Atopic dermatitis is a chronic, relapsing, very pruritic inflammation of the skin with a worldwide prevalence of 10-20% in children and 1-3% in adults. Topical steroids or a calcineurin inhibitor, such as tacrolimus or pimecrolimus, are used to treat atopic dermatitis. Although various factors cause the skin disease, the cutaneous Malassezia species have drawn attention during the last decade (4, 5). Malassezia are basidiomycetous yeasts that colonize not only patients with atopic dermatitis but also healthy individuals. As the microorganisms require lipids for growth, they are especially common on the head and neck, which are lipid-rich areas. Currently, 11 species are accepted in the genus Malassezia. Of these, M. globosa and M. restricta have been isolated from almost every patient with atopic dermatitis, whereas the other species have been found in fewer than 40% of cases (8). This distribution frequency is identical in both patients and healthy subjects. However, anti-Malassezia-specific IgE antibody is produced in patients with atopic dermatitis but not in healthy subjects (1,8). The main cause of this specific sensitization might be the disrupted skin barrier, facilitating allergen uptake. Based on these findings, antifungal therapy, such as itraconazole and ketoconazole, has been demonstrated to decrease the number of cutaneous Malassezia species in patients with atopic dermatitis (6, 7, 10). Azole agents have proven effective for treating atopic dermatitis in several clinical trials, including randomized, double-blind, placebo-controlled trials. Given that the dosage and period of administration of azole therapy differ in these studies, the therapy method has not yet been standardized.To increase our understanding, we examined the in vitro pharmacodynamics of the effects of itraconazole against Malassezia, which is one of the factors exacerbating atopic dermatitis, using a time-kill method. This study examined 24 Malassezia clinical isolates, representing five isolates each from the two major components of the cutaneous Malassezia flora, M. globosa (strains AD25, AD49, AD50, AD63, and AD75) and M. restricta (strains AD13, AD15, AD23, AD33, and AD35), and two isolates each from M. dermatis (strains M9928, M9929), M. furfur (strains M11009, and M11010), M. japonica (strains M9966, and M9967), M. obtusa (strains M11011, and M11012), M. slooffiae (strains M11013, and M11014), M. sympodialis (strains AD42, and M11016), and M. yamatoensis (strains M9985, and M9986).Before the time-kill studies, the isolates were subcultured and grown for 3 days at 32 C on modified Leeming and Notman agar (mLNA). Some colonies were suspended in sterile physiological saline solution, and the suspension was vortexed with sterile glass beads, 0.45 mm in diameter. After vortexing for 20 sec to disperse the Malassezia clumps, the inoculum was adjusted Abstract: The in vitro pharmacodynamic activity of itraconazole against Malassezia was determined by time-kill methods. Itraconazole showed fungistatic activity at concentrations grea...