Infant Skin: Routine Care, Microflora, and Dermatologic...

View this activity online at:http://www.medscape.org/viewarticle/804338

Infant Skin: Routine Care, Microflora, and Dermatologic Conditions CME/CELawrence F. Eichenfield, MD

Supported by an independent educational grant from Johnson & Johnson Consumer & Personal Products Worldwide

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Infant Skin: Routine Care, Microflora, and Dermatologic Conditions CME/CE

This article is a CME/CE-certified activity.To earn credit for this activity visit:

http://www.medscape.org/viewarticle/804338

CME/CE Released: 05/30/2013 Valid for credit through 05/30/2014

Target AudienceThis activity is intended for pediatricians, dermatologists, primary care physicians, physician assistants, nurse practitioners, nurses, pharmacists, and other healthcare practitioners involved in infant care.

GoalThe goal of this activity is to designed to educate clinicians about infant skin development and microflora in health and disease so that they can educate patients and their caregivers about optimal skin care practices to support skin barrier function.

Learning ObjectivesUpon completion of this activity, participants will be able to:

1. Discuss currently available data regarding the evolution of microflora in infant skin and dermatologic innate immunity

2. Describe the impact of microflora on the role of bacterial growth in dermatologic conditions seen in infants, such as atopic dermatitis

3. Evaluate how skin care products can affect the skin microbiome and the potential impact on infant skin

4. Outline the fundamental principles of the formulation of safe and effective skin care products for infants and children to preserve microflora

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Physicians should claim only the credit commensurate with the extent of their participation in the activity.


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Faculty and DisclosuresItisthepolicyoftheUniversityofCalifornia,SanDiegoSchoolofMedicinetoensurebalance,independence,objectivity,andscientific rigor. All persons involved in the selection, development, and presentation of content are required to disclose any real or apparent conflicts of interest. All conflicts of interest will be resolved prior to an educational activity being delivered to learners through one of the following mechanisms: 1) altering the financial relationship with the commercial interest, 2) altering the individual’s control over CME content about the products or services of the commercial interest, and/or 3) validating the activity content through independent peer review. All persons are also required to disclose any discussions of off label/unapproved uses of drugs or devices. Persons who refuse or fail to disclose are disqualified from participating in the CME activity.

Lawrence F. Eichenfield, MDChief, Pediatric and Adolescent Dermatology; Professor of Pediatrics and Dermatology, Rady Children’s Hospital and, University of California, San Diego

Disclosure: Lawrence F. Eichenfield, MD has disclosed no relevant financial relationships.

Dr Eichenfield does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

Dr Eichenfield does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

Nafeez Zawahir, MDCME Clinical Director, Medscape, LLC

Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

Laurie E. Scudder, DNP, NPNurse Planner, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor, School of Nursing and Allied Health, George Washington University, Washington, DC

Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.

Raegan D. Hunt, MD, PhDFellow, Pediatric & Adolescent Dermatology University of California San Diego Rady Children’s Hospital-San Diego

Disclosure: Raegan D. Hunt, MD, PhD, has disclosed no relevant financial relationships.

The CME staff, meeting planners, planning committee and CME committee reviewers, peer reviewers, and medical writers do not have any relevant financial relationships to disclose.

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Infant Skin: Routine Care, Microflora, and Dermatologic Conditions Lawrence F. Eichenfield, MD CME/CE Released: 05/30/2013; Valid for credit through 05/30/2014

INFANT SKIN AND INNATE IMMUNITY

Lawrence F. Eichenfield, MD: WelcometotheMedscapevideolecturetitled,“InfantSkinCare,RoutineCase,Microflora,andDermatologicConditions.”IamDr.LawrenceEichenfield,ProfessorofPediatricsandDermatologyattheUniversityofCalifornia,SanDiego.Inthislecture,Iwillbediscussingnewinsightsintoinfantskinandsomeofthedynamicprocessesthathappenwithskin at birth, infancy, and in early childhood. There are new insights in the biology of skin in infancy, and we will discuss how these might influence our care of infant skin.

Infantskin,includingtheevolutionofmicrofloraandinnateimmunity,isreallyabroadtopicarea,sowearegoingtostartatthebeginning.Iwouldliketolookatthechangesthathappenasaninfantisborn,includingtheevolutionoforganismsontheskin,and the influence of the innate immune system on microbes and skin function.


