Farmer's lung: a study of an early acute fatal case

Abstract

The clinical and pathological findings in a fatal case of farmer's lung in a 17-year-old youth are described. His lungs were uncomplicated by chronic disease, and his first exposure to mouldy hay probably occurred only weeks before his death. As this was an acute attack, whose duration could be measured in days, the changes seen are probably the earliest to be recorded, and the probable nature of the sensitivity reaction can be deduced. The pathological process is seen to be an acute centrilobular bronchopneumonia of a special type and is associated with an obstructive bronchiolitis. There is a focal interstitial pneumonia with much proliferation of alveolar epithelium, and there is a necrotic exudate in which neutrophils and eosinophils are seen along with mononuclears, some lymphocytes, and plasma cells. The alveolar spaces are in many cases obscured, but others contain a haemorrhagic fluid. Alveolar capillaries show an acute vasculitis, with platelet and fibrin deposition, and with acute neutrophil infiltration. Serological and mycological data are included. Precipitins to mouldy hay and to Thermopolyspora polyspora were found in the serum. In dusts collected from his habitat T. polyspora was found. We think the bronchiolitis explains the severe dyspnoea, and the vasculitis accounts for the malaise, fever, and haemoptysis. The histological findings are compared with accounts of experimentally produced Arthus reactions and tuberculin reactions, and we give our reasons for believing the fundamental lesion to be an Arthus reaction.There is good evidence that farmer's lung is the result of a hypersensitivity reaction caused by antigens found in mouldy hay or cereals (Pepys and Jenkins, 1965). In a typical case of several years' duration the histological picture of granulomata, with scarring and distortion of both bronchioles and lung parenchyma, gives no clue as to the aetiology of the condition. Nor does material obtained by lung biopsy from cases of shorter duration, which often show giant-cell granulomata (Totten, Reid, Davis, and Moran, 1958; Seal, Thomas, and Griffiths, 1963). No descriptions of patients who have died in the first attack of the disease have been published, although the account by Hoer, Horbach, and Schweisfurth (1964) of the death of a 15-year-old boy after a three-week illness said to have been caused by Aspergillus fumigatus could well have been of an acute attack of farmer's lung. HISTORYThe deceased schoolboy was a 17-year-old farmer's son, who first complained of symptoms in September 1964. Previously in perfect health, he had been awarded the victor ludorum in his school sports earlier that summer. He had spent the summer helping his father, and his first known exposure to mouldy hay occurred only weeks before his death.When first seen at the beginning of October 1964 he admitted to having felt tired and to looking ill for about eight weeks. For one week he had experienced a constricting pain across the chest, had sweated at night, and had coughed up some faintly blood-stained sputum. ...

Inter- and Intraspecific Genetic Analysis of the Genus Saccharomonospora with 16S to 23S Ribosomal DNA (rDNA) and 23S to 5S rDNA Internally Transcribed Spacer Sequences

“…Strains of S. viridis have been implicated as causal agents of farmer's lung disease (1,6). It is, therefore, important to distinguish S. viridis from other Saccharomonospora species.…”

“…The results of recent numerical phenetic studies (11) and results obtained by nucleic acid techniques (12,(39)(40)(41) suggest that the strains of "S. caesia" are very closely related to S. azurea K161T. It has been determined that strains of S. viridis cause farmer's lung disease ( 1,6) and are significant agents of hypersensitivity pneumonitis (12,39). (14).…”

Hypersensitivity pneumonia: the role of lung biopsy in diagnosis and management

“…Rapid recovery of pulmonary function is typical of acute hypersensitivity pneumonia, although rare fatal episodes have been documented. 25 Corticosteroids are useful in accelerating the rate of recovery, but do not affect the long-term outcome, independent of eliminating antigenic exposure. 26,27 Lung function improves over a period of months and years, but abnormalities may persist in nearly half of patients.…”

“…Rare reports describe a patchy airspace filling process resembling bronchopneumonia, in which both neutrophils and eosinophils are present with an associated necrotizing small vessel vasculitis. 25,33 Lung biopsy often has a critical role in separating chronic hypersensitivity pneumonia from other forms of diffuse interstitial lung disease, especially in patients for whom no specific antigenic exposure is identified. 6 Histological diagnosis of hypersensitivity pneumonia is predicated on recognition of a classical triad: 1) bronchiolocentric cellular chronic interstitial pneumonia, 2) chronic bronchiolitis, and 3) non-necrotizing granulomatous inflammation affecting the peribronchiolar interstitium.…”

Hypersensitivity Pneumonia: Role of Surgical Lung Biopsy

“…Autopsy of a patient who died during an episode of acute farmer's lung published more than 40 years earlier demonstrated similar alveolar exudates as well as a small-vessel vasculitis. 45 Chronic hypersensitivity pneumonia is usually characterized by a classic triad of pathologic features (Table). This triad includes a bronchiolocentric cellular chronic interstitial pneumonia, chronic bronchiolitis, and nonnecrotizing granulomatous inflammation largely confined to the peribronchiolar interstitium.…”