Bagassosis _TOP_

Historically bagassosis was first described by Jamison and Hopkins in 1941 after it was reported in a hard-board factory in New Orleans, USA. Subsequently, other reports followed from other American states (mainly in the south) and other countries such as Italy, India, and the Philipines. Castleden and Hamilton-Paterson were the first to use the term 'bagassosis' after observing it in four factory workers in London in 1942.

bagassosis

In the past, bagasse was processed manually, in a time-consuming process, before the technological revolution in the 1950s and '60s. However, the machine-processing of bagasse led to the dispersal of particle-laden dust around the machines. Soon after introducing these machines, the first cases of bagassosis were reported, predictably in those close to the machines, such as the workers who fed the machines and the engineers who supervised them. Other workers, such as those who handled the finished products, were not affected.

Bagassosis belongs to the group of respiratory conditions classified as interstitial lung diseases or hypersensitivity pneumonitis. It presents similarly to other extrinsic allergic alveolitis, such as farmer's lung. It develops in a patient due to exposure and inhalation of bagasse - the residual fibrous material after sugar is extracted from sugar cane. This activity describes the etiology, pathophysiology, and management of bagassosis and highlights the role of the interprofessional team in the prevention and treatment of the condition.

Objectives:Identify the etiology of bagassosis.Review the clinical features of bagassosis.Discuss the treatment options for bagassosis.Summarize the role of the interprofessional team consisting of clinicians, occupational health physicians, and public health officers in the prevention and treatment of patients with bagassosis.Access free multiple choice questions on this topic.

Historically bagassosis was first described by Jamison and Hopkins in 1941 after it was reported in a hard-board factory in New Orleans, USA.[3] Subsequently, other reports followed from other American states (mainly in the south) and other countries such as Italy, India, and the Philipines.[4][5] Castleden and Hamilton-Paterson were the first to use the term 'bagassosis' after observing it in four factory workers in London in 1942.[6]

In the past, bagasse was processed manually, in a time-consuming process, before the technological revolution in the 1950s and '60s. However, the machine-processing of bagasse led to the dispersal of particle-laden dust around the machines. Soon after introducing these machines, the first cases of bagassosis were reported, predictably in those close to the machines, such as the workers who fed the machines and the engineers who supervised them. Other workers, such as those who handled the finished products, were not affected.[2]

Although bagassosis is caused by the inhalation of bagasse, the specific etiological mechanism responsible for causing the disease is considered multifactorial. Historically, the disease has been attributed to irritant properties of the bagasse itself, microorganisms present in the dust, its silica content, an allergic reaction, and a combination of these factors. It most commonly occurs in those frequently in contact with this material, e.g., sugar factory workers. A study showed that 11 out of 21 bagasse-shredding workers developed the disease over 15 months.[1]

Aerobacter cloacae is a microorganism that has been seen as a possible causative organism in the etiology of bagassosis.[9] Most notably, thermophilic actinomycetes (T. sacchari and T. vulgaris) are the causative agents found in bagasse responsible for triggering a pathological response.[1]

There is no mention of the prevalence of bagassosis in recent literature, and its sex and age distribution are unknown. It is a relatively rare disease, first described in 1941. Most of the initially reported cases were in southern American states, especially Louisiana. Few cases were reported in Europe and Asia.[1] Four reported cases came from a London factory in 1942. By 1958, the total number of cases reported globally in the literature was nearing 60.[1] However, after 69 cases occurred in 140 Puerto Rican paper-mill workers in 1960, the disease was no longer regarded as very uncommon.[1]

Recent studies in India indicate clinically significant thermophilic actinomycetes are widely present in cane sugar mills, and Thermoactinomyces sacchari and Saccharopolyspora rectivirgula are the major species responsible for the sensitization of Indian bagasse workers.[10] A study carried out in Australia in 2010 revealed no evidence to believe the development of chronic bagassosis among the workers of the sugar industry. Therefore, there was no significant prevalence of bagassosis among bagasse workers in Australia.

However, other mechanisms have also been postulated in the pathophysiology of the disease, including the irritant property of bagasse itself, its silica content, other micro-organisms including fungi, or a combination of these factors.[13] In acute bagassosis, immune complexes mediate lung inflammation as evidenced by:

In subacute and chronic bagassosis, characteristic T-lymphocytic alveolitis is noted, attributable to increased T-cell migration, decreased apoptosis, and local proliferation. Immune processes leading to persistent disease and fibrotic changes are unclear but may be mediated by:

Bronchoalveolar lavage specimens from patients suffering from bagassosis show hypercellularity and neutrophilia.[14] Other findings include increased levels of TNF-alpha, IL-1beta, IL-8, and IL-6.[14] A lung autopsy shows minute needle-like spicules in the pulmonary tissue. When rotated in polarized light, these spicules have the same semblance and characteristics as bagasse fiber. Other findings are the presence of large cells with a foamy cytoplasm in the alveolar spaces and an interstitial fibroblastic tissue reaction.[13]

Physical examination of patients with bagassosis reveals crepitations, which are generally basal but could be generalized in severe cases.[7] Findings vary according to clinical presentation, such as in patients with acute disease; the usual presenting features are fever, tachypnea, and fine bibasilar crackles on auscultation. Patients with subacute bagassosis present similarly, but symptoms are generally not as severe and have lasted longer. Patients with chronic disease may demonstrate muscle wasting and weight loss. Almost half of the patients would have clubbing. These patients also have respiratory distress, tachypnea, and inspiratory crackles.

There have been many case reports where individuals with a history of work-related exposure to bagasse were found to have typical radiographic changes to suggest bagassosis as the underlying cause of their disease. In such case reports, the chest radiograph demonstrated bilateral opacities, and computed tomography revealed patchy bilateral opacification, septal thickening, and ground-glass haziness. In many cases, bronchoalveolar lavage reveals lymphocytosis. In bronchoalveolar lavage fluid (BALF) of patients with bagassosis, hypercellularity with neutrophilia is common. Moreover, raised levels of TNF-α, IL-1β, IL-8, and IL-6 are also noted in the BALF of patients with bagassosis. or bagassosis and silicosis. Further investigation is required to assess the mechanisms underlying the different cellular and cytokine compositions in bagassosis.[15][14]

Early diagnosis is critical in managing bagassosis as progression is generally preventable, and adverse effects are usually reversible. Minimizing exposure is the cornerstone of management. There is no role for drugs in the management of bagassosis; however, where elimination of antigen exposure fails at regressing the disease, corticosteroids may be warranted. Being an occupational hypersensitivity pneumonitis resulting from exposure to bagasse dust, avoiding the dust is usually all that is required to treat the condition. Reexposure to the dust is associated with the reoccurrence of the disease.[13] 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, corticosteroids have shown to be beneficial.[13]

Morbidity and mortality related to bagassosis vary widely based on several factors, such as type, duration, and severity of the exposure. Genetic factors may also play an imperative role. The prognosis is generally less favorable once fibrotic changes occur, such as in chronic cases.[26]

Educating factory workers on the clinical symptoms and signs of the disease is very important in preventing 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. Patients and their coworkers should also be informed that the disease is not contagious; however, other workers may be exposed to the same environment.

Bagassosis is now an 'almost non-existent' disease due to preventive control measures put in place to improve the storing process of bagasse.[28] For instance, dust control measures such as wetting the bagasse, thereby increasing its moisture content, improving ventilation, and using face masks led to a significant reduction in the incidence of the disease, especially in the 1970s.[13][29] 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 interprofessional 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. 041b061a72