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Whenwelookatbabyskin,weareveryimpressedwithhowsmoothitis.Itseemstobefunctioningsowell.Thisbabyissaying,“Likethewaymyskinisdeveloping?”ButIwantustothinkaboutwhatactuallyishappeninginthetransitionfromfetustoinfant.Therearesomecrucialtransitionsthatarequitefascinating.OneofthethingsIwantyoutodoistoappreciatethewonderofthetransitions that happen at birth.

The function of the skin certainly changes as it moves from an existence in a wet environment in uteroto the realities of a relatively dry, extrauterine life.[1] A lot of the things that happen involve the maturation of the epidermis and barrier function changes that happen very soon after birth.

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At birth, essentially, you will have a neutral or alkaline pH, but within a few days, there is the development of acidification of the skin, with what is called the acid mantle. This acid pH in the skin is important to improve our epidermal barrier function and it also contributes to maintaining bacterial and chemical resistance.[1]

There are changes that happen in the stratum corneum of infants as well as children and adolescents, and we now recognize that the maturation process and changes in the biology of the skin are really a dynamic process. This has been an area of quite intense research recently. For instance, we know that there are many genetic variations that influence skin function. For instance, there are a great many people with mutations in filament-aggregating protein, what is called filaggrin, an important protein in the epidermis. Those deficiencies in filaggrin are associated with compromises in the epidermal barrier function, dry skin, and much higher risk of the development of atopic dermatitis (AD).[2]

There are other factors that influence skin barrier function. These include the ambient environment. Our skin does a pretty good job of a change from a humid environment to a dry environment. Microbial exposure influences skin barrier function, as do hormones. Probably the best example of hormonal changes influencing skin function is what happens in the preadolescent or adolescent, where their skin is influenced by androgenic hormones, which impact on oil production in the skin, and sets up an increase in P. acnes, which, of course, is associated with acne.


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Elements of the innate immune system are also very important in skin function. Research has shown that we have a well-developed innate immune system. That is a set of immune responders that are, so to speak, pre-programmed to contribute to our immune defense. The innate immune system is partially a physical barrier that helps to block microbial entry and helps to minimize physical damage to the outer surface of the skin. The innate immune system is partially a chemical shield, which inhibitsmicrobialgrowthandinvasionofmicrobes.Itispartiallyarecognitionsystem.Theinnateimmunesystemissetuptoidentify foreign microbes, and it can trigger inducible anti-microbial responses. The innate immune system is set up to interact with other parts of the immune system. For instance, it will interact with the cellular immune system to amplify and enhance defenses.Ithasbeenshownthathowandwhatwegetcolonizedwithisverymuchaninterplayoftheenvironment,themicrobeswe are exposed to, and what our immune system has worked out over several years and has decided is okay to be on the skin.[3]

Part of the area of research that has really contributed to new understanding about infant skin is the skin microbiome research. Partially, this is technique-driven. New techniques have broadened our perspectives on microbes living on our skin, way beyond that of just bacterial cultures. Using genomic techniques, we know that there is a much larger set of organisms on the skin, known as the skin microbiome. We quickly come to the conclusion that the skin microbiome is this complex, symbiotic ecosystem of commensal microbes on the skin, first described in adult skin. There is a certain degree of homeostasis that exists between commensalorganismsandthehost.Inadults,thisisfairlystable,anatomic,site-specific,withcommunitiesoforganismsbeingsetup, but in infants and children, there is marked change in terms of what colonizes the skin at birth.[4]

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What bacteria is most likely to first colonize infant skin?

Lactobacillus spp.

Prevotella spp.

Streptococcus aureus

Depends on the method used to deliver the infant

Going back to infant skin, a baby enters the world from a sterile environment as a fetus. Colonization begins immediately after birth, within 24 hours, and in relatively new research, we know that it is relatively undifferentiated but affected by delivery mode. So, vaginally delivered infants acquire bacterial communities that resemble their mothers’ vaginal flora, Lactobacillus species, Prevotella species and others, as compared to an infant who might be delivered by caesarian section, in which case the bacterial communities are similar to those found on the skin surface of adults: Staphylococcus aureus, Corynebacterium species and Propionibacterium species.[5]

Over the first few months of life, there is a site-specific evolution of the infant’s skin microbial communities, which really begins within the first few months. Streptococci and Staphylococci dominate the early infant skin colonization up to 6 months of age. There are other species that can colonize the skin, such as Malassezia species. Basically, the infant skin microbiome becomes less stable than an adult over the first few months of life but evens out afterwards.[6]


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But how does the skin microbiome function interact with the skin function in the innate immune system? This is a really fascinating area of research.

