Mushrooms,fungi,yeastsContaminatedwood,humidifiers,centralhotairheatingducts,peatmossplants
MycobacteriaMetalworkingfluids,sauna,hottub
BirdsPigeons,dovefeathers,ducks,parakeets
ChemicalsIsocyanates(autopainters),zinc,dyes
FromLacasseY,GirardM,CormierY:Recentadvancesinhypersensitivitypneumonitis,Chest 142:208,2012.
Several lines of evidence suggest that hypersensitivity pneumonitis is an immunologically mediated disease:
Bronchoalveolar lavage specimens consistently show increased numbers of CD4+ and CD8+ T lymphocytes.
Most affected patients have specific antibodies against the offending antigen in their serum.
Complement and immunoglobulins have been demonstrated within vessel walls by immunofluorescence.
Noncaseating granulomas are found in the lungs of two-thirds of affected patients.
MORPHOLOGYThehistopathologicpictureinbothacuteandchronicformsofhypersensitivitypneumonitisincludespatchymononuclearcellinfiltratesinthepulmonaryinterstitium,withacharacteristicperibronchiolaraccentuation.Lymphocytespredominate,butplasmacellsandepithelioidmacrophagesalsoarepresent.Inacuteformsofthedisease,variablenumbersofneutrophilsalsomaybeseen.“Loose,” poorly formed granulomas, withoutnecrosis,arepresentinmorethantwo-thirdsofcases,usuallyinaperibronchiolarlocation(
Fig.13.22 ).Inadvancedchroniccases,bilateral,upper-lobe–dominantinterstitialfibrosis(UIPpattern)occurs.
Fig. 13.22 Hypersensitivitypneumonitis,histologicappearance.Looselyformedinterstitialgranulomasandchronicinflammationarecharacteristic.
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Hypersensitivity pneumonitis may manifest either as an acute reaction, with fever, cough, dyspnea, and constitutional signs and symptoms arising 4 to 8 hours after exposure, or as a chronic disease characterized by insidious onset of cough, dyspnea, malaise, and weight loss. With the acute form, the diagnosis is usually obvious because of the temporal relationship of symptom onset and exposure to the incriminating antigen. If antigenic exposure is terminated after acute attacks of the disease, complete resolution of pulmonary symptoms occurs within days. Failure to remove the inciting agent from the environment eventually results in an irreversible chronic interstitial pulmonary disease.
A number of disorders are characterized by pulmonary infiltrates rich in eosinophils, which are recruited to the lung by local release of chemotactic factors. These diverse diseases generally are of immunologic origin, but the etiology is not understood. Pulmonary eosinophilia is divided into the following categories:
Acute eosinophilic pneumonia with respiratory failure, characterized by rapid onset of fever, dyspnea, hypoxia, and diffuse pulmonary infiltrates on chest radiographs. The bronchoalveolar lavage fluid typically contains more than 25% eosinophils. There is prompt response to corticosteroids.
Simple pulmonary eosinophilia (Loeffler syndrome), characterized by transient pulmonary lesions, eosinophilia in the blood, and a benign clinical course. The alveolar septa are thickened by an infiltrate containing eosinophils and occasional giant cells.
Tropical eosinophilia, caused by infection with microfilariae and helminthic parasites
Secondary eosinophilia, seen, for example, in association with asthma, drug allergies, and certain forms of vasculitis