Purpureocillium lilacinum (P. lilacinum) is a rare opportunistic mold that predominantly affects immunocompromised hosts and exhibits intrinsic resistance to several conventional antifungal agents. Pulmonary infection is uncommon, and only a limited number of cases have been reported in patients with autoimmune connective tissue diseases receiving immunosuppressive therapy. We report a 37-year-old male hospital social worker with anti-Jo-1-positive myositis-associated interstitial lung disease receiving corticosteroids and mycophenolate mofetil who presented with hemoptysis and dyspnea. Computed tomography of the thorax demonstrated bilateral ground-glass opacities, multilobar consolidation, tree-in-bud nodularity, and mediastinal lymphadenopathy. Bronchoalveolar lavage fungal culture yielded P. lilacinum, with species identification confirmed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Because second-generation triazoles were unavailable at the time of diagnosis, treatment was initiated with oral itraconazole (200 mg twice daily) together with temporary cessation of immunosuppressive therapy. The patient experienced rapid clinical improvement, with resolution of the acute pulmonary infiltrates on follow-up computed tomography after three months and a negative follow-up sputum fungal culture after six months of therapy. Immunosuppressive treatment was subsequently reintroduced without recurrence of infection or progression of interstitial lung disease during follow-up. This case highlights the diagnostic challenge of probable pulmonary P. lilacinum infection in immunosuppressed patients with myositis-associated interstitial lung disease. It demonstrates a favorable clinical course during prolonged oral itraconazole therapy when preferred antifungal agents were unavailable. However, treatment outcomes should be interpreted with caution, as this is a single case, and concomitant antibacterial therapy, along with temporary modification of immunosuppressive therapy, may also have contributed to recovery.

Nocardiosis is an uncommon infection that presents as a chronic, debilitating illness with radiographic manifestations simulating lung cancer or tuberculosis. Immunocompromised hosts may develop a fulminant disease resembling acute bacterial pneumonia or disseminated disease. We report a case of a juvenile lupus who developed disseminated Nocardia pseudobrasilienisis infection in form of necrotizing pneumonia, subcutaneous nodules and central nervous system (CNS) lesion in the right parietal lobe, following inadvertent hiking of steroids after a minor organ flare. This case was successfully treated with intravenous meropenem, amikacin, and oral cotrimoxazole therapy for 6 weeks which lead to resolution of pneumonia, and partial resolution of of the cutaneous and CNS lesion. As the patient was immunosuppressed, and had disseminated nocardiosis, we planned to put her on oral cotrimoxazole for the next 1 year.

Total chemical synthesis of two trisaccharides related to the O-antigens from Burkholderia cepacia serotype E (O2), the causative pathogen of pneumonia in immunocompromised patients with underlying cystic fibrosis, is accomplished through rational protecting group manipulations followed by stereoselective glycosylations. The target trisaccharides in the form of their 2-aminoethyl glycoside are particularly useful for further conjugation with suitable aglycons and potential vaccine design against the multidrug-resistant species. All new compounds are well characterized by NMR and HRMS.

Invasive pneumococcal disease (IPD) is a life-threatening infection caused by Streptococcus pneumoniae, particularly in immunocompromised individuals, such as those with asplenia. Although pneumococcal vaccination has reduced the incidence of vaccine-covered serotypes, non-vaccine serotypes, including serotype 23B, have emerged as the predominant cause of IPD. This case report describes a 67-year-old woman with asplenia who developed IPD caused by multidrug-resistant Streptococcus pneumoniae serotype 23B, which led to meningitis, septic arthritis, and endophthalmitis. The patient, who had declined pneumococcal vaccination after her splenectomy, presented with fever, pain in her left hip and right shoulder, and visual issues. The diagnosis confirmed S. pneumoniae serotype 23B, resistant to multiple antibiotics. The treatment involved a combination of vancomycin, ceftriaxone, and rifampicin, followed by vitrectomy for the eye infection. Despite severe complications, including worsening vision, the patient's vision in the right eye improved after surgery, and the joint pain subsided with long-term antibiotic therapy. This case underscores the challenges posed by non-vaccine S. pneumoniae serotypes, particularly in asplenic patients. Currently, we can use the 21-valent pneumococcal conjugate vaccine (PCV21), which includes the 23B serotype. Vaccination and early recognition, combined with a multidisciplinary treatment approach involving both antimicrobial therapy and surgical intervention, are crucial for improving the outcomes of patients with severe IPD.

We assessed the Pneumocystis jirovecii PCR accuracy on non-invasive oropharyngeal wash (OW) specimens for the diagnosis of Pneumocystis jirovecii pneumonia (PJP) in non-HIV immunocompromised patients. In this retrospective study, 134 patients with suspected PJP undergoing both OW and deep respiratory sampling were included. PJP was defined by composite criteria. OW P. jirovecii PCR showed a sensitivity of 61.5% (95% CI 42.5-77.6) and a specificity of 97.2% (95% CI 92.2-99.1). Positive and negative predictive values were 84.2% and 91.3%, respectively. These results suggest OW P. jirovecii PCR may support non-invasive diagnosis, but cannot be used to exclude PJP.

