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Classification and clinical manifestations of hypersensitivity pneumonitis (extrinsic allergic alveolitis)

Talmadge E King, Jr, MD
Section Editor
Kevin R Flaherty, MD, MS
Deputy Editor
Helen Hollingsworth, MD


Hypersensitivity pneumonitis (HP), also called extrinsic allergic alveolitis, is a complex syndrome of varying intensity, clinical presentation, and natural history rather than a single, uniform disease [1-5]. Numerous inciting agents have been described including, but not limited to, agricultural dusts, bioaerosols, microorganisms (fungal, bacterial, or protozoal), and certain reactive chemical species [1,6,7]. (See "Epidemiology and causes of hypersensitivity pneumonitis (extrinsic allergic alveolitis)".)

The classification and clinical manifestations of HP will be reviewed here. The epidemiology, causes, diagnostic criteria, and treatment of this disorder are discussed separately. (See "Epidemiology and causes of hypersensitivity pneumonitis (extrinsic allergic alveolitis)" and "Diagnosis of hypersensitivity pneumonitis (extrinsic allergic alveolitis)" and "Treatment, prevention, and prognosis of hypersensitivity pneumonitis (extrinsic allergic alveolitis)".)


Classically, the clinical presentations of HP have been categorized as acute, subacute, or chronic depending upon the frequency, length, and intensity of exposure and upon the duration of subsequent illness. In an attempt to address ambiguities that result from this taxonomy, several other classification schemes have been proposed (table 1) [2,4,8,9]. Unfortunately, none are completely satisfactory because of the great variability in the presentation and course of HP [4].


Acute HP may follow heavy exposure to an inciting agent. It is the most classic and easily recognized form of HP, but symptoms still may be confused with a viral or bacterial infection, and patients are frequently treated initially with antibiotics [1,2]. The course is characterized by the abrupt onset (four to six hours following exposure) of fever, chills, malaise, nausea, cough, chest tightness, and dyspnea without wheezing. Physical examination is notable for tachypnea and diffuse fine crackles. Wheezing is rarely present.

Removal from exposure to the inciting antigen in acute HP results in subsiding of symptoms within 12 hours to several days and complete resolution of clinical and radiographic findings within several weeks. The disease may recur with reexposure.

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Literature review current through: Nov 2017. | This topic last updated: Sep 09, 2016.
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