INTRODUCTION
The incidence of Candida infections has increased substantially in recent years in HIV, cancer, and immunosuppressive patients. Patients undergoing radio chemotherapy in oncology malignancies, HIV, onchomycosis, diabetic feet, and organ transplantation (kidney, bone marrow) may often manifest opportunistic superficial Candida infections. During impairment of innate defense, these infections may turn pathogenic and life threatening. Therefore, early therapeutic intervention is required. A series of azole derivatives are used topically in basic clinical practice to control infection caused by yeasts, dermatophytes, and Malassezia furfur.1 Superficial candidiasis affects the skin and nails and is caused by Candida albicans, which has a unique ability to grow in a variety of morphological forms, ie, yeast-like, hyphae, pseudohyphae, and chlamydospores (Figure 1).2,3 Candida has the ability to digest keratin present in the skin and its appendages, which may trigger an inflammatory host response.4 The molecules found in fungal cells that are mainly responsible for adhesion are called adhesins, which include Als1p-Als7p and Asl9p, Hwp1p, Int1p, Mnt1p, etc. Once the pathogen adheres to the host cell, it propagates and colonizes on the skin and penetrates deeper inside the body.5 Recently, several reports have indicated the emergence of resistance of this opportunistic fungal pathogen. Mutations and over expression in the gene ERG11 that encodes lanosterol 14α-demethylase can affect the binding of drugs to this enzyme, resulting in the increased drug resistance of the cells.6 Furthermore, drug resistance is mediated by two types of efflux pumps, ATP-binding cassette transporters and major facilitators.7 In healthy human beings, Candida infections are due to impaired epithelial barrier functions and occur most
commonly in the elderly and infants. Candidiasis of the skin can occur anywhere on the skin, but it is most likely to occur on areas where the skin is folded, eg, armpits, groin, between fingers, and under breasts. The skin infection can progress to cause cracking, soreness, blisters, and formation of pustules. Candida albicans possess the virulent hydrolytic enzymes aspartyl proteinase and phopholipases, which are released in the body during infection and cause host cell damage. The spectrum of infection may manifest in acute, chronic, or disseminated forms.8 Clinical variants of acute mucocutaneous candidiasis include erosiointerdigitalis blastomycetica, characterized by erythematous patches (thin plaques with peripheral macules and papules) often termed as satellite lesions. In cutaneous candidiasis, the majority of the mycelia and spores are situated inside the cells of the stratum corneum and many are parakeratotic. Candida commonly causes onycholysis but distinguishes itself histologically from the dermatophytes by its lack of nail plate invasion. Yeast forms may be seen along the undersurface of the nail plate.9 Candida also cause psoriasiform changes and inflammatory response as caused by dermatophytes. The pseudo hyphae of Candida are generally thick, bulbous, and irregular in appearance compared to the smooth, thin, and regular hyphae of dermatophytes.10
Miconazole is a broad-spectrum imidazole derivative used in basic clinical practice as 2% w/w in topical drug preparations for treatment of candidiasis, dermatophytosis, intertrigo (sweat rash), paronychia (nail inflammation), diaper dermatitis, onchomycosis (toe and finger nails), and mixed infection. Miconazole is also effective against species of Candida that are resistant to
