Bacteriological aspects of Darier’s disease

Background There are no established data on the prevalence of bacterial colonization of lesional skin, nares and perineum in Darier’s disease (DD), or its contribution to the clinical manifestations of the disease. Objective To determine the prevalence of bacterial colonization of lesional skin and Staphylococcus aureus (S. aureus) in nares and perineum in 75 patients with DD, the association of these parameters with disease and patient characteristics, and the features of the bacterial skin infection in this group. Methods Medical interviews and physical examinations were performed. Bacteria were isolated from swabs taken from lesional skin, nares and perineum. Results S. aureus was isolated in 68%, 47% and 22% of lesional skin, nares and perineum cultures respectively. Subjects with positive S. aureus culture from lesional skin and/or nares had a statistically significant higher percentage of skin area affected and a more severe disease than patients with negative culture. Thirty of the 75 patients (40%) recalled bacterial skin infection, most often on the chest. Conclusions Patients with DD have high prevalence of S. aureus colonization in lesional skin and nares, with a correlation between disease severity and extent of the colonization. Further studies examining the consequences of S. aureus eradication in those sites may establish the need for S. aureus lesional skin and nares colonization screening and eradication as part of the treatment of DD exacerbations.     

Staphylococcus aureus skin colonization is promoted by barrier disruption and leads to local inflammation

Experimental mouse models of bacterial skin infections that have been described show that pathogenic microorganisms can readily invade the epidermis and dermis to produce localized infections. We used an epicutaneous mouse skin infection model to determine how the level of barrier disruption by tape‐stripping correlates with persistence of Staphylococcus aureus skin colonization, concomitant induction of cutaneous inflammation and infection. Furthermore, we investigated how murine skin responds to S. aureus colonization in a physiologic setting by analysing proinflammatory cytokines and antimicrobial peptides in mouse skin. We show that previous cutaneous damage allows skin inflammation to develop and favours S. aureus persistence leading to cutaneous colonization, suggesting an interdependence of cutaneous bacteria and skin. Our study suggests that skin barrier defects favour S. aureus skin colonization, which is associated with profound cutaneous inflammation.     

The complex biology and contribution of Staphylococcus aureus in atopic dermatitis,current and future therapies

Atopic dermatitis (AD) is a complex, chronic inflammatory skin disorder affecting more than 10% of U.K. children and is a major cause of occupation‐related disability. A subset of patients, particularly those with severe AD, are persistently colonized with Staphylococcus aureus and exacerbation of disease is commonly associated with this bacterium by virtue of increased inflammation and allergic sensitization, aggravated by skin barrier defects. Understanding the complex biology of S. aureus is an important factor when developing new drugs to combat infection. Staphylococcus aureus generates exoproteins that enable invasion and dissemination within the host skin but can also damage the skin and activate the host immune system. Antibiotics are often used by dermatologists to aid clearance of S. aureus; however, these are becoming less effective and chronic usage is discouraged with the emergence of multiple antibiotic‐resistant strains. New ways to target S. aureus using monoclonal antibodies and vaccines are now being developed. This review will attempt to evaluate the key biology of S. aureus, current treatment of S. aureus infections in AD and recent advances in developing new anti‐S. aureus therapies that have potential in severe AD.     

Correlation Between Serum 25‐Hydroxyvitamin D and Virulence Genes of Staphylococcus aureus Isolates Colonizing Children with Atopic Dermatitis

The skin of children with atopic dermatitis (AD) is colonized with Staphylococcus aureus more frequently than that of their peers. We investigated the prevalence of skin and nares colonization by S. aureus in children with AD, the virulence genes of the isolates, and their association with allergy, AD severity, and serum vitamin D (25(OH)D). This was an observational, cross‐sectional study in a sample of children diagnosed with AD in two settings in Spain. The samples were collected in 2012. Swabs from affected skin and nares were taken for microbiologic culture. The prevalence of S. aureus and presence of 17 staphylococcal virulence genes were studied using polymerase chain reaction. A total of 114 patients with a mean age of 5.7 ± 4.1 (range 3 mos to 14 yrs) were included in the study. Swabs were taken from the skin of 113 individuals with AD and from the nares of 85; 28.3% had S. aureus on the skin, which was significantly associated with positive allergen‐specific immunoglobulin E antibodies and higher Scoring Atopic Dermatitis (SCORAD) scores in the multivariate analysis. The presence of virulence factors tsst‐1, eta, cna, aur, and sec in cutaneous S. aureus isolates was associated with lower serum levels of 25(OH)D. S. aureus on nasal swabs correlated with its presence on the skin and was associated with lower 25(OH)D levels. In conclusion, S. aureus colonization is associated with allergy and severity in AD, whereas certain virulence genes are associated with lower serum 25(OH)D levels.     

