Conflicts of interest None declared.
New insights into disease pathogenesis in crusted (Norwegian) scabies: the skin immune response in crusted scabies
Version of Record online: 14 APR 2008
© 2008 The Authors. Journal Compilation © 2008 British Association of Dermatologists
British Journal of Dermatology
Volume 158, Issue 6, pages 1247–1255, June 2008
How to Cite
Walton, S.F., Beroukas, D., Roberts-Thomson, P. and Currie, B.J. (2008), New insights into disease pathogenesis in crusted (Norwegian) scabies: the skin immune response in crusted scabies. British Journal of Dermatology, 158: 1247–1255. doi: 10.1111/j.1365-2133.2008.08541.x
Authors’ contributions S.F.W. participated in the design and coordination of the study, analysis of results and drafted the manuscript. D.B. carried out the immunohistochemical assays, undertook the microscopy and participated in drafting the manuscript. P.R.-T. participated in the design of the study and analysis of results. B.J.C. conceived the study, collection of the samples and coordination. All authors read and approved the final manuscript.
- Issue online: 14 APR 2008
- Version of Record online: 14 APR 2008
- Accepted for publication 30 November 2007
- immune markers;
- inflammatory skin disease;
- parasitic skin diseases;
Background Crusted scabies is a rare and severely debilitating disease characterized by infestation of the skin with up to millions of Sarcoptes scabiei mites, high total IgG levels, extremely high total IgE levels, and the development of hyperkeratotic skin crusts that may be loose, scaly and flaky or thick and adherent.
Objectives To describe crusted scabies skin pathogenesis and identify markers associated with an inappropriate immune response leading to disease progression.
Patients/methods Serial sections from skin biopsies obtained from two patients with severe crusted scabies were examined by immunohistochemistry for cell surface markers and inflammatory and regulatory cytokines. Concurrent levels of total B- and T-cell subsets and IgE, IgA, IgM, IgG and IgG subclasses were analysed in the blood. In addition antibody levels were recorded in a further 33 patients with crusted scabies and 14 patients with ordinary scabies.
Results A predomination of infiltrating CD8+ T lymphocytes in the dermis was observed compared with minimal helper T lymphocytes (CD4+) and the absence of any B cells. The proportion of T and B lymphocytes and T-cell subsets in the blood of these patients were within normal ranges, indicating a selective movement of CD8+ T cells into the dermis. Furthermore, strong staining for the inflammatory cytokine interleukin-1β and anti-inflammatory cytokine transforming growth factor-β1 was observed. Elevated levels of IgE, IgG, IgG1, IgG3 and IgG4 were recorded.
Conclusions Skin-homing cytotoxic T cells contribute to an imbalanced inflammatory response in the dermis of crusted scabies lesional skin. This, in combination with the lack of B cells, is contributing to the failure of the skin immune system to mount an effective response resulting in uncontrolled growth of the parasite.