Staphylococcus aureusand atopic eczema

What are the therapeutic

implications?

Third Edition

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Atopic eczema (synonymous with atopic dermatitis) is a

common chronic skin condition mainly affecting children and

follows a remitting and relapsing course. It is characterised by

intense itching, redness, inflammation and exudation. It affects

mainly the flexor surfaces of the elbows and knees, as well as

the face and neck.

Estimates of the prevalence of eczema vary but it has been

reported recently that the recorded incidence and lifetime

prevalence of patients with eczema has increased in England

in the new millennium. With almost 1 in 9 of the population

experiencing the condition at some point in their lives, eczema

is now one of the most common chronic conditions to affect

the English population.1

Atopic eczema may affect as many as 15 to 20% of school-age

children and 2 to 10% of adults in the United Kingdom.2 Atopic

eczema can continue into adolescence and adult life as a chronic

disease but it can be expected to clear in approximately 65%

of children by the time they are seven years of age and in

approximately 74% of children the eczema will have disappeared

by 16 years of age. 3

The severity of atopic eczema varies enormously, from an

occasional dry, scaly patch to a debilitating disease where much

of the body is covered by excoriated (scratched and abraded),

bleeding and infected lesions. Its course may be continuous for

prolonged periods or of a relapsing-remitting nature

characterised by acute flare-ups.

Atopic eczema can have a significant impact on quality of life.

In addition to the burden of daily treatment, the condition may

affect everyday activities, such as work or school and sleep

disturbance is common, especially during flare-ups.

Severe atopic eczema in children can also have a significant

impact on family life, with parents/carers having to cope with the

demands associated with caring for a child with a chronic illness.

A. INTRODUCTIONThe precise cause of atopic eczema is unknown but

immunological, genetic and environmental factors play a role.

It often has a genetic component that leads to the breakdown

of the skin barrier. This allows ingress of trigger factors such as

irritants, allergens and microorganisms which can make the

eczema worse.

Itchy skin (pruritus) is a major symptom of atopic eczema.

A vicious circle can develop, where itching and scratching damage

the skin and increase inflammation, which in turn increases the

itch. Scratching can damage the skin and cause bleeding,

secondary infection and thickening of the skin (lichenification).

The combination of a vicious itch-scratch cycle with frequent

flare-ups has long been known; however it is only relatively

recently that the extent of the involvement of Staphylococcus

aureus (S. aureus) in atopic eczema has been recognised.

This booklet provides a review of key data published on the link

between S. aureus and atopic eczema. Extracts from papers are

provided for easy reference, together with a diagrammatic

summary of the role of the bacteria in the exacerbation of

the disease. Finally, there is a review of how these recent

developments in our understanding of the pathophysiology of

atopic eczema can be of practical relevance to the successful

management of this often debilitating and distressing condition.

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CONTENTS

A. Introduction ……………………………………………………………………………………………………………………………2

B. Incidence of Staphylococcus aureus……………………………………………………………………………3

A defective skin barrier

Skin colonisation

Skin adherence of S. aureus …………………………………………………………………………………………………………4

C. The pathophysiological role of Staphylococcus aureus

in atopic eczema …………………………………………………………………………………………………………………5

S. aureus ‘vicious circle’…………………………………………………………………………………………………………………6

D. Clinical implications of Staphylococcus aureus

colonisation of the skin ……………………………………………………………………………………………………7

Severity of eczema

Transmission and recolonisation …………………………………………………………………………………………………8

E. Therapeutic implications of Staphylococcus aureus

colonisation of the skin ……………………………………………………………………………………………………9

a) Controlling S. aureus levels

b) Development of bacterial resistance ……………………………………………………………………………………11

F. Rationale for using the Dermol range of antimicrobial emollients ………………13

a) Importance of formulation to patient compliance

b) Clinical evaluation of the Dermol range

i) Dermol Lotion ……………………………………………………………………………………………………………14

ii) Dermol Cream ……………………………………………………………………………………………………………15

iii) Dermol Bath Emollient

c) Antimicrobial efficacy of the Dermol range …………………………………………………………………………16

i) Dermol Lotion ………………………………………………………………………………………………………………17

ii) Dermol Bath Emollient…………………………………………………………………………………………………18

d) Avoiding antimicrobial resistance …………………………………………………………………………………………19

e) Efficacy of the Dermol range against resistant strains of S. aureus ………………………………………20

f ) Dermol Lotion used as an antimicrobial soap substitute ……………………………………………………21

g) Dermol range prescribing information …………………………………………………………………………………23

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Noble W.C. British Journal of Dermatology 1998;139:9-12

‘The normal bacterial skin flora in humans is composed of three major groups of Gram-positive bacteria, the coryneformbacteria, the micrococci and the staphylococci, with only aminor component of Gram-negative bacilli. This is chieflybecause the skin is a comparatively dry habitat, with availablewater as the chief factor controlling growth; occlusion of skin is a potent way to increase the number of bacteria on the skin.Gram-negative bacilli require more available water than Gram-positive bacteria and this probably controls theirpopulation density.’

‘The factors that permit skin colonization in eczema, orconversely prevent colonization in normal individuals, are notknown, but since the essential fatty acids are more toxic to S. aureus than to the coagulase-negative species, and since a deficit of essential fatty acids may result in a poor skinstructure, this may form part of the equation.’

Roll A., Cozzio A., Fischer B. & Schmid-Grendelmeier P. Current Opinion in Allergy and Clinical Immunology2004;4(5):373-378

‘S. aureus can be isolated from lesional skin, especially fromintertriguous regions, the nose (‘nasal carriage’), as well as unaffected atopic skin. Next to mechanical triggers(scratching), predominantly alkaline pH and decreased IgA secretion through sweat production, there are severalimportant pathophysiological features leading to thedisruption of the primary skin defence system. Various factorscontributing to increased numbers of S. aureus in atopic skinand the perpetuation of inflammation have recently beendiscovered: altered lipid composition within the stratumcorneum; exposed extracellular matrix adhesins; changes inimmune response; bacterial superantigens and increasedspecific IgE production.’

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A defective skin barrier

The skin acts as an effective barrier to the external environment preventing the ingress of allergens and microbes while preventing water

loss through the skin. In atopic eczema the skin barrier is compromised, in part due to decreased production of skin lipids leading to dryness,

fissuring and penetration of environmental toxins, allergens and microbes such as S. aureus. This results in inflamed, itchy and possibly infected skin.

Skin colonisation

In patients with atopic eczema there is an increased incidence of S. aureus in both lesional and non-lesional skin. Nasal carriage of S. aureus

is also higher in patients with atopic eczema.

Aly R., Maibach H.I. & Shinefield H.R. Archives of Dermatology 1977;113:780-782

B. INCIDENCE OF STAPHYLOCOCCUS AUREUS

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Patel S.D. & Noble W.C. Microbial Ecology in Health & Disease 1993;6:181-184

‘Patients with atopic dermatitis, who are invariably colonisedwith Staphylococcus aureus, showed changes in the lipidcompositions before and after treatment. Skin lipids whichmoderate microbial growth may be suppressed in atopicdermatitis permitting the overgrowth of S. aureus.’

‘Staphylococcus aureus is usually transient on the normal skin surface, the common resident sites are the nose, axillae,perineum and toewebs. The relative rarity of colonisation by S. aureus on normal skin sites contrasts dramatically with thehigh carriage rate in all patients with atopic dermatitis andcutaneous infection is one of the factors that plays a role in the aggravation of this condition.’

‘The role of S. aureus may be to aggravate atopic dermatitis or prevent the resolution of the lesions. Not only is it found inlesions, where it may be recovered with an average density ofabout 2 x 107 organisms/cm2 in acute lesions, but it is also thedominant organism on the clinically normal skin of thesepatients, although the density is lower.’

NON ATOPICS Nasal carriage (10-45%)

Reported colonisation of S. aureus

NON ATOPICS Skin excl. perineum (<10%)

ATOPICS Nasal carriage (79%)

ATOPICS Eczematous lesion (93%)

ATOPICS Non Involved skin (76%)

= S. aureus presentKey: = S. aureus absent

Leyden J.J., Marples R.R. & Kligman A.M. British Journal of Dermatology 1974;90:525-530

‘Atopic dermatitis is thought to be a multifactorial disease.Staph. aureus overgrowth appears to be a neglected component.More than 90% of patients with chronic lichenified plaquescarried this pathogen. Indeed, Staph. aureus was overwhelminglythe dominant species with counts exceeding 106/cm2 in abouthalf of the patients. The affinity of Staph. aureus for atopicdermatitis was even more pronounced in the acute, exudativeform of the disease. Staph. aureus was recovered 100% of thetime with a mean density of 18,417,000 organisms per cm2 inacute lesions. In only five of twenty patients was the density lessthan 107/cm2. Despite these huge numbers, the lesions did notlook infected. Only in the acute exudative form was there anyhint of a harmful effect of Staph. aureus, visible as a slightserous exudate and thin crust.’

‘A question of major importance is whether these extraordinarilyhigh numbers of Staph. aureus represent secondary infection orharmless colonization. Staph. aureus is not a customary memberof the cutaneous microflora except for occasional resident statusin the perineum.’

Skin adherence of S. aureus

Increased colonisation of atopic eczema patients with S. aureus may be due to increased adherence of the bacteria to the stratum corneum.

Skin surface lipid deficiency in atopic eczema patients may also play a critical role in S. aureus colonisation.

Cole G.W. & Silverberg N.L. Archives of Dermatology1986;122:166-169

‘Staphylococcus aureus has a peculiar ability to colonize the skinof patients with atopic dermatitis. We examined the possibilitythat this might be due to a specific ability of this pathogenicstaphylococcus to adhere to atopic stratum corneum. We used an in vitro model to show that S. aureus does have an unusualability to adhere to atopic corneocytes when compared withcorneocytes obtained from patients with other cutaneousdiseases, including psoriasis. Protein A – a component of thestaphylococcal cell wall – may be responsible in part for thisadherence phenomenon. This trait did not extend to other gram-positive bacteria tested.’

