eMedicine Specialties > Pediatrics: General Medicine > Allergy & Immunology

Severe Combined Immunodeficiency: Differential Diagnoses & Workup

Author: Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Coauthor(s): Smeeta Sinha, MD, Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Aug 18, 2009

Differential Diagnoses

Agammaglobulinemia
Human Immunodeficiency Virus Infection
Atopic Dermatitis
Hyperimmunoglobulinemia E (Job) Syndrome
B-Cell and T-Cell Combined Disorders
Lymphohistiocytosis
Bruton Agammaglobulinemia
Lymphoproliferative Disorders
Cartilage-Hair Hypoplasia
T-Cell Disorders
Cystic Fibrosis
X-linked Immunodeficiency With Hyper IgM

Other Problems to Be Considered

When patients first present with common bacterial infections such as otitis media and pneumonia, a diagnosis of agammaglobulinemia often is considered. In fact, early descriptions of severe combined immunodeficiency (SCID) were termed Swiss agammaglobulinemia.

In almost all cases, flow cytometry immediately distinguishes between B-cell deficiencies and lack of mature T cells. Other immunodeficiency syndromes, particularly DiGeorge syndrome, may lack T-cell function completely and look clinically like severe combined immunodeficiency. The nonimmunologic features of these T-cell disorders usually distinguish them. CD40 ligand (CD154) deficiency, that is, X-linked hypogammaglobulinemia with hyper–immunoglobulin M (IgM), may present with recurrent otitis media and Pneumocystis pneumonia, as does severe combined immunodeficiency; the former has normal populations of mature T cells, B cells, and NK cells, unlike most variants of severe combined immunodeficiency. Table 1. Primary Immunodeficiency Diseases With T-Lymphocyte Dysfunction

