The Malassezia sp. (previously known as Pityrosporum) is a lipophilic lipase-producing yeast [16]. The lipase splits triglycerides into fatty acids. The yeast organism ingests the saturated fatty acids, allowing the unsaturated fatty acids to penetrate the stratum corneum, causing inflammation [17]. A study of 31 Japanese adults showed that the population of genus Malassezia found was approximately three times more on SD skin than on non-lesional skin [18]. Studies have also shown good correlation between the Malassezia sp. count and severity of SD [19]. There is furthermore strong evidence of clinical response of SD to antifungal treatment in adult studies [20].

In a Chinese study carried out on adult patients with SD, M. globosa and M. restricta were found in 87.0 and 81.5 % of patients, respectively. 82.9 % of these patients also showed colonisation of two or more Malassezia sp. [21]. Similar results have been observed in infants with SD. A study done on Japanese infants aged 1 month showed that M. furfur and M. globosa were isolated from affected patients at significantly higher rates than from healthy infants [22].

Other studies have shown that M. furfur (previously known as P. ovale or P. orbiculae in the oval and round forms, respectively) has been isolated more frequently in infants with SD compared to controls [23]. Prolonged stay in the intensive care unit, parenteral nutrition, insertion of central lines in neonates are risk factors for colonisation of the infant skin with M. furfur [24, 25].

Infants with active SD have been found to have significant levels of a rare essential fatty acid 20:2w6. It is postulated that there is transient abnormal function of the enzyme delta-6-desaturase causing the elevated levels of 20:2w6. The normalisation of the high essential fatty acid levels correlated with a resolution of their SD [26].

Most infants will not require any treatment due to the self-limiting nature of SD. Thick scales can be softened through the application of a sterile mineral oil to the scale which is massaged into the scalp for 5–10 min before washing the hair. In a cohort study on 34 children aged between 1 month and 10 years, 97 % of patients treated with bifonazole shampoo 1 % three times weekly for 4 weeks had good to complete resolution of their scalp SD [27]. There is a small study of 13 infants with scalp SD treated with ketoconazole shampoo for 4 weeks. During the course of the treatment, measured serum ketoconazole were undetectable and liver enzymes were not elevated, showing no evidence of significant systemic absorption of topical ketoconazole among infants [28]. Adult studies show that ketoconazole cream or shampoo for 3–4 weeks is efficacious and well tolerated in patients with SD [29, 30].

Alternatively, coal tar shampoo can be used to treat SD although coal tar use on the trunk may be limited by its odour and staining of skin and clothing. Selenium sulphide shampoo has been shown to be effective in treating SD in all regions in older children [31] but is generally not used for application to the face. Older children with thicker scalp scales may also benefit from salicylic acid 2 % cream for 2–3 h before shower. From the authors’ experience, the use of mild topical steroids such as hydrocortisone 1 % cream combined with topical antifungals (e.g. Daktacort^®) can help to reduce the erythema associated with SD. Other options include application of desonide lotion in the morning and topical antifungals in the evenings.

For patients of Black or African American descent, it may be difficult to shampoo more frequently than once a week due to intrinsic dryness of the hair shaft. In these patients, usage of pomades with selenium sulphide and/or oil-based mid-potency topical corticosteroids (e.g. fluocinolone) may be less damaging to the hair shaft (Table 31.1).

The prognosis in infants is generally good as SD resolves on its own. For adolescents, a course of ketoconazole shampoo and cream for scalp and facial SD, respectively, often leads to excellent clinical improvement. Studies also show that the recurrence rate of SD in adults 3–4 months post-antifungal treatment is similar to those treated with topical steroids [29, 32, 33]. Although no formal studies have been done in adolescents, recurrence is not uncommon and patients will benefit from a repeat course of treatment.

In view of the diagnostic challenge in differentiating infantile SD from other chronic conditions such as AD and psoriasis, clinicians must always consider these possible differential diagnoses in patients who do not improve with standard treatment.

There has been recent research on the use of topical pimecrolimus and tacrolimus for facial and truncal SD. Topical calcineurin inhibitors were found to be as effective as topical steroids and antifungals in adults [32–35]. A small study also showed that the pimecrolimus group were associated with fewer and less severe relapses compared to topical steroids [35]. Patients on pimecrolimus tend to have more side effects than those treated with topical steroids. Mild transient burning sensation and skin irritation were reported in 10–45 % of patients on pimecrolimus and 0.1 % tacrolimus ointment which usually subsides within the first 72 h [36–40]. Due to the transient side effects, patients often do not discontinue treatment but they should be advised of these adverse effects especially as SD often affects the eyebrows and forehead. Rosaceiform dermatitis is also a rare side effect of pimecrolimus cream which has been reported in the literature [41]. Tacrolimus may cause acne formation if used on facial locations in acne prone pre-teens and teenagers. Furthermore, these agents bear a black box warning in the United States stating that they may be associated with cancer and should not be used in children under the age of 2 years.