Baker B.S. Clinical and Experimental Immunology2006;144:1-9

‘Various factors are involved in the altered skincolonization by S. aureus in AD including an alteredepidermal barrier, increased bacterial adhesion, defective bacterial clearance, and decreased innateimmune responses.’

‘S. aureus are tightly attached to the uppermost corneocytes,and can penetrate the epidermis via the intercellular spacesprobably as a result of lipid deficiencies in AD skin. In AD,the average pH of the skin is slightly more alkaline, andsphingosine levels are decreased in both lesional andnonlesional stratum corneum. In addition, the dryness andcracking of AD skin, as a result of transepidermal water losscaused by altered lipid content, may facilitate bacterialcolonization. Furthermore, Th-2 cytokines such as IL-4 inatopic skin increase expression of fibronectin and fibrinogen,receptors that mediate the adhesion of S. aureus to stratum corneum.’

Morishita Y., Tada J., Sato A., Toi Y., Kanzaki H., Akiyama H. & Arata J. Clinical and Experimental Allergy1999;29:1110-1117

‘The current study revealed that the bacterial cells tightly attached to the uppermost corneocytes and could penetrate theepidermis via the intercellular spaces. Fibrillar and amorphousstructures, which were positive for ruthenium red stain and might be derived from products of S. aureus cells, plasmacomponents, or a mixture of both, were found between the S. aureus cells in contact with each other and between S. aureuscells and corneocytes.’

The findings in this study, especially penetration of S. aureus intointercellular spaces of the epidermis, strongly suggest that skinsurface lipids in AD patients are deteriorated.’

Breuer K., Häussler S., Kapp A. & Werfel T. British Journal of Dermatology 2002;147:55-61

‘The susceptibility of the atopic skin to colonization with S. aureus may be for several reasons: S. aureus cell wallsexhibit receptors, the so-called adhesins, for epidermal anddermal fibronectin and fibrinogen. As the skin of patients withAD lacks an intact stratum corneum, dermal fibronectin mightbe uncovered and increase the adherence of S. aureus. Fibrillarand amorphous structures have been traced between S. aureuscells and corneocytes and may result in a bacterial biofilm thatcontributes to the adherence of S. aureus. Skin surface lipidssuch as free fatty acids and polar lipids have been shown toexhibit antibacterial activity. The observation that S. aureuspenetrates into intracellular spaces of the epidermis suggeststhat skin surface lipids are deteriorated in patients with AD.Furthermore, immunological factors might also enhancesusceptibility to S. aureus.’

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Cardona I.D., Cho S.H. & Leung D.Y.M. American Journal of Clinical Dermatology 2006;7(5):273-279

‘A defective skin barrier does not entirely account for theincreased susceptibility that AD patients have to skin infectionbecause patients with psoriasis have also been reported to havereduced skin barrier function. However, patients with ADexperience four times more skin infections than patients withpsoriasis. Importantly, decreased innate immune responses have been found in AD, as compared with psoriatic skin.’

Leung D.Y.M., Harbeck R., Bina P., Reiser R.F., Yang E., Norris D.A., Hanifin J.M. & Sampson H.A. Journal of Clinical Investigation 1993;92:1374-1380

‘These findings suggest the possibility that local production ofexotoxin at the skin surface could cause IgE-dependent mast celldegranulation. This could have several important consequences.First, the acute release of histamine and other mediators couldtrigger the itch-scratch cycle which can exacerbate AD. Moreimportant, mast cell degranulation results in the local release ofmediators, cytokines, and leukocyte chemotactic factors that resultin late-phase inflammatory reactions. Since patients with AD arecolonized with S. aureus, the continuous release of exotoxins intothe skin may promote the chronic inflammation found in AD.’

‘These data may also explain the clinical observation that many flares of eczema correlate with high colonization counts of S. aureus on the skin and that the skin rash frequently resolveswhen S. aureus is eradicated or drastically reduced following antibiotic therapy.’

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Birnie A.J., Bath-Hextall F.J., Ravenscroft J.C., Williams H.C. Cochrane Database of Systematic Reviews. 2008 Jul 16;(3):CD003871.

‘…several possible mechanisms for a pathogenic role have alsobeen suggested. There may be a direct chemical irritation or a non-specific reaction of the protein A component of thebacterium with immune cells. Great interest has been shown inpossible mechanisms involving superantigens. The superantigentheory proposes that S. aureus exacerbates or maintains skininflammation in atopic eczema by secreting a group of toxins,which are capable of stimulating large populations of T-lymphocytes distant from the eczematous site, giving rise towidespread activation of existing lesions. Several lines ofinvestigation support a role for superantigens in atopic eczema. First, it has been shown that such toxins can be produced by S. aureus isolated from atopic eczema patients, and that in thesepatients a T-lymphocyte expansion consistent with superantigenstimulation has occurred. Second, most atopic eczema sufferersmake specific IgE antibodies directed against superantigen toxinsfound on their skin. Third, a correlation has been found betweenthe presence of these antibodies and the severity of the eczema.Finally, the application of one specific superantigen to the skinhas been shown to induce skin changes of erythema andthickening of the skin.’

‘As a consequence of such findings, it is not surprising that anumber of products with anti-staphylococcal properties havebeen developed for the treatment of atopic eczema, both clinically infected and uninfected, ranging from antibacterialsoaps, impregnated clothing, to additives to bath oils and topical corticosteroids.’

Leung D.Y.M., Hauk P., Strickland I., Travers J.B. & Norris D.A. British Journal of Dermatology 1998;139:17-29

‘To study the mechanisms by which S. aureus might exacerbateAD, Leung et al characterized the toxins produced by S. aureusisolates from the skin of AD patients. More than half of the ADpatients had S. aureus that secreted identifiable toxins, primarilythe superantigenic toxins SEA, SEB and TSST-1. As a proof ofconcept, Strange et al studied the effects of SEB applied to intactnormal skin and the uninvolved skin of patients with AD. Theyreported significant erythema and induration followingapplication of SEB to uninvolved normal-appearing AD skin. Three of the six AD subjects studied experienced a flare of theirdisease in the elbow flexure ipsilaterally to where the SEB patchwas applied. These authors concluded that superantigens canexacerbate and sustain the inflammation associated with AD.’

‘...These findings raise the possibility that epicutaneoussuperantigenic toxins induce specific IgE in AD patients, leadingto mast-cell degranulation in vivo when the toxins penetrate thedisrupted epidermal barrier, thereby promoting the scratch-itchcycle prominent in atopic patients. In addition, recent studiesindicate that staphylococcal superantigens can trigger B cells toproduce allergen-specific IgE, providing a novel mechanism bywhich microbial superantigens could aggravate allergic responses.’

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A number of studies investigating the pathogenic role of S. aureus in atopic eczema have been published. Findings show that S. aureus releases

exotoxins that act as superantigens and are potent immunostimulators. The exact role of these exotoxins and the subsequent immune reaction

stimulated have been widely investigated and reported.

C. THE PATHOPHYSIOLOGICAL ROLE OF STAPHYLOCOCCUS AUREUS

Morishita Y., Tada J., Sato A., Toi Y., Kanzaki H., Akiyama H. & Arata J. Clinical and Experimental Allergy 1999;29:1110-1117

‘Further studies and our previous report revealed that 70-80% of allthe patients tested had a significantly higher incidence of circulatingIgE antibodies specific for SEA and/or SEB (P<0.001) compared withthose in two control groups. Because the staphylococcal enterotoxinsseem to penetrate the injured skin barrier in patients with AD moreeasily than they do an intact skin barrier these findings stronglysupport the possibility that in the majority of AD patients SEA andSEB have a role in exacerbation and prolongation, and/or act as atrigger of AD through IgE-dependent immunoreaction. Even inpatients with mild AD, staphylococcal toxins might have similareffects on the lesions as those in patients with severe AD.’

It is known that S. aureus causes a ‘vicious circle’ in atopic eczema. Release of superantigenic exotoxins activates large populations of T cells,

resulting in release of cytokines, IgE and inflammatory mediators. This contributes to the exacerbation and maintenance of skin inflammation

in atopic eczema patients. This also permits more S. aureus to infiltrate the inflamed and disrupted epidermal barrier thus reinforcing the cycle.

The vicious circle caused by Staphylococcus aureus in atopic eczema

S. aureusS. aureus

S. aureus

S. aureus

EPIDERMIS

T cell activation

INFLAMMATIONON ECZEMA LESION

INFLAMMATORYMEDIATORS

MASSIVE CYTOKINEINTERLEUKIN-4 (IL-4)

PRODUCTION

MASTCELL

B

IgE

T

Genetic predisposition in atopic eczema to produce high levels of cytokine IL-4 in response to environmental triggers.

B cells release IgE instead of IgM following stimulation by IL-4.

Increased population of S. aureus especially if skin exudative or excoriated.

Exotoxins (▼) are superantigens (potent immunostimulatory molecules).

IgE bindsto mast cells.

Degranulation of activated mast cell on exposure to antigen (staphylococcal exotoxin).

Kemp A.S. & Campbell D.E. Journal Paediatric Child Health1996;32:4-6

‘Atopic dermatitis is a chronic pruritic inflammatory disordercharacterized by infiltration of the skin by T cells, monocytes and macrophages. Although atopic dermatitis forms part of theatopic spectrum and is accompanied by marked elevations inimmunoglobulin E (IgE) antibodies, the cutaneous infiltrate is suggestive of a cell-mediated immune reaction with apredominance of T cells. Inflammatory stimuli leading to thedevelopment of the skin lesions are poorly understood and may relate to cytokine imbalance. It is believed that children with atopic dermatitis have cytokine imbalance with increasedsecretion of interleukin-4 (IL-4) and decreased secretion ofinterferon gamma (γ-IFN).’

