Utilization of matrix‐assisted laser desorption and ionization time‐of‐flight mass spectrometry for identification of infantile seborrheic dermatitis‐causing Malassezia and incidence of culture‐based cutaneous Malassezia microbiota of 1‐month‐old infants

Matrix‐assisted laser desorption and ionization time‐of‐flight mass spectrometry (MALDI‐TOF‐MS) has been utilized for identification of various microorganisms. Malassezia species, including Malassezia restricta, which is associated with seborrheic dermatitis, has been difficult to identify by traditional means. This study was performed to develop a system for identification of Malassezia species with MALDI‐TOF‐MS and to investigate the incidence and variety of cutaneous Malassezia microbiota of 1‐month‐old infants using this technique. A Malassezia species‐specific MALDI‐TOF‐MS database was developed from eight standard strains, and the availability of this system was assessed using 54 clinical strains isolated from the skin of 1‐month‐old infants. Clinical isolates were cultured initially on CHROMagar Malassezia growth medium, and the 28S ribosomal DNA (D1/D2) sequence was analyzed for confirmatory identification. Using this database, we detected and analyzed Malassezia species in 68% and 44% of infants with and without infantile seborrheic dermatitis, respectively. The results of MALDI‐TOF‐MS analysis were consistent with those of rDNA sequencing identification (100% accuracy rate). To our knowledge, this is the first report of a MALDI‐TOF‐MS database for major skin pathogenic Malassezia species. This system is an easy, rapid and reliable method for identification of Malassezia.     

Seborrheic dermatitis—Looking beyond Malassezia

Seborrhoeic Dermatitis (SD) is a very common chronic and/or relapsing inflammatory skin disorder whose pathophysiology remains poorly understood. Yeast of the genus Malassezia has long been regarded as a main predisposing factor, even though causal relationship has not been firmly established. Additional predisposing factors have been described, including sebaceous activity, host immunity (especially HIV infection), epidermal barrier integrity, skin microbiota, endocrine and neurologic factors, and environmental influences. Genetic studies in humans and mouse models—with particularly interesting insights from examining the Mpzl3 knockout mice and their SD‐like skin phenotype, and patients carrying a ZNF750 mutation—highlight defects in host immunity, epidermal barrier and sebaceous activity. After synthesizing key evidence from the literature, we propose that intrinsic host factors, such as changes in the amount or composition of sebum and/or defective epidermal barrier, rather than Malassezia, may form the basis of SD pathobiology. We argue that these intrinsic changes provide favourable conditions for the commensal Malassezia to over‐colonize and elicit host inflammatory response. Aberrant host immune activity or failure to clear skin microbes may bypass the initial epidermal or sebaceous abnormalities. We delineate specific future clinical investigations, complemented by studies in suitable SD animal models, that dissect the roles of different epidermal compartments and immune components as well as their crosstalk and interactions with the skin microbiota during the process of SD. This research perspective beyond the conventional Malassezia‐centric view of SD pathogenesis is expected to enable the development of better therapeutic interventions for the management of recurrent SD.     

Distribution of Malassezia species in patients with psoriasis and healthy individuals in Tehran, Iran

Background: Psoriasis is a non‐contagious disorder that affects the skin as red scaly patches. Although the role of Malassezia species in the pathogenesis of psoriasis is still not fully understood, it is thought that these lipophilic yeasts might be a trigger factor in the exacerbation of psoriatic lesions. Methods: Using culture in a specific medium followed by the polymerase chain reaction‐restriction fragment length polymorphism method, the presence of Malassezia species in the skin of 110 patients with psoriasis was compared with that in a control group of 123 healthy patients. Results: The recovery rate of Malassezia species from the skin of patients with psoriasis was significantly lower than that in the controls. In both psoriatic and healthy skin, Malassezia globosa was isolated as the predominant species. In psoriatic patients, the rate of colonization of Malassezia furfur and Malassezia restricta was almost twice that in the controls, whereas M. globosa was isolated more frequently from healthy individuals than from patients. Conclusions: Considering the higher lipase activity secretion by M. furfur in comparison with other Malassezia species, the enzymatic release of arachidonic acid and its metabolites by M. furfur may exacerbate the inflammatory and hyperproliferative changes observed in psoriasis.     