IfyoutakeyourhandandputitinavatofE. coli, and put it down on a culture plate, you will actually get very little growth of the E. colionthecultureplate.IfyoutakeyourhandandputitinagloveandputitonE. coli and then put it on the culture plate, the E. coligrowsout.Thisisanexampleoftheinfluenceoftheinnateimmunesystem,decidingwhatorganismsitlikesontheskin.Inother words, we are programmed to have an anti-E. coli set of immune defense protein agents on our skin, so that a skin is keeping off E. coli as compared to a gloved hand. Now this can be very different than Staphylococcus species, which may very easily grow on the skin.[7,8]

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We also know that the microbiome interacts with the innate immune system. For instance, Staphylococcus epidermidis, a normal commensal on the skin, benefits your innate immune system. Staphyloccus epidermidis stimulates antimicrobial peptide production, which can protect against wound infection, and it also helps to suppress uncontrolled inflammatory reactions during wound healing. We can think of the group of commensal organisms on the skin as something that has set up shop with the approval of the innate immune system and that helps the innate immune system to protect the organism over time.[9,10,11]

BARRIER FUNCTION AND DERMATOLOGIC CONDITIONS

Now let us look at some aspects of dermatologic conditions that may be associated with aspects of skin development over time as well as microflora on the skin.


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Let us start off with one of the most common skin conditions we see in infants, atopic dermatitis, presented here in a typical image of a child who has diffuse dry skin as well as inflammation of the skin and, as you will see, the evident secondary pruritus that is associated with atopic dermatitis.

This is an example of a disease state that is associated with genetic barrier dysfunction, an area of rapidly evolving research. We are discovering more and more specific genetic factors that are essentially giving a higher risk of development, or are involved in thepathogenesisofthedevelopmentofspecificdiseases:atopicdermatitis,whichIwilldiscussinmoredetailinaminute,aswellas acne, rosacea, psoriasis, and allergic contact dermatitis.

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Eczema,oratopicdermatitis,affects15%to20%ofchildren.Decadesago,itwasonly5%.Itisnowknownthatthefilaggrinmutations are associated with atopic dermatitis, such that 20% to 40% of children with atopic dermatitis have this innate, genetically programmed deficiency in filaggrin. Having this deficiency in filaggrin makes it harder for the skin to hold onto water. Itcreatesaleakierskinthatcannotkeepoutthemicrobes.Itisassociatedwithhigherriskofskininfection,aswellasthedevelopmentofIgE-mediatedallergicdisease,whichhassecondaryconsequences,includingnewresearchshowinghigherratesof attention deficit hyperactivity disorder associated with atopic dermatitis.[12,13,14]

Amanifestationoffilaggrinabnormalitiesishavingincreasedlinesonyourskin.Ifyoulookatyourhypothenareminence,andyoulook a little wrinkled, there is a good chance that you have filaggrin abnormalities. This is also associated with common dry skin or what is called ichthyosis vulgaris, presenting as a fine, dry skin on the extensor surfaces.


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Thiscorrelateshistologicallywithhavingdeficientfilaggrin.Intheimageatthebottomofyourscreen,youseehalfofanepidermis stained for filaggrin in a normal individual, and you see these black dots that are present in the epidermis. The biopsy justtothesideofthatisalsostainedforfilaggrin.Ithappenstobeapatientwithcommonichthyosisvulgarisandatopicdermatitis, stained also for filaggrin, and you see it stains negative. There is no filaggrin in the skin.[15] A significant percentage of patients have fundamental defects in filaggrin. They have more permeable skin. They have an inability to keep their acid pH. They haveasetupfornotonlyinflammation,buthigherratesinthedevelopmentofIgE-sensitization,asthma,allergicrhinitis.Thefilaggrin abnormalities are also associated with persistent atopic dermatitis over time.[2]

Interestingly,theinnateimmunesystemisalsoaffectedinatopicdermatitis.Inatopicdermatitis,theskinhaslowexpressionofsome of the innate immune system factors, such as cathelicidins and beta-defensins. Having a decrease in this innate immune system is a setup for bacterial colonization and infection. We know Staphylococcus aureus is commonly a problem with atopic dermatitis in patients. Similarly, rosacea and psoriasis also show alterations of innate immunity.[3,16] These abnormalities can impact on skin function and the disease state.

