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Also called a Hypersensitivity Alveolitis or Hypersensitivity Pneumonitis.The spores that cause Farmer's Lung are not infectious. Instead, they trigger an allergic reaction. Similar to other disease but Bird fancier's lung has a worse prognosis than farmer's lung

About

• This is not an infection but all allergic response to allergen
• This is probably the most common occupational form of EAA
• Outcome of an allergic response to a group of microbes
• These form mould on vegetable matter in storage.

Aetiology

• Exposure to organochlorines and carbamate pesticides may also be risk factors for farmer's lung
• Farmer's lung - one of the most common forms. Due to exposure to mouldy hay. The major antigen is Saccharopolyspora rectivirgula.

Background

• During the handling of mouldy straw, hay or grain, particularly in a confined space such as a poorly ventilated building, inhalation of spores and other antigenic material is very likely.
• There also appears to be a clear relationship between the water content of crops, heating (through mould production) and microbial growth, and this would apply to various crops and vegetable matter, with the spores produced likely to cause EAA.

Clinical

• Acute Illness: intense attack about 4 to 8 hours after the person breathes in a large amount of dust from mouldy crops consists of Onset of shortness of breath, dry cough, malaise, Fever and chills., tachycardia
• Sub-Acute Farmer's Lung: develops slowly, responding to continual exposure to small amounts of mouldy dust. The signs and symptoms include: cough, breathlessness, mild fever, chills, arthralgia, myalgia, malaise, loss of appetite
• Chronic Farmer's Lung: Over years. Increasing dyspnoea, mild fever, weight loss, permanent lung damage and gradually worsen as exposure to mouldy dust continues. Cyanosis, CLubbing.

Investigations

• FBC: Normal. CRP and ESR may be elevated
• CXR: show diffuse micronodular interstitial shadowing. In the subacute form, there may be micronodular or reticular opacities in the mid/upper lung fields. In the chronic form, there may be features of fibrosis with loss of lung volume.
• HRCT: can help evaluate the stage of disease and usually shows typical changes and fibrosis
• Evidence of antigen-specific IgG antibodies can be useful as supportive evidence for diagnosis
• Pulmonary function testing: normal early on but progresses to a restrictive defect in acute and subacute forms and a mixed restrictive/obstructive picture in late chronic form
• Bronchoalveolar lavage: usually a lymphocytosis and the CD4/CD8 ratio is reduced to less than 1.0
• Transbronchial or open lung biopsy: this may show characteristic histopathological features

Management

• Oxygen for acute episode or ongoing hypoxemia. Corticosteroids may be indicated for the treatment of severe acute and subacute forms and for chronic forms that are severe or progressive. Azathioprine and mycophenolate mofetil has been used as steroid-sparing agents and also in resistant cases. Systemic corticosteroids represent the only reliable pharmacologic treatment of HP but do not alter the long-term outcome. The use of inhaled steroids is anecdotal. Treatment of chronic or residual disease is supportive.
• Farmer's lung can be prevented by drying crops adequately before storage and by ensuring good ventilation during storage. Respiratory protection should also be worn by farm workers when handling stored crops, particularly if they have been stored damp or are likely to be mouldy.
• Untreated it is regarded as a more treatable cause of pulmonary fibrosis, but it can cause progressive symptoms and become hard to treat.

References

• Predictors of survival in coexistent hypersensitivity pneumonitis with autoimmune features