Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis (EAA) is a syndrome caused by the repetitive inhalation of antigens from the environment in susceptible or sensitized people.

[3] People affected by this type of lung inflammation (pneumonitis) are commonly exposed to the antigens by their occupations, hobbies, the environment and animals.

[4][3] The inhaled antigens produce a hypersensitivity immune reaction causing inflammation of the airspaces (alveoli) and small airways (bronchioles) within the lung.

Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache.

[1] Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy.

[7] 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.

[11] Because different people react variably to antigen exposure, the exact mechanism is unclear but genetic and host factors are likely at play.

[2] 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.

[8] The diagnosis is made through clinical judgement using a combination of findings because there does not exist a single, universal diagnostic criteria for the disease.

[1][12] Acute presentation may reveal poorly defined a micro-nodular interstitial pattern and ground-glass opacities in the lower and mid lung zones.

The non-fibrotic form is typically characterized by ground glass opacities, mosaic attenuation, ill-defined centrilobular nodules (<5 mm), and air trapping.

[1] The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.

[8] Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen.

The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma.

[7][22] When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias.

This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated.

[3] 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.

[24][25] 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 [1] In chronic disease, HP must be differentiated from very similarly presenting idiopathic pulmonary fibrosis.

[3] In addition to steroids for fibrotic disease, other immunosuppressants (Azathioprine, Mycophenolic acid) and anti-fibrotic agents (Nintedanib) may be used although their effectiveness is unclear[2] There are few studies examining longitudinal outcomes in patients diagnosed with hypersensitivity pneumonitis.

[8] Most of the outcomes collected are from patients diagnosed with farmer's or bird breeder's lung and thus the degree to which this data can be extrapolated to other types of HP is uncertain.