‘An obvious question that arises is what is the stimulus for theactivation of T cells in atopic dermatitis? A likely candidate isStaphylococcus aureus; S. aureus skin colonization is an almostuniversal feature of severe atopic dermatitis ... Staphylococcusaureus secretes exotoxins, called superantigens, which stimulate

a large proportion of T cells through interaction with the Vß region of the T cell receptor and MHC class II molecules. Thesesuperantigens stimulate larger numbers of peripheral lymphocytesthan normal antigens as they are not dependent on recognition by a specific binding site on the hypervariable region of the T cell receptor. ...In addition to the stimulation of T cells, S. aureusantigens also may promote B cell growth and differentiation andthus many contribute to the elevated IgE levels characteristic ofatopic dermatitis. Staphylococcus aureus superantigens are potent activators of B cells through cytokines released by T cells.’

‘Paediatricians have long known that treatment of children with severe atopic dermatitis with anti-Staphylococcal antibioticscan produce a rapid and significant improvement. The recentunderstanding of the inflammatory response implicates a majorrole for T cells in this disorder. Thus the effectiveness of antibiotictreatment may not be simply due to control of secondaryinfection, but also due to the removal of antigens and superantigenswhich initiate specific and non-specific T cell stimulation.’

MHC = major histocompatibility complex.

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Leyden J.J., Marples R.R. & Kligman A.M. British Journal of Dermatology 1974;90:525-530

‘High numbers of Staph. aureus may not only intensify pre-existing lesions but may have great importance in relation to public health. Inflamed skin has been recognised as a majorsource of dissemination of Staph. aureus in hospital wards. Fatal infections have been traced to dermatitic skin. We witnessed one such epidemic of Staph. aureus woundinfections in a gynaecology ward, the source in this instancebeing atopic dermatitis in the resident physician. Phage typingand antibiotagram established the identity of the organism in each wound with that of the atopic lesion. On severaloccasions, we observed primary pyodermas (furuncles) inmembers of families of patients with atopic dermatitis, theidentity of the organism being validated as above.’

Williams J.V., Vowels B.R., Honig P.J. & Leyden J.J. Paediatric Dermatology 1998;15:194-198

‘Staphylococcus aureus colonization is common in atopicdermatitis (AD) and can exacerbate the disease. Additionally,some evidence shows that patients with AD may act asreservoirs for S. aureus transmission to others. This studycompared S. aureus colonization in AD patients and theircaregivers with control patients and their caregivers... ADpatients had a significantly greater carriage of S. aureus fromlesional and clinically normal skin as well as the hand.Significant increases in carriage of S. aureus were found in theanterior nares and hands of caregivers to AD patients comparedwith control caregivers. Topical corticosteroid use did not affect recovery of S. aureus. There was a significant correlationbetween recovery of S. aureus from lesional skin and recoveryform the anterior nares (p=.002) and hands (p<.0001). Thesefindings suggest that the anterior nares and the hands may be important reservoirs and vectors for the transmission of S. aureus to lesional skin and to close contacts of these patients.’

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D. CLINICAL IMPLICATIONS OF STAPHYLOCOCCUS AUREUS

COLONISATION OF THE SKIN

Severity of eczema

Colonisation of atopic eczema patients with S. aureus has been well documented as has the role of S. aureus derived superantigens in atopic

eczema. In this section the clinical implications of S. aureus colonisation and the effects this may have on disease severity are reported.

Goodyear H.M., Watson P.J., Egan S.A., Price E.H., Kenny P.A. & Harper J.I. Clinical and Experimental Dermatology1993;18:300-304

‘The bacterial flora of the skin was assessed quantitatively in 50 children with eczema, aged 6 months to 14 years, referred tothe hospital for the first time. Twenty non-atopic controls with an unrelated non-infective disorder were also studied.’

‘Bacterial colonization of the skin was consistently more commonand greater in amount from patients compared with controls.Staphylococcus aureus was the most common pathogen isolatedfrom patients only; from the worst affected area of eczema in74% of patients and from an uninvolved skin site in 30% ofpatients. Quantitative assessment showed that the density ofcolonization was proportional to the severity of eczema.’

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Motala C., Potter P.C., Weinberg E.G., Malherbe D. & Hughes J.Journal of Allergy and Clinical Immunology 1986;78:583-589

‘In this study the group of patients with anti-S. aureus IgEantibodies had a higher prevalence of superficial pustules. The70% nasal carriage of S. aureus in the group with anti-S. aureusIgE antibodies was higher than reported in normal subjects (30%to 40%). This may be a contributing factor to the high prevalenceof skin sepsis in these patients. The eradication of S. aureus fromthe nasal reservoir and eczematous skin would appear to be alogical step in the treatment of these patients. Our results alsoindicate that patients with atopic dermatitis who have developedthese antibodies tend to have more severe disease. Adult patientswho had anti-S. aureus IgE invariably had a history of long-standing severe disease since childhood. It is likely that thepresence of anti-S. aureus IgE antibodies may predict a morechronic course and less favourable outlook for patients withatopic dermatitis.’

Gong J.Q., Lin L., Lin T., Hao F., Zeng F.Q., Bi Z.G., Yi D. & Zhao B. Clinical and Laboratory Investigations2006;155:680-687

‘On the whole, the colonization rate of bacteria and the positive rate of S. aureus were distinctly higher in lesional than in nonlesional skin of patients with eczema and AD. The differences were highly significant. There were positivecorrelations between the bacterial colonization density and theseverity of eczema and AD. By comparing the flora distributionand constituent ratio in patients with eczema and AD, we foundthat the positive rate of S. aureus in the AD group was distinctlyhigher than in the eczema group, not only in lesional skin butalso in nonlesional skin. This shows that S. aureus infectionplays a more important role in the pathogenesis of AD.’

Ricci G., Patrizi A., Neri I., Bendandi B. & Masi M. Pediatric Dermatology 2003;20(5):389-392

‘The goal of this study was to evaluate the frequency and role ofStaphylococcus aureus infection in patients with atopic dermatitis(AD). In 81 children, ages 2 months to 9 years, affected withmoderate to severe AD, 308 samples from the cutaneous lesionswere obtained and analyzed. S. aureus was isolated in 52 children(64.2%).’

‘Our data demonstrate the importance of S. aureus in the clinicalmanifestation of AD and, in particular, its role in worsening theeczematous lesions of the face, neck, and perineum in children less than 1 year of age.’

‘S. aureus colonization and infection of the skin are thought toplay an important role in the pathogenesis of AD. Many studiesshow that the extent of S. aureus colonization of the skin of ADpatients correlates with disease severity, and in our study theinfection rate of AD was higher in patients with severe AD(SCORAD > 40, 70.2% of infected patients) than in patients with moderate AD (55.8%).’

Bunikowski R., Mielke M., Skarabis H., Herz U., BergmannR.L., Wahn U. & Renz H. Journal of Allergy and ClinicalImmunology 1999;103:119-124

‘The skin of patients with atopic dermatitis exhibits a strikingsusceptibility to colonization and infection with Staphylococcusaureus. In this context it has been previously shown that S. aureus-derived superantigens could function as classicallergens, inducing production of functionally relevant specificIgE antibodies.’

‘Twenty of 58 children (34%) were sensitized to superantigens(45% to SEB, 10% to SEA, 45% to SEA and SEB). In thisgroup, severity of atopic dermatitis and levels of specific IgE tofood and air allergens were significantly higher. The degree ofdisease severity correlated to a higher extent with the presence of SEA/SEB-specific antibodies than with total serum IgE levels.Density of colonization with superantigen-secreting S. aureusstrains was higher in the superantigen IgE-positive group. Sixty-three percent of these children experienced repeatedepisodes of superficial S. aureus skin infections.’

‘Sensitization to S. aureus-derived superantigens may be involved in disease exacerbation. The presence of SEA/SEB-specific antibodies had additional explanatory value for disease severity and therefore may be helpful in thecharacterization of children with severe atopic dermatitis.’

Atopic eczema patients colonised with S. aureus may act as carriers or ‘reservoirs,’ leading to transmission of the bacteria and possible infection

to other subjects. Similarly, these S. aureus ‘reservoirs’ may lead to recolonisation of patients following S. aureus eradication therapy.

Transmission and recolonisation

Breuer K., Häussler S., Kapp A. & Werfel T. British Journal of Dermatology 2002;147:55-61

‘Our results confirm the possible role of colonization with S. aureus as an aggravating factor in AD. S. aureus wasisolated from the majority (94%) of our patients, either from the skin (11%) or the anterior nares (6%) or, as inmost cases (77%) from both sites, suggesting the nose mayact as a reservoir of S. aureus strains, which are spread overthe skin surface by autotransmission. The fact that the nasaland cutaneous strains produced the same toxins in mostcases supports this hypothesis. Of our patients, 50% carriedS. aureus on both clinically affected and unaffected skin, and cultures could be grown from both acute and chroniclesions, which is in keeping with the data reported by other groups.’

Patel G.K., Wyatt H., Kubiak E.M., Clark S.M. & MillsC.M. Acta Dermato-venereologica 2001;81:366-367

‘Nasal carriage of S. aureus is common among the generalpopulation (up to 35% carriage rate) and is higher amongpatients with atopic eczema (39-82% colonized). Of the 17patients with nasal S. aureus carriage in this study, only twodid not have S. aureus on skin swab culture; one of thesehad previously been treated with antibiotics. A furtherpossible explanation for the persistence of S. aureus despiteprior antibiotic treatment is colonization of the parentleading to re-colonization of the child. Only 6 of the 46parents had nasal carriage of S. aureus; however, in all thesecases the children were also colonized with S. aureus. It seems likely that parental S. aureus carriage influences S. aureus colonization in the child.’

