Demonstration of synergy with fluconazole and either ibuprofen, sodium salicylate, or propylparaben against Candida albicans in vitro

Scott, Eileen; Tariq, Vicki; McCrory, Roisin M.

doi:10.1128/aac.39.12.2610

Cited by 60 publications

(49 citation statements)

References 11 publications

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“…In the current investigation, combining ibuprofen with either nikkomycin Z or econazole produced an antifungal effect which was significantly greater than that obtained with each compound on its own (i.e., it resulted in synergism), while combining it with amphotericin B resulted in additivity. These results support observations by Scott et al (13), who reported synergistic interactions between ibuprofen and the azoles miconazole and fluconazole against C. albicans NCYC 610 by the checkerboard titration method. Combining ibuprofen with an antifungal drug may not only result in increased antifungal efficacy, but the recognized anti-inflammatory properties of ibuprofen could also prove to be clinically useful in the topical treatment of candidiasis and other fungal The results presented here indicate that the DAA is a useful method for initial assessments of the interactions between antifungal compounds, since it provides a more complete description of the interactions detected.…”

Section: Discussionsupporting

confidence: 82%

Use of decimal assay for additivity to demonstrate synergy in pair combinations of econazole, nikkomycin Z, and ibuprofen against Candida albicans in vitro

Tariq

Scott

McCain

1995

Antimicrob Agents Chemother

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Interactions between six compounds (econazole, miconazole, amphotericin B, nystatin, nikkomycin Z, and ibuprofen) were investigated for their antifungal activities against Candida albicans by using pair combinations in an in vitro decimal assay for additivity based on disk diffusion. Additive interactions were observed between miconazole and econazole, amphotericin B and nystatin, and amphotericin B and ibuprofen, while an antagonistic interaction was observed between econazole and amphotericin B. Synergistic interactions were recorded for the combinations of econazole and ibuprofen, econazole and nikkomycin Z, and ibuprofen and nikkomycin Z.Candida albicans is an opportunistic fungal pathogen responsible for causing candidiasis in individuals with an underlying pathological process or deficiency state. Increases in the numbers of immunocompromised individuals have resulted in concomitant increases in the occurrence of Candida infections (9). For more than two decades the fungicidal polyene compounds, such as amphotericin B and nystatin, provided the most effective treatment of candidiasis, despite their potential toxicity to humans. More recently, the azole antifungal compounds have emerged as the principal drugs used in the treatment of candidiasis, although their activities are fungistatic rather than fungicidal (2). Improvements in the efficacy of antifungal drug therapy and reductions in toxicity may be achieved by using combinations of drugs. To date there have been few investigations of the interactions between antifungal agents (1,3,4,(6)(7)(8).One of the limitations to such studies on the evaluation of antifungal activity has been the lack of an adequate in vitro methodology capable of yielding reproducible results. Sanders et al. (11) pointed out the inherent methodologic limitations of the two most widely used methods for assessing drug interactions, namely, the time-kill technique and the checkerboard titration, and went on to describe a new in vitro test for antibacterial agents designed to avoid many of the problems previously described (11). This new test, the decimal assay for additivity (DAA), was based on the disk diffusion assay and was designed to have a precisely defined endpoint for additivity so that interactions greater or less than additivity (i.e., synergism or antagonism, respectively) could be accurately identified. The DAA involves initially performing disk diffusion assays with each antibiotic on its own over a range of drug masses in order to obtain a standard dose-response curve. A target zone of inhibition for each drug combination, representing a zone in the midrange of the standard curve for each drug, is selected so that increases or decreases in zones of inhibition resulting from drug interactions can be reliably detected. The mass of each drug on its own required to produce this target zone (i.e., the biologic equivalence factor [BEF]) is calculated by using the linear regression equation for the standard doseresponse curve. Once the two BEFs for a combination of a pair of d...

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Section: Discussionsupporting

confidence: 82%

Use of decimal assay for additivity to demonstrate synergy in pair combinations of econazole, nikkomycin Z, and ibuprofen against Candida albicans in vitro

Tariq

Scott

McCain

1995

Antimicrob Agents Chemother

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“…The increase of antifungal resistance increase the need for new antifungals. Many studies showed that NSAID showed activity against Candida [37,38,39] that led us to undergo this study on the activity of three non-steroidal antiinflammatory drugs on C. albicans and 2 non-albicans strains…”

Section: Discussionmentioning

confidence: 99%

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of <i>Candida spp</i><i>.</i>

