Figure 1. Proposed mechanisms in the pathogenesis of hypersensitivity pneumonitis. exaggerated immune reaction activation of the fibroblast accumulation of extracellular matrix TNF-α IFN-γ IL-12 mild increase of local lymphocytes without clinical consequences

acute formchronic form

ill-defined nodules mosaic perfusion extensive bronchiolar obstruction secondary to shunting of blood away from poorly ventilated regions of lung patchy areas of air trapping on expiratory scans indirect signs of small airways obstruction  subacute/chronic HP

bronchiolocentric septal thickening consolidation with traction bronchiectasis architectural distortion subpleural predominant distribution irregular reticular opacities traction bronchiectasis architectural distortion central distribution  chronic HP

two key histopathologic features lymphocytic interstitial pneumonitis poorly formed granuloma around a small airway typical interstitial HP granuloma small, non-necrotizing, poorly formed, loosely arranged  subacute HP

fibrosis, architectural remodeling in peribronchiolar pattern fibrosis, architectural remodeling with septal fibrosis -- as seen in usual interstitial pneumonia (UIP) but without the honeycombing and fibroblastic foci  chronic HP

Figure 5. Algorithmic approach for the diagnosis of subacute/chronic hypersensitivity pneumonitis