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Table
Lymphocyte ProfileDisease or PhenotypeGene Mutation
T-, B+, NK- X-linked severe combined immunodeficiencyCommon g chain receptor on chromosome band Xq13.1
Autosomal recessive (AR) severe combined immunodeficiency (AR SCID)JAK3 at chromosome band 19q13.1
T-, B+, NK+ AR severe combined immunodeficiencyInterleukin (IL)-7 a chain receptor on chromosome band 5p13
AR severe combined immunodeficiencyCD3 d and CD3 e chain on chromosome band 11q23
T-, B-, NK- AR severe combined immunodeficiencyAdenosine deaminase (ADA) on chromosome band 20q13.2-q13.11
T-, B-, NK+ AR severe combined immunodeficiencyRecombinase-activating genes RAG1 or RAG2 on chromosome band 11p13
AR severe combined immunodeficiencyArtemis gene on chromosome band 10p13
Omenn syndromeRAG1 or RAG2 genes
T+, B+, NK+ AR severe combined immunodeficiencyp56 lck
T-/CD45-, B+, NK- AR severe combined immunodeficiencyCD45 tyrosine phosphatase
Proliferative T
cells/CD25- 		With autoimmunityIL-2 a chain receptor on chromosome band 10p14-15
Proliferative T and NK, CD8+ With EBV infectionSH2D1A (SAP; Duncan syndrome) on chromosome band Xq25
Activated T cells/CD69+/DR+ With autoimmunityIPEX on chromosome band Xp11.2-q13
CD4+, CD8- T; B+, NK+ AR severe combined immunodeficiencyZAP70 tyrosine kinase on chromosome band
2q12
CD4-, CD8+; B+/DR- AR severe combined immunodeficiency - Bare lymphocyteMajor histocompatibility complex (MHC) class II deficiency: RFXAP on 13q; CIITA on chromosome band 16p13; RFXANK
CD4+, low CD8: ratio 4-8WAS: low platelet volume, numberChromosome band Xp11.22
T+/TCR-, B+ With autoimmunityCD3 g or e on chromosome band 11q23
T+, B+, NK+; chromosome breakage+ AT: high a fetoprotein; low IgAATM on chromosome band 11q22.3
Nl profile, mild lymphopeniaDiGeorge: facial, cardiac, low Ca++ DGCR at chromosome band 22q11.2
T+/CD154-, B+, NK+ With hyper-IgM; low IgG,
IgA		CD40 ligand on chromosome band Xq26.3-q27.1
Lymphocyte ProfileDisease or PhenotypeGene Mutation
T-, B+, NK- X-linked severe combined immunodeficiencyCommon g chain receptor on chromosome band Xq13.1
Autosomal recessive (AR) severe combined immunodeficiency (AR SCID)JAK3 at chromosome band 19q13.1
T-, B+, NK+ AR severe combined immunodeficiencyInterleukin (IL)-7 a chain receptor on chromosome band 5p13
AR severe combined immunodeficiencyCD3 d and CD3 e chain on chromosome band 11q23
T-, B-, NK- AR severe combined immunodeficiencyAdenosine deaminase (ADA) on chromosome band 20q13.2-q13.11
T-, B-, NK+ AR severe combined immunodeficiencyRecombinase-activating genes RAG1 or RAG2 on chromosome band 11p13
AR severe combined immunodeficiencyArtemis gene on chromosome band 10p13
Omenn syndromeRAG1 or RAG2 genes
T+, B+, NK+ AR severe combined immunodeficiencyp56 lck
T-/CD45-, B+, NK- AR severe combined immunodeficiencyCD45 tyrosine phosphatase
Proliferative T
cells/CD25- 		With autoimmunityIL-2 a chain receptor on chromosome band 10p14-15
Proliferative T and NK, CD8+ With EBV infectionSH2D1A (SAP; Duncan syndrome) on chromosome band Xq25
Activated T cells/CD69+/DR+ With autoimmunityIPEX on chromosome band Xp11.2-q13
CD4+, CD8- T; B+, NK+ AR severe combined immunodeficiencyZAP70 tyrosine kinase on chromosome band
2q12
CD4-, CD8+; B+/DR- AR severe combined immunodeficiency - Bare lymphocyteMajor histocompatibility complex (MHC) class II deficiency: RFXAP on 13q; CIITA on chromosome band 16p13; RFXANK
CD4+, low CD8: ratio 4-8WAS: low platelet volume, numberChromosome band Xp11.22
T+/TCR-, B+ With autoimmunityCD3 g or e on chromosome band 11q23
T+, B+, NK+; chromosome breakage+ AT: high a fetoprotein; low IgAATM on chromosome band 11q22.3
Nl profile, mild lymphopeniaDiGeorge: facial, cardiac, low Ca++ DGCR at chromosome band 22q11.2
T+/CD154-, B+, NK+ With hyper-IgM; low IgG,
IgA		CD40 ligand on chromosome band Xq26.3-q27.1