Bacterial colonization,overgrowth, and superinfection in atopic dermatitis

Staphylococcus aureus infection is a major burden for individuals with moderate-to-severe atopic dermatitis and a known inducer of disease exacerbation. This increased susceptibility to staphylococcal infections has been attributed to abnormalities in the innate immune system of atopic dermatitis (AD) skin, including deficits in barrier proteins and lipids, and a muted response in generating antimicrobial peptides, all of which is further impaired by the activation of Th2 and Th22 immune pathways, which characterizes AD. Skewing of the immune response with a reduced Th1:Th2 ratio and increased adherence of bacteria to AD skin are also thought to contribute. Bacterial species diversity is reduced with flares, concomitant with increases in S. aureus and sometimes clinical infection, which has recently been linked to the finding that commensal bacteria produce anti–S. aureus factors that contribute to the endogenous response. S. aureus produces several virulence factors affecting the skin barrier and immune system, including promoting Th2 cell activation. Best practices for the management of staphylococcal infections include systemic antibiotics, initiation of antiseptics (particularly dilute bleach baths), and sometimes periodic intranasal mupirocin. Newer evidence suggests the possibility that treatment of the skin with commensal bacterial species could also reduce S. aureus growth and increase diversity.     

Colonization with community-acquired methicillin-resistant Staphylococcus aureus in children with atopic dermatitis: a cross-sectional study

Background Bacterial infection with Staphylococcus aureus is a common complication of atopic dermatitis (AD). The incidence of community‐acquired methicillin‐resistant S. aureus infection (MRSA) in the AD population is unknown. Objectives This study aimed to assess the prevalence of S. aureus and MRSA in pediatric patients with AD, to compare disease severity, and to characterize the clonal diversity of the isolates. Methods We carried out a prospective, cross‐sectional study of 200 patients with AD. The severity of AD was defined as mild, moderate, or severe depending on a composite AD severity score. A swab was taken from the nares of each patient and another from affected skin or folds. Genotyping of all S. aureus isolates was conducted by polymerase chain reaction (PCR) amplification of the S. aureus protein A (spa) gene. Results According to the severity score, 66.5% of subjects were ranked as having mild AD, 29.5% as having moderate and 4% as having severe AD. Staphylococcus aureus colonization was seen in 61.5% of all patients, represented by 43.7% of skin swabs and 48% of nares swabs. Only one of the isolations represented MRSA. Older age and higher AD severity scores were associated with S. aureus colonization (P = 0.03 and P < 0.001, respectively). No significant associations were noted for attendance at day care, family members with frequent skin infections, or family members working in healthcare. Isolates from spa CC015 were cultured in 19.2% of patient samples. The single MRSA culture showed a new spa type that belonged to CC127. Conclusions The results of this study confirm a high rate of S. aureus colonization of pediatric patients with AD. The low rate of MRSA requires further proof from larger prospective studies.     

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.     