Gilani S.J.K., Gonzalez M., Hussain I., Finlay A.Y. & Patel G.K.Clinical and Experimental Dermatology 2005;30:10-13

‘Patients with atopic dermatitis (AD) are often heavily colonizedby Staphylococcus aureus, which adversely affects eczemaseverity. Strategies to control S. aureus in AD include antibioticand or antiseptics. However long-term efficacy is unclear. In this study we consider extra-cutaneous factors that may causeS. aureus re-colonization in adult AD. Twenty-one patients with AD were recruited and were assessed for: duration of AD,use of topical or oral antibiotic within the preceding 3 months,the number of hospital admissions during the preceding year andcurrent treatment. The types of topical treatments used, vehicle,container and the expiry dates were also recorded. The severity

of AD was assessed by SCORAD index. Microbiologicalassessment for S. aureus carriage from affected skin, anteriornares, emollient and topical steroid was undertaken usingculture, Staphaurex test and antibiotic resistance. Of the patients 86% had S. aureus colonization. The median SCORADscore were greater in those colonized with S. aureus (P=0.02) and those with contaminated treatments (P=0.05). Priorantibiotic treatment, prior hospital admission and nasal carriage did not influence the median SCORAD. Three extra-cutaneous mechanisms by which S. aureus can re-colonize the skin were identified: antibiotic resistance, nasal carriage and treatment contamination.’

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 7

Huang J.T., Abrams M., Tlougan B., Rademaker A. & Paller A.S. Pediatrics 2009;123(5):e808-e814

‘We show here that the concurrent use of intermittentintranasal mupirocin treatment and dilute bleach baths led tosignificant improvement in the severity of moderate/severe AD.Decreased EASI scores at the 1-month visit, after a 2-weekcourse of cephalexin therapy, might have been predicted.However, the continued improvement in EASI scores in thetreatment arm at the 3-month visit, as well as the significantdifferences in the extent of involvement and severity of ADbetween the treatment and placebo groups despite the courseof antibiotic therapy, supports the therapeutic benefits ofsodium hypochlorite baths and intranasal mupirocin treatmentin AD. Furthermore, the statistically significant reductions inEASI scores at 1 month and dramatically at 3 months forbody sites exposed to the dilute bleach baths but not for theunexposed head and neck regions provide clear evidence thatthe addition of dilute bleach baths to intranasal mupirocintreatment decreased the severity of AD.’

‘The use of this easy nonantibiotic approach to inhibitovergrowth of organisms is preferable to the use of antibiotics,which may promote further S. aureus resistance. The potentialfor development of bacterial resistance to mupirocin ointment,however, should not be neglected.’

10

E. THERAPEUTIC IMPLICATIONS OF STAPHYLOCOCCUS AUREUS

COLONISATION OF THE SKIN

a) Controlling S. aureus levels

Treatment guidelines for atopic eczema in children have been published recently by the National Institute for Health and Clinical Excellence

(NICE).4 A stepwise approach for the management of atopic eczema is advocated by tailoring the treatment step to the severity of the

condition. Emollients should form the basis of atopic eczema management supplemented with topical corticosteroids and possibly leading

on to more potent topical immunomodulatory preparations in severe disease.

When S. aureus is involved, NICE recommends the following management strategies.

Recommendations for the management of S. aureus eradication in non-clinically infected atopic eczema, however, are not given. In this situation

systemic or topical antibiotics may be used but have the potential for development of resistance. Antimicrobial emollients offer a therapeutic

option by reducing bacterial load and repairing the defective skin barrier. This breaks not only the S. aureus superantigen induced ‘vicious circle’

in atopic eczema but also the ‘itch/scratch cycle’.

9

Treatment Use for Time

Systemic antibiotics activeagainst S. aureus andstreptococcus

Widespread bacterial infections 1-2 weeks

Topical antibiotics, includingthose combined with topicalcorticosteroids

Localised clinical infection Maximum of 2 weeks

Flucloxacillin First-line treatment of S. aureus and streptococcal infections As indicated

ErythromycinFirst-line treatment of S. aureus and streptococcal infections in the case of allergy to flucloxacillin or flucloxacillin resistance

As indicated

ClarithromycinFirst-line treatment of S. aureus and streptococcal infections in the case of allergy to flucloxacillin or flucloxacillin resistance and intolerance toerythromycin

As indicated

Antiseptics such as triclosanor chlorhexidine

Adjunct therapy for decreasing bacterial load in cases of recurrent infectedatopic eczema

Avoid long-term use

Abeck D. & Mempel M. British Journal of Dermatology1998;139:13-16

‘Discussion on the importance of microbial factors on thepathogenesis of eczema and the therapeutical implications for the treatment of eczema began more than 100 years ago.Since then, our knowledge concerning the complex interactionsbetween microbes and skin inflammation has improveddramatically and today the Gram-positive bacterium,Staphylococcus aureus, is recognized as an important triggeringfactor for the maintenance of skin inflammation and acuteexacerbations of the genetically determined skin disease atopic dermatitis (AD).’

‘The improved knowledge of the pathophysiological importanceof S. aureus in AD, combined with the positive correlationbetween the severity of eczematous lesions and the colonizationwith S. aureus, forms the rationale for an anti-staphylococcaltherapy in patients with AD.’

‘Even in the absence of clinical signs of active infection, patientswith AD profit from a reduction of S. aureus density due to thepresence of these bacteria on the skin. In those cases antisepticssuch as chlorhexidin or triclosan can be added to emollients andsuccessfully used for the treatment of larger skin areas.’

Lever R., Hadley K., Downey D. & Mackie R. British Journal of Dermatology 1988;119:189-198

‘Quantitative bacteriological assessment before treatmentshowed that heavy colonization of the skin with Staphylococcusaureus was present in nearly all patients even in the absence ofovert infection.’

‘During the present study a reduction in the bacterial load wasnoted to be associated with clinical improvement, suggesting that control of skin colonization with staphylococci may proveclinically beneficial in the treatment of atopic dermatitis.’

Veien N.K. British Journal of Dermatology 1998;139:30-36

‘A typical programme for the reduction of staphylococcalcolonization consists of chlorhexidine or topical antibiotics such as mupirocin applied in the nares.’

‘Patients with atopic dermatitis almost invariably harbour S. aureus on their skin. The microorganism could be isolatedfrom 93% of the skin lesions of 41 children with atopicdermatitis compared with 32% of non-atopic controls. Sudden aggravation and ‘weeping’ should alert the clinician to the possibility of S. aureus infection.’

Bieber T. New England Journal of Medicine 2008;358:1483-1494

‘Since the barrier dysfunction of the skin and chronicinflammation are characteristic of atopic dermatitis, long-termclinical management should emphasize prevention, intensified and individually adapted skin care, reduction of bacterialcolonization by means of local application of lotions containingantiseptics such as triclosan and chlorhexidine, and – mostimportant – the control of inflammation by the regular use of topical corticosteroids or topical calcineurin inhibitors.

In children, before and after the diagnosis of IgE-mediatedsensitization, measures that prevent exposure to allergens shouldbe beneficial. The current therapy of atopic dermatitis is reactive – treating the flares – but management should include early andproactive intervention with effective and continuous control of the skin inflammation and S. aureus colonization. This strategy has proved to be effective in reducing the number of flares. When applied early in infancy, it could potentially help to reducelater sensitization to environmental antigens and autoallergens.’

Leung D.Y.M., Hauk P., Strickland I., Travers J.B. & NorrisD.A. British Journal of Dermatology 1998;139:17-29

'A multipronged approach is required for treatment of chronic inflammatory skin diseases such as AD and psoriasis.Characterization of each patient’s skin disease reaction patternand the reduction of exacerbating factors are critical foreffective management. Factors that must be considered andeliminated include infection, irritants, allergens and emotionalstresses. Appropriate use of anti-inflammatory agents andimmunomodulatory agents to reduce skin inflammation iscritical for a successful outcome.’

‘Recently, we have found that when T-cells are stimulated with bacterial superantigens, as compared with other stimuli,they become insensitive to the immunosuppressive effects of corticosteroids… Taken together, these data indicate the importance of combining immunomodulatory and/or anti-inflammatory therapy with the eradication of bacteriasecreting superantigens to effectively treat inflammatory skindiseases such as AD. In this regard, it is also important tomaintain skin barrier function by using intensive skinhydration and emollient regimens that reduce invasion ofsurface bacteria and the itch/scratch cycle that can also lead to cytokine release and inflammation.’

Cardona I.D., Cho S.H. & Leung D.Y.M. American Journal of Clinical Dermatology 2006;7(5):273-279

‘Since S. aureus infection can exacerbate acute AD, and colonizationmay promote chronic skin inflammation, use of anti-staphylococcaltherapy should be considered in patients with poorly controlled AD.However, antibacterials should be reserved for the patient who isheavily colonized or infected with S. aureus and where it is clear thatinfection with S. aureus is an important trigger factor. Antibacterialsknown to be effective against S. aureus include erythromycin,azithromycin, clarithromycin, and the cephalosporin cefuroxime axetil.’

‘Unfortunately, the increasing prevalence of MRSA in the communityhas made treatment options more difficult for some patients. In suchpatients, clindamycin, fusidic acid, or combination therapy withtrimethoprim-sulfamethoxazole and intranasal mupirocin can beeffective in eliminating MRSA infection. Other therapies for AD thatmay be useful in suppressing bacterial infection include 0.3% gentianviolet, antiseptics such as chlorhexidine or triclosan, and phototherapy.’

‘Because of the increased risk of MRSA that may occur with frequentuse of antibacterials, it is important to combine antibacterial therapywith effective skin moisturization and anti-inflammatory agents since it is well established that the excoriated inflamed skin of ADpredisposes patients to S. aureus colonization and infection.’

