The objective was to examine the pooled effects of antibiotic–probiotic combinations by examining the cure rate and recurrence rate for bacterial vaginosis (BV). A systematic literature search was conducted from electronic databases. All parallel randomized controlled trials (RCTs) that focused on the effects of antibiotics combined with intravaginal probiotics were included. Cure rate and recurrence rate were the primary and secondary outcomes to be analyzed. Meta-analysis was conducted following the Cochrane handbook for Systematic Reviews of Interventions. As a result, of 923 studies identified, 11 articles involving 1,493 BV patients met the inclusion criteria and nine were available for meta-analysis. A meta-analysis of two studies evaluated the recurrence rate 12–16 weeks after treatment. Results showed a statistically significant difference favoring the antibiotics plus probiotics group vs the antibiotics plus placebo group (relative risk 0.62, 95% confidence interval [CI]: 0.45–0.85). The narrative review in one study indicated that the cure rate was higher in the antibiotics plus probiotics group, giving a significant HR ratio of 0.73 (95% CI 0.54–0.98) (p = 0.042). In conclusion, vaginal application of Lactobacillus in combination with antibiotics for the treatment of BV could be a promising method for both reducing the recurrence rate and relieving symptoms of BV.

Background. Quinolones are commonly used for reducing the duration of diarrhea, infection severity, and limiting further transmission of disease related to Vibrio cholerae, but V. cholerae susceptibility to quinolone decreases over time. In addition to mutations in the quinolone-resistance determining regions (QRDRs), the presence of qnr and other acquired genes also contributes to quinolone resistance. Results. We determined the prevalence of quinolone resistance related genes among V. cholerae O139 strains isolated in China. We determined that eight strains carried qnrVC, which encodes a pentapeptide repeat protein of the Qnr subfamily, the members of which protect topoisomerases from quinolone action. Four qnrVC alleles were detected: qnrVC1, qnrVC5, qnrVC12, and qnrVC9. However, the strains carrying qnrVC1, qnrVC5, and qnrVC12 were ciprofloxacin (CIP)-sensitive. Contrastingly, the strain carrying qnrVC9 demonstrated high CIP resistance. qnrVC9 was carried by a small plasmid, which was conjugative and contributed to the high CIP resistance to the receptor V. cholerae strain. The same plasmid was also detected in V. vulnificus. The qnrVC1, qnrVC5, and qnrVC12 were cloned into expression plasmids and conferred CIP resistance on the host V. cholerae O139 strain. Conclusions. Our results revealed the contribution of quinolone resistance mediated by the qnrVC9 carried on the small plasmid and its active horizontal transfer among Vibrio species. The results also suggested the different effects of qnrVC alleles in different V. cholerae strains, which is possibly due to differences in sequences of qnrVC alleles and even the genetic characteristics of the host strains.

The management of carbapenem-resistant Acinetobacter baumannii (CRAB) infections remains a formidable clinical challenge. This study evaluated the in vitro antimicrobial activities of sulbactam-durlobactam (SUL-DUR) and eravacycline (ERV) against CRAB isolates and elucidated the genomic landscapes of resistance and virulence determinants in SUL-DUR-resistant strains to inform therapeutic decision-making. A total of 233 clinical CRAB isolates were collected and screened for susceptibility to SUL-DUR and ERV using the Kirby-Bauer (K-B) disk diffusion assay. Isolates exhibiting resistance to SUL-DUR were further characterized via metagenomic next-generation sequencing (mNGS) to identify key resistance and virulence factors. SUL-DUR and ERV demonstrated robust in vitro activity, with susceptibility rates of 92.3% and 91.4%, respectively. Notably, no isolates exhibited concurrent non-susceptibility to both agents. Genomic analysis of 14 SUL-DUR-resistant strains revealed a complex and heterogeneous distribution of genetic determinants. The presence of bla _NDM-1 was identified as a critical driver of SUL-DUR resistance. Additionally, reduced susceptibility was potentially associated with specific mutations in bla _OXA-23 , bla _OXA-66 , and bla _TEM-1 , while hyperactive efflux systems and altered membrane permeability further synergized to enhance the resistance phenotype. Despite the extensive-drug-resistant (XDR) nature of current CRAB isolates, they maintain high sensitivity to SUL-DUR and ERV. Our findings underscore that SUL-DUR and ERV represent highly promising therapeutic options with significant development potential and broad clinical application prospects for the management of CRAB-related infections.