Antimicrobial and antibiofilm efficacy of triclosan and DispersinB(R) combination

Darouiche, Rabih O.; Mansouri, Mohammad D.; Gawande, Purushottam V.; Madhyastha, Srinivasa

doi:10.1093/jac/dkp158

Cited by 190 publications

(131 citation statements)

References 20 publications

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“…An in vivo model using a medical-grade silicone elastomer with an NO-storing film implanted in rats led to a reduction in bacterial colonization after S. aureus challenge (see below for the effects of NO on dispersal) (270). Other vascular catheter coatings have been studied, such as the association of triclosan (an antiseptic) and dispersin B (an antibiofilm enzyme) (see below) to prevent S. aureus colonization in vitro and in vivo (271). Triclosan-loaded urinary catheters have also been studied successfully in vivo for the prevention of Proteus mirabilis CAUTI (272).…”

Section: Targeting Biofilm Recalcitrance: Progress and Perspectivesmentioning

confidence: 99%

Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics

Lebeaux

Ghigo

Beloin

2014

Microbiol Mol Biol Rev

998

862

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International audienceSurface-associated microbial communities, called biofilms, are present in all environments. Although biofilms play an important positive role in a variety of ecosystems, they also have many negative effects, including biofilm-related infections in medical settings. The ability of pathogenic biofilms to survive in the presence of high concentrations of antibiotics is called "recalcitrance" and is a characteristic property of the biofilm lifestyle, leading to treatment failure and infection recurrence. This review presents our current understanding of the molecular mechanisms of biofilm recalcitrance toward antibiotics and describes how recent progress has improved our capacity to design original and efficient strategies to prevent or eradicate biofilm-related infections

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Section: Targeting Biofilm Recalcitrance: Progress and Perspectivesmentioning

confidence: 99%

Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics

Lebeaux

Ghigo

Beloin

2014

Microbiol Mol Biol Rev

998

862

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“…The halo diameters produced by the combination were predominantly larger than ones produced by single-drug treatments. The sizes of the inhibition zones increased to 19.2, 18, 15.6, and 10.8 mm when 16 g/ml fluconazole was combined with 16,8,4, and 2 g/ml of triclosan, respectively.…”

mentioning

confidence: 98%

“…However, the increase in azole use has precipitated a rise in drug resistance in clinical isolates. Triclosan, a chlorinated aromatic compound, has antimicrobial (4,8,20), antiparasitic (26), and anti-inflammatory (1,24) activities. It has been used in personal care products (2).…”

mentioning

confidence: 99%

In Vitro Interaction between Fluconazole and Triclosan against Clinical Isolates of Fluconazole-Resistant Candida albicans Determined by Different Methods

Ling

Deng

et al. 2011

Antimicrob Agents Chemother

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The in vitro interaction between triclosan and fluconazole against 24 azole-resistant clinical isolates of Candida albicans was evaluated by the microdilution checkerboard technique. The synergisms were verified by time-killing curves and agar diffusion tests in selected strains. Antagonistic activity was not detected.Candida albicans is the primary cause of opportunistic fungal disease in humans. It is predominantly found at low levels among the normal oral flora but can thrive in immunocompromised individuals (16,25). Fluconazole has been used successfully as a prophylactic and a first-line therapeutic antifungal agent (5,6,19). However, the increase in azole use has precipitated a rise in drug resistance in clinical isolates. Triclosan, a chlorinated aromatic compound, has antimicrobial (4,8,20), antiparasitic (26), and anti-inflammatory (1, 24) activities. It has been used in personal care products (2). Combination therapy can improve the efficacy of antimicrobial therapy for infections recalcitrant to most treatments. Therefore, we aimed to assess the presence of combination effects with triclosan and fluconazole in C. albicans.A total of 24 clinical isolates of fluconazole-resistant C. albicans were used in this study, and C. albicans ATCC 10231, C. parapsilosis ATCC 90018, and C. krusei ATCC 6258 were used as quality controls. The drugs were purchased from Sigma (Sigma-Aldrich).The drug MICs were determined by broth microdilution according to CLSI method M27-A (3) with an inoculum of 2.5 ϫ 10 3 CFU/ml. The plates were incubated at 35°C, and the optical density (OD) value was determined at 492 nm after 48 h, a modification to the CLSI reference method. All experiments were conducted in triplicate, and the median MIC-1 endpoint value, which represents an 80% reduction in turbidity, and MIC-2 endpoint value, which represents a 50% reduction in turbidity, were calculated (3). The drug interactions were analyzed using the fractional inhibitory concentration index (FICI) and ⌬E models based on the Loewe additivity and Bliss independence theories, respectively (14, 21). The FICIs were defined as the sum of the MICs of each drug used in the combination divided by the MIC of the drug used alone. Synergy and antagonism were defined by FICIs of Յ0.5 and Ͼ4, respectively (15). The ⌬E model was calculated as the sums of the percentages of all statistically significant (SS) synergistic (ΑSYN) and antagonistic (ΑANT) interactions. Interactions that were Ͻ100% and Ͼ200% SS interactions were considered weak and strong, respectively. Interactions that were 100 to 200% SS interactions were considered moderate (14). The numbers of SS synergistic and antagonistic combinations were calculated for each strain.A 100-l sample of 10 6 CFU/ml C. albicans YL345, which exhibited the best synergistic effect, was spread onto a yeast extract-peptone-dextrose agar surface. Subsequently, 6-mmdiameter paper disks, impregnated with drugs or dimethyl sulfoxide (DMSO) alone, were placed onto the surface. The inhibition zones were measured usi...