Susceptibility testing and resistance phenotype detection in Staphylococcus aureus strains isolated from patients with atopic dermatitis, with apparent and recurrent skin colonization

Background Staphylococcus aureus colonization is accepted to be an important triggering factor in patients with atopic dermatitis (AD) and antibiotic resistance has been recognized to be a serious problem as a consequence and for the management of AD treatment. Objectives To investigate the antibiotic resistance pattern of S. aureus strains isolated from patients with AD with apparent (lesional and nonlesional skin areas) and recurrent skin colonization and strains obtained from healthy nasal carriers. Methods Eighty‐seven patients (age 23 ± 11·5 years) with mild to severe AD (SCORAD 46·9 ± 16·6), 21 patients (age 19·8 ± 6·7 years) before antistaphylococcal treatment and 177 healthy nasal carriers (age 27·5 ± 8·4 years) were microbiologically assessed for carriage of S. aureus. Colonization of lesional and nonlesional skin areas was quantified by counting the number of colony forming units on the skin surface (log₁₀ CFU cm^?2). Antimicrobial susceptibility and resistance phenotypes of 179 S. aureus strains were assessed with the agar disc‐diffusion method. Results Staphylococcus aureus was isolated from 87% of lesional and 44% of nonlesional skin samples from patients with AD. The colonization density of S. aureus was markedly higher in lesional than in nonlesional skin (P < 0·001), and was positively correlated with AD severity (P < 0·001) and total serum IgE (P < 0·05). Patients with AD had a significantly higher prevalence of chloramphenicol‐resistant S. aureus than nasal carriers (P < 0·01). Similar rates of resistance were expressed to tetracycline, erythromycin, mupirocin, clindamycin and penicillin. Nearly 35% of S. aureus strains from the lesional skin demonstrated different antimicrobial sensitivity pattern compared with strains from nonlesional skin of the same patients with AD. The trend of increasing resistance to chloramphenicol, erythromycin and fusidic acid was observed among S. aureus strains recovered from patients after approximately 75 days of antibiotic treatment. Methicillin‐resistant S. aureus isolates were cultured from two patients, one during exacerbation and the other after subsequent bacterial recolonization. Conclusions Discrepancies in antibiotic sensitivity pattern were observed among S. aureus strains colonizing different sites of AD skin (lesional and nonlesional areas), and also in AD patients with prior antibiotic treatment. Therefore, clinicians should consider repeat microbial susceptibility testing on different body sites of patients with AD when clinically indicated.     

Malassezia yeasts activate the NLRP3 inflammasome in antigen‐presenting cells via Syk‐kinase signalling

Although being a normal part of the skin flora, yeasts of the genus Malassezia are associated with several common dermatologic conditions including pityriasis versicolour, seborrhoeic dermatitis (SD), folliculitis, atopic eczema/dermatitis (AE/AD) and dandruff. While Malassezia spp. are aetiological agents of pityriasis versicolour, a causal role of Malassezia spp. in AE/AD and SD remains to be established. Previous reports have shown that fungi such as Candida albicans and Aspergillus fumigatus are able to efficiently activate the NLRP3 inflammasome leading to robust secretion of the pro‐inflammatory cytokine IL‐1β. To date, innate immune responses to Malassezia spp. are not well characterized. Here, we show that different Malassezia species could induce NLRP3 inflammasome activation and subsequent IL‐1β secretion in human antigen‐presenting cells. In contrast, keratinocytes were not able to secrete IL‐1β when exposed to Malassezia spp. Moreover, we demonstrate that IL‐1β secretion in antigen‐presenting cells was dependent on Syk‐kinase signalling. Our results identify Malassezia spp. as potential strong inducers of pro‐inflammatory responses when taken up by antigen‐presenting cells and identify C‐type lectin receptors and the NLRP3 inflammasome as crucial actors in this process.     

