Infection最新文献

Background: Ventilator-associated pneumonia (VAP) affects 30-50% of mechanically ventilated patients with acute brain injury (ABI), exceeding general ICU rates (10-20%) due to aspiration risks and immunosuppression, prolonging ICU stays and morbidity. Although short-course antibiotic prophylaxis (AP; e.g., ceftriaxone) targets early VAP, efficacy in ABI remains debated amid mixed evidence, resistance concerns, and non-endorsement by IDSA/ATS guidelines.

Methods: We searched PubMed, Cochrane Library, and Web of Science (inception to October 2024) for RCTs and non-RCTs on systemic AP (short-course beta-lactams) for VAP prevention in ABI (TBI, SAH, stroke, post-arrest coma) requiring ventilation ≥ 48 h.

Primary outcomes: early-onset VAP (≤ 96 h), late-onset VAP (> 96 h), overall VAP, ICU mortality. Secondaries: mechanical ventilation duration, ICU/hospital length of stay (LOS), time to first VAP. Random-effects meta-analysis; heterogeneity via I²; risk of bias (RoB 2.0/ROBINS-I).

Results: Ten studies (5 RCTs [n = 586], 5 non-RCTs [n = 1,087]; total n = 1,673) were included. AP reduced overall VAP (RR = 0.65, 95% CI: 0.48-0.90, P < 0.001; I² = 75.9%) and early-onset VAP (RR = 0.41, 95% CI: 0.33-0.52, P < 0.001; I² = 0%; events: 88/754 AP vs. 240/832 control). No effect on late-onset VAP (RR = 1.13, 95% CI: 0.72-1.78, P = 0.07; I² = 64.8%) or ICU mortality (RR = 0.91, 95% CI: 0.76-1.08, P = 0.27; I² = 0%). Secondaries: Reduced ICU LOS (MD = - 2.05 days, 95% CI: - 3.73 to - 0.37, P = 0.01; I² = 46%) and hospital LOS (MD = - 5.02 days, 95% CI: - 9.20 to - 0.85, P = 0.02; I² = 70.8%); no difference in ventilation duration (MD = - 1.36 days, 95% CI: - 2.91 to 0.19, P = 0.09) or time to VAP (MD = 1.04 days, 95% CI: - 0.87 to 2.95, P = 0.29). RCTs showed low-moderate bias; non-RCTs moderate-serious (confounding).

Conclusion: Short-course AP reduces early/overall VAP and LOS in ABI without impacting late VAP or mortality, supporting targeted use in high-risk cases (e.g., GCS < 8) per stewardship principles. However, heterogeneity, resistance gaps, and guideline caution warrant larger RCTs with non-ABI comparatives to mitigate selection bias and confirm specificity.

Background: Hypervirulent Klebsiella pneumoniae (HvKp) causes severe invasive infections, but the lack of a standardized definition complicates surveillance. The emergence of carbapenem-resistant HvKp (CR-HvKp) poses a "dual-risk" threat whose impact is poorly quantified. This meta-analysis aimed to determine pooled proportions of severe outcomes stratified by diagnostic criteria and quantify the mortality risk associated with CR-HvKp.

Methods: Following PRISMA guidelines, we systematically searched five databases for studies published up to July 2025 reporting clinical outcomes of HvKp infection. A random-effects model was used to calculate pooled proportions of liver abscess, metastatic spread, septic shock, microbiological failure and mortality, with subgroup analyses by HvKp definition (phenotypic, molecular, combined, or clinical). Odds ratios (OR) for mortality in CR-HvKp versus carbapenem-susceptible (CS)-HvKp were pooled.

Results: From 4413 records, 79 studies involving 4240 patients were included. The pooled proportion of liver abscess was 24% (95% CI 17-32%) and metastatic spread was 22% (95% CI 12-32%), both significantly influenced by the diagnostic criteria used (p < 0.0001). Pooled mortality for HvKp was 21% (95% CI 15-27%). In stark contrast, pooled mortality for CR-HvKp was 57% (95% CI 35-78%). The frequency of microbiological failure among HvKp infected patients was reported to be 39%. A meta-analysis of six studies revealed CR-HvKp infection was associated with over 12-fold higher odds of death compared to CS-HvKp infection.

