26. Microbiology in Atopic Eczema

  1. Alan D. Irvine MD, FRCPI, FRCP3,4,
  2. Peter H. Hoeger MD5,6 and
  3. Albert C. Yan MD, FAAP, FAAD7,8
  1. Christina Schnopp MD1 and
  2. Martin Mempel MD2

Published Online: 24 MAY 2011

DOI: 10.1002/9781444345384.ch26

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

How to Cite

Schnopp, C. and Mempel, M. (2011) Microbiology in Atopic Eczema, in Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition (eds A. D. Irvine, P. H. Hoeger and A. C. Yan), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444345384.ch26

Editor Information

  1. 3

    Trinity College, Dublin, Ireland

  2. 4

    Our Lady's Children's Hospital, Dublin, Ireland

  3. 5

    University of Hamburg, Hamburg, Germany

  4. 6

    Catholic Children's Hospital Wilhelmstift, Hamburg, Germany

  5. 7

    University of Pennsylvania School of Medicine, Philadelphia, PA, USA

  6. 8

    The Children's Hospital of Philadelphia, Philadelphia, PA, USA

Author Information

  1. 1

    Department of Dermatology and Allergy, Biederstein, Technische Universität München, München, Germany

  2. 2

    Allergic Diseases, and Infectious Diseases, Department of Dermatology, Venereology, and Allergology, Georg - August - Universität Göttingen, Göttingen, Germany

Publication History

  1. Published Online: 24 MAY 2011
  2. Published Print: 3 JUN 2011

ISBN Information

Print ISBN: 9781405176958

Online ISBN: 9781444345384

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Keywords:

  • atopic eczema;
  • colonization;
  • IgE;
  • Malassezia;
  • Staphylococcus aureus;
  • superantigens

Summary

The colonization of lesional and non-lesional atopic eczema skin with Staphylococcus aureus represents an important trigger for the severity and exacerbation frequency of skin symptoms. Atopic skin is preferentially prone to bind Staphylococcus aureus and this binding is followed by a perepetual stimulation of the atopic immune system, mainly by staphylococcal superantigens, that leads to enhanced T-cell homing as well as increased IgE-synthesis. Atopic skin shows reduced induction of the crucial skin defence peptides such as LL37, HBD2 and HBD3. Sensitivity to Malassezia antigens is a phenomenon specific to atopic eczema. Up to 50% of adult patients and more than 30% of paediatric patients are sensitized to Malassezia, with higher rates in adults who have a predominance of head and neck involvement, more severe atopic eczema and high total IgE. Higher rates of Malassezia sensitization in adults can be attributed to a higher proportion of extrinsic-type (atopic) eczema. Thus, sensitization to Malassezia and other microbial allergens seems to reflect the tendency towards a Th2-immune response in extrinsic-type atopic eczema rather than being a specific response.