Clinical Microbiology and Infection最新文献

Background: Patients treated with glucagon-like peptide-1 (GLP-1) receptor agonists and sodium glucose co-transporter 2 (SGLT2) inhibitors often have underlying conditions that predispose them to infection. While these agents offer cardiometabolic benefits, concerns persist regarding their impact on infectious risk. Existing literature has not comprehensively assessed their dose-dependent influence on severe infections such as sepsis.

Objectives: To investigate the effect of GLP-1 receptor agonists and SGLT2 inhibitors on infection risk.

Data sources: PubMed, Embase, ClinicalKey, Cochrane CENTRAL, ProQuest, ScienceDirect, Web of Science, and ClinicalTrials.gov up to December 18, 2024.

Study eligibility criteria: Randomized controlled trials reporting target infection outcomes related to GLP-1 receptor agonists or SGLT2 inhibitor prescription.

Participants: Individuals without evidence of ongoing infection at study initiation.

Interventions: GLP-1 receptor agonists or SGLT2 inhibitors.

Assessment of risk of bias: Cochrane risk of bias tool version 2.0.

Methods of data synthesis: A frequentist random-effects model was used to assess the comparative incidence of infectious complications-classified as sepsis, abscess/gangrene, or other infections (e.g., pneumonia and urinary tract infection). Drop-out rates served to reflect acceptability. Sensitivity analyses included Bayesian modelling and subgroup analyses of diabetic status and treatment duration.

Results: Based on 105 randomized controlled trials with 219 283 participants, no significant association was found between GLP-1 receptor agonists or SGLT2 inhibitors and controls, except for high-dose canagliflozin (300 mg/day), which was the only intervention significantly associated with reduced sepsis risk versus control. This effect persisted in participants with diabetes. No significant associations were found between any other GLP-1 receptor agonist or SGLT2 inhibitor and risk of sepsis, abscess, gangrene, or other infections. Subgroup and meta-regression analyses confirmed robustness. Bayesian modelling yielded comparable results. Treatment duration had minimal influence on primary outcomes.

Conclusions: This analysis identifies no significant evidence of infection-related adverse events related to GLP-1 receptor agonist or SGLT2 inhibitor prescription.

Objectives: Nearly a million people have received the recombinant vesicular stomatitis virus-based vaccine expressing the surface glycoprotein of Ebola virus (rVSVΔG-ZEBOV-GP), whose immune durability is unknown. We evaluated the safety and immunogenicity of the DNA vaccine candidate INO-4201 in volunteers primed with the rVSVΔG-ZEBOV-GP vaccine.

Methods: This investigator-initiated phase Ib double-blind, placebo-controlled, single-centre trial randomly assigned healthy adults (≥18 years) primed with rVSVΔG-ZEBOV-GP to intradermal INO-4201 (1 mg) or placebo (4:1), both followed with electroporation. The coprimary outcome was incidence of adverse events at 14 days and geometric mean EBOV-GP-binding antibody titres (GMT) at 28 days (clinicaltrials.gov NCT04906629).

Results: Forty-six participants were enrolled. Median age was 52 years (interquartile range 44-57); 26 (57%) were male. Thirty-six participants received INO-4201 and 10 participants received placebo. No serious adverse events occurred. There was little reactogenicity. At 14 days, 20 of 36 (56%) vaccinees versus 5 of 10 (50%) placebo recipients (relative risk 1.11 [95% CI 0.56-2.20]) experienced adverse events. Peak T-cell responses were significantly increased in INO-4201 recipients (median percentage of CD4 cells producing interferon-gamma at postboost peak versus day 0: 0.09 [range 0.00-14.48] versus 0.00 [0.00-1.33], p 0.004). Filovirus Animal Non-Clinical Group-based EBOV-GP-binding titres were significantly higher after boosting for vaccinees at all time points (GMT at 4 weeks versus day 0: 3221.7 [95% CI 2629.8-3946.8] vs 704.3 [513.8-965.3]). Neutralizing antibody titres were also significantly higher after boosting for vaccinees at all time points measured (GMT at 4 weeks versus day 0: 21.3 [95% CI 13.8-32.7] versus 2.4 [1.5-3.9]).

Conclusions: In adults primed with rVSVΔG-ZEBOV-GP, INO-4201 demonstrated favourable safety and significant immunogenicity.

Background: Colonisation of the gastrointestinal tract by multidrug-resistant organisms (MDROs) is a precursor to endogenous infection and onward transmission. The gut microbiome provides colonisation resistance (CR) - the ability to prevent or limit the establishment of pathogens, including MDROs - through nutrient and niche competition, production of inhibitory metabolites, and immune modulation. However, its integrity is threatened by antibiotics, adverse diet, and healthcare exposures.

Objectives: To describe mechanistic, epidemiological, and interventional evidence on the role of the gut microbiome in MDRO colonisation and infection, and to highlight implications for clinical practice, policy, and research.

Sources: PubMed/MEDLINE, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov were searched from 1 January 2000 to 30 September 2025, supplemented by hand-searching of key international guidelines (EUCIC/ESCMID, WHO, CDC/ECDC, NICE/UKHSA) and reference lists.

Content: CR is shaped by microbial and host factors, including metabolic interactions, immune responses, and environmental exposures. Antimicrobials, non-antimicrobial drugs, diet, travel, and healthcare contact can disrupt the microbiota, predisposing to MDRO acquisition and infection. Observational data link gut microbial composition to risk of colonisation and infection outcomes, but predictive models are imperfect. Interventions to preserve or restore CR - such as diet-based strategies, probiotics, and faecal microbiota transplant - show promise but require robust and repeated, context-specific evaluation.

Implications: Protecting the microbiome must be a clinical and policy priority. Short-course, microbiome-sparing antimicrobial regimens, microbiome-aware diagnostics, and public health measures that support microbiome resilience could reduce MDRO burden and infections. Rigorous trials of microbiota-based therapies and integration of microbiome stewardship into antimicrobial resistance strategies are essential for translating mechanistic insights into patient benefit.

Objectives: The implementation of the European in vitro medical devices regulation (IVDR) poses significant challenges, yet its impact has not previously been quantified in clinical microbiology. The aim of this study was to quantify the number of tests in a large clinical microbiology laboratory that may be affected by IVDR.

Methods: The study was performed in a clinical microbiology laboratory of a large academic hospital in the Netherlands. We calculated proportion of CE-marked tests and laboratory-developed tests (LDTs), and we calculated the number of test results generated by these tests.

Results: We found that CE-IVD-labelled tests accounted for 55% (57/104) of the available tests in bacteriology but represented 82.8% (99 521/120 254) of all test results generated in this specialty. Among tests in mycology, 38% (6/16) were LDTs. Most LDTs were PCR assays targeting specific microorganisms, such as Bordetella spp. and Candida auris. In contrast, only 29% (7/24) of parasitology tests had a CE-IVD label, and these accounted for 38.3% (1612/4209) of all test results in this specialty.

Conclusions: We showed the potential burden in complying with IVDR 2017/746 in a clinical microbiology laboratory and the need for LDTs in certain setting. The results of this study may initiate informed discussion on a balanced implementation of the IVDR, ensuring compliance while minimizing unnecessary burden for clinical microbiology laboratories and also manufacturers.