Lung transplant recipients are at risk of opportunistic infections because of immunosuppression. We report a case of Burkholderia vietnamiensis bacteraemia that occurred 3 months after bilateral lung transplantation for diffuse panbronchiolitis. Persistent bacteraemia developed despite apparent in vitro susceptibility to meropenem. Therefore, antimicrobial therapy was reassessed and modified according to the clinical course rather than susceptibility results alone, which resulted in clearance of bacteraemia. The patient recovered without recurrence during a short-term follow-up. This case highlights an important clinical lesson that antimicrobial susceptibility testing may not reliably predict the treatment response in Burkholderia cepacia complex infections after lung transplantation. Early reassessment of therapy should be considered when bacteraemia persists despite apparently active antimicrobial agents.

Primary ciliary dyskinesia (PCD) presents various clinical manifestations, including bronchiectasis, chronic sinusitis, situs inversus, and infertility. PCD is diagnosed through multiple methods, including transmission electron microscopy (TEM), high-speed video microscopy analysis (HSVA), immunofluorescence (IF), and genetic testing. Recent reports show that a homozygous deletion involving exons 1-4 of DRC1 is common in Japanese patients with PCD. We report the case of a 29-year-old male without situs inversus previously diagnosed with diffuse panbronchiolitis, who underwent PCD testing. TEM appeared almost normal, and HSVA showed motile cilia with reduced amplitude. Genetic testing revealed a homozygous deletion involving exons 1-4 of DRC1. Due to lack of a suitable DRC1 antibody for IF, we used the DRC3 antibody as in previous studies. IF showed the absence of DRC3 in the cilia, suggesting a DRC1 deletion affects DRC3 localization in the cilia. To the best of our knowledge, this case represents one of the earliest reports to perform IF and ciliary movement analysis in PCD with a homozygous deletion involving exons 1-4 of DRC1.

Objective To determine the clinical significance of sputum Pasteurella multocida in adults with structural lung disease by operationally distinguishing infection from colonization and describing outcomes of pathogen-directed therapy. Methods We performed a single-center, retrospective case study. Infection was defined a priori by new or worsening lower -respiratory symptoms at the time of culture, supported by inflammatory or radiologic changes; isolation without symptoms was classified as colonization. Two pulmonologists blinded to the clinical data reviewed the chest CTs scans. Antibiotic selection and clinical responses within 2-4 weeks were extracted from the charts. Results Seven adults (five women; mean age, 67.1 years) with structural airway disease were included. Middle lobe syndrome and diffuse panbronchiolitis were predominant, while bronchiectasis was present in two patients. Five of the seven patients (71.4%) reported regular dog/cat exposure. Sputum cultures were obtained for acute symptom exacerbations in four patients and for incidental imaging abnormalities in three. Three symptomatic patients received penicillin-class therapy and all improved. One symptomatic patient improved without antibiotics. No recent animal bites or scratches were reported. No severe treatment-related adverse events were observed. Conclusion In elderly patients with structural airway disease, sputum P. multocida during symptomatic episodes likely represents true infection and responds to targeted narrow-spectrum therapy, whereas asymptomatic isolates may reflect colonization. These observations provide a pragmatic framework to distinguish infection from colonization, support susceptibility-aligned narrow-spectrum management, and offer small-series evidence to inform antimicrobial stewardship in structural lung diseases.

This case report describes a Japanese woman in her 70s who was initially diagnosed with diffuse panbronchiolitis (DPB) and treated with long-term macrolide therapy. The patient presented with a persistent cough and purulent sputum, and a CT of the chest showed centrilobular opacities. The clinical course, which included the detection of Pseudomonas aeruginosa and obstructive impairment, was consistent with DPB. However, the treatment was ineffective, and the opacities worsened over time. Subsequently, 6 years after the initial presentation, yellow nails were observed, leading to a revised diagnosis of yellow nail syndrome (YNS). This noteworthy case, presenting with centrilobular opacities closely resembling DPB, is an important example suggesting that lymphatic dysfunction in YNS may be involved in the formation of centrilobular opacities.

Bronchiolitis is a heterogeneous group of disorders, each with its own clinical and radiographic presentation, treatment options, and prognosis. Until now, classifications were based on pathology and radiology.

Primary ciliary dyskinesia (PCD) is a hereditary disorder characterized by defects in cilia that impair mucociliary clearance. This study focuses on PCD caused by mutations in the Cyclin O (CCNO) gene and reports on three cases involving Chinese children. Case 1 was an 8-year-and-3-month-old boy who presented with respiratory distress after birth and later developed a recurrent productive cough and purulent nasal discharge. He was initially diagnosed with diffuse panbronchiolitis (DPB) due to the presence of diffuse micronodules in lung CT scans. Case 2 was the younger sister of case 1. She also presented with respiratory distress after birth, with a chest radiograph revealing atelectasis. She required oxygen supplementation until the age of 2 months. Case 3 was a 4-year-and-4-month-old girl with a history of neonatal pneumonia, persistent pulmonary atelectasis, and recurrent lower respiratory tract infections. Her chest radiograph also showed diffuse micronodules. In all three cases, the final diagnosis of PCD was confirmed by genetic testing. Cases 1 and 2 exhibited homozygous c.248_252dup TGCCC (p.G85Cfs*11) mutations in the CCNO gene, while case 3 harbored a homozygous c.258_262dup GGCCC (p.Q88Rfs*8) mutation. A literature review indicated that the common clinical features of CCNO-PCD include neonatal respiratory distress (40/49, 81.6%), chronic cough (31/33, 93.9%), rhinosinusitis (30/35, 85.7%), bronchiectasis (26/35, 74.3%), and low nasal nitric oxide (nNO, 40/43, 93.0%). Notably, situs inversus has not been reported. In CCNO-PCD patients, cilia may appear structurally normal but were severely reduced in number or entirely absent. Lung CT scans in these patients may exhibit diffuse micronodules and "tree-in-bud" signs, which can lead to a clinical misdiagnosis of DPB. nNO screening combined with genetic testing is an optimized diagnostic strategy. Treatment options include the use of anti-infective and anti-inflammatory agent, along with daily airway clearance. This study underscores the importance of genetic testing in neonates and children with suspected PCD or those clinically diagnosed with DPB to enable an early diagnosis and prompt intervention, thereby enhancing the prognosis for these patients.