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Exposure to fungi in the work place may lead to lung damage

April 15 2016

A recent review of occupational hypersensitivity pneumonitis (OHP) has highlighted the number of different agents which can cause lung damage across a variety of occupations. In particular, moulds and fungi are shown to be the leading cause of this disease. Fungal agents implicated include Aspergillus, Penicillium, Trichosporon and regular inhalation of these agents in a workplace environment that can lead to serious lung damage. Occupations carrying a high risk of exposure to fungi include farmers, wood workers, tobacco growers, cheese workers, wine makers and florists.

OHP is an immunologic lung disease which develops as the result of an allergic reaction to a large variety of causal agents, including bacteria, fungi, animal and plant proteins, chemicals and metals. Symptoms are also highly variable, and can be separated into two broad groups: Acute OHP (characterised by recurrent systemic symptoms including chills and body aches) and chronic OHP (characterised by clubbing, hypoxemia and fibrosis on HRCT scan). Data from the German Statutory accident insurance institutions (covering approx. 40 million workers) shows that moulds and fungi were the etiological agents in 45.9% of new OHP cases.

Lung biopsy from a patient with chronic HP showing mild expansion of the alveolar septa (interstitium) by lymphocytes. A multinucleated giant cell, seen within the interstitium to the right of the picture halfway down, is an important clue to the correct diagnosis. By Mutleysmith - Taken with a microscope for education https://goo.gl/bdXGE6
 
 
 
 
Establishing a diagnosis of HP is not easy as the variety of clinical and radiologic findings can mimic a wide range of lung diseases. A multidisciplinary approach, from clinicians, radiologists, pathologists and occupational physicians/hygienists is therefore required, both to diagnose HP and importantly, to establish the causal role of the workplace. The key diagnostic procedure for HP is high-resolution computed tomography (HRCT) though a high proportion of patients with HP may have a normal scan. Predominant findings are ground-glass opacities, poorly defined small centrilobular nodules, mosaic attenuation and gas trapping on expiratory CT images. The authors of the review propose a set of criteria for the diagnosis of both acute and chronic OHP based on previously published criteria and consensus amongst experts (see table 5 of the original article).

The recommended treatment for acute OHP is early removal from exposure to the agent. Identification of the source is therefore crucial, both for diagnosis and for treatment. Treatment with supplemental oxygen and/or corticosteroids may be required for more severe acute cases. For chronic OHP, treatment is corticosteroids until no further improvement is observed. Immunosuppresants may be added to treatment in progressive cases and lung transplantation may be required in the most severe instances. The authors stress that removing the patient from further exposure is the most important treatment option, whether by removing the antigen from the workplace or removing the patient from the environment. 

Original article