Mushroom Worker Lung

Mushroom worker lung is hypersensitivity pneumonitis in workers who cultivate mushrooms, caused by inhaling spores of the cultivated fungus (Agaricus bisporus, Pleurotus ostreatus, Lentinula edodes) and by thermophilic actinomycetes (Saccharopolyspora rectivirgula, Thermoactinomyces vulgaris) and moulds that proliferate in composted substrate of straw, horse manure and chicken litter. The highest exposures occur during spawning, casing, picking and spent compost removal in enclosed growing rooms at high humidity.

Sensitisation produces a combined immune complex and cell mediated alveolitis. Prevalence among exposed workers is 2 to 5 percent. Acute and subacute forms resolve after antigen removal; chronic exposure leads to upper lobe fibrosis, emphysema and honeycombing. Mushroom growing is expanding in Kenya as a small holder enterprise, so exposed workers are increasingly seen outside industrial settings.

• Acute: fever, chills, malaise, dry cough, dyspnoea and myalgia 4 to 8 hours after entering growing rooms; resolves within 24 to 72 hours.
• Subacute: progressive cough, breathlessness, fatigue, anorexia and weight loss over weeks.
• Chronic: persistent dyspnoea, clubbing, weight loss, end inspiratory squeaks, crackles.
• Symptoms recur at work and improve on leave.
• Asthma like wheeze and rhinitis occur from spore allergy, a separate process.
• Red flags: resting hypoxaemia, haemoptysis, rapid decline, pneumothorax.

• Exposure history with symptom timing; ask about humidity, composting tasks and respirator use.
• Chest radiograph: diffuse nodular or ground glass opacities, often normal in mild disease.
• High resolution CT: ground glass opacity, poorly defined centrilobular nodules, mosaic attenuation with expiratory air trapping (three density sign); fibrosis with upper and mid zone traction bronchiectasis in chronic disease.
• Spirometry: restrictive, obstructive or mixed; DLCO reduced.
• Serum IgG precipitins to Saccharopolyspora rectivirgula, Thermoactinomyces vulgaris and mushroom spore extracts; a positive result shows exposure and is not diagnostic alone.
• Bronchoalveolar lavage: lymphocytes exceeding 30 percent with low CD4/CD8 ratio.
• Biopsy when unclear: non-necrotising granulomas, peribronchiolar lymphocytic inflammation.
• Inhalation challenge in a specialist unit only.
• Exclude tuberculosis, atypical pneumonia, organic dust toxic syndrome, sarcoidosis, and idiopathic pulmonary fibrosis.

• Remove from the exposure. Complete avoidance is the only reliable preventive measure; partial control with respirators usually does not prevent recurrence in sensitised workers.
• Mild acute disease: avoidance alone; symptoms usually settle within 3 days.
• Moderate to severe disease or hypoxaemia: oxygen to maintain SpO2 92 percent or more; prednisolone 0.5 to 1 mg/kg orally once daily (usual 40 mg) for 2 to 4 weeks, tapered by 5 mg weekly to stop over 8 to 12 weeks.
• Chronic fibrotic or relapsing disease: prednisolone for 3 to 6 months; add azathioprine 1 to 2 mg/kg orally once daily, or mycophenolate mofetil 500 mg orally twice daily increased to 1 g twice daily. Monitor full blood count and liver function every 2 weeks for 3 months, then every 3 months.
• Prophylaxis during steroids over 20 mg/day for more than 4 weeks: co-trimoxazole 480 mg orally once daily, omeprazole 20 mg once daily, calcium 1000 mg and vitamin D 800 IU daily.
• Progressive fibrosis: long term oxygen for resting PaO2 below 7.3 kPa; transplant referral.
• Workplace measures: lower humidity, steam pasteurise compost, use enclosed spawn handling, use powered air purifying respirators for unavoidable tasks.
• Follow up: spirometry, DLCO and CT at 1, 3 and 12 months.
• Counselling: redeployment, and re-exposure risk; compensation notification.