Antibiotic treatment of cutaneous infections with Staphylococcus aureus in patients with atopic dermatitis: current antimicrobial resistances and susceptibilities

Background/aims: Atopic dermatitis (AD) is a common chronic inflammatory skin disease. In many patients, the disease is complicated by enhanced susceptibility to skin infections, especially with Staphylococcus aureus. The aim of this study was to determine the antimicrobial susceptibility of skin‐colonizing S. aureus strains in patients with AD and consecutively to recommend the first‐line antibiotic therapy. Methods: We studied S. aureus‐positive skin swabs (n = 102) from lesional skin of children, adolescents and adults with AD presenting to our inpatient and outpatient departments from January 2005 to June 2006. Results: Antimicrobial susceptibility testing revealed resistance against oxacillin, amoxicillin/clavulanic acid, cephalexin and cefuroxim in 3%, against tetracycline in 17%, against gentamicin in 16%, against erythromycin and clindamycin in 21%, against trimethoprim/sulfamethoxazol in 23%, against levofloxacin in 23%, against fusidic acid in 25%, against fosfomycin in 12% and against rifampicin in 16%. All strains isolated were susceptible to vancomycin. Conclusion: Currently, the first generation cephalosporin cephalexin appears to be the preferential first‐line antibiotic for the treatment of bacterial superinfections with S. aureus in children and adults with AD due to its restricted antimicrobial spectrum to Gram‐positive bacteria and a limited number of Gram‐negative strains. Cefuroxim and amoxicillin/clavulanate, which also showed 3% resistances in our patients, cover a broader range of bacterial micro‐organisms. However, a broader coverage is not required in case of AD, as S. aureus is the most frequent bacterial micro‐organism causing skin infections.     

S. Aureus Isolation from the Lesions,the Hands,and the Anterior Nares of Patients with Atopic Dermatitis

Abstract: Staphylococcus aureus colonization is common in atopic dermatitis (AD) and can exacerbate the disease. Additionally, some evidence shows that patients with AD may act as reservoirs for S. aureus transmission to others. This study compared S. aureus colonization in AD patients and their caregivers with control patients and their caregivers. Quantitative cultures were obtained from the lesions, clinically normal skin, hands, and anterior nares of 100 patients with AD, 100 controls with other cutaneous disorders, and 200 caregivers. AD patients had a significantly greater carriage of S. aureus from lesional and clinically normal skin as well as the hand. Significant increases in carriage of S. aureus were found in the anterior nares and hands of caregivers of AD patients compared with control caregivers. Topical corticosteroid use did not affect recovery of S. aureus. There was a significant correlation between recovery of S. aureus from lesional skin and recovery from the anterior nares (p = .002) and hands (p < .0001). These findings suggest that the anterior nares and the hands may be important reservoirs and vectors for transmission of S. aureus to lesional skin and to close contacts of these patients.     

Encoding a superantigen by Staphylococcus aureus does not affect clinical characteristics of infected atopic dermatitis lesions

Background Bacterial infection with Staphylococcus aureus is a known trigger for the worsening of atopic dermatitis (AD). Staphylococcal superantigens have been theorized to make a potential contribution to this worsening of AD seen with infection. Objectives We sought to assess whether encoding a superantigen by S. aureus affects the inflammatory characteristics of impetiginized AD skin lesions. Methods Fifty‐two children with clinically impetiginized lesions of AD which were positive for S. aureus were enrolled in this study. A lesion was graded clinically using the Eczema Area and Severity Index (EASI), and then wash fluid was obtained from the lesion for quantitative bacterial culture, and measurement of bacterial products lipoteichoic acid and staphylococcal protein A and cytokines. The staphylococcal isolate was tested for antibiotic susceptibilities and the presence of a superantigen. Results Fifty‐four per cent (28 of 52) of the staphylococcal isolates encoded a superantigen. The presence of a superantigen had no significant effect on EASI score, amounts of bacterial products or inflammatory cytokines in the AD lesion. Conclusions These studies suggest that the expression of a superantigen by S. aureus alone does not play an important role in the increased skin inflammation associated with staphylococcal infection in childhood AD.     

