Allergic alveolitis


  • Recurrent fever and dyspnoea may be caused by exposure to environmental organic particles or biological dusts, such as mould spores or bird droppings, in patients with allergic alveolitis. It is, however, fairly common that the predisposing factor cannot be identified.
  • Allergic alveolitis is nowadays divided into fibrotic and nonfibrotic form.


  • Allergic alveolitis is caused by repeated or continuous exposure to organic particles or biological dusts. In some countries the condition is known as hypersensitivity pneumonitis. Several causative factors are known.
  • A common form of the disease is farmer's lung, which is caused by handling mouldy hay, litter or straw. In Finland the incidence of farmer's lung has nowadays decreased.
  • Allergic alveolitis may also be caused by exposure to mouldy sawdust, wood chippings or mushroom compost.
  • Cage bird droppings may cause allergic alveolitis known as bird fancier’s lung (bird breeder's lung). It is in many countries one of the most common forms of allergic alveolitis.
  • New causes of allergic alveolitis may be found even nowadays.


  • The symptoms of acute allergic alveolitis develop about four to eight hours after exposure.
    • The most common symptoms are cough, dyspnoea and fever.
    • Muscle and joint pains, headache and nausea may also appear.
    • If the condition persists, loss of appetite and weight loss may occur.
  • The symptoms associated with farmer’s lung usually occur during the cattle indoor feeding season. The symptoms generally appear after the working day in the evening or at night, and they abate within a few days. With repeated exposure, the attacks recur.
  • Symptoms may manifest as febrile episodes, bronchitic symptoms, malaise, loss of appetite, weight loss and exertional dyspnoea.
  • In cases where the symptoms are of a long duration a careful history should direct towards the possible diagnosis.
  • Fibrotic allergic alveolitis may resemble idiopathic pulmonary fibrosis (Idiopathic pulmonary fibrosis), and exposure to some factor cannot always be found.

Clinical findings

  • Lung auscultation often reveals fine inspiratory crackles.

Imaging and laboratory tests

  • A chest x-ray may be normal or show an increased micronodular pattern, most prominent in the basal lobes, or more diffuse infiltrates. In the chronic form, signs suggesting pulmonary fibrosis may be found.
  • Typical findings of high resolution CT scanning (HRCT) include air trapping and, in particular, centrilobular ground glass opacities. Reticular abnormalities are rarely seen in the acute and subacute nonfibrotic phase, but they are common in the fibrotic form. Honeycombing and traction bronchiectasis can also be encountered in the fibrotic phase, whereby the finding may be classified as so-called usual interstitial pneumonia (UIP). Sometimes the HRCT finding may resemble that of so-called nonspecific interstitial pneumonia (NSIP). The newest international guideline recommends classifying HRCT findings as typical of allergic alveolitis, compatible with it or indeterminate for it.
  • ESR and CRP may be increased at the early stages. Leucocytosis may also be present.
  • The patient’s serum often contains allergen-specific IgG antibodies against mould dust or other antigens. The presence of antibodies indicates prior exposure but does not necessarily represent disease.
  • A bronchoalveolar lavage (BAL) will show lymphocytosis and the T cell CD4/CD8 ratio may be reduced.

Pulmonary function tests

  • Oxygen saturation when measured with a pulse oximeter may be reduced.
  • The partial pressure of oxygen in an arterial sample is often reduced.
  • Diffusing capacity is usually reduced.
  • Restrictive changes are often evident on spirometry.


  • Diagnosis is based on history, clinical examination, exposure information and/or serum IgG determination, HRCT finding and BAL findings.
  • Lung biopsy is recommended if the diagnosis remains unclear, or in accordance with the clinic's practice in certain circumstances already in the initial phase when in the nonfibrotic type standard transbronchial lung biopsy may be sufficient.
    • In the fibrotic form, it is recommended to take the lung biopsy either as cryobiopsy in bronchoscopy or as a so-called surgical lung biopsy in a surgical endoscopic procedure.
    • The findings should be discussed in a multidisciplinary meeting in which a pulmonary specialist, radiologist and, as needed, pathologist participate.
  • If an acute case is suspected, expertise in pulmonary medicine should be sought immediately in order to arrange for diagnostic investigations as soon as possible. If these investigations are not done until, for example, after the sick leave period, the results may have returned back to normal.

Differential diagnoses


  • Measures to eliminate allergen exposure and avoidance of further exposure are the cornerstones of treatment.
  • Glucocorticoids are used in severe cases to accelerate recovery, for example prednisolone with a starting dose of 30–60 mg a day followed by gradual dose reduction. The duration of drug treatment is usually about 2–4 weeks, and it does not alter long-term prognosis.
  • Exposure leading the recurrence of allergic alveolitis should be prevented, for example by using an air-supplied helmet respirator.
  • Allergic alveolitis due to occupational exposure, for example in farmers, may be considered an occupational disease entitling the patient to compensation.
  • In the fibrotic form, treatment methods of other types of pulmonary fibrosis are applied.
  • Nintedanib has been found to slow down the rate of decline in the forced vital capacity (FVC) in some patients with a progressive lung fibrosis, such as fibrotic allergic alveolitis, for example. Nintedanib may be used in the treatment of fibrotic allergic alveolitis if the criteria for progressive lung fibrosis are fulfilled.


  • Long-term, untreated illness can become chronic and may cause, for example, pulmonary fibrosis and emphysema.
  • Usually lung function will more or less normalise, provided that the disease is diagnosed and treated in time.


1. Raghu G, Remy-Jardin M, Ryerson CJ et al. Diagnosis of Hypersensitivity Pneumonitis in Adults. An Official ATS/JRS/ALAT Clinical Practice Guideline. Am J Respir Crit Care Med 2020;202(3):e36-e69.  [PMID:32706311]
2. Quirce S, Vandenplas O, Campo P et al. Occupational hypersensitivity pneumonitis: an EAACI position paper. Allergy 2016;71(6):765-79.  [PMID:26913451]
3. Flaherty KR, Wells AU, Cottin V et al. Nintedanib in progressive fibrosing interstitial lung diseases. N Engl J Med 2019;381(18):1718-1727.  [PMID:31566307]
4. Raghu G, Remy-Jardin M, Richeldi L et al. Idiopathic Pulmonary Fibrosis (an Update) and Progressive Pulmonary Fibrosis in Adults: An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline. Am J Respir Crit Care Med 2022;205(9):e18-e47.  [PMID:35486072]

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