Workup

Laboratory Studies

  • Lymphopenia is the classic hallmark of severe combined immunodeficiency (SCID); however, normal or even elevated lymphocyte counts can be seen in a significant proportion of patients. A complete absence of T-cell function by mitogen tests can occur in association with a normal lymphocyte count for age in some forms of severe combined immunodeficiency, including X-linked (XL) severe combined immunodeficiency, in which all the lymphocytes are B cells. DiGeorge syndrome is another example in which lymphocytes may be more than 2000 cells/dL with no T-cell function, or, conversely, normal T-cell function may be observed in spite of lymphopenia.
  • Severe combined immunodeficiency is typically diagnosed by fluorocytometric analysis of T-cell, B-cell, and NK cell populations. See Table 1, which differentiates the lymphocyte profile of various T-cell disorders.
  • Enumeration of lymphocytes is followed by DNA-sequencing of genes suggestive of the particular profile. Lymphocyte function should be assessed by measuring responses to phytohemagglutinin, a nonspecific stimulant of T-cell proliferation, concanavalin A directed at T-cell proliferation, and pokeweed mitogen directed at T-cell and B-cell proliferation.
    • Specific antigens, such as tetanus and Candida, stimulate lymphocyte proliferation and represent a later step in lymphocyte function than responses to the nonspecific mitogens. Healthy young infants may not respond well to these specific antigens due to lack of exposure and/or immature T-cell functions.
    • Another T cell function used for screening is their ability to proliferate in response to allogeneic cells; this response aids in defining the type of severe combined immunodeficiency but also is relevant to determining the need for immunosuppressive therapy in preparation for stem cell reconstitution.
    • Additional activators of lymphocyte proliferation are phorbol myristate acetate (PMA) with ionomycin or anti-CD3 and anti-CD28.
  • Measurement of leukocyte adenosine deaminase (ADA) enzyme activity is both sensitive and specific for the detection of ADA deficiency severe combined immunodeficiency.
  • Even when severe combined immunodeficiency is not suspected until the infant's death, lymphocyte markers, mitogen responses, and DNA studies can be carried out. Anticoagulated blood should be saved because lymphocytes are viable for at least 48 hours after death. An autopsy to assess the thymus and peripheral lymphoid tissues, including the spleen, gut, and tonsils, is needed.
  • Compromise of other hematopoietic cell lines is observed in reticular dysgenesis, in which myeloid cells are decreased, and platelets and erythrocytes may be deficient. Autoimmune hemolytic anemia can complicate forms of severe combined immunodeficiency in which autoimmune phenomena are present. Hypoplastic anemia occurs in cartilage-hair hypoplasia.
  • Patients with severe combined immunodeficiency are anergic. However, the reliability of delayed hypersensitivity skin testing depends on adequate exposure to the antigen. Candida and tetanus are the most useful antigens, but exposure requires 4-6 weeks, and more than one immunization is required in the case of tetanus. Mumps and Trichophyton antigens are of minimal use in infants.
  • T-cell defects can be difficult to define. The clinical manifestations of T-cell–associated opportunistic infections, such as mycobacteria, cytomegalovirus (CMV) and associated viruses, and P jiroveci, are usually interpreted by immunologists as defining a T-cell defect, even in the presence of apparently adequate mitogen responses (eg, IKK-γ deficiency for which impaired T-cell receptor [TCR]–mediated signaling is present despite normal mitogen responses).
  • Somech and Roifman suggest mutation analysis in patients with apparently normal immunologic tests to diagnose atypical cases of gC deficiency.3
  • When a T-cell disorder is suspected, the Immune Deficiency Foundation has a consultative service for physicians. Laboratories in Seattle (the University of Washington), Boston (Children's Hospital), and New York City are funded to provide molecular analysis (Jeffrey Modell Foundation) or they can assist in contacting other research facilities.
  • Prenatal diagnosis may be attempted when the family history is positive for severe combined immunodeficiency. Available DNA tests allow for the identification of mutations in genes for ADA, RAG1/RAG2, JAK3, gC, IL-7R, Artemis and many other gene mutations associated with SCID phenotype.
    • Amniocentesis and chorionic villus sampling enable DNA analysis of fetal cells.
    • Percutaneous umbilical blood sampling is performed to examine fetal blood for T-cell deficiency as well as ADA enzyme levels.

Imaging Studies

  • Chest radiographs in classic severe combined immunodeficiency show a small or absent thymus. However, infants who are immunologically normal may have no visible thymus if they have an overwhelming infection, such as sepsis or meningitis. Other T-cell defects, especially DiGeorge syndrome, also lack thymic tissue. Presence of thymic tissue does not exclude severe combined immunodeficiency. Patients with severe combined immunodeficiency who have mutations in ZAP70 or CD3 typically have normal size thymuses.
    • Chest radiographs are essential for early recognition of pneumonitis caused by viral pathogens and P jiroveci.
    • Patients with ADA deficiency and cartilage-hair hypoplasia may have bony abnormalities observed in the ribs and vertebrae on chest radiography.

