Ask The Expert
January 8, 2014
When should a child with repeated skin infection of moderate to severe atopic dermatitis (4 to 6 courses of antibiotics annually), but with no infections elsewhere, be investigated for immunodeficiency?
From the Editors:
Children with severe atopic dermatitis can be challenging to manage. Our experts have given us a very valuable synopsis of a very complex question. This will be one article you will want to save to your office computer to refer to when complicated issues arise with your atopic dermatitis patients. Furthermore, this would be an excellent review article from which to study when it comes time to renew your allergy boards.
By Dr. Punchama Pacharn and Prof. Pakit Vichyanond:
Atopic dermatitis (AD) is a chronic inflammatory disease with defects of the innate immune system, including in the production of antimicrobial peptides, diminished recruitment of cells to the skin, and epidermal barrier abnormalities (1). Furthermore, the skin colonization of S. aureus and Malassezia species has been reported (2, 3). Therefore, AD patients are susceptible to recurrent skin infections from S. aureus, fungus, and several viruses (3, 4). Severe systemic infections with Herpes simplex, i.e., disseminated eczema herpeticum (EH) could occur in AD patients (3). This group of patients has more severe symptoms, higher numbers of circulating eosinophil, higher levels of serum CCL17, higher incidents of asthma and a higher specific IgE sensitization to inhaled and food allergens (5).
However, most infections in AD patients would require systemic antibiotic treatment in less than 50%, and are predisposed to EH in less than 5% (6). Therefore, an evaluation for immunodeficiency should be considered when patients have severe or difficult to treat skin infections or those with infections in organ systems other than skin.
By Dr. Juan Aldave Becerra:
Severe atopic dermatitis has several genetic and environmental pathogenic factors that affect the normal function of the immune system within the skin. I summarize them in the following list:
- Skin barrier defects: scratching; reduced synthesis of epidermal proteins such as filaggrin, loricrin, involucrin, corneodesmosin, S100 proteins, antiproteases and tight junction proteins (e.g. claudin-1).
- Innate immune dysregulation: increased number of inflammatory dendritic cells, altered TLR signalling, reduced production of antimicrobial peptides (e.g. cathelicidin, defensins), keratinocyte activation by environmental factors (e.g. allergen proteases, pollutants, microbes), increased keratinocyte production of cytokines that promote TH2 environment (e.g. TSLP, IL-25, IL-33), increased production of neuropeptides.
- Adaptive immune dysregulation: increased TH2 and TH22 inflammation, altered TH1 responses (predisposition to viral and bacterial infections), altered TH17 responses (predisposition to bacterial and fungal infections), and reduced Treg responses.
- Exaggerated immune responses to food allergens (e.g. milk, egg), aeroallergens (e.g. house dust mites), microbial molecules (e.g. from S aureus or Malassezia sp) or self antigens (e.g. human thioredoxin).
- Abnormal skin colonization by microbes: S aureus colonizes the skin in 90% of AD patients (staphylococcal enterotoxins induce polyclonal T-cell and B-cell activation).
By Dr. Mark Ballow
The organism in eczema is almost always Staphylococcus. However, if cultures show a gram negative organism, e.g. Proteus, Klebsiella, etc that should trigger an immune workup for a phagocytic abnormality. There are approaches to reduce Staph colonization in patients with eczema such as bleach baths 2-3x per week. Patient also needs aggressive treatment of the eczema to avoid 2nd infections. Also if in an adult may consider culturing for a fungal infection (see Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report and Recent insights into atopic dermatitis and implications for management of infectious complications- both in JACI.)
Mark Ballow, MD
Chief, Division of Allergy and Clinical Immunology
Medical Director, Immunology Laboratory at the Women and Children’s Hospital
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