Conclusion: HvKp continues to cause severe invasive infections, though outcome estimates vary due to inconsistent definitions. Mortality increases markedly when carbapenem resistance co-exists with virulence, indicating that poor outcomes are driven by both pathogenic and resistance mechanisms. Standardized diagnostic criteria and expanded genomic surveillance are essential to improve epidemiological comparability and guide early detection and containment of high-risk HvKp strains.

Background: Nosocomial pneumonia (NP), including hospital-acquired (HAP) and ventilator-associated pneumonia (VAP), remains a leading cause of morbidity, mortality, and antimicrobial resistance worldwide. Data from Eastern Europe and the Caucasus are scarce, limiting region-specific infection control strategies.

Methods: We conducted a prospective multicenter surveillance study across five tertiary hospitals in Georgia from May 2020 to December 2023. A total of 484 respiratory specimens were obtained from 397 adult patients with microbiologically confirmed NP. Pathogen identification was performed using culture and MALDI-TOF MS, with antimicrobial susceptibility testing according to CLSI guidelines. PCR assays detected major resistance genes. Epidemiological, molecular, and clinical outcomes were evaluated, including temporal trends and comparisons between ICU and non-ICU patients.

Results: Gram-negative bacteria predominated (71.7%), with Pseudomonas aeruginosa (41.9%) as the leading pathogen, followed by Staphylococcus aureus (21.3%), Acinetobacter baumannii (13.4%), Klebsiella pneumoniae (13.0%), and Streptococcus pneumoniae (9.3%). Multidrug resistance (MDR) was identified in 80% of isolates, extensively drug-resistant (XDR) phenotypes in 18.4%, and pandrug-resistant (PDR) phenotypes in 1.4%. ESBL prevalence increased from 48.3% in 2020 to 79.8% in 2023 (p < 0.001), carbapenemase expression doubled from 15.0% to 30.2% (p < 0.01), and colistin resistance rose from 2.5% to 8.5% (p < 0.05). ICU isolates showed significantly higher MDR and XDR rates than those from non-ICU settings (p < 0.001). Thirty-day mortality correlated with resistance phenotype, ranging from 18.2% in susceptible infections to 71.4% in PDR cases.

Conclusions: This four-year study shows high and increasing antimicrobial resistance among NP pathogens in Georgia, especially in ICU settings. The rise in ESBL, carbapenemase, and colistin resistance highlights the need to strengthen antimicrobial stewardship, infection prevention, and genomic surveillance to control the spread of high-risk strains and improve patient outcomes in resource-limited settings.

Typhoid fever, a systemic disease caused by Salmonella enterica serovar Typhi (S. Typhi), remains a major global health problem, particularly in regions with poor sanitation. Despite advancements in diagnostics and treatment, S. Typhi continues to impose a heavy disease burden, worsened by the emergence of multidrug-resistant (MDR) strains. Chronic carriers, accounting for 2-5% of infections, play a crucial role in disease transmission. These carriers are often asymptomatic but intermittently shed bacteria, sustaining S. Typhi within the human population. Gallstones are strongly associated with the chronic carrier state, providing a niche for bacterial biofilm formation that enhances persistence and antibiotic resistance. Furthermore, long-term colonisation of the gallbladder is linked to an increased risk of gallbladder cancer, a condition common in typhoid-endemic areas. The pathogenesis of typhoid fever involves bacterial invasion of the gastrointestinal mucosa, evasion of innate immunity, and systemic spread. Biofilm formation on gallstones promotes long-term persistence within the gallbladder, while immune responses and intestinal microbiota dynamics influence disease progression and bacterial shedding. Current diagnostic methods, including culture and serology, often fall short in identifying carriers, necessitating the development of innovative approaches for effective surveillance and control. Treating chronic carriers remains difficult due to the biofilm-associated resistance of S. Typhi. Although cholecystectomy combined with targeted antimicrobial therapy shows promise, it does not guarantee the elimination of the carrier state. This review emphasises the importance of integrating strategies that combine improved diagnostic tools, targeted therapies, and public health interventions to reduce the burden of typhoid fever and its chronic carriers.