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FascinatingresearchhascomeoutoftheNationalInstitutesofHealthinthelastfewyears,lookingathowourmicrobesontheskinchangeindiseasestates.Inatopicdermatitis,whenapatientisnotflared,thereisaverydiversesetoforganismsthatarepresent on the skin. However, when a patient starts to flare in atopic dermatitis, the diversity goes down, and there is a dominance of Staphylococcus aureus that ispresent in the skin.[17]

So one of the implications for treatment of atopic dermatitis is that it might make sense to not prophylax atopic dermatitis patients with systemic antibiotics or with topical antimicrobials too aggressively, because, in fact, there is a diversity of organismsatthattime.Ifyouhaveinfectedatopicdermatitis,itmightbeperfectlyreasonabletouseantibioticstohelptodecrease the Staphylococcus aureus colonization, of course with concurrent anti-inflammatory therapy.

Do you use prophylactic antibiotics in your pediatric patients with atopic dermatitis?

Always

Never

Sometimes


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Let us go back to infant skin. How does the care of infant skin influence the skin over time?

We are looking at skin care practices and their impact on infant skin. There is a broad set of cultural factors that influence skin care, andtheyalsoinfluenceskinfunction.Forinstance,bathingandsoakingcanhavesignificantimpactsontheskin.Ifyoubathetheskin and do not moisturize it afterwards, you actually dry out the skin. Over-bathing can impact on your ability to hold onto water, it impacts on what is called the natural moisturizing factor content of skin.

Do you ask or advise your patients/their caregivers about skin care practices?

Yes

No

OnlyifIbelievethepatienthasaskinbarrierproblem

PRACTICAL IMPLICATIONS OF SKIN MICROBIOME RESEARCH

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There have been questions raised over the years over whether having overly clean skin might be a bad thing.

One interesting theory that has been proposed as an explanation for the increased rates of atopic dermatitis and other allergic disease that we see now as compared to decades ago, is what has been called the hygiene hypothesis. The hygiene hypothesis states that if you are exposed to endotoxin, if you are exposed to infections early on, perhaps exposed to animals on farms or a dog, that exposure is creating a certain push on the immune system that is associated with less development of allergic disease. The hygiene hypothesis is positing that maybe we are too clean, that in our new modern society, having less exposure to certain things on the skin or in our everyday lives, less exposure to endotoxins, less exposure to infectious agents, perhaps having skin that is too clean, is creating an immunologic stress that it is creating a higher risk of the development of atopic phenomena, such as atopic dermatitis over time.[18]


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Ithinkitisreasonabletoapproachinfantskinwithanunderstandingofthenaturaldefensesthatareinplayandgenerallytakingthe approach of trying not to do too much damage to the skin in the name of cleanliness. We do not want to strip the natural defenses. Cleansing infant skin is probably reasonable, but we do not want too harsh cleansing, we do not want cleansing that is too drying.[19] We know that you can bathe pre-term infants fairly infrequently without increasing the risk of infections. We know that watery lotions and some cleansers can harm skin barrier function.[20]Inchildrenwithestablishedatopicdermatitis,itisveryimportant to moisturize them after bathing to keep the hydration present in the skin.[21]

Wehavenoticedthatthereisabroadsetofproductsthatareavailableonthemarketfortakingcareofinfantskin,andIhavepersonal concerns about some of the organic skin care products, because they have chemicals that are untested in them, several ofwhichareknownsensitizers,thatis,agentsthatcancauseallergiccontactdermatitis.Ihaveseenproductsinthemarketplacethat have organic almond and nut and macadamia and certain oils that we know can create more problems with contact allergy overtime.Itisdifficulttoreadlabels,sincetheycontainsomanyingredients,anditisveryhardforclinicianstobeexpertenoughto advise individuals and mothers in terms of what might be sensitizing products or what might not be.[22]Thegeneralrule,Ithink,is that it is a best bet to stick with products that have been extensively tested.

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We have gone through a lot of information on infants skin development, on the microbial colonization and changes over time, the interrelationshipofthehostdefensesystemwithwhatispresentonourskin,andIthinkitisreasonabletosaythatweareatthebeginning stages of understanding the impact of microbes on infant skin development and host defense. A logical strategy, for, now in terms of skin care is to try to maintain or repair the existing barrier (physical, chemical and microbiologic); to recognize that skin care practices can influence skin colonization and impact on skin health and disease development; and to use reasonable, good skin-care practices that support normal skin barrier function.

Thank you for participating in this educational activity. You may now take the post-test by clicking on the “Earn CME/CE credit”link. Please also take a moment to complete the program evaluation that follows.