Immunophenotyping of inflammatory cells in subacute prurigo

Background Subacute prurigo (SP) is a relatively common disease of papular cutaneous lesions that itch intensely. However, there is a lack of systematic clinical and histological studies on SP. Objectives We aimed to immunophenotype inflammatory cells in SP using immunohistochemistry and flow cytometry. Methods Lesional and non‐lesional skin of 21 patients with SP was investigated. Immunohistochemical staining for CD1a, CD3, CD4, CD8, CD15, CD34, CD68, and anti‐human tryptase (AHT) was performed. In order to evaluate the absolute counts and percentages of CD4+ and CD8+ lymphocytes in the peripheral blood of SP patients, flow cytometric methods were used. Results Compared to non‐lesional skin, there was a significant increase of the median percentage of CD3+, CD4+, and CD8+ cells in the lesional dermis (12.6% vs. 19.7%, P = 0.044; 0.8% vs. 3.7%, P = 0.016; and 1% vs. 15.6%, P = 0.0039, respectively). The mean ± SD CD4+/CD8+ ratio was 0.58 ± 0.6. Median percentage of CD15+ cells was significantly increased in lesional skin as compared to non‐lesional skin (11.7 vs. 1%, P = 0.027). Median percentage immunoreactivity of CD68+ cells was significantly increased in lesional dermis as compared to non‐lesional skin (32.5% vs. 9.4%, P = 0.0005). CD1a, CD34, and AHT positive cells did not significantly differ between lesional and non‐lesional skin. T lymphocyte subsets in the peripheral blood of SP patients did not show significant pathologies. Conclusions We observed that the inflammatory cell infiltrate in SP mainly consists of T lymphocytes, particularly CD8+ cells, CD15+ neutrophils, and CD68+ macrophages.     

Increased lysophosphatidylcholine content in lesional psoriatic skin

Various cell stimuli occur via activation of phospholipase A₂, which hydrolyses polyunsaturated fatty acids from the sn-2 position of membrane phospholipids, resulting in the formation of polyunsaturated fatty acids and lysophospholipids. The level of lysophospholipids is determined by the balance between phospholipase A₂ activity and the rate of catabolism of the lysophospholipids. One of the lysophospholipid classes, lysophosphatidylcholine, has been shown to stimulate certain leucocyte activities which are of importance for the induction and maintenance of inflammation. In addition, it has been demonstrated that phospholipase A₂ activity is increased in psoriatic skin. In the present study, we analysed the levels of lysophosphatidylcholine, by thin layer chromatography, in lesional psoriatic skin, uninvolved psoriatic skin and normal skin. The lysophosphatidylcholine content, expressed as μmol lysophosphatidylcholine/μmol phosphatidylcholine, was 1.55, 0.21 and 0.12% in lesional psoriatic skin, uninvolved psoriatic skin and normal skin, respectively. The level of lysophosphatidylcholine was significantly elevated in lesional compared with uninvolved psoriatic skin (P= 0.004) and normal skin (P= 0.002). The increased lysophosphatidylcholine levels in psoriatic skin indicate that the phospholipase A₂ activation is not accompanied by a corresponding increase in the activity of enzymes catabolizing lysoPC. If present in biologically active concentrations, lysophosphatidylcholine may contribute to the induction and maintenance of the inflammatory and immunological processes occurring in lesional psoriatic skin.     