Adenovirus may cause life-threatening infections. While outcomes in immunocompromised patients are well documented, data on critically ill, immunocompetent adults remain limited. To describe the clinical characteristics and outcomes of adenovirus infection in adult intensive care unit (ICU) patients and to identify factors associated with 30-day mortality. This retrospective observational study included adult patients (≥ 16 years) admitted to ICUs between January 2020 and May 2025 with PCR-confirmed adenovirus infection and compatible clinical syndromes, with a primary focus on describing patient characteristics rather than analyzing virological features of the infection. Data were collected from 24 centers in 11 countries. Demographics, comorbidities, clinical characteristics, laboratory findings, treatments, and outcomes were recorded. The primary outcome was 30-day all-cause in-hospital mortality. Variables associated with mortality in univariate analyses were entered into a stepwise multivariable logistic regression model. A total of 126 patients were included; 40 (31.7%) died within 30 days of PCR positivity. The mean age of the entire cohort of patients was 44.9 ± 20.4 years (median 48; 16-95), and 38.9% were female. Pneumonia was the most common presentation (108/126, 85.7%), followed by upper respiratory tract infection (18.3%), gastroenteritis (6.3%), conjunctivitis (4.8%), meningoencephalitis (2.4%), and cystitis (1.6%). Significant immunosuppression was present in 29.4%. In multivariable analysis, independent predictors of 30-day mortality included mean arterial pressure ≤ 65 mmHg, SOFA score ≥ 5, increasing Charlson Comorbidity Index, central venous catheter placement, platelet count <50,000/µL (borderline significance), procalcitonin ≥ 0.1 ng/mL, and significant immunosuppression. The final model had 84.9% accuracy, 72.5% sensitivity, and 90.7% specificity. A high percentage of ICU patients with PCR-confirmed adenovirus infection died within 30 days. Hemodynamic instability, organ failure severity, comorbidity burden, inflammatory response, thrombocytopenia, and immunosuppression are key determinants of poor outcome.

Patients with mantle cell lymphoma (MCL) who undergo chemotherapy are at high risk of developing opportunistic pulmonary infections. Concurrent infection with cytomegalovirus (CMV) and the rare pathogen Aspergillus tamarii (A. tamarii) has never previously been reported in MCL patients. In this case report, we present the first documented instance of concurrent CMV and A. tamarii pneumonia in a MCL patient. A 69-year-old man with MCL developed a cough, chills, exertional dyspnoea, and hypoxemia after five cycles of rituximab-bendamustine (R-Benda) chemotherapy. Chest computed tomography (CT) showed bilateral ground-glass opacities. Metagenomic next-generation sequencing (mNGS) of the blood and bronchoalveolar lavage fluid (BALF) simultaneously revealed CMV and A. tamarii infections. The patient initially achieved rapid clinical improvement with ganciclovir and voriconazole. However, the infection relapsed following unauthorised premature discontinuation of ganciclovir and voriconazole without medical advice. Long-term oral voriconazole with regular TDM and close monitoring of ganciclovir-related myelosuppression resulted in sustained remission. This is the first reported case of concurrent CMV and A. tamarii pulmonary coinfection in a MCL patient, and mNGS enables the rapid and accurate diagnosis of mixed rare infections. Voriconazole is effective against A. tamarii; TDM and full-course treatment are essential for preventing relapse. We present a practical workflow for managing immunocompromised patients with rare mixed pulmonary infections to improve outcomes.

Vaccines against SARS-CoV-2 and influenza require reformulation due to viral evolution. It remains unclear how vaccination against evolving antigens influences T-cell responses and the impact of reformulation on T-cell responses to new variants in immunocompromised hosts. Solid organ transplant recipients (SOTRs) had significantly lower antibody levels following vaccination and required repeated boosting during the COVID-19 pandemic.

Pulmonary disease caused by Mycobacterium avium complex (MAC) most often occurs in patients with structural lung disease or immunocompromising conditions and typically follows recognized fibrocavitary or nodular-bronchiectatic radiographic patterns. Advanced cavitary disease discovered incidentally in an asymptomatic patient represents an uncommon and diagnostically challenging presentation that may be initially attributed to malignancy, aspiration pneumonia, or endemic fungal infection. We report the case of a 45-year-old man without known immunodeficiency who had alcohol use disorder and active deep vein thrombosis treated with apixaban and presented with acute right groin pain secondary to a reducible inguinal hernia. Abdominal computed tomography performed during hernia evaluation incidentally demonstrated a 6.9 × 5.3 cm thick-walled cavitary opacity in the left lower lobe with an air-fluid level and bilateral reticulonodular opacities. The patient denied cough, dyspnea, hemoptysis, fever, night sweats, and weight loss. Serial sputum acid-fast bacillus smears were positive, and mycobacterial cultures grew MAC. In the setting of compatible cavitary imaging, these findings fulfilled the American Thoracic Society/European Respiratory Society/European Society of Clinical Microbiology and Infectious Diseases/Infectious Diseases Society of America (ATS/ERS/ESCMID/IDSA) diagnostic criteria for pulmonary MAC disease. Tuberculosis and HIV testing were negative. A respiratory molecular panel was also positive for Haemophilus influenzae. Because bacterial cultures showed no growth, this finding was interpreted as a possible coinfection rather than a confirmed bacterial infection. Given the leukocytosis and bilateral infiltrates, intravenous ceftriaxone was initiated empirically. However, MAC-directed multidrug therapy was complicated by two pharmacologic barriers: the risk of reduced apixaban exposure with rifabutin-containing therapy and a baseline corrected QT interval of 512 ms, limiting routine macrolide use. The patient was therefore transferred to a tertiary care center for multidisciplinary regimen selection. This case underscores that incidental cavitary pulmonary lesions demand systematic microbiologic evaluation regardless of symptom burden and that early pharmacologic risk assessment is essential when standard MAC therapy is constrained.