Suh L., Coffin S., Leckerman K.H., Gelfand J.M., Honig P.J. & Yan A.C. Pediatric Dermatology2008;25(5):528-534

‘Although most atopic dermatitis patients studied were colonized with S. aureus (43/54 [80%]),methicillin-resistant S. aureus was isolated from onlyseven atopic dermatitis patients (7/43 [16%]). Patientscolonized with S. aureus were more likely to be male,to have been previously hospitalized, to have used atopical calcineurin inhibitor in combination with atopical steroid, and less likely to have used topicalantibiotics. Bivariable analysis, however, revealed thatonly previous hospitalization was independentlyassociated with an increased risk of methicillin-resistantS. aureus colonization. We observed that 80% of atopicdermatitis patients were colonized with S. aureus, andthat of these patients, 16% of colonized patients werecolonized with a methicillin-resistant strain. Methicillin-resistant S. aureus colonization was found to besignificantly associated with previous hospitalization.Evidence also indicates that topical calcineurininhibitors used in conjunction with topical steroids is associated with increased S. aureus colonization, while topical antibiotic use appears to decrease S. aureus colonization.’

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 9

Arkwright P.D., Daniel T.O., Sanyal D., David T.J. & Patel L. Archives of Dermatology 2002;138:939-941

‘Skin staphylococci and streptococci are known toexacerbate atopic dermatitis, but the prevalence changes that occur with age are unknown. This study examined theage-related prevalence and antibiotic resistance of thesepathogenic bacteria in children with atopic dermatitis andsuspected skin infections.’

‘Medical records of 150 children with atopic dermatitisreferred to a regional center, who had skin swabs taken forsuspected infection, were studied retrospectively. All patientscarried Staphylococcus aureus. The prevalence of methicillinsodium-resistant (P=.05) and fusidic acid-resistant (P=.001)S. aureus tripled from infancy to school age.’

12

Treatment of widespread infected eczema relies on the use of systemic antibiotics or topical antibiotics if the infection is confined to a smaller

area. However, as the disease involves periods of exacerbation which may be frequent or prolonged, the regular or long term use of antibiotics

can lead to development of resistance. Resistance to the antibiotic fusidic acid has been increasingly reported in the UK and appears to be

correlated with increased topical use and with an increased incidence in dermatology patients.

Use of alternative topical antimicrobials such as antiseptics reduces the risk of resistance developing due to their generally non-specific modes

of action. Antiseptics are not generally prone to development of bacterial resistance because they work by several mechanisms, including

physical means, in contrast to antibiotics which tend to rely on a single mode of attack such as interfering with a specific enzymatic function.

b) Development of bacterial resistance

Thestrup - Pedersen K. British Journal of Dermatology1998;139:1-3

‘Any doctor using antibiotics should be aware of the increasingworldwide problem with multi-resistant bacteria, with themajority of hospital-based infections in some countries beingcaused by these bacteria. Proper use of antibiotics is thereforemandatory for any physician, including for dermatologists, who treat bacterial infections of the skin. Detailed knowledge is needed of when to use topical versus systemic antibiotics, and for how long such treatments should be given.’

‘It is likely that the anatomy and physiology of normal skin is a sophisticated defense system against the growth of pathogenicmicroorganisms. This is shown indirectly through the bacterialcontamination of atopic skin, where the normal skin barrier isbroken both physically through scratching and because of achanged content of lipids and sebum secretion.’

‘Thus, a recent study of patients admitted with atopic dermatitisshowed a colonization of 74% among the patients; 88% of the S. aureus were penicillin resistant and resistance was observedagainst two or more antibiotics in 38% of the isolated strains.’

Aycliffe G.A.J. Journal of Hospital Infection 1980;1:111-124

‘Skin disinfectants, such as chlorhexidine or povidone-iodinereduce the numbers of all organisms, and emergence ofresistance is unlikely following application to the skin.Although often less effective than antibiotics in the treatment of skin infections, every effort should be made to use skindisinfectants when an antibacterial effect is required. New non-toxic effective topical disinfectants are required, andmore controlled trials on older agents may be worthwhile.Topical use of antibiotics should be discouraged, and thosewhich are valuable for systemic treatment of severe infections,e.g. gentamicin and fusidic acid, should preferably not beused topically at all.’

Espersen F. British Journal of Dermatology 1998;139(Suppl 53):4-8

‘The increased prevalence of bacterial resistance is one of the major problems of medicine today.Antibiotic resistance can be defined as the situation where the minimal inhibitory concentration isgreater than the concentration obtainable in vivo. Resistance genes are easily transferred amongbacteria, especially bacteria on skin and mucous membranes. In dermatological patients the mostimportant resistance problems are found among staphylococci, Propionibacterium acnes and, to some extent, streptococci. Staphylococcus aureus strains have developed worldwide resistance to penicillin due to betalactamase production in > 90% of cases, and methicillin resistance is now amajor problem with resistance levels of > 50% in certain areas of the world. These resistant strainsare often multiresistant, and include resistance to erythromycin and tetracycline, with resistance toquinolone developing rapidly. …To limit the development of antibiotic resistance, it is necessary toestablish an antibiotic policy (prescription rules, reimbursement strategy, development of bothnational and local guidelines, and limitations on non-medical use).’

Shah M. & Mohanraj M. British Journal of Dermatology2003;148:1018-1020

‘The results from our study suggest there is an almostidentical level of fusidic acid resistance in both non-dermatological hospital and community patients which is10%. This compares with a statistically significant differentlevel of 50% for dermatological patients (P<0.001 whenanalysed using the t-test). Our results suggest that patientswith eczema are more likely to show cultures of fusidic acid-resistant S. aureus. This may be as a result ofinappropriate use of topical antibiotics.’

‘Although topical fusidic acid has been available for over 20 years, we feel this rapidly emerging resistance is a recentphenomenon. The resistance rate is nearly 10% in ourgeneral population and 50% in dermatology patients. This seems to be the correct time to convey the message ofrestrictive use of fusidic acid to health care professionals.’

‘In our own area we have reminded our general practitionercolleagues about the problems of antibiotic resistance andthe need to restrict use of fusidic acid. We suggest thatfusidic acid-containing preparations are used to treat acuteskin infections in the short term only. Dermatologists andgeneral practitioners should consider alternatives to topicalantibiotics for treating chronic eczema. Topical fusidic acid should only be used for short periods and not on aregular or prolonged basis. If possible, topical antisepticpreparations should be used to treat skin infection. If action is not taken now, the future use of fusidic acid will be compromised.’

11

Mitra A., Mohanraj M. & Shah M. Clinical andExperimental Dermatology 2008;34:136-139

‘In 2001, a study carried out over 4 months inDewsbury and District Hospital showed that FRSA wassignificantly higher in dermatology patients comparedwith other hospital patients and primary-care patients(P<0.001). In patients whose cultures showed FRSA,96% had been given topical FA compared with only29% of patients whose cultures showed fusidic acid-sensitive S. aureus (P<0.001). It was concluded that high use of topical FA may have contributed to highlevels of resistance.’

‘A local education campaign followed to try to reduce inappropriate prescriptions of topical FA.Written guidelines were issued to general practitionersencouraging use of antiseptics and restriction of topicalFA to short periods to treat skin infection. The presentstudy was carried out 3 years later in the same hospital.The aims were to assess whether the guidelines hadaffected the number of prescriptions and the use oftopical FA, and whether there had been any effect on the level of FRSA.’

‘One new finding was the emergence of methicillin-resistant S. aureus (MRSA) in 11% of dermatologypatients (5 of 46) in 2004 compared with 0% in 2001.Only one of these patients had both MRSA and FRSA.’

‘Although we have showed a significant fall in hospitaland community prescriptions as well as use of topicalFA in dermatology between 2001 and 2004, there has not been a corresponding drop in FRSA seen indermatology patients. In addition, there has been anincrease in FRSA seen in the community and otherhospital specialities.’

‘We suggest that the reason for the remaining high levels of FA resistance is the development of an FRSAreservoir in our community. This is an observationalstudy and therefore a direct cause and effect between FA use, and resistance cannot be established. There maybe a lag period before FA resistance clears from ourcommunity. We still advocate continued close control of topical FA prescriptions even though restriction inour area has not shown a decrease in FA resistance. This advice seems safest in order to avoid possiblefurther rises in FRSA- and FA-resistant MRSA, pending future studies to establish a cause betweencontinued use of topical FA and resistance.

Limited topical FA treatment for 2 weeks was shownnot to increase the rate of FRSA in post-treatment skin and nasal swabs in one small study. However, we suggest the use of topical FA should be avoided inareas where there is already a high level of resistance,particularly in patients with atopic eczema.’

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 11

The Dermol range of antimicrobial emollients has been

especially formulated to offer significant convenience and ease

of use – advantages designed to maximise patient compliance.

They also benefit from the inclusion of benzalkonium chloride

and chlorhexidine dihydrochloride which work synergistically as

antimicrobial agents. This is discussed further on page 16.

On dry skin…

Dermol Lotion is specially formulated to

be absorbed rapidly into dry skin to relieve

symptoms quickly, without being messy or

greasy. It is also a pleasant, easy to use and

cosmetically acceptable soap substitute.

On very dry skin…

Dermol Cream is a highly emollient cream

formulated with the humectant glycerol to

preserve moisture in the skin. It also works

well as a soap substitute.

Under the shower…

Dermol Shower Emollient as well as being

an effective emollient, is also a non-ionic

soap-substitute cleanser, helping to remove

scalar debris from the skin, without stripping

it of natural oils.

In the bath water…

Dermol Bath Emollient is a liquid bath

additive which, formulated as a true emulsion,

disperses thoroughly in warm water, to evenly

coat the whole body.

■ 40 children (average age 6 years) receiving emollients for

eczema/dermatitis were enrolled in a single centre GP study.

■ Patients substituted their previous emollient for Dermol Lotion

for two weeks.

