[A case of allergic bronchopulmonary mycosis caused by Triodiomyces crassus]

There are few published cases of non-aspergillus allergic bronchopulmonary Mycosis (ABPM) worldwide. Here we report the first case where the fungus Triodiomyces crassus was found to be the causative pathogen of non-aspergillus ABPM. This study provided an overview of the diagnosis, treatment and follow-up of the case. In May 2018, a 60-year-old male patient presented with a 1-month history of dry cough with mild chest tightness. He had no history of asthma and no clinically reported illness. The routine pulmonary auscultation on admission revealed no abnormalities. Subsequent laboratory tests revealed marked peripheral blood eosinophilia and an increased level of serum total IgE. However, the specific IgE antibody test for Aspergillus fumigatus was negative. A chest CT scan showed peribronchial consolidation in the right upper lobe with high-attenuation mucoid impaction in the corresponding bronchi. Bronchoscopy confirmed these mucus plugs. The bronchoscopic biopsy specimen showed a large number of eosinophils and fungal hyphae. The fungal smear from the bronchial lavage fluid showed fungal hyphae, although the fungal culture showed no growth. A CT-guided transthoracic needle biopsy was performed on the lesion in the right upper lung, which showed significant eosinophil infiltration in the pulmonary parenchyma. The biopsy specimen was cultured and yielded colonies with a yeast-like appearance. Microscopic examination of these colonies revealed yeast-like fungi and pseudohyphae. The fungal morphology observed in the bronchial wash smear and the pathology of the bronchoscopic biopsy were consistent with that seen in the cultured colonies. The organism was identified as Triodiomyces crassus through sequencing of the internal transcribed spacer (ITS) region of its ribosomal DNA (rDNA). The patient was initially treated with a 2-week course of voriconazole, 200 mg orally twice daily, but there was no significant improvement in symptoms. Follow-up bronchoscopy revealed persistent obstructive mucus plugs. Based on these findings, the diagnosis was revised to ABPM caused by Triodiomyces crassus rather than an invasive fungal infection, and corticosteroid treatment was added, with prednisone administered at 20 mg/day. After two weeks, the patient coughed up a mung-bean-sized gelatinous substance (mucus plug), and there was a marked improvement in cough and chest tightness. Treatment continued for a further two weeks, but was then discontinued by the patient's own decision. The patient returned for the first follow-up, 77 days after the initial admission. Clinical symptoms had subsided. Repeat tests showed normal eosinophil counts and total IgE levels, and a chest CT scan showed significant absorption of the lesions, with only mild bronchiectasis remaining. As the patient had discontinued steroid therapy and there were no recurrent symptoms, no further medication was prescribed, but continued observation was suggested. At the second follow-up, 6 months after the initial admission, routine blood tests and total IgE levels remained normal, and a chest CT scan showed only minor streaky shadows, with no recurrent symptoms. The clinical characteristics of ABPM caused by non-Aspergillus fungi differ from those of ABPA. If ABPA is clinically suspected but tests for specific IgE antibodies to Aspergillus fumigatus are negative, the possibility of ABPM caused by rare non-Aspergillus fungi should be considered. Early and proactive mycological investigation is crucial for the diagnosis of this condition and the identification of rare pathogenic fungi.