Purpose: This study aimed to analyse COVID-19-related mortality during the pandemic, stratified by groups at risk of severe COVID-19.

Methods: Patients with COVID-19 between March 2020 and February 2023 were enrolled using the international multicentric Lean European Open Survey on SARS-CoV-2-Infected Patients (LEOSS). The COVID-19 in-hospital mortality was calculated using a multivariable logistic regression model adjusted for age and sex.

Results: A total of 11,765 patients were included, with an overall mortality rate of 13.1% (N = 1541). Mortality decreased from 14.4% during the wildtype (wt) period to 10.6%, 9.5%, and 6.3% in the alpha (α), delta (δ), and omicron (Ω) periods, respectively. Patients aged 66-75, 76-85, and > 85 years had 11.4-, 19.3-, and 34.7-fold higher mortality odds than patients aged 26-35 years (p < 0.001 in all comparisons). This increase in mortality between younger and older patients decreased with the shift from wt (increase of 39.4%) to Ω (15.5%). The overall adjusted mortality rate in males (18.4%) was higher than in females (10.6%); however, this sex-specific difference levelled off with the shift from wt (m: 18.9%, f: 10.1%) to Ω (m: 5.9%, f: 5.3%). Referring to comorbidities, adjusted mortality increased significantly with the number of comorbidities in patients during the wt but remained stable in patients with Ω-period. Among severely immunosuppressed patients, mortality declined markedly throughout the pandemic (wt vs. Ω: p < 0.001).

Conclusion: Overall mortality decreased during the pandemic, even among severely immunosuppressed patients. Age, sex, and the number of comorbidities were key mortality risk factors, although their impact lessened as the pandemic progressed.

Purpose: Diphtheria is a re-emerging vaccine-preventable disease, mainly caused by toxigenic Corynebacterium diphtheriae.

Methods: Here, we report a fatal respiratory diphtheria infection in a Polish woman travelling to Germany possibly linked to a cutaneous diphtheria infection in a homeless man living in the same geographic area. Laboratory diagnostics involving MALDI-TOF MS, tox-gene PCR, Lateral Flow Immuno Assay, a modified Elek test and Next Generation Sequencing (NGS) identified the causative strain as cotrimoxazole-resistant toxigenic Corynebacterium diphtheriae biotype mitis, sequence type ST574. Moreover, a review on the diphtheria situation in Poland is presented.

Results: NGS data suggest a common source of infection in Poland and a possible link to the Europe-wide outbreak of imported diphtheria with C. diphtheriae since 2022. This is the first diphtheria case in Poland since 2000.

Purpose: Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. It is a major cause of morbidity and mortality. A contemporary overview of sepsis epidemiology in England is long overdue. This study provides an update on the incidence of sepsis-coded hospital admissions and mortality following the COVID-19 pandemic, focusing on the relative contribution of different bacterial pathogens to sepsis-coded admissions.

Methods: We undertook a descriptive study of all hospital admissions from April 1998 to March 2024 using routinely collected health data. Information on sepsis admission episodes, causative pathogens, age, sex, length-of-stay and mortality were collected.

Results: Sepsis-coded hospital admissions increased from 27.9 admissions per 100,000 in 1998 to 210.4 in 2023, a 7.5-fold increase. The incidence of sepsis-coded admissions due to most pre-specified pathogens of interest increased. The largest increases were seen for sepsis due to Enterococci, Streptococcus pyogenes, gram-negative bacteria, Streptococcus agalactiae, Staphylococcus aureus and Listeria spp. Sepsis due to meningococcus decreased. The percentage of patients aged ≥ 75 years admitted with sepsis increased from 32.4 to 52.5% of sepsis cases. Median length-of-stay was 6.1 days. Sepsis-coded admissions and mortality decreased during the COVID-19 pandemic. These have now returned to pre-pandemic levels.

Conclusion: The recorded incidence of sepsis-coded hospital admissions has risen. This may have been impacted by coding changes and improved disease recognition. The decrease in meningococcal sepsis may reflect the success of vaccination campaigns. Further research is needed to explore concurrent trends in sepsis severity, predict who is at greatest risk and improve prevention efforts.