Malassezia species in healthy skin and in dermatological conditions

The genus Malassezia comprises lipophilic species, the natural habitat of which is the skin of humans and other warm‐blooded animals. However, these species have been associated with a diversity of dermatological disorders and even systemic infections. Pityriasis versicolor is the only cutaneous disease etiologically connected to Malassezia yeasts. In the other dermatoses, such as Malassezia folliculitis, seborrheic dermatitis, atopic dermatitis, and psoriasis, these yeasts have been suggested to play pathogenic roles either as direct agents of infection or as trigger factors because there is no evidence that the organisms invade the skin. Malassezia yeasts have been classified into at least 14 species, of which eight have been isolated from human skin, including Malassezia furfur, Malassezia pachydermatis, Malassezia sympodialis, Malassezia slooffiae, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia dermatis, Malassezia japonica, and Malassezia yamatoensis. Distributions of Malassezia species in the healthy body and in skin diseases have been investigated using culture‐based and molecular techniques, and variable results have been reported from different geographical regions. This article reviews and discusses the latest available data on the pathogenicity of Malassezia spp., their distributions in dermatological conditions and in healthy skin, discrepancies in the two methods of identification, and the susceptibility of Malassezia spp. to antifungals.     

Effects of Malassezia yeasts on serum Th1 and Th2 cytokines in patients with guttate psoriasis

Background Systemic and focal infections caused by microorganisms have been known to induce or exacerbate psoriasis. Although the role of yeast species of the genus Malassezia in the pathogenesis of psoriasis is not fully understood, it is thought that these lipophilic yeasts may represent a triggering factor in the exacerbation of psoriatic lesions. Objectives This study investigated the effects of Malassezia yeasts on serum Th1 and Th2 cytokines in patients with guttate psoriasis (GP) in order to define their role in the pathogenesis of psoriasis. Methods Fifty patients with GP and 29 clinically healthy individuals were included in the study. All samples consisted of scales and scrapings taken from the scalps, trunks, and upper limbs of both psoriasis patients and healthy subjects. Psoriasis patients and healthy subjects were grouped according to their positivity or negativity for Malassezia yeasts as ascertained by direct microscopy and/or culture. An enzyme‐linked immunosorbent assay (ELISA) was used to measure serum levels of Th1 and Th2 cytokines in these groups. Results No significant differences in positivity for Malassezia yeasts were found between psoriatic skin and healthy skin in samples taken from different body sites. Serum interleukin‐13 (IL‐13) levels were significantly lower in the psoriasis group compared with the control group (P = 0.04). Levels of other cytokines did not differ significantly between the psoriasis and control groups. Mean levels of Th2 cytokines (IL‐4, IL‐10, IL‐13), but not of Th1 cytokines (IL‐2 and IFN‐γ), were significantly lower in psoriasis patients positive for Malassezia yeasts compared with those negative for Malassezia yeasts and control subjects (P = 0.04, P < 0.001 and P = 0.01, respectively). Conclusions The isolation of Malassezia yeasts from GP lesions does not necessarily mean that these species are pathogenic, but their downregulating effects on anti‐inflammatory Th2 cytokines may contribute to the occurrence of GP.     

Platelet activating factor (PAF) and lyso-PAF in psoriasis

Previous studies have shown that scale from lesional psoriatic skin contains substantial amounts of platelet activating factor (PAF). In this study, PAF and its immediate precursor, lyso-PAF, were measured in exudates from abrasions on lesional and uninvolved psoriatic skin, and from skin of healthy subjects. The mean amounts of PAF recovered from lesional and uninvolved psoriatic skin (n=13) and from healthy skin (n=14) were not significantly different (range 0.05–2.14 pmol/sample). Mean recoveries of lyso-PAF from lesional psoriatic skin (n=9) and skin of healthy subjects (n=13) were also similar (9.5 ± 1.9 and 11.0 ± 1.9 pmol/sample, respectively), but significantly less lyso-PAF was found in exudates from the uninvolved psoriatic skin (n=9; 3.1 ± 0.4 pmol/sample; P<0.01 relative to both lesional psoriasis and healthy skin). The finding of reduced lyso-PAF in uninvolved psoriatic skin was unexpected because increased phospholipase-A₂ activity is associated with psoriasis. These results do not support the hypothesis that extracellular PAF contributes significantly to the inflammation associated with psoriasis.     

