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Category: Environmental Microbiology; Microbial Genetics and Molecular Biology
Biofilm Antimicrobial Resistance, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817718/9781555818944_Chap14-1.gif /docserver/preview/fulltext/10.1128/9781555817718/9781555818944_Chap14-2.gifAbstract:
This chapter describes the phenomenon of biofilm-reduced susceptibility to antimicrobial agents, discusses factors that influence biofilm tolerance, and outlines possible protective mechanisms. Microorganisms that band together in biofilms are protected from killing by biocides, disinfectants, and antibiotics. The phenomenon of biofilm resistance to drugs and antimicrobials is easily reproduced in the laboratory. The antimicrobial agents range from brute-force oxidants, such as chlorine, to antibiotics with exquisitely specific cellular targets. The microorganisms range from bacteria to yeast and from obligate aerobes to sulfate reducing bacteria and other finicky anaerobes. When microorganisms are dispersed from a biofilm, their antimicrobial susceptibility is usually rapidly restored. Fungal biofilms are commonly encountered in cases of invasive catheter-related infections as well as superficial infections like denture stomatitis. Biofilm susceptibility is influenced significantly by such factors as biofilm thickness, biofilm age, biofilm areal cell density, antimicrobial dose concentration, biofilm species composition, and genotype. In bacterial biofilms, it has been suggested that the thick extracellular matrix (ECM) may contribute to antimicrobial resistance by preventing the diffusion of drugs to target cells. The cellular target of fluconazole in Candida albicans is a cytochrome P-450 hemoprotein involved in the ergosterol biosynthetic pathway. Microorganisms are equipped with numerous genetic and biochemical systems for responding to environmental stresses. Reduced antimicrobial susceptibility of microorganisms in biofilms is thought to be due to a combination of antimicrobial depletion through reactions with biofilm constituents, poor antimicrobial penetration, slow growth or stationary-phase existence in the biofilm, adaptive stress responses, and the formation of protected persister cells.
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Comparison of biofilm (●) and planktonic (○) killing by antimicrobial agents. (A) S. epidermidis challenged with 0.1 μg of rifampin per ml (from Zheng and Stewart, 2002 ). (B) P. aeruginosa challenged with 50 mg of glutaraldehyde per liter (reprinted from Grobe et al., 2002, with permission from Springer Verlag ). (C) P. aeruginosa challenged with 10 μg of tobramycin per ml (from Walters et al., 2003 ).
Comparison of biofilm (●) and planktonic (○) killing by antimicrobial agents. (A) S. epidermidis challenged with 0.1 μg of rifampin per ml (from Zheng and Stewart, 2002 ). (B) P. aeruginosa challenged with 50 mg of glutaraldehyde per liter (reprinted from Grobe et al., 2002, with permission from Springer Verlag ). (C) P. aeruginosa challenged with 10 μg of tobramycin per ml (from Walters et al., 2003 ).
Correlation of biofilm development and metabolic activity with antifungal resistance Antifungal susceptibility of C. albicans at different stages of biofilm development against FLU (A), AMB (B), NYT (C), CHX (D), respectively, are represented as histograms. The line curves show percent metabolic activity of growing C. albicans biofilms exposed to FLU (64 μg/ml), AMB (4 μg/ml), NYT (8 μg/ml) or CHX (64 μg/ml). Metabolic activity was normalized to the control without drugs, which was taken as 100%. Redrawn with permission from Journal of Bacteriology ( Chandra et al., 2001a ).
Correlation of biofilm development and metabolic activity with antifungal resistance Antifungal susceptibility of C. albicans at different stages of biofilm development against FLU (A), AMB (B), NYT (C), CHX (D), respectively, are represented as histograms. The line curves show percent metabolic activity of growing C. albicans biofilms exposed to FLU (64 μg/ml), AMB (4 μg/ml), NYT (8 μg/ml) or CHX (64 μg/ml). Metabolic activity was normalized to the control without drugs, which was taken as 100%. Redrawn with permission from Journal of Bacteriology ( Chandra et al., 2001a ).
Effect of amphotericin B (a), flucytosine (b), and fluconazole (c) on C. albicans biofilms grown statically (●) or with gentle shaking (○). [3H]Leucine incorporation by biofilms was determined as a percentage of that for control biofilms incubated in the absence of the antifungal agent. Redrawn from Baillie and Douglas, 2000, by permission of Oxford University Press.
