Chronic pulmonary aspergillosis (CPA) is predominantly found alongside cavitating or bullous lung diseases. Although pulmonary embolism may cause cavitation, an association with CPA has not been well described. We describe a case of CPA in a 79-year-old female following bilateral pulmonary emboli. The clinical implications are numerous, including the dilemma of anticoagulation. This link suggests that a lower threshold for suspecting CPA following pulmonary embolus is required, even in the absence of other respiratory disease.

Aspergillus fumigatus is a saprophytic fungus that is a major causative pathogen for aspergillosis. Only a few classes of antifungals are used for treating this life-threatening fungal infection. Azoles are the first-line drugs and are widely used for the management and prophylaxis of aspergillosis. An emerging issue is the increasing incidence of resistant isolates worldwide. In particular, environmentally derived tandem-repeat-type azole-resistant mutations, such as Cyp51A TR34/L98H, and Cyp51A TR46/Y121F/T289A, have emerged over the last decade. In particular, azole-resistant isolates were prevalent in clinical settings in European countries; many of the reports are from the Netherlands, UK, and Germany. In contrast, reports on azole-resistant A. fumigatus isolates from East Asian countries are still few and have only recently begun to increase. Herein, all literature on East Asian azole-resistant A. fumigatus isolates were reviewed, and a complete list of resistant isolates from China, Japan, Taiwan, and Korea is provided. As of this report, the total numbers of tandem-repeat-type azole-resistant isolates are 26, 3, 32, and 1 in China, Japan, Taiwan, and Korea, respectively.

Stress responses and pathogenicity have been extensively studied in Aspergillus fumigatus, the main causative pathogen of life-threatening aspergillosis. The heterogeneity in this pathogen's biology has recently attracted increasing attention. In the present work, we used 16 clinically isolated strains to investigate several properties relevant to the pathogenicity of A. fumigatus, namely, gliotoxin production, elastase activity, hypoxia growth, adaptation to iron-limiting conditions, and growth upon nitrosative, oxidative, and high osmotic stresses. The range of phenotypes was diverse across the strains, with gliotoxin production and elastase activity being negatively correlated at an intermediate index (R=-0.4717). Notably, there were strains that showed extraordinary high production of gliotoxin or elastase activity and hypersensitivity to nitrosative or oxidative stresses. Clustering analysis showed that the 7 potentially pathogenicity-related phenotypes were not correlated with the genetic sub-group or pathotype. These results contribute to the growing awareness of the genetic and phenotypic diversity in A. fumigatus isolates.

Aspergillus species are a major cause of life-threatening infections in immunocompromised hosts, and the most common pathogen of invasive aspergillosis is Aspergillus fumigatus. Recently, the development of molecular identification has revealed cryptic Aspergillus species, and A. felis is one such species within the Aspergillus section Fumigati reported in 2013. We describe a case of invasive pulmonary aspergillosis caused by A. felis in a 41-year-old Japanese woman diagnosed with myelodysplastic syndrome. She presented with fever 19 days after undergoing autologous peripheral blood stem cell transplantation and was clinically diagnosed with invasive pulmonary aspergillosis. Bronchoscopy and bronchoalveolar lavage were performed for definitive diagnosis. The β-tubulin genes of the mold isolated from the bronchoalveolar lavage fluid, and sequenced directly from the PCR products using a primer pair were found to have 100% homology with A. felis. We successfully treated the patient with echinocandin following careful susceptibility testing. To the best of our knowledge, this is the first published case reporting the clinical course for diagnosis and successful treatment of invasive aspergillosis by A. felis.

Invasive aspergillosis is a common fungal infection in immunocompromised individuals. Some studies have shown that toll-like receptor and dectin-1 genetic polymorphisms may alter signaling pathways, thus increasing an individual's susceptibility to invasive aspergillosis. We investigated the pertinent literature to determine whether polymorphisms in the genes encoding toll-like receptors and dectin-1 increase the susceptibility to invasive aspergillosis. This study systematically reviewed the literature using the databases PubMed/PMC, Scopus, and Web of Science using the keywords invasive aspergillosis, polymorphism, Toll-like, and Dectin-1. From the initial search, 415 studies were found and according to our inclusion and exclusion criteria, eight studies were selected. Several studies described single-nucleotide polymorphisms (SNPs) that are associated with a greater susceptibility to invasive aspergillosis. These SNPs were found in the genes that encode toll-like receptors 1, 3, 4, and 5 and the gene that encodes dectin-1; upon activation, both cellular receptors initiate a signaling cascade that can result in the production of cytokines and chemokines. Thus, our literature review uncovered a significant association between polymorphisms in the genes that encode toll-like receptors and dectin-1 and invasive aspergillosis. More studies should be performed to better understand the relationship between toll-like receptor and dectin-1 genetic polymorphisms and invasive aspergillosis susceptibility.