Non‐invasive imaging of mid‐dermal elastolysis

Mid‐dermal elastolysis (MDE) is a rare disease that is characterized histopathologically by selective loss of elastic tissue in the mid dermis. We aimed to assess MDE using noninvasive skin imaging techniques in vivo. We examined both the lesional and adjacent healthy skin of a woman with the reticular variant of MDE, using confocal scanning laser microscopy, optical coherence tomography (OCT) and high‐frequency ultrasound (HFUS). The median diameter of blood vessels at the top of dermal papillae was significantly increased in erythematous lesional skin compared with healthy skin. The mid‐dermal signal intensity detected by OCT was higher in healthy skin than in lesional skin. With HFUS, mid‐dermal density values were significantly higher in healthy skin than in lesional skin. Our preliminary findings indicate that noninvasive skin imaging methods such as OCT and HFUS might be suitable techniques for the evaluation and monitoring of elastolytic skin disorders such as MDE.     

Immunohistological pointers to a possible role for excessive cathelicidin (LL-37) expression by apocrine sweat glands in the pathogenesis of hidradenitis suppurativa/acne inversa

Summary Background The cause of follicular occlusion, a key early event in the pathogenesis of hidradenitis suppurativa (HS), also known as acne inversa, remains unknown. Objectives To identify changes, if any, in the antimicrobial peptide (AMP) and cytokine expression profile of HS affected human skin. Methods Quantitative immunohistomorphometry was used to compare the in situ protein expression of selected AMPs and cytokines in lesional HS skin from 18 patients with that in healthy skin (n = 12). The lesional skin from patients with HS was histologically subclassified based on the predominance of inflammation vs. scarring. Results Compared with healthy controls, significantly increased immunoreactivity for cathelicidin (LL‐37) was noted in the apocrine sweat gland and distal outer root sheath (ORS) of the hair follicle (HF) epithelium in lesional HS skin. Immunoreactivity for LL‐37, psoriasin, human β‐defensin 3 (hBD3), α‐melanocyte stimulating hormone (α‐MSH), macrophage migration inhibitory factor (MIF), tumour necrosis factor (TNF)‐α and interleukin (IL)‐8 was significantly increased in HS epidermis. LL‐37 and TNF‐α immunoreactivity was also increased in the dermis of lesional HS skin. In contrast, lysozyme expression was decreased in the epidermis of lesional HS skin, while that of TNF‐α and IL‐8 was decreased in the proximal ORS of HFs in HS lesions. These differences were most pronounced in HS with predominant inflammation. Conclusions Our observations raise the question as to whether excessive secretion of AMPs by the skin, in particular by the apocrine sweat glands, distal HF epithelium, and epidermis, may attract inflammation and thus facilitate or promote HS development.     

Evaluation of zinc level in skin of patients with necrolytic acral erythema

Summary Background Necrolytic acral erythema (NAE) is considered a cutaneous sign of hepatitis C virus infection. Its exact pathogenesis is still not fully understood, with some reports about decreased serum zinc levels but none about its level in the skin. Objectives To assess skin (lesional and perilesional) and serum zinc levels in patients with NAE and compare them with levels in control subjects. Methods Fifteen patients with NAE and 10 healthy controls were included in this study. Assessment of zinc level, in serum by graphite furnace atomic absorption spectrophotometry and in lesional and perilesional skin biopsies by flame atomic absorption spectrometry, was done in all subjects. Re‐evaluation of serum and lesional skin zinc level was done after oral zinc treatment. Results Mean ± SD zinc levels were significantly lower in patients (serum 0·44 ± 0·13 mg L^?1; lesional skin 42·6 ± 18·9 mg L^?1; perilesional skin 32·5 ± 17·2 mg L^?1) than controls (serum 1·17 ± 0·29 mg L^?1; skin 100·1 ± 2·77 mg L^?1), with a positive correlation between lesional and perilesional skin zinc (r = 0·91, P < 0·01). Oral zinc supplementation significantly increased serum and skin zinc levels (by 159% and 4%, respectively; P < 0·05). Conclusions NAE is associated with decreased serum and skin zinc levels. Oral zinc supplementation corrects decreased levels of plasma and skin zinc much earlier than the desired clinical benefits appear.     

