Search

Background: An association between the bacterium Staphylococcus aureus and atopic eczema has been recognized for many years. Although few would dispute the benefit of systemic antibiotics in people with overtly clinically infected eczema, the clinical role of S. aureus in causing inflammatory flares in clinically uninfected eczema is less clear., Objectives/methods: To see if atopic eczema can be improved by antistaphylococcal agents, we performed a systematic review of randomized controlled trials (RCTs) using Cochrane Skin Group's Specialised Register, the Cochrane Central Register of Controlled Trials, MEDLINE (from 2000), EMBASE (from 1980), the metaRegister of Current Controlled Trials (to March 2009), plus manual searching of references and conference proceedings. RCTs that compared interventions to reduce S. aureus in people with atopic eczema with no treatment, vehicle, or another active compound were included. Publication status and language were not barriers to inclusion., Results: Twenty-six studies involving 1229 participants were included. The studies were generally short term and of poor quality. There was no significant difference in global outcome for clinically infected eczema when oral antibiotics were compared with placebo [one study, relative risk (RR) 0.40, 95% confidence interval (CI) 0.13-1.24] or when topical steroid antibiotic combinations were compared with steroid alone (two studies, RR 0.52, 95% CI 0.23-1.16). One study of children with infected eczema that added bleach to bathwater showed a significant improvement in eczema severity when compared with bathwater alone, although the difference could have been explained by regression to the mean. Although antistaphylococcal interventions reduced S. aureus numbers in people with clinically uninfected eczema, none of the studies showed any clinical benefit., Conclusions: We failed to find any evidence that commonly used antistaphylococcal interventions are clinically helpful in people with eczema that is not clinically infected. Their continued use should be questioned in such situations, until better and longer-term studies show clear evidence of clinical benefit.

Background: Staphylococcus aureus can cause secondary infection in atopic eczema, and it may promote inflammation in eczema that does not look infected. Many antimicrobial products exist for eczema, but it is unclear if they work or if they promote bacterial resistance., Objectives: To assess the effects of interventions to reduce Staphylococcus aureus for treating infected or uninfected atopic eczema., Search Strategy: We searched the Cochrane Skin Group Specialised Register (March 2008), the Cochrane Central Register of Controlled Trials (Cochrane Library Issue 1, 2008), MEDLINE (OVID) (from 2002 to March 2008), EMBASE (OVID) (from 2002 to March 2008), Ongoing trials registers (March 2008). References from trials and reviews were searched, pharmaceutical companies were contacted for unpublished trials. There were no language restrictions., Selection Criteria: Randomised controlled trials (RCTs) of people with atopic eczema who have been treated with a product intended to reduce S. aureus on the skin., Data Collection and Analysis: Two people independently performed the study selection, data abstraction and quality assessment., Main Results: We included 21 studies (1018 participants) covering 7 treatment categories. Most studies were poorly reported and study differences limited pooling of results. Adverse effects were especially poorly reported, and only one study reported the emergence of resistant bacterial strains following oral antibiotics. Oral antibiotics were not associated with benefit in non-infected (2 trials, 66 participants) or infected eczema (1 trial, 33 participants). We did not find any benefit for antibacterial soaps (1 trial, 50 participants), or antibacterial bath additives (2 trials, 41 participants), or topical antibiotics/antiseptics (4 studies, 95 participants). Adding antibiotics to topical corticosteroids reduced numbers of Staphylococcus aureus in 4 trials (302 participants), but there was no evidence of any clinical benefit in 9 trials involving 677 participants: betamethasone plus neomycin vs clobetasol (MD 1.2; 95% CI 0.25, 2.15), prednicarbate plus antimicrobial vs prednicarbate (RR 0.64; 95% CI 0.25, 1.68), or betamethasone valerate plus gentamicin vs betamethasone (RR 0.31; 95% CI 0.07, 1.35). One trial (30 participants) showed no significant improvement in eczema for those using silver textiles (RR 2.67; 95% CI 0.98, 7.22), despite using 10 times the amount of topical steroids., Authors' Conclusions: We failed to find clear evidence of benefit for antimicrobial interventions for people with atopic eczema, despite their widespread use. This does not necessarily mean they do not work because the studies were small and poorly reported. Further large studies with long-term outcomes and clearly defined participants are urgently required.

Background: Staphylococcus aureus has a role in the pathophysiology of atopic eczema. Topical fusidic acid is widely used in its treatment. There is concern that topical use of fusidic acid may be driving the selection and dissemination of fusidic acid-resistant (FusR) S. aureus., Objectives: To test the hypothesis that treatment of atopic eczema for 2 weeks with topical fusidic acid/steroid combination can increase carriage of FusRS. aureus., Methods: Forty-six patients with atopic eczema were allocated randomly to one of two treatment groups. Group 1 (28 patients) were treated with topical 2% fusidic acid plus 0.1% betamethasone cream, and group 2 (18 patients) with topical 2% mupirocin and 0.1% betamethasone cream. The clinical response and nasal and skin colonization with S. aureus were recorded before treatment and after 1 and 2 weeks of therapy., Results: Baseline samples from the site of worst eczema showed S. aureus (sensitive and resistant) in 76% of patients, and FusRS. aureus in 26%, with no significant difference between treatment groups. After 1 and 2 weeks, both groups showed similar significant clinical improvement. The overall median clinical improvement was paralleled by a reduction in prevalence and population density of S. aureus (sensitive and resistant) at the worst eczema site (P < 0.0001). However, for FusRS. aureus there was no significant change in the prevalence of carriage, or population density in either group compared to baseline. Over 50% of patients carried S. aureus in the nerves and over 20% carried FusRS. aureus. Neither regimen affected either the prevalence or population density of S. aureus or FusRS. aureus in the nerves., Conclusions: In this small study there is no evidence to support the hypothesis that short-term treatment of atopic eczema with fusidic acid/steroid combination increases fusidic acid resistant S. aureus during a 2-week period.

A retrospective study was carried out to investigate possible reasons for a marked increase in fusidic acid-resistant Staphylococcus aureus (FusR S. aureus) identified by our routine hospital microbiology service. Information was obtained on a sample of 64 consecutive patients from whom resistant S. aureus had been cultured. The source of isolates was found to be diffuse within the hospital and community. The site of sample was most frequently chronic cutaneous infections (68%). All the S. aureus isolates were resistant to both fusidic acid and penicillin and many were resistant to multiple antibiotics. Topical fusidic acid had been used by 40% of patients in the preceding 6 months and none had received oral fusidic acid (sodium fusidate). Most (80%) had received an oral antibiotic in the preceding 2 years. Information from the Prescriptions Pricing Authority revealed that the total number of prescriptions for fusidic acid-containing preparations for the period September 1997 to August 1998 was markedly higher in Harrogate than in five other local areas where increases in (FusR) S. aureus have not been observed.