Coinfection in COVID-19 patients is associated with worsening outcome. Among patients with COVID-19, Legionella pneumophila, a common cause of pneumonia, has been reported as a co-occurring respiratory infection. A nonspecific clinical presentation, however, makes an early diagnosis difficult. Bronchoalveolar lavage fluid was collected from a patient suffering from COVID-19 and presenting with pneumonia and sent for metagenomic analysis. Differential abundance analysis was carried out by comparing each taxon reads per million between the bronchoalveolar lavage fluid sample and the negative control. Two replicates of metagenomic sequencing were conducted on bronchoalveolar lavage fluid samples. Within each replicated sequencing, one negative control was sequenced for comparison of taxon abundance in the BALF sample. In both replicates, Legionella pneumophila was the only taxon with significantly higher abundance when compared with the negative control. PCR of the bronchoalveolar further confirmed the presence of L. pneumophila. Several studies have estimated that the incidence of Legionnaires’ disease co-infection in patients with COVID-19 infection is approximately 0% to 1.5%. There are some common characteristics of COVID-19 and co-infection with Legionnaires’ disease, making it difficult to diagnose bacterial infection early. The diagnosis of these cases is important due to the different treatments used. Current diagnostic tests for Legionnaires’ disease include conventional culture, urinary antigen for L. pneumophila serogroup 1, polymerase chain reaction, direct fluorescent antibody stain, and paired serology. The current study demonstrated that metagenomics is a promising approach that facilitated the diagnosis of Legionnaires’ disease.

Purpose: Burkholderia cepacia complex (Bcc) is a known significant opportunistic pathogen causing morbidity and mortality, particularly in those with cystic fibrosis, chronic granulomatous disease, or immunocompromising host. Mortality of Bcc bloodstream infections among non-cystic fibrosis patients remained high. The antibiotic treatment for Bcc infection is quite challenging due to its intrinsic resistance to most antibiotics, and the resistance to carbapenems was the biggest concern among them. We aimed to realize the mechanism of carbapenem resistance in Bcc. Patients and Methods: Ten strains of Bcc were identified by the MALDI-TOF MS, and the drug susceptibility test was using VITEK 2 system. The Burkholderia cepacia complex genomes were sequenced via Nanopore GridIon. We also downloaded another ninety-five strains of Bcc from the National Center for Biotechnology Information database to evaluate the divergence between carbapenem-resistance and carbapenem-sensitive strains. Results: The genetic organization between carbapenem-sensitive and carbapenem-resistant strains of Bcc showed no difference. However, in the carbapenem-sensitive strain, E151V substitution in PenR was detected. In addition, a novel specific OXA family subgroup, bla_OXA-1043 in Burkholderia cenocepacia was discovered. Conclusion: The E151V substitution in PenR may be associated with carbapenem-sensitive in Bcc. Moreover, the V151E mutation in PenR may be related to the activation of PenB, leading to Bcc resistance to carbapenems. Besides, a novel OXA family subgroup, bla_OXA-1043, was found in Burkholderia cenocepacia, which differs from the previous OXA family.

Background: Pulmonary aspergillosis remains highly lethal despite modern therapy. Although polymerase chain reaction (PCR) has enhanced detection, the clinical significance of its cycle threshold (Ct) values is unclear. The key problem is the lack of validation of Ct values for assessing fungal burden or predicting outcomes, limiting their diagnostic and prognostic utility. Methods: We conducted a retrospective cohort study of 154 adult patients diagnosed with pulmonary aspergillosis at a tertiary medical center in Taiwan (2021– 2024). All patients had a positive Aspergillus PCR from a respiratory specimen. We used receiver operating characteristic (ROC) curve analysis to determine an optimal Ct cutoff for predicting 30-day all-cause mortality and multivariable logistic regression to identify independent predictors. Results: Among 154 patients (mean age 70.5 ± 13.5 years; 48.1% female), the optimal Ct cutoff for predicting 30-day mortality was 30.7 (AUC = 0.65, 95% CI 0.56– 0.73). Patients with a Ct value < 30.7 had significantly higher 30-day mortality than those with a Ct ≥ 30.7 (71.2% vs 43.1%, p = 0.002). After adjusting for clinical and laboratory confounders, a Ct value < 30.7 remained the independent predictor of mortality (adjusted OR 3.07; 95% CI 1.27– 7.39; p = 0.012). Conclusion: A low Aspergillus PCR Ct value is an independent predictor of 30-day mortality in patients with pulmonary aspergillosis. While its discriminative ability is moderate, the Ct value may serve as a valuable predictor to aid in early risk stratification, when interpreted within the overall clinical context.

