Aspergillus tracheobronchitis is defined as an Aspergillus infection which is limited entirely or predominantly confined to the tracheobronchial tree. In addition, Denning suggested the term be applied to patients in whom there is evidence of bronchial and/or tracheal inflammation, excess mucus production, with Aspergillus as the only pathogen and without invasion of bronchial mucosa on biopsy (Denning 1995), but full criteria for this diagnosis have not been validated.
Aspergillus infection of the large airways has several manifestations. Many authors try to propose a classification to describe the disease, but to date; there is still no ideal classification. Overlapping clinical features can make cases difficult to classify. Interestingly Young et al. described a non-invasive form of infection, with the bronchial mucosa is usually preserved, but this contrasts with many reported invasive cases in patients with immunosuppression and poor immunological host responses (Young 1970).
Aspergillus tracheobronchitis was probably first described by Wheaton et al. (Wheaton 1890) in a 2.5 year old girl who died of pneumonia. He described it as “In the main bronchus were several white gelatinous patches like those upon the tongue, which peeled off with difficulty, leaving a raw surface…The white patches in the bronchus were found to consist of the mycelium of a fungus mixed with flat epithelial cells…”.
In 1926, Mary Lapham described two general types of pulmonary aspergillosis; bronchitic and pleuritic type. Bronchitic type is being described as the mucous membranes of the bronchi become almost black from congestion, ulcerations may be eaten out and patches of membranes formed (now termed pseudomembranous Aspergillus tracheobronchitis). In the pleuritic type, Aspergillus spores are carried to the periphery of the lung, become deposited there and causing congestion, thickening and adhesions of the pleura (Lapham 1926).
In 1963, Campbell and Clayton described ‘aspergillary bronchitis’ which is bronchial infection by Aspergillus spp. with or without allergic manifestations. In this type, the Aspergillus only grows as sporing mycelium with mild inflammation of the mucosa and/or excess production of mucus without invasion of the mucosa (Campbell & Clayton 1963).
Young et al. from autopsy studies, found 8 out of 98 (8%) patients had localized Aspergillus bronchitis without accompanying bronchopneumonia. In five out of eight patients, the infection was limited to this site is confirmed histologically. It was characterized by bronchial casts containing mucus and mycelia. All had superficial erosions and ulcerations and only three had focal parenchymal involvement with consolidation and abscess formation, in one case chronic cavitary pulmonary aspergillosis in a 29 year old man, without any recognized immunodeficiency (Young 1970).
Clarke et al. in 1991 reviewed nine cases of fungal tracheobronchitis (of which eight were histologically positive for Aspergillus) described two morphological manifestations: firstly intraluminal, circumferential pseudomembrane and exudate with only superficial mucosal invasion or as mucus plugs which may results in airway occlusion and secondly single or multiple discrete plaques on the airway wall, sometimes associated with invasion of the adjacent lung parenchyma or pulmonary artery. This may result in broncho-oesophageal and fatal haemorrhage from bronchoarterial fistula (Clarke 1991).
In 1991, Kramer et al. described the invasive forms of Aspergillus tracheobronchitis based on autopsy biopsies showing hyphae invading the cartilage under the necrotic material covering the ulcers or inflamed mucosa, in lung transplant recipients. They divided cases into two types: invasive and saprophytic (noninvasive). The invasive one was further subdivided into three morphological forms: tracheobronchitis, ulcerative bronchitis and pseudomembranous bronchitis. The saprophytic one was subdivided into two morphological forms: mucoid impaction of the bronchi and obstructing bronchial aspergillosis (Kramer 1991).