Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Anton C. de Groot in Monographs in Contact Allergy, 2021
Naftifine is a synthetic allylamine derivate with broad-spectrum antifungal activity. It can be fungicidal or fungistatic depending on the concentration and the organisms involved. Naftifine is indicated for the topical treatment of tinea pedis, tinea cruris, and tinea corporis caused by the organisms Trichophyton rubrum, Trichophyton mentagrophytes, Trichophyton tonsurans and Epidermophyton floccosum. Naftifine is also effective against gram-negative and gram-products, positive bacteria and has anti-inflammatory activity by targeting the prostaglandin pathway. In pharmaceutical naftifine is employed as naftifine hydrochloride (CAS number 65473-14-5, EC number not available, molecular formula C21H22ClN) (1).
Use of Essential Oils in Agriculture
K. Hüsnü Can Başer, Gerhard Buchbauer in Handbook of Essential Oils, 2020
Cymbopogon citratus (Poaceae) was able to kill Aspergillus flavus, a fungus that can produce very toxic aflatoxins and harms stored products, to 100%. It has to be applied at about 1000 ppm to inhibit Aspergillus flavus. Besides A. flavus, it has the ability to kill many other fungi, as well, for about 210 days in storage. The EO of Cymbopogon citratus, especially if it was produced between May and November, also appeared to be more successful in fighting fungi than several synthetic products (Mishra et al., 1994). Lemongrass EO also showed activity against colony development of Cladosporium herbarum and Rhizopus stolonifer. A concentration of 500 ppm was lethal for Colletotrichum coccodes, Cladosporium herbarum, Rhizopus stolonifera, and Aspergillus niger. The fungal colony growth of Botrytis cinerea was only inhibited up to 60%. The fungal spore production could be inhibited in all five fungi (Tzortzakis et al., 2007). Lemongrass EO can also be used against A. flavus in parboiled rice. It causes fungistatic and fungicidal effects (Paraganama et al., 2003).
Antifungal Drugs and Susceptibility Testing of Fungi
Rossana de Aguiar Cordeiro in Pocket Guide to Mycological Diagnosis, 2019
The azole derivatives encompass compounds with both imidazole and triazole moieties. They are the most widely used class of antifungal in clinical practice, due to their safety and availability in both oral and intravenous formulations. These drugs interfere with ergosterol synthesis by blocking the enzyme 14-α-demetilase present in the P-450 cytochrome of the fungal cell, hampering lanosterol demethylation into ergosterol. This interference results in ergosterol depletion and the accumulation of toxic sterol intermediates, which stops cellular growth and division and induces severe membrane stress. Most of the antifungal imidazoles are formulated for topical use, as they are more toxic and less bioavailable, limiting their systemic use. On the other hand, triazoles, which include fluconazole, itraconazole, voriconazole, posaconazole, ravuconazole, and isavuconazole, are licensed for the treatment of invasive fungal diseases. The azoles are mostly fungistatic, with the exception of the fungicidal activity of itraconazole and voriconazole against some species of filamentous fungi, such as A. fumigatus (Table 2.1).
Lactobacillus casei reduces the extracellular matrix components of fluconazole-susceptible Candida albicans biofilms
Published in Biofouling, 2021
Beatriz H. D. Panariello, Marlise Inez Klein, Luana Mendonça Dias, Amanda Bellini, Vitoria Bonan Costa, Paula Aboud Barbugli, Ana Claudia Pavarina
The antifungal effect of probiotic bacteria, focusing on Lactobacillus spp., has been evaluated in vitro using standard biofilm assays, solid medium agar diffusion, and microscopy (Verdenelli et al. 2014; Chew et al. 2015; Vilela et al. 2015). The fungicidal or fungistatic effects underlying probiotics may involve the production of secondary metabolites with antimicrobial activity (Zakaria Gomaa 2013; Ceresa et al. 2015). Furthermore, the fungistatic effect is also affected by adhesion sites, stimulation of the immune system, and competition for nutrients (Servin and Coconnier 2003; Fidan et al. 2009). Other studies have also shown that probiotic bacteria can suppress the formation of C. albicans biofilms on various surfaces, such as silicon and biomaterials (Orsi et al. 2014; Ceresa et al. 2015). The inhibitory effects of cells and supernatants of probiotic Lactobacillus species (L. rhamnosus LR32, L. acidophilus NCFM, and L. casei) at different stages of the development of the C. albicans biofilm involved cell-cell interactions and secretion of exometabolites that may affect pathogenic attributes associated with colonization of C. albicans on host surfaces and yeast filamentation. However, no studies have characterized the extracellular matrix of the mixed biofilm of these microorganisms.