Results after 14 days

Table 1 - Clinical effectiveness of Dermol Lotion

■ 72% of users (or parents) ranked Dermol Lotion as more

effective, 23% equivalent and 5% as less effective than their

previous emollient treatment.

■ In the opinion of the investigator, 9 of the 17 patients

receiving adjunctive treatment were able to reduce its potency

and/or frequency.

Table 2 - Cosmetic acceptability of Dermol Lotion

*12 patients did not use as a soap substitute

Conclusions

■ These results confirm the effectiveness and ease-of-use/

acceptability of Dermol Lotion in the management of these

skin conditions.

■ Dermol Lotion provided significant relief of itching and dryness

in over 75% of cases where these symptoms were present.

■ Dermol Lotion was generally well liked by patients in terms of

effectiveness and ease-of-use, when compared with those they

had used previously.

■ Dermol Lotion was also found to be satisfactory by all patients

who used it as a soap substitute.

See back page for Prescribing Information

An open study to evaluate patient acceptability/tolerabilityand effectiveness of Dermol Lotion in the management ofchronic dry and pruritic skin conditions, especially eczemaand dermatitis, in infants and young children.5

Cosmetic acceptability As a skin lotion As a soap substitute*

Overalleffectiveness

No comment 5 0 2

Excellent 8 1 2

Very good 14 4 15

Good 3 5 0

Poor 2 0 2

Clinicaleffectiveness

Itchinglimbs/trunk

Itchingface/neck

Drynesslimbs/trunk

Dryness face/neck

Absent 2 18 0 18

Completely better 7 6 5 6

Much better 13 8 18 7

Better 11 4 11 4

No change 6 3 4 4

Worse 0 0 1 0

Much worse 0 0 0 0

b) Clinical evaluation of the Dermol Rangei) Evaluation of Dermol Lotion

14

F. RATIONALE FOR USING THE DERMOL RANGE

OF ANTIMICROBIAL EMOLLIENTS

Complete emollient therapy is widely accepted as the mainstay of

treatment for dry eczematous skin by rehydrating the skin, reducing

local pruritus and restoring the skin’s barrier function. Owing to

their hydrating and occlusive effects, emollients can also increase

the permeation of topically applied medicines. Thus, if emollients

are used regularly, they can help to reduce the reliance on topical

corticosteroids.

Various emollient preparations are available for this purpose,

designed for use either by direct application to the skin, or indirectly

as a bath water additive, or in the shower. However, many of these

preparations are entirely oily in character and are unpopular with

patients due to their messiness and greasiness, which may soil

clothing and the bath surrounds.

In the 2007 NICE review on atopic eczema in children, the following

guidelines were given in relation to patient choice of emollients and

wash products.4

‘Healthcare professionals should offer child ren with atopiceczema a choice of unperfumed emollients to use every day for moisturising, washing and bathing. This should be suited to the child’s needs and preferences, and may include a combination of products or one product for all purposes.’

Similarly guidelines for the management of atopic eczema developed

by the Primary Care Dermatology Society (PCDS) and British

Association of Dermatologists (BAD)2 state the following.

‘Continual treatment with complete emollient therapy(combinations of cream, ointment, bath oil and emollient soap substitute) will help provide maximal effect.’

Empowering the patient to choose a product they like will improve

compliance and lead to improvements in the skin condition as

illustrated in the following study.

a) The importance of formulation to patient compliance

Cork M.J., Timmins J., Holden C., Carr J., Berry V., Tazi-Ahnini R. & Ward S. The Pharmaceutical Journal2003;271:747-748

‘Compliance with the complex treatment regimens formanaging atopic eczema is likely to be much less than 50 percent. An audit of new referrals to our paediatric dermatologyclinic revealed that none of the children was being treatedwith emollients or topical steroids in accordance with bestpractice guidelines. Intensive education from specialistdermatology nurses resulted in an 800 per cent increase inthe use of emollients and an appropriate use of mild andmoderate potency topical steroids. This resulted in an 89 per cent reduction in the severity of the eczema.’

‘In order to enhance children’s compliance with theirtreatment regimens we have developed a child-orientatedapproach – “Skin Wars!” – to teach them about eczema and its treatment.’

‘Part of this education allows children to pick their favouriteemollient from a tray containing all of the emollients in theBNF. This method empowers them to use their chosenemollients.’

13

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 13

Staph. aureuscolonisation

Exacerbationof the eczema

Water lossfrom epidermis

Dry skin

ATOPIC ECZEMA

Furtherskin damage

ANTIMICROBIALACTS HERE

EMOLLIENTACTS HERE

Studies previously listed in this booklet confirm the important role

S. aureus plays in the pathogenesis of atopic eczema. The Dermol

range of products has been designed not only to provide ideal

emollient characteristics but also, importantly, to include antimicrobial

activity, so as to help reduce the viability and proliferation of

S. aureus, and thereby improve the prospects for treatment.

Dermol Shower Emollient, Dermol Lotion and Dermol Cream

employ the advantageous combined (synergistic) effect of two

antimicrobial agents, benzalkonium chloride 0.1% and chlorhexidine

dihydrochloride 0.1%. Together they provide effective and

synergistic antimicrobial activity when applied directly to the skin,

or used as a soap substitute, and with both at low concentration,

the risk of skin irritation is minimised.

c) Antimicrobial efficacy of the Dermol range

Dermol Bath Emollient contains benzalkonium chloride 0.5%,

which is powerfully antibacterial in its own right, particularly against

gram-positive organisms. Its activity resides in the large, positively

charged cation, which is mobilised in the bath water towards the

negatively charged surface of the skin and bacterial cell walls as

soon as the patient immerses in the bath. This affinity helps to

concentrate the antibacterial agent precisely where it is needed,

to provide effective antimicrobial activity.

The antibacterial activities of the Dermol range of products against

S. aureus have been confirmed both in vitro and in vivo in the

following studies.

16

■ 100 patients (adult, elderly or children ≥2 years) receiving

prescribed emollients for dry/pruritic skin conditions were

enrolled in this four centre GP study.

■ Patients substituted their previous emollient for Dermol Cream

for two weeks.

Results after 14 days

Table 3. Clinical effectiveness of Dermol Cream in reducingdryness and itching (%)

Table 4. Patient acceptability of Dermol Cream (%)

For relief of dry skin – 66% of patients preferred the new

emollient compared to 12% who preferred their previous

treatment (p<0.001).

For relief of itching – 60% of patients preferred the new

cream compared to 13% who preferred their previous

treatment (p<0.001).

Use as a soap substitute – 66% of patients rated

Dermol Cream as excellent or good as a soap substitute.

Conclusions

■ Dermol Cream was generally well liked by patients.

■ A statistically significant number of patients preferred Dermol

Cream to their previous emollient for the relief of itching,

dryness and in terms of cosmetic acceptability.

■ It performed well as a soap substitute.

Characteristic Excellent Good Satisfactory Poor

Odour 33 38 27 1

Consistency 25 51 23 1

Ease-of-use 30 50 19 1

Time to absorb 25 49 22 4

Soothing 36 44 17 3

Smoothing 39 42 18 1

Moisturising 39 41 19 1

Dryness Itching

Excellent 36 30

Good 44 33

Satisfactory 18 30

Poor 2 6

A study to evaluate hydration, acceptability and clinicalefficacy of Dermol Cream in patients with dry skinconditions such as eczema/dermatitis.6

ii) Evaluation of Dermol Cream

■ 54 patients (aged 1-88 years) attending a hospital out-patient

clinic with dry skin conditions e.g. eczema, ichthyosis or psoriasis

were recruited.

■ Patients added 30ml to their baths and continued using regular

adjunctive topical therapy for up to 12 weeks.

Results

Figure 1

■ Patients found the preparation convenient and easy to use

and 76% patients rated the bath emollient as ‘much better’

or ‘better’ than previously used preparations.

■ 70% of patients reported that they were ‘pleased’ or

‘very pleased’ with the effectiveness of the product.

■ 98% patients found the bath emollient to have ‘good’ or

‘very good’ dispersal in water.

■ 87% patients experienced satisfactory cleansing with

the product.

Conclusions

■ In the opinion of the supervising Consultant Dermatologist,

enhanced patient compliance helped to reduce the quantity and

potency of adjunctive topical steroid use.

■ Dermol Bath Emollient was found to have a useful role to play

in the management of patients with dry skin conditions.

See back page for Prescribing Information

0

5

10

15

20

25

30

0

3

6

9

12

15

18

0

5

10

15

20

25

05

10152025303540

Film on skin Softening effect

Comparison with previous preparations State of bath after use

CleanMuchbetter

Better Equal Lesseffective

Noprevious

treatment

12

17

3

6

16

Slightlygreasy

Tide mark Nocommentsreceived

37

7 6 4

8

25

16

5

Justright

Notgreasy

Not greasyenough

Slightlytoo greasy

Excellent Good Moderate Poor

27

18

81

Num

ber o

f pat

ients

Num

ber o

f pat

ients

Num

ber o

f pat

ients

Num

ber o

f pat

ients

An open clinical study to evaluate Dermol Bath Emollientas an adjunct in the treatment of dry skin conditions. 7

iii) Evaluation of Dermol Bath Emollient

15

Breaking the Itch Scratch Vicious Circle Using an Antimicrobial Emollient

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 15

■ S. aureus inoculum was added to various aqueous dilutions

of Dermol Bath Emollient thus simulating use in the bath.

■ Bacterial kill rates were determined at 10 and 30 minutes.

Results

■ A 1 in 500 dilution achieved complete bactericidal activity

against S. aureus within 10 minutes.

■ A higher dilution of 1 in 1000 achieved a reduction in viable

count in excess of 97% within 10 minutes and greater than 99%

within 30 minutes.

Conclusions

■ Even at extended dilution in the patient's bath water Dermol

Bath Emollient achieved substantial bactericidal activity against

S. aureus, the micro-organism implicated in atopic dermatitis.

■ In normal clinical usage, the bactericidal activity might be even

greater, because a proportion of the antimicrobial remains on

the patient’s skin after bathing.