Recent Microbiological Shifts in Perianal Bacterial Dermatitis: Staphylococcus aureus Predominance

Abstract: Traditionally, bacterial infections of the anal skin have been found to be caused by Streptococcus. The aim of this study was to determine the breakdown of bacterial isolates and the current presentation of bacterial diseases involving the perineum. From the chart review of children who had bacterial cultures of the anus from 2005 to 2008 in a pediatric dermatology practice population in New York City, 26 pediatric patients (ages 5 months to 12 yrs) who had the indications of anal erythema or recurrent buttocks dermatitis were identified. Bacterial cultures of 17 patients grew pathogens, that of 14 (82% of identifiably infected patients) grew Staphylococcus aureus, in 11 as a solo pathogen (6 MSSA and 5 MRSA in 2 family clusters). Streptococcus was identified in three patients, two on culture and one on latex agglutination test; and two patients were identified as having both group A beta hemolytic Streptococcus and Staphylococcus aureus (2 MSSA and 1 MRSA). In patients with S. aureus perianally, concurrent small papules and pustules of the buttocks or extension of the erythema to adjacent buttock skin was the primary clinical feature distinguishing this condition from isolated streptococcal disease. Whereas Streptococcal infections of the anus and buttocks occur commonly, Staphylococcus aureus has become the leading cause of anal bacterial infection in the setting of skin involvement; therefore, antibacterial therapy for anal and buttock bacterial infections should be tailored accordingly.     

Local steroid therapy and bacterial skin flora in atopic dermatitis

A double-blind, randomized trial was conducted to determine the influence of topical steroid therapy on atopic skin flora. The bacteriological and clinical effects of desonide (Locapred®), compared with those of its excipient, were studied in 40 children. Clinical scoring and bacteriological sampling were performed before the start of the trial and after 7 days of once-daily topical treatment. Before treatment, no differences in clinical score or Staphylococcus aureus colonization were noted between the two groups. After treatment, the clinical score improved (P<0.001) in the desonide group, and S. aureus density decreased dramatically (P<0.001). In the excipient group, no significant differences in clinical score or S. aureus density were noted. A comparison of the two groups demonstrated statistically significant differences with regard to clinical score (P<0.001) and S. aureus density (P<0.05). These results show the efficacy of topical corticosteroid treatment alone on S. aureus colonization in atopic skin, and confirm the critical role of inflammation in bacterial colonization.     

The clinical significance of fungi in atopic dermatitis

Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases and is caused by multiple factors including genetic factors, skin barrier defects, host immune responses, allergen sensitivity, environmental effects, and infections. Commonly, bacterial and viral infections are present in the eczematous lesions of AD patients and clearly aggravate the symptoms. However, studies of fungal infections in AD are limited in spite of the fact that there are reports showing that Malassezia, Candida, and some dermatophytes can affect the symptoms of AD. Moreover, certain fungal infections are sometimes overlooked and need to be considered particularly in AD patients with treatment failure as clinical features of those fungal infections could mimic eczematous lesions in AD. Here, we review the epidemiology, pathogenesis, clinical manifestations, and overlooked features of fungal infections associated with the symptoms of AD including the diagnosis and effectiveness of fungal treatments in AD patients.     

Interleukin-18 is elevated in the horny layer in patients with atopic dermatitis and is associated with Staphylococcus aureus colonization

Background An increase in interleukin (IL)‐18 production from epidermal cells has been reported in an atopic dermatitis (AD) mouse model, and subsequent topical application of Staphylococcus aureus results in severe dermatitis. Objectives To reveal the relationship between S. aureus colonization of skin lesions and keratinocyte IL‐18 production, particularly in AD with relatively low serum IgE levels. We also aimed to establish a simple and noninvasive method of assaying IL‐18 produced by epidermal keratinocytes to evaluate local skin inflammation and therapeutic effects in patients with AD. Methods IL‐18 in the horny layer of the skin was collected via a tape‐stripping method and measured in 95 patients with AD and 40 healthy controls by enzyme‐linked immunosorbent assay (ELISA). Clinical severity, blood data and S. aureus skin colonization were evaluated before and after treatment. Results IL‐18 levels in the horny layer were significantly higher in the skin lesions of patients with AD than in healthy controls and correlated with SCORAD, levels of serum IL‐18, IgE, lactate dehydrogenase, thymus and activation‐regulated chemokine, blood eosinophils and transepidermal water loss. In the AD group with serum IgE < 1500 IU mL^?1, significantly higher IL‐18 levels were observed in the horny layer of patients colonized with S. aureus compared with those who were not. Conclusions Epidermal IL‐18 production was associated with the severity of AD. Staphylococcus aureus colonization seems to contribute to this IL‐18 production, especially in the AD group with relatively low IgE production. Tape stripping provides an easy and noninvasive method to assess epidermal IL‐18 production by ELISA.     