Ashraf¹,

Yousri²,

Taha³

et al. 2015

AJMR

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Candida spp. are the most common cause of fungal diseases and the fourth commonest cause of nosocomial invasive infections which are considered in many cases as life threatening. Among Candida spp., C. albicans is the most common cause of many fungal diseases, but non-albicans spp. infections are in increase. Nonsteroidal anti-inflammatory drugs have previously been shown to have antifungal activity. In this study we determine the antifungal activity of the tested NSAIDs using agar well diffusion method, their effect on the dimorphic transition of C. albicans by testing their ability to form germ tube in the presence of human serum. Determining the effect of NSAIDs on the adherence to plastic surfaces and on the mature biofilms formed by the tested Candida spp.. The results indicated that Sodium Diclofenac showed lower MIC against C. albicans and C. glabrata while Ibuprofen had lower MIC against C. krusei. upon examining the effect of Diclofenac sodium, Ibuprofen and ketoprofen on biofilm formed on polyurethane segments by Scanning electron microscope (SEM), a damage to membranes of the tested species was observed. Sodium Diclofenac showed the highest inhibitory effect on the adherence (51.1-76.9% at MIC and 56.6-83.3% at 2XMIC) of C. albicans and C. glabrata but Ibuprofen showed a higher inhibitory effect against the adherence of C. krusei. For mature biofilms, the highest disruptive effect on mature biofilms formed by all tested Candida Spp. .06% at 2XMIC) was observed by Diclofenac sodium. Sodium Diclofenac inhibited dimorphic transition of C. albicans but a decrease in germ tube formation was shown by others. In conclusion, the tested drugs showed antifungal, anti-adherent and antibiofilm activity that make them useful in the treatment of fungal infection and the prevention of biofilm formation on the surface of medical devices.

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“…Perhaps this is because echinocandins are typically fungicidal and have potent activity against most Candida species when administered alone. Other agents with limited antifungal activity on their own, including metronidazole (52), fluvastatin and pravastatin (41,136), nonsteroidal antiinflammatory agents (155,188,224), and quinolones (135), have been studied in combination with amphotericin B or triazoles, with a suggestion of positive effects occurring in all cases. The results of a recent report also suggested that when combined with fluconazole, terbinafine, or caspofungin, combinations of calcineurin inhibitors such as cyclosporine A and tacrolimus are highly synergistic for fungicidal effects (142).…”

Section: (D) Other Combinationsmentioning

confidence: 99%

Combination Antifungal Therapy

Johnson

MacDougall

Ostrosky-Zeichner

et al. 2004

Antimicrob Agents Chemother

485

368

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5 RATIONALEThe availability of new antifungal agents with novel mechanisms of action has stimulated renewed interest in combination antifungal therapies. In particular, and despite the limited clinical data, the high mortality of mold infections and the relatively limited efficacy of current agents have produced significant interest in polyene-, extended-spectrum azole-, and echinocandin-based combinations for these difficult-to-treat infections. With the recent publication of the first large randomized trial of antifungal combination therapy to be conducted in two decades (166) and the rapid proliferation of new in vitro and in vivo data on antifungal combinations, we have sought to review the recent work and future challenges in this area.The focus of this review is on the efficacy of antifungal drugs in combination with respect to the extent or rate of killing of the fungal pathogen, although other potential interactions (such as pharmacokinetic drug interactions) can impact efficacy when these agents are used together. The value of giving two drugs because each is separately effective against a group of organisms exhibiting a variety of types of resistance is not specifically discussed, but this also is an obvious and straightforward reason to use a combination of agents.It cannot be simply assumed that the use of two or more effective drugs with different mechanisms of action will produce an improved outcome compared to the results seen with a single agent. Combination antifungal therapy could reduce antifungal killing and clinical efficacy, increase potential for drug interactions and drug toxicities, and carry a much higher cost for antifungal drug expenditures without proven clinical benefit (106). Thus, it is important to critically evaluate the role of combination therapy as new data become available.Conceptual models and terminology. Methods for studying antifungal combinations in vitro and in vivo have differed considerably over time and among investigators. These tools do not differ with respect to their application to combination antibacterial or antiviral therapies and have been discussed extensively and elegantly in the landmark 1995 review by Greco (79). In brief, all approaches to evaluating combinations can be reduced to two elements: (i) a conceptual model for predicting the expected result for a combination and (ii) a set of phrases used to categorize results that are better than expected, worse than expected, or as expected. Although many subtle variations are possible, the underlying mathematical model is based on either the assumption of additive interactions or the assumption of probabilistic (multiplicative) interactions. On the basis of the terminology employed by the author who first carefully described each of these models, the two models can be usefully referred to as the Loewe additivity model and the Bliss independence model (79).The terminology used to place results into interpretive categories is often the subject of debate and confusion. Greco et al. (79) have proposed a set ...

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Demonstration of synergy with fluconazole and either ibuprofen, sodium salicylate, or propylparaben against Candida albicans in vitro

Cited by 60 publications

References 11 publications

Use of decimal assay for additivity to demonstrate synergy in pair combinations of econazole, nikkomycin Z, and ibuprofen against Candida albicans in vitro

Use of decimal assay for additivity to demonstrate synergy in pair combinations of econazole, nikkomycin Z, and ibuprofen against Candida albicans in vitro

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of <i>Candida spp</i><i>.</i>

Combination Antifungal Therapy

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