Cheese Washer's Lung

Cheese washer's lung is hypersensitivity pneumonitis caused by inhaling mould and mite antigens in cheese ripening rooms. Penicillium casei and Penicillium roqueforti and the cheese mite Acarus siro are the usual sources.

Exposure. Cheese ripening, rind washing, brushing and packing, especially of mould ripened and washed rind cheeses.

Epidemiology. Uncommon and found in cheese producing regions. Cases follow months to years of exposure.

Forms. Acute, subacute and chronic. Early disease is usually reversible with antigen avoidance.

Related condition. Cheese workers can also develop occupational asthma or rhinitis from mite and mould allergens.

Pathophysiology.

High airborne concentrations of mould spores and mite particles in humid ripening rooms are inhaled. In susceptible people they induce a type III and type IV hypersensitivity reaction with granulomatous bronchiolitis and alveolitis.

Persistent exposure can lead to fibrosis.

• Acute: fever, chills, cough and dyspnoea 4 to 8 hours after exposure, resolving within a few days.
• Subacute and chronic: progressive dyspnoea, cough, fatigue and weight loss.
• Basal crackles, and clubbing in fibrotic disease.

Red flags.

• Resting hypoxaemia or rapid deterioration.
• Weight loss, haemoptysis or progressive fibrosis.

• Exposure history including cheese type, task and room conditions.
• HRCT: ground glass centrilobular nodules, mosaic attenuation with air trapping, fibrosis in chronic disease.
• Spirometry with gas transfer: restrictive or mixed, reduced DLCO.
• Serum IgG precipitins to Penicillium species and Acarus siro show exposure.
• Bronchoalveolar lavage lymphocytosis over 20 to 30%.
• Biopsy when atypical; exclude tuberculosis and fungal infection.

Differential diagnosis. Sarcoidosis, other hypersensitivity pneumonitis, organic dust toxic syndrome, occupational asthma, idiopathic pulmonary fibrosis, infection.

• Avoid the antigen. Remove from ripening areas, or control mould and mite growth, humidity and ventilation; respirators as an adjunct.
• Prednisolone 0.5 mg/kg orally once daily in the morning, maximum 40 mg daily, for 4 weeks. If symptoms, spirometry, gas transfer and imaging improve, taper to the lowest effective dose over 8 to 12 weeks, then stop. If there is no improvement, taper over 2 weeks and reconsider the diagnosis. Monitor glucose, blood pressure, weight, mood and infection, with bone protection if therapy exceeds 3 months. Exclude active tuberculosis first. Caution in diabetes and peptic ulcer; no renal adjustment.
• Chronic fibrotic disease with progression: nintedanib 150 mg orally twice daily with food, long term. Maximum 300 mg daily; reduce to 100 mg twice daily for adverse effects or mild hepatic impairment. Monitor liver enzymes monthly for 3 months, then every 3 months; manage diarrhoea. Avoid in moderate or severe hepatic impairment and in pregnancy; avoid when eGFR is under 30.
• Long term oxygen when resting PaO2 is under 7.3 kPa, or 7.3 to 8 kPa with polycythaemia or cor pulmonale.
• Lung transplant assessment in advanced fibrosis.

Monitoring. Symptoms, spirometry and gas transfer at 4 to 6 weeks, then every 3 to 6 months; HRCT at 6 to 12 months.

Referral and escalation. Respiratory and occupational physician; workplace assessment; transplant assessment for advanced disease; notification and compensation where required.