in the expression of proteins during the hydrogen peroxide- or superoxide ion-induced oxidative stress response in

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.4

Classification of active-transporter systems

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.5

Examples of bacterial efflux systems that have been shown to extrude biocides and antibiotics

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.6

Protective cell surface structures external to the bacterial cell wall

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.7

Typical bacteria and fungi associated with biofilm formation

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.8

Biofilms and microbial response to antimicrobial agents

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.9

Examples of known extreme resistance to biocides and biocidal processes

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.10

Spore-forming bacteria and their significance

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.11

Sporistatic and sporicidal concentrations of liquid biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.12

Structures, components, and activities of endospores and their vegetative cells

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.13

Examples of revival mechanisms that have been described following biocidal exposure

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.14

Ranges of MICs and MBCs of chlorhexidine and triclosan against and sp. isolates

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.15

MICs of various biocides (determined in test media) for grampositive and gramnegative bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.16

Possible transport mechanisms of some biocides into gramnegative bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.17

Acquired mechanisms of resistance to antimicrobial drugs

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.18

Examples of RND efflux pumps associated with biocide resistance in due to overproduction

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.19

Examples of mutations causing increased sensitivity to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.20

Identified and possible mechanisms of plasmid-encoded resistance to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.21

Examples of acquired (plasmid or transposon) resistance to mercury in bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.22

Examples of plasmid-mediated resistance to silver and copper in bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.23

Plasmid-mediated resistance to various toxic metals in bacteria

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.24

Examples of genes and susceptibilities of strains to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.25

genes and resistance to QACs and other biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.26

Viral classification and response to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.27

Effects of various disinfection and sterilization methods on prions

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.28

Possible mechanisms of fungal resistance to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.29

Comparison of the relative resistances of bacteria and fungi to biocides

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.30

Fungicidal concentrations of biocides for yeasts and molds

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.31

Various cell wall structures of fungi Presence of cell wall component

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.32

Parameters affecting the response of to chlorhexidine

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.33

Examples of spores produced by fungi

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8
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TABLE 8.34

Minimum amoebicidal concentrations for trophozoites and cysts

Citation: McDonnell G. 2007. Mechanisms of Microbial Resistance, p 253-334. In Antisepsis, Disinfection, and Sterilization. ASM Press, Washington, DC. doi: 10.1128/9781555816445.ch8

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