Infection and Atopic Dermatitis
Infection is a major complication of atopic dermatitis.1,2 Factors that contribute to the higher frequency of infection include a defective skin barrier facilitating microbial entry, a compromised immune system impairing recognition of active infection, and reduced antimicrobial peptide production.1-4 Genetic variants in the innate immune response may predispose patients with atopic dermatitis to an increased risk of skin infections.5 Abnormalities in the cutaneous microbial environment have also been documented that may play a role.6-9
Increased Staphylococcus aureus (S aureus) Colonization
Colonization of atopic dermatitis lesions with S aureus is common, with as many as 80% to 100% of patients with atopic dermatitis demonstrating colonization compared to 5% to 30% of non-atopic individuals.10 Rates of bacterial colonization are higher at more severely affected and inflamed sites, while overall microbial diversity is reduced.6,10 Such findings suggest that the absence of beneficial organisms in the skin microbiome of patients with atopic dermatitis may facilitate colonization and infection. Adequate atopic dermatitis therapy is associated with greater bacterial diversity7 and reduced rate of skin infection.11 In one study, treatment with topical corticosteroids, alone or combined with bleach baths, restored microbial diversity to control skin levels and normalized bacterial composition on lesional skin to resemble that of nonlesional skin.6
A Cochrane review identified no benefit to routine antistaphylococcal therapy in individuals with atopic dermatitis in the absence of clinical infection.12 Current guidelines recommend systemic antibiotics for overt secondary infection and bleach baths and intranasal mupirocin to reduce atopic dermatitis severity and infectious episodes.3,13
Participants should read the activity information, review the activity in its entirety, and complete the online post-test and evaluation. Upon completing this activity as designed and achieving a passing score on the post-test, you will be directed to a Web page that will allow you to receive your certificate of credit via e-mail or you may print it out at that time.The online post-test and evaluation can be accessed at http://tinyurl.com/atopicdermsupl2017.
Inquiries about CME accreditation may be directed to the University of Louisville Office of Continuing Medical Education & Professional Development (CME & PD) at email@example.com or (502) 852-5329.
Lawrence F. Eichenfield, MD
Linda F. Stein Gold, MD
Wynnis L. Tom, MD
Physicians: This activity has been planned and implemented in accor- dance with the requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of the University of Louisville and Global Academy for Medical Education, LLC. The University of Louisville is accredited by the ACCME to provide continuing medical education for physicians.
The University of Louisville Office of Continuing Medical Education & Professional Development designates this enduring material for a maximum of 1.75 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Nurses: Postgraduate Institute for Medicine is accredited with distinction as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.This educational activity for 1.6 contact hour is provided by the Postgraduate Institute for Medicine. Designated for 0.8 contact hours of pharmacotherapy credit for Advance Practice Nurses.
Recent research into the pathophysiology of atopic dermatitis has yielded two new treatments—the first ones to receive US Food and Drug Administration (FDA) approval for management of this condition in more than a decade. Both new therapies offer novel mechanisms of action. Crisaborole, a topical medi- cation that inhibits the phosphodiesterase-4 (PDE-4) enzyme, is approved for the treatment of mild to moderate disease in adults and children as young as 2 years old. Dupilumab, the first biologic therapy approved for use in atopic dermatitis, inhibits interleukin (IL)-4 and IL-13. It is indicated for the treatment of moderate to severe disease in adults whose disease is inadequately controlled with topical prescription therapies, or when those therapies are inadvisable.
Awareness of the substantial impact atopic dermatitis can have on quality of life can facilitate patient-clinician conversations about treatment goals. Such discussions may influence shared decision-making about therapeutic choices.
Therapeutic patient education has been applied to a variety of conditions and is now being studied in atopic dermatitis.
Food allergy and infection represent common comorbidities in patients with atopic dermatitis. New information about the benefit of the early introduction of peanuts to the diet has surfaced in recent years. Alterations in the skin microbiome may underlie the association of colonization and infection in atopic dermatitis. Preliminary research attempts to deploy the atopic patient’s “good” bacteria to reduce Staphylococcus aureus colonization.
Brief, expert reviews of the literature in these areas can help busy providers stay current in a rapidly evolving field, and can facilitate the translation of research into clinical practice to improve outcomes.
By reading and studying this supplement, participants should be better able to:
- Demonstrate an understanding of how atopic dermatitis can affect patient sleep, quality of life, daily activities, risk of comorbidities, and health care utilization/cost
- Explain the mechanism of action and clinical trials data supporting recently approved treatments for atopic dermatitis
- Discuss investigation therapies for atopic dermatitis
- Apply recent recommendations for evaluation of candidates for systemic treatment of atopic dermatitis
- Explain the benefit of providing patients with a written action plan
- Analyze the relationships of food allergy and infection to atopic dermatitis.
Individuals in a position to control the content of this educational activity are required to disclose: 1) the existence of any relevant financial relationship with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients with the exemption of non-profit or government organizations and non-health care related companies, within the past 12 months; and 2) the identification of a commercial product/device that is unlabeled for use or an investigational use of a product/device not yet approved.
