They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present. In fact, hypersensitivity pneumonitis can often resemble (IPF) in terms of pulmonary fibrosis and that many patients experience hypoxemia. Epidemiology
Although the prevalence of hypersensitivity pneumonitis is not established it is thought to be low. Data collection limitations are a result of difficulty in diagnosis, sub-clinical presentations that go undetected and variability in climate, region and proximity to local industries. The most common types are bird fanciers and farmers lung. Interestingly, cigarette smoking appears to be protective against the disease. Pathophysiology
Hypersensitivity pneumonitis is caused by an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity can both occur depending on the cause. In general, acute HP is suspected to be attributed to a type III hypersensitivity while the subacute and chronic types are suspected to be caused by T cell infiltration and granuloma formation. Because different people react variably to antigen exposure, the exact mechanism is unclear but genetic and host factors are likely at play. The two hit hypothesis is often toted in the literature to explain why some people have a normal reaction to an antigenic exposure without clinical findings while others experience an exaggerated immune response.
False negatives are often common with serum precipitins because of lack of testing reagents for many antigens.Precipitating IgG antibodies against fungal or avian antigens can be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein precipitin lines form on agar plate. The ImmunoCAP technology has replaced this time-consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmers lung or for ABPA) or avian antigens (Bird Fanciers Lung). Differential Diagnosis
Organic dust toxic syndrome presents similarly with fevers, chills a few hours after exposure to bioaerosols with toxins from fungi, however this is not a true hypersensitivity reaction because it occurs on initial exposure without a preceding sensitization In chronic disease, HP must be differentiated from very similarly presenting idiopathic pulmonary fibrosis.Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.Similarly, sarcoidosis has noncaseating granuloma formation, however hilar adenopathy is often seen on chest radiographs. Treatment
The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage and acute disease is often self-limiting. The identification of the provoking antigen and its location must be ascertained by conducting an exposure assessment. Home cleaning is one method of antigen avoidance.