The onset of the disease may be acute or insidious. The acute onset is usually after exposure to a very large concentration of the bagasse dust. In other cases, symptoms start to appear about four months to 12 years after exposure to the dust.[1] Classical presenting complaints include a worsening and severe shortness of breath, cough, fever, malaise, and weight loss.[1][3] The cough is usually dry but maybe productive of mucoid sputum. Cyanosis, clubbing, wheezing, and signs of consolidation are generally absent.[1]

Physical examination of these patients reveals crepitations, which are usually basal but may be generalized in severe cases.[1][3] 

The diagnosis is clinical and based on a positive occupational history, characteristic clinical features, and chest X-ray findings, and after the exclusion of other possible conditions.[4]

Blood tests are usually unremarkable; normal white cell counts, normal PCO2, and slightly elevated ESR.[1] The chest X-ray shows fine micronodular shadowing, but may be normal in some patients.[1][3] Pulmonary function tests show a restrictive picture, including reduced lung volumes, ventilatory capacity, and gas transfer.[3] FEV1 and FVC will both be reduced while the FEV1/FVC ratio will be normal.[1] There is no evidence of airway reversibility after inhalation of a bronchodilator.[1]

There is no role for drugs in the management of bagassosis. Being an occupational hypersensitivity pneumonitis resulting from exposure to the bagasse dust, avoiding the dust is usually all that is required to treat the condition. Re-exposure to the dust is associated with the re-occurrence of the disease.[4] Symptomatic treatment with antitussives, antipyretics, fluid rehydration, rest, nutrition, and in some cases, oxygen supplementation, may be required. In very severe forms of the disease, the use of steroids has shown to be beneficial.[4] 

The differential diagnoses of the disease are numerous. They include other causes of extrinsic allergic alveolitis, such as those occurring after exposure to other organic dust (such as silicon, hay, cotton, and compost dust) and other non-allergic types of pneumonia, such as infective causes.[6][7]

Examples of hypersensitivity pneumonia that could mimic bagassosis include Farmer's lung, suberosis, Pigeon breeder's/bird fancier's disease, and fungal pneumonitis.[8] Other differential diagnoses include asthma, chronic obstructive pulmonary disease (COPD), eosinophilic pneumonia, community-acquired pneumonia, miliary tuberculosis, silicosis, pulmonary edema, and idiopathic interstitial lung disease.[4][8] 

After stopping the patient from contact with the offending bagasse dust, complete resolution of symptoms usually occurs in 1 to 6 months. The chest X-ray returns to normal in 2 to 6 months while pulmonary function normalizes in 2 to 4 months.[1][3][4] The mortality rate of the disease is reported to be 7.5% but is likely much lower as much milder forms of the disease go undetected.[4]

Bagassosis usually resolves completely without any long-standing complications. However, similar to other pneumoconioses, several complications can arise in these patients, including interstitial lung fibrosis, chronic obstructive pulmonary disease, hemoptysis, pneumothorax, pleuritis, chronic interstitial pneumonia, and malignancy.[9]

Educating factory workers on the clinical symptoms and signs of the disease is very important in the prevention of bagassosis. Early recognition of the disease leads to immediate separation of the worker from the offending dust leading to complete recovery. Patients should be informed of warning symptoms of recurring disease or worsening features indicative of lung fibrosis and advised to seek medical care urgently. Workers should also receive training on the importance of personal protective equipment, and its use should be mandatory. Work schedules should encourage the rotation of patients working close to bagasse to limit contact.

Bagassosis is now an 'almost non-existent' disease due to preventive control measures that were put in place to improve the storing process of bagasse.[10] For instance, dust control measures such as wetting the bagasse, thereby increasing its moisture content, improving ventilation, and the use of face masks led to a significant reduction in the incidence of the disease, especially in the 1970s.[4][11] As such, there is now little mention of bagassosis in recent literature.

The diagnosis of bagassosis is often clinical. Other investigations and radiological imaging studies are only supportive. Once diagnosed, the most effective treatment involves removing the patient from the offending dust. As an occupational health issue, the main focus is prevention. From an occupational and public health perspective, this involves a much broader multi-disciplinary team including clinicians, occupational therapists, public health workers, social workers, health and safety professionals, physiotherapists and even a medicolegal team. Since the management of the condition involves prolonged absenteeism from work, the social welfare of the patients becomes essential; this is why the disease is fraught with medicolegal issues. Unfortunately, due to the lack of information on the condition when it was first described, it was not covered under the Workman's Compensation Act; hence sufferers could not make any claims.[12] However, the American College of Occupational and Environmental Medicine (ACOEM) now updates its guidelines on the investigation and management of the disease every three years. [Level 1]