Lawrence F. Eichenfield, MD, Advisory Board/Speaker: Valeant Pharmaceuticals North America LLC. Consultant: Eli Lilly and Company, Genentech, Inc., Otsuka America Pharmaceutical, Inc./Medimetriks Pharmaceuticals, Inc., Pfizer Inc., Sanofi Genzyme/Regeneron Pharmaceuticals, TopMD, Valeant. Investigator: Sanofi Genzyme/Regeneron.
Linda F. Stein Gold, MD, Consultant: Pfizer. Grant/Research: GlaxoSmithKline and Pfizer. Data Monitoring Committee: Otsuka.
Wynnis L. Tom, MD, Consultant: Pfizer. Grant/Research: Pfizer, Celgene Corporation, Pfizer, and Regeneron.
University of Louisville CME & PD Advisory Board and Staff Disclosures:
The CME & PD Advisory Board and Staff have nothing to disclose.
CME/CE Reviewers: University of Louisville Cindy England Owen, MD, has nothing to disclose. The Postgraduate Institute of Medicine planners and managers Trace Hutchison, PharmD; Samantha Mattiucci, PharmD, CHCP; Judi Smelker-Mitchek, MBA, MSN, RN; and Jan Schultz, MSN, RN, CHCP, have nothing to disclose.
Global Academy for Medical Education Staff: Eileen McCaffrey, MA; Tristan M. Nelsen, MNM, CMP, HMCC; Sylvia H. Reitman, MBA, DipEd; and Ron Schaumburg have nothing to disclose.
Off-Label/Investigational Use Disclosure
This CME/CE activity discusses the off-label use of certain approved medica- tions as well as data from clinical trials on investigational agents. Any such material is identified within the text of the articles.
This continuing medical education (CME/CE) supplement was developed from a satellite symposium held at the Skin Disease Education Foundation’s 18th Annual Las Vegas Dermatology Seminar, November 3, 2017, in Las Vegas, Nevada. The Guest Editors acknowledge the editorial assistance of Global Academy for Medical Education and Eileen McCaffrey, MA, medical writer, in the development of this supplement. The manuscript was reviewed and approved by the Guest Editors as well as the Editors of Seminars in Cutaneous Medicine and Surgery. The ideas and opinions expressed in this supplement are those of the Guest Editors and do not necessarily reflect the views of the supporter, Global Academy for Medical Education, the University of Louisville, Postgraduate Institute for Medicine, or the Publisher.
Sun D, Ong PY. Infectious complications in atopic dermatitis. Immunol Allergy Clin North Am. 2017;37(1):75-93.
David TJ, Cambridge GC. Bacterial infection and atopic eczema. Arch Dis Child. 1986;61(1):20-23.
Kim KH. Clinical pearls from atopic dermatitis and its infec- tious complications. Br J Dermatol. 2014;170(Suppl 1):25-30.
Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic derma- titis with topical therapies. J Am Acad Dermatol. 2014;71(1):116-132.
Ong PY, Leung DY. Bacterial and viral infections in atopic dermatitis: a comprehensive review. Clin Rev Allergy Immunol. 2016;51(3):329-337.
Gonzalez ME, Schaffer JV, Orlow SJ, et al. Cutaneous micro-biome effects of fluticasone propionate cream and adjunctive bleach baths in childhood atopic dermatitis. J Am Acad Dermatol. 2016;75(3):481-493.e488.
Kong HH, Oh J, Deming C, et al. Temporal shifts in the skin microbiome associated with disease flares and treat- ment in children with atopic dermatitis. Genome Res. 2012;22(5):850-859.
Nakatsuji T, Chen TH, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis. Sci Transl Med. 2017;9(378).
Totte JE, van der Feltz WT, Hennekam M, van Belkum A, van Zuuren EJ, Pasmans SG. Prevalence and odds of Staphylococcus aureus carriage in atopic dermatitis: a systematic review and meta-analysis. Br J Dermatol. 2016;175(4):687-695.
Gong JQ, Lin L, Lin T, et al. Skin colonization by Staphylococcus aureus in patients with eczema and atopic dermatitis and relevant combined topical therapy: a double-blind multicentre randomized controlled trial. Br J Dermatol. 2006;155(4):680-687.
Fleming P, Drucker AM. Risk of infection in patients with atopic dermatitis treated with dupilumab: A meta-analysis of randomized controlled trials. J Am Acad Dermatol. 2017. [Epub ahead of print]
Bath-Hextall FJ, Birnie AJ, Ravenscroft JC, Williams HC. Interventions to reduce Staphylococcus aureus in the management of atopic eczema: an updated Cochrane review. Br J Dermatol. 2010;163(1):12-26.
Sidbury R, Davis DM, Cohen DE, et al. Guidelines for the management of atopic dermatitis: section 3. Management and treatment with polytherapy and systemic agents. J Am Acad Dermatol. 2014;712(2):327-349.
Leung DY. Why is eczema herpeticum unexpectedly rare? Antiviral Res. 2013;98(2):153-157.
Glatz M, Bosshard PP, Hoetzenecker W, Schmid-Grendelmeier P. The role of Malassezia spp. in atopic dermatitis. J Clin Med. 2015;4(6):1217-1228.