Background/Objectives: Hypersensitivity pneumonitis (HP), a subtype of interstitial lung disease (ILD), is often misdiagnosed as idiopathic pulmonary fibrosis (IPF), particularly when the causative antigen cannot be identified. Typically resulting from chronic exposure to inhaled organic particles smaller than 5 microns, HP presents a diagnostic challenge. This report outlines a case of fibrotic HP initially misclassified as asthma. No triggering antigen was identified despite extensive investigation. The disease progressed despite corticosteroid, immunosuppressive, and antifibrotic therapy, ultimately leading to an advanced fibrotic stage and requiring lung transplantation. This clinical course is rare and infrequently reported, particularly in cases requiring lung transplantation without an identifiable causative antigen. Such progression is uncommon and underreported, especially in patients initially misclassified as having asthma. Methods: Medical records of 24 patients diagnosed with HP were reviewed. Only one case demonstrated progression to fibrotic HP; this case was selected for detailed analysis. Results: Clinical and functional deterioration occurred despite standard therapy. Given the advanced stage of fibrosis and treatment resistance, lung transplantation was deemed the next appropriate therapeutic option. Conclusions: HP remains underdiagnosed due to difficulties in identifying the causative antigen and overlapping features with other ILDs. Early and accurate differentiation from IPF is essential, particularly in progressive fibrotic forms unresponsive to conventional therapies.

Background and Clinical Significance: Extrapulmonary tuberculosis (TB) remains a diagnostic challenge, particularly when affecting rare sites such as the oral cavity and digestive tract. We report the case of a 55-year-old woman with disseminated (miliary) tuberculosis presenting with atypical oral lesions initially suspected to represent a malignant tumor. Case Presentation: The patient had a history of recurrent depressive disorder, cognitive impairment, sleep disturbances, and nicotine/alcohol dependence. She presented with painful ulcerations of the oral cavity, dysphagia, odynophagia, and glossodynia. Otolaryngologic examination revealed reduced tongue mobility and an ulceroinfiltrative lesion involving the floor of the mouth and the lower alveolar ridge. Fibroscopic evaluation confirmed infiltrative ulcerative lesions, and biopsy samples were obtained. Histopathologic examination revealed a chronic necrotizing granulomatous inflammation with multinucleated giant cells, consistent with a mycobacterial infection. Further investigations confirmed disseminated (miliary) tuberculosis with oral and digestive involvement. Antituberculous therapy was initiated; however, despite temporary stabilization, the patient’s condition progressively worsened and the outcome was fatal. Conclusions: Oral and digestive tuberculosis, although rare, should be considered in the differential diagnosis of ulceroinfiltrative lesions of the oral cavity, particularly in patients with systemic symptoms or risk factors for TB. Early histopathologic confirmation and initiation of specific therapy are essential for favorable outcomes and prevention of misdiagnosis as malignant disease.

Background: Non-Hodgkin lymphoma (NHL) is a malignancy of the immune system that includes several subtypes, most commonly diffuse large B-cell lymphoma and follicular lymphoma. Its etiology is multifactorial, with risk factors such as immunosuppressive therapy, infections, chemical exposure, and advanced age. A key aspect is the bidirectional relationship between lymphoma and immunodeficiency, which increases susceptibility to recurrent infections and complicates disease management. Case presentation: One particularly challenging case during the COVID-19 pandemic involved a patient with a personal history of diffuse B-cell non-Hodgkin lymphoma, diagnosed 5 years earlier, who had undergone eight cycles of rituximab-based chemotherapy. The patient tested positive for SARS-CoV-2 for three consecutive months and experienced repeated urinary tract infections warranting more in-depth investigations. The uniqueness of this case lies in the rare association of non-Hodgkin lymphoma, suspected post-rituximab immunodeficiency, severe COVID-19 infection, and recurrent urinary tract infections, which complicated clinical management. Despite appropriate treatment for both respiratory and urinary infections, as well as eight cycles of chemotherapy, the patient’s condition continued to deteriorate significantly, ultimately requiring intravenous immunoglobulin replacement therapy. Following the treatment, the patient presented a remarkable clinical improvement, with resolution of the signs and symptoms, and an absence of further recurrent infections. The patient remained clinically stable under regular immunoglobulin replacement therapy, with sustained infection control and improved quality of life. Conclusions: This case highlights the importance of assessing immune status in patients with a hematological malignancy, especially when recurrent infections persist.

