Vulvovaginal candidiasis (VVC) is the second most common cause of vaginitis after bacterial vaginosis and affects millions of women globally every year. VVC is most commonly caused by Candida albicans, followed by other species of Candida such as C. glabrata and C. parapsilosis. In a recent study, out of 100 clinical isolates of Candida spp. obtained from patients with VVC, 84 were identified as C. albicans. The remaining isolates were non-albicans Candida strains. A large number of the C. albicans strains produced phospholipases and proteinases while esterases and hemolysins were produced by a minority of these strains. Only a few of the non-C. albicans strains produced these proteins. Almost all the isolates formed biofilms. Butoconazole, clotrimazole, and fluconazole were found to be active against C. albicans and less active against the non-albicans Candida strains. The MIC90 of amphotericin B and nystatin were 2 and 4 μg/ml, respectively, against either C. albicans or non-albicans Candida spp. Representative ceragenins (CSA-13, CSA-131, and CSA-138), developed as mimics of endogenous antimicrobial peptides, were shown to be active against fluconazole-resistant strains, both alone and in combination with fluconazole. The results of this study thus suggest the potential use of ceragenins in treating VVC, including infections caused by fluconazole-resistant isolates. The findings of the study are published online in Medical Mycology.