Intrinsic alterations of pro-inflammatory mediators in unstimulated and TLR-2 stimulated keratinocytes from atopic dermatitis patients

Abstract: In many patients with atopic dermatitis (AD), the disease is complicated by their enhanced susceptibility to bacterial skin infections, especially with Staphylococcus aureus (S. aureus). Resistance to bacterial skin infections, e.g. S. aureus, is based on the function of intact innate immune mechanisms in the epidermis, mainly provided by keratinocytes. Toll‐like receptor (TLR)‐2 recognizes components of S. aureus and is known to be expressed on keratinocytes. The aim of this study was to investigate intrinsic TLR‐2 expression and cytokine secretion upon TLR‐2 stimulation with peptidoglycan (PGN), lipoteichoic acid (LTA) and N‐palmitoyl‐S‐[2,3‐bis(palmitoyl)‐(2RS)‐propyl]‐(R)cysteinyl‐alanyl‐glycine (Pam3Cys) in keratinocytes from patients with AD compared to healthy controls. Human primary keratinocytes (HPKs) were cultivated from hair follicles of patients with AD and non‐atopic healthy controls and stimulated with Pam3Cys, LTA and PGN. TLR‐2, TLR‐1 and TLR‐6 expression were investigated at the mRNA level. IL‐6, IL‐8, chemokine C‐C motif ligand (CCL)‐20 and MMP‐9 production were studied at the protein level. TLR‐2, TLR‐1 and TLR‐6 were expressed on both HPKs from patients with AD as well as healthy controls without significant differences between these groups. HPKs from patients with AD had an intrinsically reduced capacity to produce IL‐6, IL‐8, CCL‐20 and MMP‐9 and responded less to TLR‐2 stimulation compared to HPKs from healthy controls. Our findings show evidence for intrinsic alterations in HPKs from patients with AD compared to healthy controls and diminished responses upon TLR‐2 stimulation that might contribute to the enhanced susceptibility to skin infections with S. aureus.     

Analysis of Colonization and Genotyping of the Exotoxins of Staphylococcus aureus in Patients with Atopic Dermatitis

Background

The skin of atopic dermatitis (AD) patients has a high susceptibility to Staphylococcus aureus colonization, and the toxins produced by S. aureus may aggravate AD by acting as superantigens.

Objective

The purpose of this study was to evaluate the relationship of the skin barrier function, colonization of S. aureus, and the clinical severity of AD. We also examined the predominant toxin genes produced in Korean AD patients.

Methods

Thirty-nine patients with AD were evaluated for clinical severity and skin barrier function by using Severity Scoring of Atopic Dermatitis (SCORAD) index and transepidermal water loss (TEWL). S. aureus was isolated from the forearm, popliteal fossa, and anterior nares of AD patients (n=39) and age-matched controls (n=40); the toxin genes were analyzed by performing multiplex polymerase chain reaction.

Results

TEWL showed a statistically significant correlation with clinical severity in patients with AD (p<0.05). TEWL was correlated with the number of S. aureus colonization sites and the presence of nasal colonization, but these results were not statistically significant. S. aureus strains were isolated in 64.1% of the 39 AD patients. The SCORAD index and AD severity were strongly correlated with the number of colonization sites. The predominant toxin gene found in AD patients was staphylococcal enterotoxin a (sea) only, which was produced in 52.6% of patients. The toxin genes sea and toxic shock syndrome toxin-1 (tsst-1) were found together in 42.1%, while tsst-1 only was found in 5.3% of the patients.

Conclusion

S. aureus strains were isolated in 64.1% of the 39 AD patients. Skin barrier function, as measured by TEWL, revealed a statistically significant correlation with clinical severity in AD patients. The SCORAD index and severity of AD was strongly correlated with the number of colonization. The most common toxin gene was sea in the Korean AD patients and this gene might have an important role in the pathogenesis of AD.     