Prolactin level is significantly elevated in lesional skin of patients with psoriasis

Background Accumulating data point to a potential role of prolactin in the pathogenesis of psoriasis. Methods We initiated a study including psoriasis patients (n = 15) and healthy volunteers (n = 15) as controls. Psoriasis area and severity index (PASI) score was evaluated, and prolactin levels in serum and blister fluid were assessed by enzyme‐linked immunosorbent assay (ELISA). Results Prolactin levels were significantly (P < 0.01) elevated in blister fluid of psoriatic lesional skin. Correlations between PASI score and different serum prolactin levels in lesional and non‐lesional skin were insignificant. Significant positive correlations of prolactin level were observed between lesional and non‐lesional skin in psoriasis (P < 0.05) and between serum and clinically normal skin in both psoriasis and control subjects (P < 0.05). Conclusions Locally produced prolactin may be involved in the pathogenesis of psoriatic lesions.     

Increased CCL18 expression in patients with cutaneous T‐cell lymphoma: association with disease severity and prognosis

Background CC chemokine ligand (CCL) 18 is expressed by monocytes and dendritic cells (DCs), and has potent chemotactic activity for T cells, B cells and DCs. CCL18 expression is up‐regulated in lesional skin of atopic dermatitis and bullous pemphigoid, suggesting its important roles in the development of these skin diseases. Objective To investigate roles of CCL18 in cutaneous T‐cell lymphoma (CTCL). Methods The CCL18 messenger RNA (mRNA) expression in CTCL skin (n = 21) and in normal skin (n = 7) was examined by quantitative RT‐PCR. CCL18 expression was also examined by immunohistochemistry. Serum CCL18 levels were measured in 38 patients with CTCL and 20 healthy controls by enzyme‐linked immunosorbent assay. We also analysed correlation between serum CCL18 levels and other clinical and laboratory data. Results The CTCL lesional skin contained higher levels of CCL18 mRNA than normal skin. CCL18 was expressed by dermal macrophages and DCs in CTCL skin. Serum CCL18 levels in patients with CTCL were significantly higher than those of healthy controls and correlated with types of skin lesions. They also significantly correlated with modified severity‐weighted assessment scores, serum sIL‐2R, LDH, IL‐4, IL‐10, IL‐31, CCL17 and CCL26 levels. Patients with high serum levels of CCL18 showed significantly poor prognosis compared with those with low CCL18 levels. Conclusion CCL18 mRNA is up‐regulated in CTCL lesional skin, and serum CCL18 levels are significantly increased and correlated with the severity of CTCL. These results suggest that CCL18 may be associated with the development of CTCL.     

Characteristics of Staphylococcus aureus colonization in patients with atopic dermatitis in Sri Lanka

Background. Colonization of the skin of patients with atopic dermatitis (AD) by Staphylococcus aureus (SA) is associated with more severe disease. Aim. To determine the association of SA colonization patterns and densities in lesional and nonlesional skin in patients with varying severities of AD, and to determine the antibiotic sensitivity patterns of SA isolates from Sri Lanka. Methods. Skin and nasal swabs collected from 100 patients with AD and 120 controls were used to investigate the presence of SA. Severity of AD was graded using the Nottingham Eczema Severity Score. Colony counts were obtained for skin samples, and antibiotic sensitivity testing was performed in cases positive for SA. Results. Skin colonization was seen in 57 patients (57%) but in only 10 controls (8%). Lesional skin of most patients (52/57; 91%) had SA densities of > 300 colony‐forming units/cm². Colonization rates with SA significantly increased with increasing age (Spearman correlation coefficient R = 0.9, P < 0.05) and increasing duration of lesions in patients with AD (Spearman R = 0.87, P < 0.05). Isolates from eight patients (13.5%) were found to be methicillin‐resistant S. aureus (MRSA). Only 6 isolates (10%) were susceptible to penicillin and 22 (37%) to erythromycin, while 28 (47%) isolates had erythromycin‐induced resistance to clindamycin. Conclusions. SA colonization rates were significantly associated with increasing age and severity of AD, and particularly with duration of lesions. Patients with severe disease were also more likely to be colonized with SA strains resistant to conventional antibiotics.     