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“…For example, several investigators are examining the antibiofilm activities of combining antibiotics or biocides with biofilm-specific agents that primarily target the extracellular matrix of biofilms, such as N-acetylcysteine (21), protamine sulfate (13), and dispersin B (12). In addition, the utility of coatings containing biological agents, such as bacteriophages, in preventing biofilm formation on medical devices has been investigated (11).…”

mentioning

confidence: 99%

Aryl Rhodanines Specifically Inhibit Staphylococcal and Enterococcal Biofilm Formation

Opperman

Kwasny

Williams

et al. 2009

Antimicrob Agents Chemother

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Staphylococcus epidermidis and Staphylococcus aureus are the leading causative agents of indwelling medical device infections because of their ability to form biofilms on artificial surfaces. Here we describe the antibiofilm activity of a class of small molecules, the aryl rhodanines, which specifically inhibit biofilm formation of S. aureus, S. epidermidis, Enterococcus faecalis, E. faecium, and E. gallinarum but not the gram-negative species Pseudomonas aeruginosa or Escherichia coli. The aryl rhodanines do not exhibit antibacterial activity against any of the bacterial strains tested and are not cytotoxic against HeLa cells. Preliminary mechanism-of-action studies revealed that the aryl rhodanines specifically inhibit the early stages of biofilm development by preventing attachment of the bacteria to surfaces.Indwelling medical devices have become integral components of modern health care. The surfaces of these devices can be colonized by bacterial pathogens that are capable of forming biofilms. Resulting biofilms frequently compromise the function of the device or cause serious systemic infections. These device-related infections are often very difficult to eradicate with conventional antibiotics, as bacteria and fungi growing in the biofilm mode of growth are extremely resistant to antibiotics, biocides, and attack from the immune system (9). Consequently, device-related infections result in increased patient morbidity, mortality, and health care costs (7,46).Because device colonization precedes device-related infections, several approaches have been used to prevent biofilm colonization of indwelling devices, such as central venous catheters. These include the implementation of stringent infection control measures by health care workers during the insertion and maintenance of vascular access devices. Such measures have been shown to decrease the incidence of catheter-related bloodstream infections when there is strict compliance with established protocols (38). Alternatively, medical devices coated with antimicrobial compounds have been tested for prevention of bacterial colonization. Central venous catheters impregnated with a combination of antibacterial agents (rifampin [rifampicin] and minocycline) or coated with a combination of antiseptics (chlorhexidine and silver sulfadiazine) have been shown to be effective in reducing catheter colonization and catheter-related bloodstream infections in clinical studies (reviewed in reference 45). However, there are lingering concerns related to the use of antiseptics and antibiotics as coatings for medical devices. For example, it is possible that the use of antibiotic-impregnated catheters could lead to increases in the occurrence of strains resistant to antimicrobial agents. While increased resistance to antibiotics used as catheter coatings has not been detected in several in vitro and in vivo studies (14,27,32,45), evidence suggests that rifampinminocycline-impregnated catheters are more susceptible to colonization when challenged with a rifampin-resistant str...

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Antimicrobial and antibiofilm efficacy of triclosan and DispersinB(R) combination

Cited by 190 publications

References 20 publications

Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics

Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics

In Vitro Interaction between Fluconazole and Triclosan against Clinical Isolates of Fluconazole-Resistant Candida albicans Determined by Different Methods

Aryl Rhodanines Specifically Inhibit Staphylococcal and Enterococcal Biofilm Formation

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