Expression of the sweat‐derived innate defence antimicrobial peptide dermcidin is not impaired in Staphylococcus aureus colonization or recurrent skin infections

Antimicrobial peptides are an integral part of innate immunity, and contribute to the protection of human skin from Staphylococcus aureus colonization and infection. We sought to investigate whether the expression of the eccrine sweat‐derived staphylocidal antimicrobial peptide dermcidin might influence S. aureus colonization or recurrent skin and soft‐tissue infections (SSTIs). Eccrine sweat was collected from 18 patients with recurrent S. aureus SSTIs, 28 patients who were intermittent or permanent S. aureus carriers, and 32 noncarriers. Expression and proteolytic degradation of dermcidin was investigated using ELISA and surface‐enhanced laser desorption ionization time‐of‐flight mass spectrometry (SELDI‐TOF‐MS). We found no significant differences in the overall amount or the proteolytic degradation pattern of dermcidin‐derived peptides between healthy noncarriers, intermittent and permanent carriers, and patients with recurrent S. aureus SSTIs. S. aureus colonization or recurrent SSTIs do not seem to be associated with diminished dermcidin expression in eccrine sweat.     

Emergence of Multiresistant Methicillin‐Resistant Staphylococcus aureus in Two Patients with Atopic Dermatitis Requiring Linezolid Treatment

We report two patients with atopic dermatitis who developed methicillin‐resistant Staphylococcus aureus (MRSA) skin infections resistant to clindamycin and trimethoprim‐sulfamethoxazole requiring repeated linezolid treatment. For one patient and family members who received an aggressive regimen of staphylococcal decolonization, including intranasal mupirocin, dilute bleach baths, and bleach cleansing of household items and surfaces, subsequent culture results demonstrated methicillin‐susceptible S. aureus colonization and infection. These findings underscore the challenges presented by multiresistant MRSA infections in children with atopic dermatitis.     

Chronic wound infection: Facts and controversies

Chronic wound infections are responsible for considerable morbidity and significantly contribute to the escalation in the cost of health care. Wound infection may initially be manifest as bacterial colonization, and it is only when colonization is combined with other factors, such as decreased vascular supply, intrinsic virulence of specific bacteria (eg, Staphylococcus aureus), and host immune factors, that true infection occurs. The microbiology of chronic wounds is complex, and it is difficult to discern which bacteria are culpable. Deep cultures or quantitative biopsies of wound tissue may be necessary. In some instances, such as in the presence of certain mycobacteria, isolation of specific organisms confirms causation. In many instances, it is appropriate to treat these wounds empirically with a combination of topical antiseptics and systemic antibiotics, especially in the presence of invasive infections.     

Cutaneous colonization with staphylococci influences the disease activity of Sézary syndrome: a potential role for bacterial superantigens

It has previously been shown that circulating Sézary cells respond in vitro to superantigenic staphylococcal exotoxins in a manner that is restricted by their Vß usage. This study was conducted to examine whether cutaneous colonization with Staphylococcus aureus influences the activity of the skin lesions of Sézary syndrome, and whether S. aureus isolated from patients with Sézary syndrome stimulates circulating Sézary cells in vitro. Two patients with Sézary syndrome, whose skin was colonized with S. aureus, were treated with antibacterial agents, and the relation between the severity of the skin disease and the degree of S. aureus colonization was assessed. In addition, the patients' peripheral blood mononuclear cells were cultured in the presence of mitomycin C-treated S. aureus or superantigenic staphylococcal toxins. The antibacterial treatment improved the skin disease, and eliminated S. aureus in both patients. In one patient, 98% of the peripheral blood mononuclear cells bore Vα2Vß17 of the T-cell receptor, indicative of the presence of an extremely high percentage of circulating Sézary cells. The peripheral blood lymphocytes from this patient responded well in vitro to superantigenic staphylococcal enterotoxin (SE), but not to SEA or toxic shock syndrome toxin-1, or to mitomycin-treated S. aureus isolated from the same patient. Cutaneous colonization by S. aureus influences the disease activity of CTCL, possibly by activation of Sézary cells by bacterial superantigenic exoproteins.