The full underlying pathogenesis is not completely understood. Most people with<unk>  have functional immune status, but usually have underlying structural damage to the lungs from an underlying process or disease. Most commonly, pre-existing<unk>  cavities from other diseases such as tuberculosis become colonised with Aspergillus conidia which have been inhaled—humans inhale between 1,000 and 10 billion spores per day, of which A. fumigatus is the most common. Aspergillomas themselves usually form in existing cavities but the cavities may form directly from<unk> . People with<unk>  tuberculosis with a cavity larger than 2 cm appear to have a 20% increased risk of developing<unk> . It is postulated that conidia, once inhaled, are attacked by the host immune defences—specifically phagocytes and alveolar macrophage resident in the small airways. It is unknown whether these defences are sufficient to clear conidia or whether they are directly responsible for the inflammation leading to<unk> . Some Aspergillus have the ability to inhibit phagocyte nicotinamide adenine dinucleotide phosphate oxidase activation which is one of the core defence systems against filamentous fungi, which may increase susceptibility of the host to<unk> .
Chronic pulmonary aspergillosis
Lung cancer
Tuberculosis
Allergic bronchopulmonary aspergillosis
Miliary tuberculosis
Primary inoculation tuberculosis
Primary pulmonary coccidioidomycosis
Extrapulmonary tuberculosis