Risks for Staphylococcus aureus colonization in patients with psoriasis: a systematic review and meta‐analysis

Evidence on whether patients with psoriasis have a higher risk for staphylococcal colonization than healthy controls remains controversial. To synthesize the current literature, we performed a systematic review on the prevalence and relative risk (RR) of Staphylococcus aureus colonization in patients with psoriasis. We modified the QUADAS‐2 instrument to assess the reporting quality of individual studies and applied random‐effects models in meta‐analysis. Overall we identified 21 eligible studies, of which 15 enrolled one or more comparison groups. The pooled prevalence of staphylococcal colonization in patients with psoriasis was 35·3% [95% confidence interval (CI) 25·0–45·6] on lesional skin and 39·2% (95% CI 33·7–44·8) in the nares. Patients with psoriasis were 4·5 times more likely to be colonized by S. aureus than healthy controls were on the skin (RR 5·54, 95% CI 3·21–9·57) and 60% more in the nares (RR 1·60, 95% CI 1·11–2·32). Cutaneous and nasal colonization by meticillin‐resistant S. aureus also appeared higher in patients with psoriasis (pooled prevalence 8·6%) than in healthy controls (2·6%), yet the difference was not statistically significant (P = 0·74). In contrast, despite of a similar risk for nasal staphylococcal colonization (RR 0·67, 95% CI 0·38–1·18), patients with psoriasis were less likely to carry S. aureus on lesional skin than atopic patients (RR 0·64, 95% CI 0·40–1·02). In summarizing the current literature, we found that patients with psoriasis were at an increased risk for staphylococcal colonization compared with healthy individuals. Prospective studies on how bacterial loads correlate with disease activity can guide the clinical management of bacterial colonization while preventing the emergence of drug‐resistant strains.     

Antibiogram testing of pediatric skin infections in the era of methicillin‐resistant Staphylococci aureus: an Egyptian University Hospital‐based study

Background Community‐associated methicillin‐resistant Staphylococci aureus (CA‐MRSA) pediatric skin infections have been reported worldwide. However, little is known about pathogens' implications in Egyptian children, and beta‐lactams are still the empiric antimicrobials prescribed. This warrants Egyptian studies on antibiogram testing of pediatric skin infections. Objectives To determine antibiotic susceptibility patterns of bacterial isolates from Egyptian pediatric skin infections to find out if we need reconsideration of the empiric beta‐lactam antimicrobial therapy. Materials and methods Throughout an eight‐month cross‐sectional study, antibiogram testing was conducted on bacterial isolates from pediatric skin infections. Determination of inducible resistance to clindamycin using D‐test was performed for isolates susceptible to clindamycin and resistant to erythromycin. Results One‐hundred and 21 children (mean age 6.9 years ± 3 SD) presented with pyogenic skin infections. Methicillin‐sensitive Staphylococci aureus (MSSA) were isolated from 114 children, associated with group A Streptococci (GAS) in four of them, while GAS were the only isolates in three patients. A diagnosis of CA‐MRSA was fulfilled in four children. Antibiotic susceptibilities differed between isolated organisms but with no statistically significant differences between susceptibility patterns of isolates from primary skin infections and those from secondary infection of skin diseases. Positive D‐test was detected in five MSSA isolates. Conclusions CA‐MRSA skin infections are not common among Egyptian children and, therefore, beta‐lactams are still effective empiric antimicrobial therapy for most infections. Antibiogram testing from suppurative skin lesions are, however, better to be recommended to guide individual therapy. Clindamycin should not be considered for susceptible isolates unless they are erythromycin susceptible or D‐test negative.