<i>Saccharomonospora viridis</i> Precipitating Antibodies, IgG
| Saccharomonospora viridis Precipitating Antibodies, IgG | | | |
| Number | | 660019 |
| CPT | | 86602 |
| Related Information | | Hypersensitivity Pneumonitis Profile |
| Synonyms | | Hypersensitivity Pneumonitis ; Thatched Roof Disease |
| Specimen | | Serum |
| Volume | | 0.2 mL |
| Container | | Red-top tube or gel-barrier tube |
| Storage Instructions | | Refrigerate |
| Causes for Rejection | | Excessive hemolysis |
| Reference Interval | | Normal: negative |
| Use | | Confirm the presence of precipitating antibodies to Saccharomonospora viridis |
| Limitations | | A positive test does not establish the diagnosis of hypersensitivity pneumonitis, nor does the absence of precipitins eliminate the diagnosis. |
| Methodology | | Double diffusion (Ouchterlony) |
| Additional Information | | Hypersensitivity pneumonitis (HP), also referred to as extrinsic allergic alveolitis (EAA), is an inflammatory lung disease resulting from the inhalation and subsequent sensitization to a wide variety of inhaled organic dusts.1,2,3,4,5 Exposure to Saccharomonospora viridis can result from contact with dried grasses and leaves causing a condition referred to as thatched roof disease.1 HP is not mediated by IgE. It is associated with progressive pulmonary disability, irreversible lung damage, and mortality in some occupational settings.1,2,3,4,5 Patients often present with intermittent chills, fever, cough, and shortness of breath that begin 4-8 hours after exposure to the offending dust. No single laboratory test is diagnostic for hypersensitivity pneumonitis.1,2,3,4,5 Diagnosis is based on a complete environmental history supported by result of chest x-ray, spirometry, and in vitro immunologic tests.1,2,3,4,5 Identification of the causative agent is important to allow avoidance of exposure.2,5 Double diffusion (Ouchterlony) assays are typically used to determine antigen-specific IgG antibodies.5 The appearance of precipitin arcs confirms the presence of precipitating antibodies to specific antigens. These antibodies may also be present in individuals not afflicted with HP.2,3,5 The presence of antibodies to the offending dust or antigen confirms exposure but is not diagnostic of HP. However, upon repeated or prolonged exposures, high levels of precipitating IgG antibodies are typically observed. |
| Footnotes | | - Richerson HB, Bernstein IL, Fink JN, et al, “Guidelines for the Clinical Evaluation of Hypersensitivity Pneumonitis. Report of the Subcommittee on Hypersensitivity Pneumonitis,” J Allergy Clin Immunol, 1989, 84(5 Pt 2):839-44.
- Patel AM, Ryu JH, and Reed CE, “Hypersensitivity Pneumonitis: Current Concepts and Future Questions,” J Allergy Clin Immunol, 2001, 108(5):661-70.
- Kurup VP and Fink JN, “Immunological Tests for Evaluation of Hypersensitivity Pneumonitis an Allergic Bronchopulmonary Aspergillosis,” Manual of Clinical Immunology, 6th ed, Rose NR, Hamilton RG, and Detrick B, eds, Washington, DC: ASM Press, 2002, 910-9.
- Zacharisen MC and Fink JN, “Hypersensitivity Pneumonitis,” Patterson's Allergic Disease, 6th ed, Grammar LC and Greenberger PA, eds, Philadelphia, PA: Lippincott Williams and Wilkins, 2002, 515-28.
- Greer Technical Bulletin #47, Hypersensitivity Pneumonitis/Extrinsic Allergic Alveolitis
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| References | | Yi ES, “Hypersensitivity Pneumonitis,” Crit Rev Clin Lab Sci, 2002, 39(6):581-629. |
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