In vitro antimicrobial efficacy of Dermol Bath Emollient.8

100

80

60

40

20

0

1:500 dilution

(1 exposurea)

>99%

1:1000 dilution

(1 exposureb)

>99%

1:5000 dilution

(3 exposuresb)

>95%

Antib

acte

rial e

ffect

ivene

ss**

Dermol Bath Emollient – antibacterial effectiveness

** Shown as percentage reduction in S. aureus count, after 10(a) and 30(b) minutes exposure.

Figure 3

ii) Antimicrobial efficacy studies on Dermol Bath Emollient both in vitro and in vivo

■ Dermol Bath Emollient was applied to the toe webs of one foot

and a non-antimicrobial bath emollient applied to the other foot

in 18 healthy volunteers.

■ Swabs were taken immediately before, at 1 hour and 6 hours

post application.

Results

Conclusions

■ After 6 hours, Dermol Bath Emollient significantly reduced the

population of viable colony-forming bacteria, compared to the

bland emollient (p=0.007).

■ The bactericidal activity is sustained for at least 6 hours.

See back page for Prescribing Information

In vivo cutaneous antimicrobial activity of Dermol BathEmollient compared with a non-antimicrobial proprietarybath emollient.9

100

80

60

40

20

01 hour 5-6 hours

Dermol bath emollient formulation

Proprietary bath emollient without antibacterial agent

Antib

acte

rial e

ffect

ivene

ss*

Dermol Bath Emollient – antibacterial effectiveness

22%

55%

74%82%

* Shown as percentage median reduction in S. aureus count, 1 and 5-6 hours after application.

Figure 4

18

■ Test samples of each emollient were inoculated with S. aureus.

■ Samples were taken at regular intervals over a 30 minute period.

Results

Conclusions

■ The study confirmed the rapid bactericidal effect of Dermol

Lotion, important in order to combat the colonising bacteria

known to be implicated in conditions such as atopic eczema.

■ By contrast, the reduction in viable bacterial count obtained

with the bland emollient was much slower, and likely attributable

to the carry over from the preservative ingredient necessarily

present in all such water-containing emulsified preparations.

In vitro antimicrobial activity of Dermol Lotion comparedwith a bland emollient cream (containing a preservative).5

Table 5In vitro antimicrobial activity of Dermol Lotion and bland emollient

cream (containing a preservative) against S. aureus. Values are log

reductions in viable counts (>5 is equivalent to 100% mortality).

Sampling time (min)

Preparation 0 5 10 20 30

Dermol Lotion 1 >5 >5 >5 >5

Bland emollient cream 1 3 4 >5 >5

i) Antimicrobial efficacy studies on Dermol Lotion both in vitro and in vivo

■ This in vivo test used direct application of Dermol Lotion or a

bland emollient cream, to the toe webs of each foot of healthy

volunteers as a recognised model for S. aureus colonisation in

atopic patients.

■ Bacterial cell counts were estimated from microbial samples

taken immediately before and 6 hours after application.

Results

Conclusions

■ Dermol Lotion produced a significant reduction in the

indigenous population of viable colony-forming bacteria,

including staphylococci, which was sustained even 6 hours

after application.

■ In contrast, bacterial overgrowth actually increased after

treatment with the bland emollient cream (containing only

a preservative).

■ Given that bacteria proliferate rapidly on the skin and would

be expected to recover over such a 6 hour period, the observed

reductions in viable counts confirm the persistent bactericidal

activity of Dermol Lotion.

See back page for Prescribing Information

In vivo cutaneous antimicrobial activity of Dermol Lotioncompared with a bland emollient cream (containing a preservative).5

Table 6Determination of antimicrobial activity of Dermol Lotion in vivo.

Values are median counts x10–3.

Total count S. aureus count

After 6h After 6hInitial contact Initial contact

Phase 1Dermol Lotion(right foot) 2000 25.2 204 7.2

Bland emollient cream(left foot) 1260 1600 360 360

Phase 2Dermol Lotion(left foot) 3000 76 184 8.8

Bland emollient cream(right foot) 2160 1040 640 460

17

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 17

■ The Dermol range was tested against FRSA and MRSA

according to the rigorous European Standard (EN1276) normally

applied to disinfectants and antiseptics used in non-clinically

sensitive circumstances.

■ Neat samples of Dermol Lotion, Shower and Cream and

1% dilution of Dermol Bath were inoculated with MRSA or

FRSA either in the presence of bovine serum albumin (BSA)

to mimic clinically ‘dirty’ conditions or without BSA to mimic

‘clean’ conditions.

■ Samples were taken at specified intervals over a 30 minute period.

Results

Table 7: Activity of Dermol Cream, Dermol Lotion and DermolShower against FRSA and MRSA

≥ 99.999% (5 log) reduction ≥ 99.99% (4 log) reduction*mean result of two tests

Dermol Cream, Lotion and Shower met the standard criteria of

≥5 log reduction (99.999% reduction) in microbial counts within

5 minutes against both FRSA and MRSA under ‘clean’ conditions

and within 10 minutes under ‘dirty’ conditions against MRSA.

Contacttime (min)

FRSA MRSA

Log kill(clean)

Log kill(dirty)

Log kill(clean)

Log kill(dirty)

Dermol Cream(undiluted)

0 <4.6* <3.5* <3.6 <3.6

5 >6.4* 4.2* 5.7 4.8

10 >6.4* 5.6* 6.0 6.0

20 >6.4* 5.6* >6.0 >6.0

30 >6.4* >6.5* >6.0 >6.0

Dermol Lotion/Dermol Shower(undiluted)

0 <2.9 <2.9 <3.6 <3.6

5 >6.4 >6.4 5.3 3.9

10 >6.4 >6.4 >6.0 >6.0

20 >6.4 >6.4 >6.0 >6.0

30 >6.4 >6.4 >6.0 >6.0

Routine infection control using a proprietary range ofcombined antiseptic emollients and soap substitutes – theireffectiveness against MRSA and FRSA.10

Summary of data presented at the 18th Congress of the EADV in Berlin, October 2009

e) Efficacy of the Dermol range against resistant strains of S. aureus

Table 8: Activity of Dermol Bath (1% dilution) against FRSA and MRSA

≥ 99.999% (5 log) reduction ≥ 99.99% (4 log) reduction

Dermol Bath even at 1% dilution achieved ≥5 log reduction against

FRSA (and very nearly the same reduction against MRSA) after

20 minutes under ‘clean’ conditions and a reasonable kill of close

to 4 log reduction (99.99%) by 20 minutes under ‘dirty’ conditions.

Conclusions

■ The Dermol range exhibited significant antimicrobial activity

against FRSA and MRSA.

■ The Dermol range of antiseptic emollients are designed for

chronic use on sensitive skins and can be used in a variety of

ways as soap substitutes, body washes, leave-on preparations

and even for bathing.

■ The Dermol range are a useful addition to the infection control

armamentarium (even against FRSA and MRSA) and being

antiseptic rather than antibiotic, they are unlikely to induce

bacterial resistance.

Contacttime (min)

FRSA MRSA

Log kill(clean)

Log kill(dirty)

Log kill(clean)

Log kill(dirty)

Dermol Bath(1% dilution)

0 <4.1 <4.1 <3.6 <3.6

5 4.8 <4.1 <3.6 <3.6

10 4.8 <4.1 4.1 <3.6

20 5.0 4.4 4.3 3.7

30 5.3 4.6 4.4 3.8

20

d) Avoiding antimicrobial resistance

Recently, concerns have been raised about the use of antimicrobial agents, particularly topical antibiotic preparations, and the development of

bacterial resistance. A number of published studies have reported increased incidences of bacterial resistance to antibiotics, such as methicillin

with the development of MRSA and resistance to fusidic acid (see Section E – Therapeutic Implications). As a result of this and in order to

preserve fusidic acid as a systemic antibiotic for the treatment of serious life threatening infections, alternative antimicrobial agents may be used.

Antiseptics are effective antimicrobial agents, which can avoid bacterial resistance by virtue of their non-specific bactericidal mechanisms of

action as illustrated in the diagram below.

Figure 5

The antimicrobial agents in Dermol Lotion, Cream and Shower Emollient are benzalkonium chloride and chlorhexidine dihydrochloride, both

present at the relatively low concentration of 0.1%. These are known to act synergistically to enhance their activity and, being antiseptic rather

than antibiotic, are most unlikely to induce resistant strains of micro-organisms.

To summarise, the Dermol range contains antiseptics at a low concentration to avoid irritation and as they are very unlikely to induce resistance

to antibiotics, they can be considered a very useful choice for routine use.

Penicillin attaches to binding proteins in thebacterial cell wall, to inactivate an inhibitor ofautolytic enzymes, resulting in damage to the cellwall and death of the bacteria.

Benzalkonium chloride has a large positivecharge which is attracted to and thendeactivates the negatively charged proteins on the cell membrane. This stops biochemicalreactions essential for the Staph to survive.

Chlorhexidine dihydrochloride damagesacidic phospholipids, which are building blocks ofthe bacterial cell membrane. The cell membranethen becomes permeable and the cytoplasmicconstituents leak out.

...and they do not need to access specific targetsites within the cell.

The shape of individual antibiotic receptors isirrelevant to their action...

Antibiotics – examples of how they workHow the two antiseptics in

Dermol can avoid resistance

Penicillin resistance develops due to geneswhich produce a ß-lactamase enzyme whichbreaks down the penicillin before it reachesthe binding site. 80% of Staph in developedcountries possess this gene.

Methicillin has the same mode of action as penicillin but is not deactivated by the ß-lactamase enzyme.

Staph originally sensitive to methicillin (MSSA)are now becoming increasingly resistant (MRSA)as the shape of the ß-lactam binding site isaltered to prevent binding of methicillin.

