A 76-year-old male presented to our institution with chronic cough and intermittent haemoptysis for 2 months. He had completed standard anti-TB therapy 10 years prior for smear positive cavitatory pulmonary Mycobacterium tuberculosis. Other past medical history was significant for rheumatic fever. He was a lifelong non-smoker. Thoracic computed tomography (CT) done 7 years previously demonstrated traction bronchiectasis and chronic scarring within the right upper lobe. He remained symptomatically well until this presentation.\nHis physical examination revealed bronchial breath sounds in the right upper lobe. Thoracic CT demonstrated fibrocystic change in an incompletely collapsed right upper lobe. There was now a large cavity with a new 2.1-cm round mass (Fig. A, C).\nWe proceeded to perform flexible bronchoscopy (Olympus 3.2 mm) under conscious sedation. After traversing two segments of the bronchi, an abnormal rounded mass was seen obstructing the anterior segment of the right upper lobe (Fig. A). Microbiological culture of bronchoalveolar lavage (BAL) from the right upper lobe cavity subsequently isolated both Staphylococcus aureus and Aspergillus fumigatus. He was commenced on a one week course of flucloxacillin as well as a prolonged course of the anti-fungal drug posaconazole. He was subsequently discharged and electively readmitted a few weeks later to facilitate bronchoscopic removal of the mycetoma.\nAt repeat flexible bronchoscopy, a flexible cryoprobe was inserted via the bronchoscope into the cavity. However, en bloc removal of the mass was not possible. The cryoprobe was removed and hot forceps was introduced to subdivide the mass into various smaller parts. Then the cryoprobe was reintroduced and the subdivided mass was removed piecemeal. Washing of the cavity was then performed with normal saline until all macroscopically visible mycetoma had been removed. Inspection of the empty cavity revealed inflamed haemorrhagic mucosa (Fig. B).\nThe obtained mass was sent for histopathological analysis. Microscopically, it demonstrated inflamed bronchial mucosa, abundant fungal organisms as well as a bacterial colony consistent with Gram-positive cocci. There was no evidence of invasive fungal infection. The case was discussed at our institution's multidisciplinary respiratory meeting, where a diagnosis of mycetoma was inferred. He was continued on oral posaconazole. Radiological and bronchoscopic surveillance at 3 months demonstrated no reoccurrence of the mycetoma (Figs. B, B, D).
A 14-yr-old girl complained of nasal blockage accompanied by yellowish mucopurulent rhinorrhea. No history of asthma, other allergic diseases, or medical or surgical treatment was identified. No potential risk factors such as diabetes mellitus, immunodeficiency, or previous facial trauma were found. Laboratory investigations revealed a white blood cell count of 15,600/mm3 with 3.7% eosinophils and a high level of serum IgE, 149 IU/mL (0-100 IU/mL). The results of the multiple antigen simultaneous test (MAST) for specific serum IgE antibodies against Aspergillus, Penicillium, Cladosporium, and Alternaria were negative. The results of the Uni-CAP system (Pharmacia, Sweden) for specific serum IgE antibodies against Aspergillus fumigatus, Cladosporium herbarum, and Alternaria tenuis were in the normal range. A non-enhanced computed tomography (CT) scan of the ostiomeatal unit revealed soft-tissue opacification in the right frontal, ethmoid, and maxillary sinuses (). Bony remodeling and destruction was found in the right lamina papyracea. Endonasal endoscopic surgery was undertaken. Mucosal swelling and polyposis were found in the right middle meatus, maxillary sinus, ethmoid sinus, and frontal sinus, which encroached on the right lamina papyracea. The frontal recess was filled with mucoid secretions, which were collected for histological and microbiological investigations. Histological examination of the material obtained from the frontal recess showed allergic mucin, characterizing Charcot-Leyden crystals, numerous eosinophils, and a few septate fungal hyphae ().\nThe material was plated onto PDA plates and incubated at room temperature, 30℃, and 37℃. Growth of a white, densely woolly mold with a yellow-to-brown reverse was observed after 3 days at all temperatures (). The fungus was sensitive to cycloheximide (400 µg/mL) and produced a tart and disagreeable smell, particularly at 37℃. Microscopic examination of the mycelia showed no conidia or sporangiospores, but revealed both narrow and wide hyphal filaments, which were hyaline, septate, branched hyphae without clamp connections and spicules (). Macroscopic examination did not reveal structures such as fruiting bodies even after 2 months of culture.\nThe ITS and D1/D2 regions of the 26S ribosomal DNA was sequenced. The ITS region (including the 5.8S rRNA gene) and the 26S rRNA gene D1/D2 domains were amplified with the following primer pairs: pITS-F (5'-GTCGTAACAAGGTTAACCTGCGG-3') and pITS-R (5'-TCCTCCGCTTATTGATATGC-3'), and NL1 (5'-GCATATCAATAAGCGGAGGAAAAG-3') and NL4 (5'-GGTCCGTGTTTCAAGACGG-3') []. The fungus was identified (Basic Local Alignment Search Tool, ) as S. commune (accession number HM595605.1) with 100% homology. The patient was given oral corticosteroids and antibiotics for 1 week after surgery. Topical nasal steroids were administered to suppress the immune response and minimize recurrence. The patient has been followed up for 3 months and shows no signs of recurrence, except mild mucosal swelling.