High Staphylococcus epidermidis Colonization and Impaired Permeability Barrier in Facial Seborrheic Dermatitis

Abstract

Background:Seborrheic dermatitis (SD) is a common inflammatory skin condition. The etiology is unclear, although overgrowth of Malassezia on the skin has been suggested to cause SD. This study investigated whether colonization with Staphylococcus plays a role in facial SD, which was not well addressed previously.Methods:The study was conducted from September 1, 2011 to February 20, 2012 in the First Hospital of China Medical University. In the first phase, the study evaluated the level of transepidermal water loss (TEWL) and the number of colony-forming units (CFU) of Staphylococcus in defined skin areas of SD patients who were human immunodeficiency virus (HIV) seropositive (HIV [+] SD [+] group, n = 13), classical SD (HIV [−] SD [+] group, n = 24) patients, HIV seropositive-non-SD (HIV [+] SD [−] group, n = 16) patients, and healthy volunteers (HIV [−] SD [−] group, n = 16). In the second phase, we enrolled another cohort of HIV (−) SD (+) patients who applied topical fusidic acid (n = 15), tacrolimus (n = 16), or moisturizer (n = 12). Changes in the Seborrheic Dermatitis Area Severity Index (SDASI), TEWL, and Staphylococcus density were evaluated 2 weeks later. Comparisons of each index were performed using analysis of variance (ANOVA) and least significant difference method.Results:The level of TEWL was greater through lesional sites in the HIV (+) SD (+) group than that in HIV (+) SD (−) and HIV (−) SD (−) groups (95% confidence interval [CI]: 18.873–47.071, P < 0.001 and 95% CI: 28.755–55.936, P < 0.001, respectively). The number of CFU of Staphylococcus was greater in the HIV (+) SD (+) group than that in HIV (+) SD (−) and HIV (−) SD (−) groups (95% CI: 37.487–142.744, P = 0.001 and 95% CI: 54.936–156.400, P < 0.001, respectively). TEWL was significantly more improved in patients treated with tacrolimus and fusidic acid than that in those treated with moisturizers (95% CI: 7.560–38.987, P = 0.004 and 95% CI: 4.659–37.619, P = 0.011, respectively). Topical tacrolimus and fusidic acid were significantly associated with decreased SDASI as compared with moisturizer (95% CI: 0.03–0.432, P = 0.025 and 95% CI: 0.033–0.44, P = 0.024, respectively).Conclusions:High colonization with Staphylococcus epidermidis, along with impaired skin permeability barrier function, contributes to the occurrence of SD.

Exploring Anti-Fungal, Anti-Microbial and Anti-Inflammatory Properties of a Topical Non-Steroidal Barrier Cream in Face and Chest Seborrheic Dermatitis

“…Here, we report that NSC treatment at W2 was able to decrease the number of SE colonies on the face by 75% compared to W0. An et al [29] have demonstrated that fusidic acid treatment, applied for 2 weeks on the face, was able to decrease the number of SE colonies from 331 to 18, achieving 95% compared to W0, whereas moisturizers increased the number of SE colonies compared to W0. It is worth mentioning that the decrease of SE colonies on the face (15.6% W1, 75% W2) was less pronounced than on the chest (92% W1, 99% W2).…”

An update on the microbiology, immunology and genetics of seborrheic dermatitis

“…Several studies have challenged the role of Malassezia in SD in HIV‐infected patients. One study done in HIV‐positive patients showed either negative or limited growth of Malassezia . On the other hand, a significantly higher number of Malassezia was cultured from HIV‐negative patients with SD.…”

“…Additional bacteria that have been implicated include Corynebacterium and Propionibacterium . One study found a higher colonization rate of S. epidermidis in both HIV‐positive and HIV‐negative patients with SD . Another recent study reported that S. aureus was the most common bacterial member of the skin flora in patients with SD, proposing an etiological role for S. aureus …”

“…These studies suggest that HIV‐positive patients may have a different pathogenic mechanism than SD in individuals with an intact immune system. These patients are also often refractory to standard SD treatments, requiring prolonged courses of topicals and systemic antifungals, and treatment failure is common …”

Clinical study on treatment of facial seborrheic dermatitis with intense pulsed light combined with 30% supramolecular salicylic acid

“…The pathogenesis of the disease is unclear. Current studies have shown that seborrheic dermatitis is closely related to the excessive sebum, the excessive reproduction of Malassezia furfur and Staphylococcus epidermidis ( 3 , 4 ), and the destruction of the skin barrier function ( 5 ). The application of antifungal drugs and glucocorticoids could alleviate the symptoms ( 6 , 7 ); however, long-term application will produce telangiectasia, epidermal atrophy, glucocorticoid dependence, and other adverse reactions ( 8 , 9 ).…”