Bagassosis

Bagassosis is hypersensitivity pneumonitis caused by inhaling mouldy bagasse, the fibrous residue left after sugar cane crushing, which is used for paper, board and fuel. The antigen is thermophilic actinomycetes, principally Thermoactinomyces sacchari (also Thermoactinomyces vulgaris, Saccharopolyspora rectivirgula), which grow in stored damp bagasse at 40 to 60 degrees C. Sugar mills in western Kenya, and bagasse board and paper plants, are potential settings.

Sensitised workers develop a type III and IV immune reaction in the lung. Acute disease follows heavy exposure; subacute and chronic forms follow repeated lower exposure and can progress to fibrosis with honeycombing and upper lobe predominance. Early disease resolves after removal from antigen. Fewer than 5 percent of exposed workers are affected.

• Acute: fever, chills, malaise, cough, dyspnoea and chest tightness beginning 4 to 8 hours after exposure and resolving over 1 to 3 days.
• Subacute: progressive cough, exertional dyspnoea, fatigue, anorexia and weight loss over weeks.
• Chronic: progressive dyspnoea, dry cough, clubbing, weight loss, crackles, fibrosis.
• Squeaks (inspiratory) in a minority; wheeze is uncommon.
• Symptoms recur on return to work and improve at weekends or on leave.
• Red flags: resting hypoxaemia, rapid progression, haemoptysis (consider tuberculosis), pneumothorax.

• Occupational history: handling of stored bagasse, timing of symptoms relative to work.
• Chest radiograph: diffuse bilateral miliary nodular or ground glass opacities (acute), upper zone fibrosis (chronic).
• High resolution CT: ground glass opacities, poorly defined centrilobular nodules, mosaic attenuation with air trapping on expiratory scans; fibrosis and honeycombing in chronic disease.
• Spirometry: restrictive or mixed; DLCO reduced; oxygen desaturation on exertion.
• Serum precipitins (IgG) to Thermoactinomyces sacchari: positive in most, although also positive in some exposed asymptomatic workers.
• Bronchoalveolar lavage: lymphocytosis above 30 percent with CD8 predominance and reduced CD4/CD8 ratio.
• Biopsy when diagnosis uncertain: non-necrotising granulomas, interstitial lymphocytic infiltrate, bronchiolitis.
• Exclude infection (including tuberculosis), organic dust toxic syndrome, sarcoidosis, idiopathic pulmonary fibrosis, and other hypersensitivity pneumonitis.

• Antigen avoidance is the definitive treatment: remove from bagasse exposure; reduce moulding by treating stored bagasse with propionic acid 2 percent, and by drying it to below 20 percent moisture.
• Acute mild disease: remove from exposure and observe; symptoms resolve in 1 to 3 days.
• Moderate to severe or hypoxaemic disease: oxygen to maintain SpO2 of 92 percent or above, and prednisolone 0.5 to 1 mg/kg orally once daily (usual 40 mg) for 2 to 4 weeks, then taper by 5 mg every week over 6 to 12 weeks.
• Severe acute respiratory failure: methylprednisolone 500 mg to 1 g intravenously once daily for 3 days, then oral prednisolone.
• Chronic or progressive 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 increasing to 1 g twice daily if steroid dependence continues. Co-trimoxazole 480 mg once daily while on prednisolone above 20 mg for more than 4 weeks.
• Fibrotic disease: long term oxygen; transplant assessment if progressive.
• Follow up: spirometry, DLCO and CT at 4 to 6 weeks, 3 months, and 12 months.
• Prevention: ventilation, masks (powered air purifying respirators for high risk tasks), storage controls.
• Counselling: re-exposure causes relapse; permanent redeployment is frequently needed.