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      Cutaneous cytomegalovirus infection in a child with hyper IgE and specific defects in antibody response to protein vaccines

      case-report

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          Abstract

          Cytomegalovirus (CMV) infection is a common opportunistic systemic infection in immunocompromised patients, but skin involvement is rare. Herein, we report a 10 year-old girl from consanguineous parents who was referred to our center because of disseminated maculopapular rash. She had history of upper and lower respiratory tract infections. In immunological studies, increased serum IgE level and decreased responses to tetanus and diphtheria were detected. Polymerase chain reaction (PCR) examination of bronchoalveolar lavage and serum sample revealed the presence of CMV. Early diagnosis of cutaneous CMV and appropriate treatment are the key actions in management of patients with underlying immunodeficiencies to avoid further complications.

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          Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndrome.

          Karin R Engelhardt, Sean A. McGhee, Sabine Winkler … (2009)
          The genetic etiologies of the hyper-IgE syndromes are diverse. Approximately 60% to 70% of patients with hyper-IgE syndrome have dominant mutations in STAT3, and a single patient was reported to have a homozygous TYK2 mutation. In the remaining patients with hyper-IgE syndrome, the genetic etiology has not yet been identified. We aimed to identify a gene that is mutated or deleted in autosomal recessive hyper-IgE syndrome. We performed genome-wide single nucleotide polymorphism analysis for 9 patients with autosomal-recessive hyper-IgE syndrome to locate copy number variations and homozygous haplotypes. Homozygosity mapping was performed with 12 patients from 7 additional families. The candidate gene was analyzed by genomic and cDNA sequencing to identify causative alleles in a total of 27 patients with autosomal-recessive hyper-IgE syndrome. Subtelomeric biallelic microdeletions were identified in 5 patients at the terminus of chromosome 9p. In all 5 patients, the deleted interval involved dedicator of cytokinesis 8 (DOCK8), encoding a protein implicated in the regulation of the actin cytoskeleton. Sequencing of patients without large deletions revealed 16 patients from 9 unrelated families with distinct homozygous mutations in DOCK8 causing premature termination, frameshift, splice site disruption, and single exon deletions and microdeletions. DOCK8 deficiency was associated with impaired activation of CD4+ and CD8+T cells. Autosomal-recessive mutations in DOCK8 are responsible for many, although not all, cases of autosomal-recessive hyper-IgE syndrome. DOCK8 disruption is associated with a phenotype of severe cellular immunodeficiency characterized by susceptibility to viral infections, atopic eczema, defective T-cell activation and T(h)17 cell differentiation, and impaired eosinophil homeostasis and dysregulation of IgE.
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            Diagnosis and treatment of a case of cutaneous cytomegalovirus infection with a dramatic clinical presentation

            Arthur Colsky, S.Manjula Jegasothy, Craig Leonardi … (1998)
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              Hyper-IgE syndrome.

              N Rezaei, A. Aghamohammadi (2010)
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                Author and article information

                Journal
                Journal ID (publisher-id): bjid
                Title: Brazilian Journal of Infectious Diseases
                Abbreviated Title: Braz J Infect Dis
                Publisher: Brazilian Society of Infectious Diseases (Salvador, BA, Brazil )
                ISSN (Print): 1413-8670
                ISSN (Electronic): 1678-4391
                Publication date (Print and electronic): October 2011
                Volume: 15
                Issue: 5
                Pages: 484-485
                Affiliations
                [03] orgnameShaheed Beheshti University of Medical Sciences orgdiv1Pediatric Infectious Research Center
                [02] Tehran orgnameShaheed Beheshti University of Medical Sciences orgdiv1Loghman Hospital Iran
                [04] Tehran orgnameTehran University of Medical Sciences orgdiv1School of Medicine Research Center for Immunodeficiencies Children's Medical Center Molecular Immunology Research Center orgdiv2Department of Immunology Iran
                [01] Tehran orgnameShaheed Beheshti University of Medical Sciences orgdiv1Mofid Children Hospital orgdiv2Department of Pediatrics Iran
                Article
                Publisher ID: S1413-86702011000500013 Publisher ID: S1413-8670(11)01500500013
                SO-VID: 45a3b8e3-cb66-404a-a5d9-b5cb1dd375f4
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                Date accepted : 09 March 2011
                Date received : 13 February 2011
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 4, Pages: 2
                Product

                SciELO Brazil

                Self URI: Full text available only in PDF format (EN)
                Categories
                Subject: Case Reports

                Keywords: common variable immunodeficiency,cytomegalovirus infections,antibody formation
                Data availability:
                Keywords: common variable immunodeficiency, cytomegalovirus infections, antibody formation

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