Effect of amphotericin B (a), flucytosine (b), and fluconazole (c) on C. albicans biofilms grown statically (●) or with gentle shaking (○). [3H]Leucine incorporation by biofilms was determined as a percentage of that for control biofilms incubated in the absence of the antifungal agent. Redrawn from Baillie and Douglas, 2000, by permission of Oxford University Press.
Effect of amphotericin B on C. albicans biofilms grown statically (a) or with shaking (b) on PVC discs cut from Faucher tubes (Vygon) (●) or vena cava catheters ( Jostra) (○). [3H]Leucine incorporation by biofilms was determined as a percentage of that for control biofilms incubated in the absence of the antifungal agent. Redrawn from Baillie and Douglas, 2000, by permission from Oxford University Press.
Effect of amphotericin B on C. albicans biofilms grown statically (a) or with shaking (b) on PVC discs cut from Faucher tubes (Vygon) (●) or vena cava catheters ( Jostra) (○). [3H]Leucine incorporation by biofilms was determined as a percentage of that for control biofilms incubated in the absence of the antifungal agent. Redrawn from Baillie and Douglas, 2000, by permission from Oxford University Press.
Variations of sterol profile of C. albicans biofilm at different developmental phases. Sterol pattern for biofilms grown to early (A), intermediate (B), or mature (C) phases were determined by gas-liquid chromatography. (D) Percentage levels of sterols identified in C. albicans biofilms and planktonic cells (chromatograph not shown), determined from the corresponding peak areas and retention times relative to ergosterol. Peaks 1 to 7 (panels A to C) represent sterols described in panel D. Redrawn with permission from Infection and Immunity ( Mukherjee et al., 2003 ).
Variations of sterol profile of C. albicans biofilm at different developmental phases. Sterol pattern for biofilms grown to early (A), intermediate (B), or mature (C) phases were determined by gas-liquid chromatography. (D) Percentage levels of sterols identified in C. albicans biofilms and planktonic cells (chromatograph not shown), determined from the corresponding peak areas and retention times relative to ergosterol. Peaks 1 to 7 (panels A to C) represent sterols described in panel D. Redrawn with permission from Infection and Immunity ( Mukherjee et al., 2003 ).
Chlorine concentration profiles in a mixed species biofilm. Chlorine at a concentration of approximately 2.5 mg/liter was flowed continuously over a biofilm, which was probed with a chlorinesensitive microelectrode. At 10 min (●), 30 min (○), and 105 min (■) of exposure, chlorine penetrated only into the surface layers of the biofilm. Redrawn with permission from Applied and Environmental Microbiology ( de Beer et al., 1994a ).
Chlorine concentration profiles in a mixed species biofilm. Chlorine at a concentration of approximately 2.5 mg/liter was flowed continuously over a biofilm, which was probed with a chlorinesensitive microelectrode. At 10 min (●), 30 min (○), and 105 min (■) of exposure, chlorine penetrated only into the surface layers of the biofilm. Redrawn with permission from Applied and Environmental Microbiology ( de Beer et al., 1994a ).
Induction of catalase in biofilms (●) and planktonic cells (○) of P. aeruginosa in response to hydrogen peroxide treatment. Biofilm cells are able to express this stress response while planktonic cells are not able to respond to the same challenge. Biofilm cells that are not exposed to hydrogen peroxide show no change in activity (■). Redrawn with permission from Applied and Environmental Microbiology ( Elkins et al., 1999 ).
Induction of catalase in biofilms (●) and planktonic cells (○) of P. aeruginosa in response to hydrogen peroxide treatment. Biofilm cells are able to express this stress response while planktonic cells are not able to respond to the same challenge. Biofilm cells that are not exposed to hydrogen peroxide show no change in activity (■). Redrawn with permission from Applied and Environmental Microbiology ( Elkins et al., 1999 ).
Microorganisms shown to exhibit reduced antimicrobial susceptibility in biofilms
Microorganisms shown to exhibit reduced antimicrobial susceptibility in biofilms
Antimicrobial agents shown to exhibit reduced efficacy against microorganisms in biofilms
Antimicrobial agents shown to exhibit reduced efficacy against microorganisms in biofilms
MICs (iAg/ml) of antifungal agents against biofilms formed by Candida albicans
MICs (iAg/ml) of antifungal agents against biofilms formed by Candida albicans