Fusidic acid inhibits protein synthesis, by acting on the RNA ribosomes inside the bacterial cell.

Resistance can develop by reducing permeability tothe antibiotic so that the target site is protected.

Antibiotics – how resistance develops

19

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 19

Antimicrobial activity of Dermol Lotion against transientmicroorganisms such as Escherichia coli (E. coli).

Micro-organisms found on the hands may be classified as ‘transients’

and ‘residents’. Transients, e.g. E. coli, do not usually grow on the skin

and are acquired by day-to-day contact with contaminated surfaces.

‘Residents’ are the normal stable microflora of the skin and are

more difficult to remove by washing or disinfection. They consist

mainly of S. epidermidis, other staphylococci, micrococci and

corynebacteria. In circumstances where elimination of ‘transient’

organisms is desired, a model involving artificial contamination can

be used to assess the effectiveness of an antibacterial agent.

■ The hands of 10 healthy volunteers were inoculated with E. coli.

■ Dermol Lotion was used as a wash and emollient on the hands.

■ Recovery of viable organisms was determined using ethanol as

a negative control, after inoculation with E. coli (positive control)

and after application of E. coli and Dermol Lotion.

■ The efficacy of Dermol Lotion was evaluated as a log10

reduction factor (RF) when compared to the positive control.

Results

Figure 6:The in vivo antimicrobial properties of Dermol Lotionwhen used as a soap substitute

■ No viable counts were detected in the negative controls.

■ The average RF value was 3.02 for Dermol Lotion.

■ Dermol Lotion killed between 99.8 and 100% of microorganisms.

Conclusions

■ The FDA recommendation for removal of bacteria is a 2 log10

reduction after 1 wash and 3 log10 reduction after 10 washes

with a medicated soap.

■ Dermol Lotion showed an average of 3 log10 reduction after

just one wash and therefore far exceeds the FDA requirements

for a medicated soap.

1 2 3 4 5 6 7 8 9 10

9

8

7

6

5

4

3

Log 10

CFU

/han

d

Subject No.

Initial inoculation of E. coli

Recovery of E. coli from untreated hands

Recovery of E. coli after washing with Dermol Lotion

3 = minimum detection

Further uses of Dermol antiseptic emollients

Potential problems arise in those patients going into hospital for

elective surgery or routine procedures who show a positive result

for carriage of MRSA following pre-hospital admission screening.

In this situation patients will not be able to undergo surgery until

the MRSA has been eradicated. In such cases, the Dermol range

may offer a useful therapeutic option due to its antimicrobial

activity against MRSA as shown previously.

Secondly, doctors and nurses working in Occupational Health

Departments within hospitals often find Dermol Lotion or Cream

useful for treating the hands of medical personnel that have become

very dry, sore and even fissured as a result of dermatitis from the

constant use of soap and/or alcoholic hand rubs and scrubs. In this

situation Dermol Lotion or Cream can be used as an antibacterial

soap substitute with the added benefit of emollient properties to

soothe and rehydrate dry, sore and chapped hands thus enabling

the healthcare staff to continue at work.

To summarise, Dermol Lotion can be considered an effective, well

tolerated hand wash to control bacterial contamination. It has been

shown to be effective even in the presence of resistant bacteria

i.e. MRSA and FRSA. With its emollient properties and low irritancy

potential, Dermol Lotion provides a useful alternative to soap for

routine hand washing, particularly for those with soap or detergent

induced hand dermatitis.

References

1. Simpson CR et al. Trends in the epidemiology and prescribing ofmedication for eczema in England. Journal of the Royal Society ofMedicine 2009:102;108-117

2. Primary Care Dermatology Society and British Association of Dermatologists2006. Guidelines on the management of atopic eczema. Available:http://www.bad.org.uk/Portals/_Bad/Guidelines/Clinical%20Guidelines/PCDSBAD-Eczema.pdf.

3. Williams HC & Strachan DP. The natural history of childhood eczema:observations from the British 1958 birth cohort study. British Journal of Dermatology 1998;139:834-839

4. National Collaborating Centre for Women’s and Children’s Health.Atopic eczema in children. Management of atopic eczema in childrenfrom birth up to the age of 12 years. NICE 2007.www.nice.org.uk/CG57

5. Whitefield M. Journal Dermatological Treatment 1998;9:103-109

6. Whitefield M. Dermal Laboratories Ltd. Data on File

7. Allenby CF. Dermal Laboratories Ltd. Data on File

8. Rosher PH. Dermal Laboratories Ltd. Data on File

9. Whitefield M. Dermal Laboratories Ltd. Data on File

10. Poster presented at the 18th EADV, Berlin October 2009

11. Whitefield M. NHS Journal of Healthcare Professionals. February 2004:62-63

22

f) Dermol Lotion used as an antimicrobial soap substitute

The emergence of antibiotic resistant pathogenic micro-organisms

is now a major problem in many hospitals. Since transmission

most frequently occurs via the hands of healthcare workers,

regular hand washing by medical personnel is a most important

precautionary measure.

Pratt RJ et al. National Evidence-Based Guidelines for PreventingHealthcare-Associated Infections in NHS Hospitals in England. J Hosp Infection 2007;65S:S1-S64

‘Overviews of epidemiological evidence conclude that handmediated cross-contamination is a major contributing factor in thecurrent infection threats to hospital in-patients. Cross-transmissionvia hands has been identified as contributing to hospitals outbreaksinvolving both methicillin-sensitive and methicillin-resistantStaphylococcus aureus (MRSA/MSSA)…’

However, numerous studies have reported that compliance is low,

averaging only about 40%, due mainly to the development of skin

irritation and dryness. These problems arise with ordinary soaps

and detergents which are anionic and can therefore act as primary

irritants. One example, sodium lauryl sulphate, is actually used as

a positive marker for skin susceptibility to irritancy.11

A non-ionic surface active agent avoids these problems and is

therefore more acceptable as a soap substitute for repeat usage

and also for those occasions when the skin is already in a sensitive

state due to a local inflammatory process. Appropriately, there is

available a licensed non-ionic antimicrobial emollient, which can

be used as a soap substitute – Dermol Lotion. This lotion has been

developed for its antibacterial action and its lack of irritancy in the

topical management of dry skin conditions such as atopic dermatitis,

where there is a high level of colonisation with S. aureus.

Dermol Lotion is formulated as a non greasy mobile emulsion in

which the two immiscible oil and water phases are stabilised with

the non-ionic emulsifier Cetomacrogol 1000, which is present at

a concentration sufficient to provide the cleansing properties of

an emollient soap substitute.

Dermol Lotion has been shown to be as effective against methicillin

resistant S. aureus (MRSA) as it is against methicillin sensitive

S. aureus (MSSA) as shown below.

In vitro antimicrobial activity of Dermol Lotion against MSSA and MRSA.

Exposure to both the neat lotion and a 10 x dilution produced

no viable counts of either MRSA or MSSA after as little as

5 minutes contact.

Table 9: Antimicrobial activity of Dermol Lotion againstmethicillin sensitive (MSSA) and methicillin resistant (MRSA)Staphylococcus aureus

Total viable count

Strain of S. aureus

Dilution of Dermol

LotionControl

Contact time (mins)

0 5 10

MSSAUndiluted 120 million 5.6 million 0 0

x10 dilution 120 million 0.7 million 0 0

MRSAUndiluted 83 million 1.3 million 0 0

x10 dilution 83 million 0.13 million 0 0

21

20787_Staphylococcus 3rd Edition_AW v2:1 3/9/09 16:28 Page 21

When the eczema is itchy...

...it may be timefor an emollient with addedantimicrobials

Dermol 200 Shower Emollient & Dermol 500 Lotioncontaining benzalkonium chloride 0.1%,chlorhexidine dihydrochloride 0.1%, liquid paraffin 2.5%, isopropyl myristate 2.5%Dermol Creamcontaining benzalkonium chloride 0.1%,chlorhexidine dihydrochloride 0.1%, liquid paraffin 10%, isopropyl myristate 10%Uses: Antimicrobial emollients for the management of dry and pruritic skinconditions, especially eczema and dermatitis, and for use as soap substitutes.Directions: Apply direct to the skin or use as soap substitutes.

Dermol 600 Bath Emollientcontaining benzalkonium chloride 0.5%, liquid paraffin 25%, isopropyl myristate 25%Uses: Antimicrobial bath emollient for the management of dry, scaly or pruritic skin conditions, especially eczema and dermatitis.

Directions: Children, adults and elderly: add up to 30ml, infants add up to 15ml to a bath of warm water. Soak for 5 to 10 minutes. Pat dry. Contra-indications, warnings, etc: Sensitivity to any of the ingredients. Pleaserefer to SPC before prescribing, particularly in relation to side-effects, precautionsand contra-indications. In the unlikely event of a reaction stop treatment. Keep away from the eyes. Take care to avoid slipping in the bath or shower. Package quantities, NHS prices & marketing authorisation numbers: Dermol 200Shower Emollient: 200ml shower pack £3.61, PL0173/0156. Dermol 500 Lotion:500ml pump dispenser £6.13, PL0173/0051. Dermol Cream: 100g tube £2.90,500g pump dispenser £6.72, PL0173/0171. Dermol 600 Bath Emollient: 600ml bottle £7.67. PL0173/0155.Legal category: P‘Dermol’ is a registered trademark.Marketing authorisation holder: Dermal Laboratories, Tatmore Place, Gosmore, Hitchin, Herts, SG4 7QR, UK. Date of preparation: June 2009.

Adverse events should be reported. Reporting forms and information can be found at www.yellowcard.gov.uk. Adverse events should also be reported to Dermal.

www.dermal.co.uk

DermolA family of antimicrobial emollientsSHOWER LOTION CREAM BATH

7004

16 D

EM30

0/OC

T09

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