Klebsiella pneumoniae is the second most common cause of urinary tract infection (UTI) in most populations; however, few cases of recurrent UTI (rUTI) have been described. In this report, we described a patient who experienced 18 episodes of community-acquired rUTI caused by extended-spectrum β-lactamase (ESBL)-producing and multidrug-resistant (MDR) K. pneumoniae over an 8-year period. All isolates were ESBL producers and MDR, with variable resistance profiles. Molecular analysis of 10 isolates also revealed variations in β-lactamase genes; however, all isolates shared the same capsular serotype (K17) and virulence gene profile. PFGE analysis identified three closely related pulsotypes, and all isolates belonged to ST101, supporting relapse events during recurrent infection. Particular attention should be paid to empirical treatment of UTI due to the high resistance rates observed in K. pneumoniae, even in community-acquired infections.

[This corrects the article DOI: 10.7759/cureus.106958.].

Diffuse alveolar hemorrhage (DAH) is a medical emergency that is known to be caused by systemic vasculitis, autoimmune conditions, coagulation disorders, and toxins. While it can be caused by chronic mitral regurgitation (MR), it has a rare association with acute MR. We report the case of a patient presenting with DAH as the first sign of acute MR. A 58-year-old man with type 2 diabetes mellitus and no cardiac history except for hypertension presented with dyspnea and cough with pink-stained white sputum for two days. On examination, bilateral crepitations and a pansystolic murmur were noticed. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was 165 ng/L, while high-resolution computed tomography (HRCT) showed diffuse bilateral ground-glass opacities with a crazy paving pattern. Transesophageal echocardiography (TEE) showed preserved left ventricular ejection fraction (>60%) and confirmed moderate-to-severe eccentric acute MR due to posterior leaflet prolapse with rupture of marginal chordae tendineae. Bronchoalveolar lavage (BAL) confirmed alveolar hemorrhage and established the diagnosis of DAH, which initially mimicked severe respiratory infection due to the presence of pink-stained sputum and bilateral infiltrates. Following stabilization, the patient was scheduled for mitral valve replacement. This case illustrates the importance of considering cardiac etiologies and performing early echocardiography in patients presenting with unexplained DAH, as these etiologies can mimic common causes of DAH.

Atypical hemolytic uremic syndrome (aHUS), also known as complement-mediated thrombotic microangiopathy (CM-TMA), is an extremely rare but potentially life-threatening disorder that presents with the triad of thrombocytopenia, hemolytic anemia, and acute renal failure. aHUS is attributed to genetic mutations in the complement regulation system and is typically triggered by events such as pregnancy, vaccination, or surgery. This case report describes a patient initially admitted for acute pancreatitis secondary to alcohol abuse who developed aHUS within 48 hours of admission. The diagnosis of aHUS was confirmed via a full diagnostic workup. Hematology recommended supportive care. The case was further complicated by acute hypoxic respiratory failure secondary to community-acquired pneumonia, which developed simultaneously with the aHUS. The patient's aHUS resolved as the acute pancreatitis resolved with supportive care, and the pneumonia resolved with antibiotics and inhaled corticosteroids, which likely helped improve the aHUS. When patients present with acute pancreatitis and hematologic abnormalities, clinicians should suspect aHUS and perform a thorough workup to distinguish between aHUS and other autoimmune hematologic conditions, such as typical hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), or drug-induced complement-mediated anemia (CMA). While most reported cases have been treated with plasma exchange therapy or eculizumab, we present one of the few cases where the patient was treated with supportive care.

Background The worldwide escalation of antimicrobial resistance poses a substantial challenge to the effective management of both community-acquired and hospital-associated infections. Among Gram-negative bacteria, resistance to β-lactam antibiotics is predominantly mediated by enzymes such as extended-spectrum β-lactamases, AmpC β-lactamases, and metallo-β-lactamases. Aim This study aimed to identify the concurrent production of these β-lactamase mechanisms in Gram-negative clinical isolates. Materials and methods A cross-sectional laboratory-based study was performed on 185 non-duplicate Enterobacteriaceae isolates obtained from clinical specimens. All the isolates underwent phenotypic screening for extended spectrum of β-lactamases (ESBL), AmpC, and metallo-β-lactamases (MBL) production using standard disk diffusion-based methods. The study adhered to ethical guidelines with institutional approval. Data were analyzed statistically using the Chi-square test, with significance set at p < 0.05. Results Out of 185 Enterobacteriaceae isolates, Klebsiella pneumoniae (90; 50.0%) and Escherichia coli (60; 33.3%) were the most prevalent. The maximum number of isolates was observed in males aged 41-60 years and females aged 21-40 years. Of 145 MDR isolates, 63 (43.4%) co-expressed two or three β-lactamases, with 28 (19.3%) showing MBL + ESBL, 13 (8.9%) MBL + AmpC, 16 (11%) ESBL + AmpC, and 6 (4.1%) concurrently producing MBL, ESBL, and AmpC. Conclusion Over the course of the study, this investigation demonstrated the substantial burden of multidrug-resistant Enterobacteriaceae, with 63 (43.4%) isolates co-expressing multiple β-lactamases and 6 (4.1%) simultaneously producing MBL, ESBL, and AmpC, highlighting a critical challenge. Incorporating routine screening for these enzymes is essential to manage infection and limit the spread of resistance.

Mycoplasma pneumoniae pneumonia (MPP) is a common form of community-acquired pneumonia in children, potentially involving multiple organ systems. Accumulating evidence suggests that dysbiosis of the respiratory microbiota is associated with various respiratory diseases. Nevertheless, it remains unclear how the respiratory microbiota varies across anatomical sites, interacts with other microbes, and correlates with host immunity in children with MPP compared to non‑MPP respiratory diseases. In this study, we collected and analyzed pharyngeal swabs, sputum, and bronchoalveolar lavage fluid samples from 401 pediatric MPP patients and 287 control subjects (MPP-negative children with other respiratory conditions).Comparative analysis revealed significant respiratory microbiome dysbiosis in MPP patients, with Mycoplasmoides constituting 30.33% of the total microbial community. A discriminative model based on Mycoplasmoides abundance demonstrated excellent performance (AUC = 0.983, sensitivity = 95.3%, specificity = 98.3%). Notably, Mycoplasmoides abundance showed significant negative correlations with Prevotella, Veillonella_A, Staphylococcus, and Rothia, suggesting potential inhibitory effects.Anatomical distribution analysis indicated distinct microbial distributions: Prevotella and Veillonella_A were predominantly enriched in the upper respiratory tract, while Mycoplasmoides showed greater abundance in the lower respiratory tract. Consistency analysis supported the hypothesis of microbial translocation from upper to lower respiratory tract in affected children.Severe MPP cases exhibited significantly higher Mycoplasmoides abundance. For correlations with clinical indicators, both Mycoplasmoides and Streptococcus showed nominal associations. Our findings elucidate the complex interplay between respiratory microbiota in pediatric MPP patients and its association with disease severity and clinical outcomes. This study highlights the need for further research to explore and validate the prognostic relevance of value of these microbial markers.