This article is a CME/CE certified activity. To earn credit for this activity visit:http://www.medscape.org/viewarticle/804338


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AbbreviationsAD = atopic dermatitis Amp = antimicrobial peptide PSM = phenol soluble modulin TLR2 = Toll-like receptor 2

References1. Rone JM, Bare DE, Pickens WL, Visscher MO, Hoath SB. Acid mantle development in the newborn infant. Pediatr Res. 1997;41:172.2. McLeanWH,IrvineAD.Heritablefilaggrindisorders:theparadigmof atopic dermatitis. J Invest Dermatol. 2012:132:E20-E21. 3. GalloRL,NizetV.Innatebarriersagainstinfectionandassociated disorders. Drug Discov Today Dis Mech. 2008;5:145-152. 4. Grice EA, Kong HH, Conlan S, et al. Topographical and temporal diversity of the human skin microbiome. Science. 2009;234:1190-1192. 5. Dominguez-Bello MG, Costello EK, Contreras M, et al. Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns. Proc Natl Acad Sci U S A. 2010;107:11971-11975. 6. Capone KA, Dowd SE, Stamatas GN, Nikolovski J. Diversity of the human skinmicrobiomeearlyinlife.JInvestDermatol.2011;131:2026-2032.7. Bevins CL. An important clue: fingerprints point to psoriasin in defense against E. coli. Nat Immunol. 2005;6:12-13. 8. Gallo RL. Gallo RL. Antimicrobial peptides in defense and inflammatory skin diseases. Presented at the 61st Annual Meeting of the Pacific Dermatologic Association. August 12-16, 2009, Portland, Oregon. Available at http://www.pacificderm.org/Powerpoints/RGallo.pdf. Accessed May 28, 20139. Gallo RL, Nakatsuji T. Microbial symbiosis with the innate immune defense system of the skin. J Invest Dermatol. 2011;131:1974-1980. 10. Lai Y, Cogen AL, Radek KA, et al. Activation of TLR2 by a small molecule produced by Staphylococcus epidermidis increases anti-microbial defense against bacterial skin infections. J Invest Dermatol. 2010;130:2211-2221. 11. Lai Y, Di Nardo A, Nakatsui T, et al. Commensal bacteria regulate TLR3-dependent inflammation following skin injury. Nat Med. 2009;15:1377-1382. A12. Simpson EL, Eichenfield LF, Ellis CN, Mancini AJ, Paller AS. Current issues in atopic comorbidities and preventing the atopic march. Semin Cutan Med Surg. 2012;31(3 Suppl):S6-S9.

13. Eichenfield LF, Ellis CN, Mancini AJ, Faller AS, Simpson EL. Atopic dermatitis: epidemiology and pathogenesis update. Semin Cutan Med Surg. 2012;31(3 Suppl):S3-S5. 14. Tsai JD, Chang SN, Mou CH, Sung FC, Lue KH. Association between atopic diseases and attention-deficit/hyperactivity disorder in childhood: a population-based case-control study. Ann Epidemiol. 2013;23:185-188. 15. IrvineAD,McLeanWH.Breakingthe(un)soundbarrier:filaggrinisamajor gene for atopic dermatitis. J Invest Dermatol. 2006;126:1200-1202. 16. Meyer-Hoffert U, Schroder JM. Epidermal proteases in the pathogenesis of rosacea. J Investig Dermatol Symp Proc. 2011;15:16-23. 17. Kong HH, Oh J, Deming C, et al. Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis. Genome Res. 2012;22:850-858. 18. Flohr C, Yeo L. Atopic dermatitis and the hygiene hypothesis revisited. Curr Probl Dermatol. 2011;41:1-34. 19. Franck LS, Quinn D, Zahr L. Effect of less frequent bathing of preterm infants on skin flora and pathogen colonization. J Obstet Gynecol Neonatal Nurs. 2000;29:584-589. 20. Simpson EL, Berry TM, Brown PA, Hanifin JM. A pilot study of emollient therapy for the primary prevention of atopic dermatitis. J Am Acad Dermatol. 2010;63:587-593. 21. Chiang C, Eichenfield LF. Quantitative assessment of combination bathing and moisturizing regimens on skin hydration in atopic dermatitis. Pediatr Dermatol. 2009;26:273-278. 22. Zissu A. Skin deep: allergies can be natural, too. N Y Times. April 27, 2011. Available at: http://query.nytimes.com/gst/fallpage.html3res=9E3DB113B F93BA15757COA9679D8B63&. Accessed April 24, 2013.

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