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Extrinsic allergic alveolitis 

Extrinsic allergic alveolitis

Chapter:
Extrinsic allergic alveolitis
Author(s):

D.J. Hendrick

and G.P. Spickett

DOI:
10.1093/med/9780199204854.003.181404

July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

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date: 29 April 2017

Extrinsic allergic alveolitis is an uncommon inflammatory disorder of the lungs that results from hypersensitivity responses to inhaled environmental agents. Most varieties are occupational in origin, but sporadic cases arise in domestic settings or from recreational activities. Causal agents chiefly comprise allergenic microbial spores that contaminate stored vegetable produce (e.g. farmer’s lung caused by Saccharopolyspora rectivirgula, previously known as Micropolyspora faeni, and Thermoactinomyces vulgaris) or reservoirs of water, but a number of animal proteins (particularly those present in feather bloom, e.g. pigeon fancier’s lung) and a few reactive chemicals are also inducers.

Pathology—acute disease is characterized by a nonspecific diffuse pneumonitis with inflammatory cellular infiltration of the bronchioles, alveoli, and interstitium; subacute disease by the formation of epithelioid noncaseating granulomas; and chronic disease by fibrosis, particularly in the upper lobes.

Acute disease—following a sensitizing period of exposure, which may vary from weeks to years, the affected subject experiences repeated episodes of an influenza-like illness accompanied by cough and undue breathlessness some hours (usually 3–9) after commencing exposure to the relevant organic dust. Fever and basal crackles are the main physical signs. Most patients recover fully from each acute exacerbation within a day or so, and if the cause is recognized and further exposure avoided there is little risk of persisting pulmonary dysfunction.

Chronic disease—typically seen following long-standing low-level antigenic exposure, e.g. in the person who keeps a single budgerigar (parakeet) in the home. Presents less dramatically than acute disease with increasing shortness of breath, but without systemic upset except for weight loss in some cases. Clinical features are similar to those of other varieties of pulmonary fibrosis, but clubbing is uncommon. Permanent fibrotic lung damage can eventually lead to hypoxaemia, pulmonary hypertension, right heart failure, and death.

Investigation—is directed towards the lungs, the relevant exposure, and determination of hypersensitivity. (1) Lungs—in acute disease the chest radiograph may be normal or show a ground-glass appearance; in subacute disease small reticular opacities may be seen; in chronic disease there is fibrosis. CT provides better images, but no single feature or pattern is pathognomonic. Lung function studies show a restrictive pattern. (2) Determination of relevant exposure—in many cases the history alone is sufficient, but industrial hygiene measurements made from personal samplers may be required when the disease is suspected in an environment not previously incriminated. (3) Determination of hypersensitivity—demonstration of a serum IgG antibody response to the inducing organic dust is unsatisfactory for ‘confirming’ hypersensitivity because it correlates with exposure better than disease, but a negative test generally excludes the diagnosis. Some form of inhalation challenge test may be necessary when there is diagnostic doubt.

Management—requires that the diagnosis is secure, and then centres on reducing any further exposure to a minimum. There is debate as to whether the use of corticosteroids for acute episodes confers any long-term benefit. In acute disease cessation of exposure usually leads to complete resolution and in chronic cases usually prevents further progression. Persistent exposure can lead to progressive and permanent fibrotic damage in some cases, but not in all.

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