Azole resistance in Aspergillus species: promising therapeutic options
Published in Expert Opinion on Pharmacotherapy, 2021
Shirisha Pasula, Pranatharthi H. Chandrasekar
It is a first-in-class agent (antifungal terpenoid) wielding a familiar mechanism of action. Like echinocandins, it inhibits 1,3-β-d-glucan synthesis to achieve antifungal effect. However, as a triterpenoid enfumafungin derivative, ibrexafungerp is structurally unique from the echinocandin class. Ibrexafungerp is highly bioavailable and can be administered as either an oral or intravenous formulation. It maintains activity against many species of Candida and Aspergillus [54]. In vitro studies have identified fungistatic activity against many Aspergillus species, including azole-resistant strains [55]. SCY-078 minimum effective concentrations₉₀ were 4-fold lower than minimum inhibitory concentrations₉₀ of voriconazole suggesting former drug might be effective as monotherapy against azole-resistant Aspergillus strains [55]. It has shown synergistic activity with an azole in vitro and in vivo neutropenic rabbit model with improved survival, mainly in wild type isolates [56]. It has been shown to be synergistic invitro when combined with amphotericin B in cyp51 mutant A. fumigatus [55]. Combination therapy of SCY-078 with an azole or amphotericin B showed no antagonism [55]. Ibrexafungerp is currently in phase II clinical trial to evaluate the safety and the efficacy of coadministration of SCY-078 with a mold-active azole (voriconazole) compared to voriconazole alone in patients with invasive pulmonary aspergillosis (NCT03672292).
Oral Ibrexafungerp: an investigational agent for the treatment of vulvovaginal candidiasis
Published in Expert Opinion on Investigational Drugs, 2020
Nkechi Azie, David Angulo, Barbara Dehn, Jack D. Sobel
Azoles, which are notably fungistatic against Candida spp [11]., are the standard of care for treatment of VVC with response rates of 55% to 80% in various studies depending on endpoints [12,13], although 44% of women experience a recurrence. Current treatment guidelines for VVC recommend a short course of topical azoles for acute uncomplicated episodes or a single 150 mg dose of oral fluconazole for nonpregnant women [3,14]. Topical azoles may provide more immediate relief because of local effect and are available as over-the-counter products, however, some patients experience hypersensitivity to topical azoles with local itching or burning. Oral fluconazole may cause systemic gastrointestinal (GI) adverse effects, but is generally well-tolerated. During pregnancy, however, only topical azoles are recommended for up to 7 days because of the risk of miscarriage or fetal malformations with oral fluconazole [3,14]. For women with rVVC, treatment recommendations are for oral fluconazole 150 mg every 3 days for three doses, then one dose weekly for 6 months [3,14,15]. While several maintenance regimens of fluconazole are effective in controlling symptomatic episodes of VVC, these long-term regimens are rarely curative, with high rates of recurrence following cessation of therapy [16]. In addition, emergence of azole resistance C. albicans results in refractory unresponsive symptomatic VVC. The success of fluconazole in managing VVC due to C. albicans is not replicated in treating patients with non-albicans Candida spp., especially C. glabrata commonly identified in complicated VVC [17,18].