Background: Tuberculous cervical lymphadenitis (scrofula) is the most common form of extrapulmonary tuberculosis, although its coexistence with massive pleural effusion is uncommon and may delay diagnosis because of its nonspecific clinical presentation. We report the case of a 47-year-old man presenting with a large right-sided pleural effusion associated with a suppurative cervical lymphadenitis, in whom rapid molecular testing established the diagnosis of disseminated extrapulmonary tuberculosis. Case Presentation: A 47-year-old male presented with progressive right-sided chest pain, exertional dyspnea, intermittent fever, night sweats, weight loss, and a progressively enlarging left laterocervical mass. Physical examination revealed multiple enlarged, fluctuant cervical lymph nodes and clinical signs of a massive right pleural effusion. Thoracic computed tomography demonstrated a large right pleural effusion with compressive atelectasis and enlarged cervical and mediastinal lymph nodes. Ultrasound-guided cervical lymph node drainage and tube thoracostomy were performed, followed by repeated pleural fluid evacuations through the chest tube. Purulent material obtained from the cervical abscess and pleural fluid were subjected to microbiological, cytological, and molecular investigations, including Xpert MTB/RIF (GeneXpert MTB/RIF). GeneXpert MTB/RIF detected Mycobacterium tuberculosis complex in both the drained cervical purulent material and pleural fluid, with no evidence of rifampicin resistance. Conventional bacterial cultures remained negative, while mycobacterial cultures were subsequently positive for M. tuberculosis. Pleural fluid analysis was consistent with an exudative lymphocytic effusion with elevated adenosine deaminase levels. Histopathological examination of the cervical tissue demonstrated necrotizing granulomatous inflammation with central caseous necrosis, epithelioid histiocytes, and Langhans-type multinucleated giant cells, supporting the diagnosis of tuberculous lymphadenitis. HIV serology was negative, and no additional immunodeficiency was identified. Standard first-line antituberculous therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) was initiated promptly following microbiological confirmation, leading to progressive regression of the cervical lesions, complete resolution of the pleural effusion, and favorable clinical evolution during follow-up. Conclusions: The simultaneous occurrence of tuberculous cervical lymphadenitis and massive pleural tuberculosis represents an uncommon presentation of extrapulmonary tuberculosis that requires a high index of clinical suspicion. The combination of histopathological examination and rapid molecular testing of extrapulmonary specimens allowed definitive and timely confirmation of tuberculosis and facilitated prompt initiation of appropriate therapy. Clinicians should consider tuberculosis in patients presenting with cervical suppurative lymphadenitis and unexplained pleural effusion, even in the absence of microbiologically confirmed pulmonary disease, to avoid diagnostic delay and improve clinical outcomes.

Background: MDRO colonization at ICU admission may identify patients at increased risk for hospital-acquired infection (HAI), but its independent predictive value remains incompletely defined. Methods: We conducted a retrospective observational study of 560 consecutive ICU admissions (July–October 2024). Admission screening assessed colonization with extended-spectrum beta-lactamase (ESBL)-producing Enterobacterales, carbapenem-resistant Enterobacterales (CRE), and vancomycin-resistant enterococci (VRE). The primary outcome was microbiologically confirmed HAI; the secondary outcome was in-hospital mortality. Associations were evaluated using multivariable logistic regression, ROC/AUC analysis, mediation analysis, and a sensitivity analysis restricted to first admissions. Results: Of 560 admissions, 223 were screen-positive and 283 screen-negative. HAI occurred in 49 patients (8.8%). Positive screening was associated with increased HAI odds, narrowly missing significance in the primary adjusted analysis (OR 1.81, 95% CI 0.96–3.41, p = 0.065) but reaching significance in the first-admission sensitivity analysis (OR 2.09, p = 0.034). CRE showed the strongest adjusted association with HAI (OR 2.33, 95% CI 1.21–4.51, p = 0.012). Screening alone showed poor discrimination (AUC 0.574); combined with clinical variables, discrimination improved substantially (AUC 0.788). Conclusions: MDRO admission screening was associated with increased HAI odds, particularly for CRE, though screening alone has limited predictive performance. Larger prospective studies are needed to confirm these findings.