Other Tests

  • Once lymphocyte populations are enumerated by flow cytometry, mutational analysis usually can be initiated based on the distribution of cell surface markers and clinical findings, including the sex of the infant. When the exact mutation cannot be found, linkage analysis and restriction fragment length polymorphism (RFLP) studies may be performed within families. The techniques for mutational analysis include screening by single-strand conformation polymorphism (SSCP), which detects about 85% of mutations, and dideoxy fingerprinting (ddF), a more sensitive test. The criterion standard to detect the exact DNA change is determination of genomic DNA; direct DNA sequencing must be carried out for some molecular defects, such as those at the 3‘ and 5‘ ends of exons and where the full exon-intron structure of the gene has not been delineated.
  • Polymorphisms in the androgen receptor are used to define nonrandom inactivation of the X chromosome in the mother and other female relatives in families in which an infant boy has severe combined immunodeficiency but no extended family pedigree is informative.

Procedures

  • Bronchoscopy frequently is indicated to identify the etiologic agent for pulmonary infection.
  • Endoscopy and biopsies are important in delineating the extent and identifying the cause of diarrhea and/or other GI symptoms.

Histologic Findings

  • In classic severe combined immunodeficiency, thymic tissue is severely deficient with few Hassall corpuscles and rare lymphocytes.
  • The skin and gut may show infiltration with histiocytes, eosinophils, and/or activated dysfunctional T cells.
  • The spleen and peripheral lymph nodes are characteristically atrophic, but, in maternal and transfusion-mediated graft versus host disease (GVHD) or in Omenn syndrome, they may be hyperplastic, with histiocytes and eosinophils.
  • Hemophagocytic lymphohistiocytosis is reported in XL severe combined immunodeficiency and cartilage-hair hypoplasia.

More on Severe Combined Immunodeficiency

Overview: Severe Combined Immunodeficiency
Differential Diagnoses & Workup: Severe Combined Immunodeficiency
Treatment & Medication: Severe Combined Immunodeficiency
Follow-up: Severe Combined Immunodeficiency
Multimedia: Severe Combined Immunodeficiency
References
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Further Reading

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Keywords

severe combined immunodeficiency, SCID, X-linked SCID, XL-SCID, MHC class II deficiency, bare lymphocyte syndrome, adenosine deaminase–deficient SCID, ADA-deficient SCID, recurrent infections, failure to thrive, dermatitis, bone marrow transplantation, DiGeorge syndrome, CHARGE syndrome, hematopoietic stem cell transplantation, HSCT, otitis media, cytomegalovirus infection, CMV, varicella, respiratory syncytial virus, RSV, rotavirus, parainfluenza virus, Epstein-Barr virus, EBV, enterovirus, adenovirus, non-Hodgkin lymphoma, herpes simplex virus, cryptosporidiosis, Crohn disease, HIV infection, graft versus host disease, GVHD, Omenn syndrome, treatment, diagnosis

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Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Smeeta Sinha, MD, Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School
Smeeta Sinha, MD is a member of the following medical societies: Alpha Omega Alpha, Phi Beta Kappa, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

James M Oleske, MD, MPH, François-Xavier Bagnoud Professor of Pediatrics, Director, Division of Pulmonary, Allergy, Immunology and Infectious Diseases, Department of Pediatrics, New Jersey Medical School
James M Oleske, MD, MPH is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Pediatrics, American Public Health Association, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

David J Valacer, MD, Consulting Staff, Hoffman La Roche Pharmaceuticals
David J Valacer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association for the Advancement of Science, American Thoracic Society, and New York Academy of Sciences
Disclosure: Nothing to disclose.

CME Editor

David Pallares, MD, Clinical Assistant Professor, Department of Pediatrics, Division of Allergy and Immunology, University of Louisville
David Pallares, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology
Disclosure: Nothing to disclose.

Chief Editor

Harumi Jyonouchi, MD, Associate Professor, Division of Pulmonary Allergy/Immunology and Infectious Diseases, Department of Pediatrics, UMDNJ-New Jersey Medical School
Harumi Jyonouchi, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association of Immunologists, American Medical Association, Clinical Immunology Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, Society for Mucosal Immunology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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