Seasonal influenza remains a major threat to healthcare facilities, where introduction of the virus can cause disproportionate morbidity and mortality among high-risk inpatients. This narrative review synthesizes current evidence and practice-oriented guidance on the prevention of hospital-acquired influenza. We conducted a targeted literature search using PubMed, guideline repositories for English-language publications from 2000 to 2025, prioritizing systematic reviews, clinical trials, and authoritative guidelines. A multifaceted strategy is emphasized: annual vaccination of healthcare personnel and eligible patients; consistent implementation of standard and transmission-based precautions; attention to environmental cleaning and disinfection; and occupational-health policies that limit presenteeism and workplace exposure. Evidence demonstrates that higher healthcare personnel (HCP) vaccination coverage is associated with lower patient influenza rates and improved survival. Reliable hand hygiene, respiratory source control, early initiation of droplet precautions, and cohorting when single rooms are limited all contribute to interrupting in-facility transmission. Ensuring that ill HCP can remain off duty without penalty further reduces the likelihood of staff-to-patient spread. Collectively, these coordinated measures provide a protective framework and underscore the central role of clinicians and infection-prevention teams in sustaining influenza control within acute-care settings.

Background: Outpatient Parenteral Antimicrobial Therapy (OPAT) has long been established as a safe and cost-effective alternative to inpatient care in Western healthcare systems. In contrast, its implementation across Asia has historically been fragmented and unstructured. A landmark multinational survey in 2017 identified OPAT in Asia as a “missed opportunity,” citing the lack of systematic oversight, standardized protocols, and outcome monitoring systems. Methods: This narrative review examines the evolution of OPAT in Asia over the past decade, synthesizing evidence from regional studies, national policies, and implementation models. Results: The findings demonstrate a clear shift from ad hoc infusion practices toward structured, multidisciplinary OPAT programs in several healthcare systems. These systems increasingly integrate antimicrobial stewardship principles, dedicated care teams, and reimbursement mechanisms. In parallel, innovative models, including hospital-at-home services and elastomeric pump–based continuous infusion, have expanded treatment feasibility while enabling the use of narrower-spectrum antibiotics. Despite these advances, substantial heterogeneity persists. Key barriers include the absence of unified national guidelines, limited monitoring infrastructure, workforce constraints, and regulatory restrictions in certain settings. Resource-limited regions continue to face challenges related to financing, laboratory capacity, and digital health integration. Conclusions: Overall, OPAT in Asia is transitioning from an underrecognized and inconsistently delivered service to an increasingly structured component of infectious disease care. Future priorities include standardized governance, integration with antimicrobial stewardship programs, sustainable reimbursement, digital outcome monitoring, and region-specific evidence on antimicrobial stability and safety.

Objectives: This review synthesizes quantitative evidence on how climate change modulates airborne and droplet-borne disease transmission and assesses hospital resilience strategies. Methods: A narrative review of global data (2000–2025) was conducted, focusing on pathogen kinetics and post-disaster hospitalization burdens. Results: Climate change alters disease dynamics by extending pathogen viability and creating prolonged transmission windows. Flood exposure increases respiratory hospitalization risk by 30% and infectious disease hospitalization risk by 26%, with burdens persisting for 60–90 days. Heat exposure increases COPD risk by 1.47% for every 1 °C above thermal thresholds. Mechanistically, low humidity favors persistent airborne droplet nuclei, whereas high humidity enhances transmission via larger droplets that require close contact. Current hospital infrastructure remains vulnerable to these compound climate-pollution crises. Conclusion: Conventional acute-phase disaster models are insufficient. Resilience requires a paradigm shift toward “climate-integrated” infection control. Critical strategies include integrating meteorological data into predictive surveillance systems and using ventilation, upper-room UVGI, and portable air cleaning as complementary engineering controls.