Aspergillus fumigatus Precipitating Antibodies, IgG

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.^1-5 HP is not mediated by IgE. It is associated with progressive pulmonary disability, irreversible lung damage, and mortality in some occupational settings.^1-5 Patients often present with intermittent chills, fever, cough, and shortness of breath that begin four to eight hours after exposure to the offending dust.

The antigen used in this assay is prepared by Greer Laboratories from a culture filtrate of #1 Reed strain of Aspergillus fumigatus. Aspergillus mode can be found in soil, foods, fresh water, and other natural sources including compost, barley, tobacco, and Esparto grass dust(stucco).^1,3,5 These organisms grow well in decaying organic material at temperatures often attained during decomposition.⁵ Aspergillus mold can also grow on ceilings and walls where water damage has occurred.⁶

No single laboratory test is diagnostic for hypersensitivity pneumonitis.^1-5 Diagnosis is based on a complete environmental history supported by result of chest x-ray, spirometry, and in vitro immunologic tests.^1-5 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.

Aspergillus infection can also result in allergic bronchopulmonary aspergillosis (ABPA), a condition where airway colonization of individuals with asthma or cystic fibrosis results in increased inflammation and destruction of bronchial structural elements.^6,7 Testing for Aspergillus precipitating IgG antibodies has been shown to be of some clinical utility in the assessment of patients with potential ABPA.⁷

1. 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 Nov; 84(5 Pt 2):839-844. PubMed 2809034

2. Patel AM, Ryu JH, Reed CE. Hypersensitivity pneumonitis: Current concepts and future questions. J Allergy Clin Immunol. 2001 Nov; 108(5):661-670. PubMed 11692086

3. Kurup VP, Fink JN. Immunological tests for evaluation of hypersensitivity pneumonitis an allergic bronchopulmonary aspergillosis. In Rose NR, Hamilton RG, Detrick B, eds.Manual of Clinical Laboratory Immunology. 6th ed. Washington, DC: ASM Press;2002:910-919.

4. Zacharisen MC, Fink JN. Hypersensitivity pneumonitis. In Grammar LC, Greenberger PA, eds. Patterson's Allergic Disease. 6th ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2002:515-528.

5. Greer Laboratories Inc. Hypersensitivity Pneumonitis/Extrinsic Allergic Alveolitis. Technical Bulletin #47. Lenoir, NC: Greer; 2004.

6. Zander DS. Allergic bronchopulmonary aspergillosis: An overview. Arch Pathol Lab Med. 2005 Jul; 129(7):924-928. PubMed 15974818

7. Bush RK, Portnoy JM, Saxon A, et al. The medical effects of mold exposure. J Allergy Clin Immunol. 2006 Feb; 117(2):326-333. PubMed 16514772

Yi ES. Hypersensitivity pneumonitis. Crit Rev Clin Lab Sci. 2002 Nov; 39(6):581-629. PubMed 12484500