Biofilm-associated infections pose a significant challenge in clinical settings due to their increased resistance to antibiotics and evasion of host immune responses. These infections are responsible for a large proportion of chronic and recurrent infections, leading to prolonged hospital stays, increased healthcare costs, and elevated morbidity and mortality rates. Vancomycin, a glycopeptide antibiotic, has long been a cornerstone in the treatment of infections caused by Gram-positive bacteria, particularly methicillin-resistant Staphylococcus aureus (MRSA). In addition, vancomycin-resistant Enterococcus (VRE) represents an important group of biofilm-forming pathogens, further complicating treatment strategies. However, its efficacy against biofilms remains a subject of ongoing research and debate. The ability of vancomycin to target biofilm-embedded bacteria is often hindered by multiple resistance mechanisms, including poor antibiotic penetration, metabolic adaptation of biofilm-associated cells, and the presence of persister cells. The aim of this review is to evaluate vancomycin’s antibiofilm activity by examining its mechanism of action, pharmacokinetics, effectiveness, limitations, and potential strategies to enhance its therapeutic outcomes. Several novel approaches have been explored to augment vancomycin’s antibiofilm activity, including combination therapies, adjuvant strategies, and nanotechnology-based drug delivery systems. Understanding these factors is crucial for optimizing therapeutic strategies and overcoming the persistent challenge of biofilm-related infections. This review synthesizes current evidence and highlights areas requiring further research to enhance vancomycin’s efficacy against biofilm-associated infections.

Burkholderia pseudomallei, a gram-negative facultative intracellular bacterium, is the causative agent of melioidosis, a life-threatening infectious disease endemic to tropical and subtropical regions, particularly Southeast Asia and Northern Australia. Key risk factors such as diabetes, alcoholism, and socioeconomic challenges were identified as major contributors to disease susceptibility and treatment outcomes in melioidosis. Globally, melioidosis accounts for approximately 89,000 deaths annually and poses a significant public health concern, particularly in resource-limited settings. B. pseudomallei exhibits remarkable environmental resilience, thrives in soil and water, and is intrinsically resistant to various antibiotics. Its pathogenicity is mediated by diverse virulence factors, including type III and VI secretion systems, a protective capsule, lipopolysaccharide (LPS), and BimA-mediated actin-based motility, which facilitate intracellular survival, immune evasion, and systemic dissemination. This bacterium can cause a wide spectrum of clinical manifestations ranging from localized skin infections to severe septicemia, pneumonia, and neurological involvement. In certain cases, B. pseudomallei may persist in a latent state for years and reactivation is often triggered by immunosuppression. The treatment of melioidosis is challenging because of its intrinsic antibiotic resistance, necessitating a two-phase approach: an intensive phase with intravenous antibiotics, such as ceftazidime or meropenem, followed by a prolonged eradication phase using trimethoprim-sulfamethoxazole. However, relapse remains a concern, particularly in patients with poor adherence to the therapy. Preventive strategies, particularly in endemic regions, focus on minimizing environmental exposure through protective measures and safe water practices. Despite advancements in therapeutic approaches, there is an urgent need for novel treatment strategies, including bacteriophage therapy and vaccine development, to enhance melioidosis prevention and control. Understanding the complex pathogenic mechanisms of B. pseudomallei is essential to improve its clinical management and reduce its global burden.

Background: The rising global threat of antimicrobial resistance, particularly among multidrug-resistant pathogens like Pseudomonas aeruginosa, has prompted research into repurposing existing drugs with established safety profiles. Cisplatin, a well-known anticancer agent, has shown preliminary antimicrobial activity but its efficacy against P. aeruginosa has not been thoroughly explored. This study aims to evaluate the antimicrobial potential of cisplatin against clinical strains of P. aeruginosa by determining the minimum inhibitory concentration (MIC). Methodology: This study assessed whether cisplatin could serve as a novel therapeutic option for treating infections caused by P. aeruginosa via broth microdilution assay, especially as the pathogen shows increasing resistance to last-resort antibiotics such as meropenem, colistin, and tigecycline. Findings from this research could contribute to expanding the arsenal of treatments for resistant P. aeruginosa infections. Results: The study found that 54.9% of isolates had an MIC of 16 μg/mL, 26.8% had 32 μg/mL, 12.7% had 64 μg/mL, and 5.6% had 8 μg/mL. While cisplatin demonstrated antibacterial activity, no statistically significant difference (p = 0.089) was observed between sensitive and resistant strains. A key limitation of this study is the small number of both resistant and sensitive strains, which limits statistical power. Increasing the sample size in future studies will allow for a more robust assessment of cisplatin’s efficacy and validate the observed MIC similarities. Additionally, further studies including resistance assays, time-kill kinetics, and in vivo models are needed to explore its bactericidal potential and efficacy in combination with β-lactams. Conclusion: Although cisplatin exhibited activity against P. aeruginosa, its clinical potential remains uncertain, and further investigation is necessary to optimize its use and overcome resistance.

Non-O1, non-O139 Vibrio cholerae (NOVC) extraintestinal infections are rare, but recently, several clinical incidents have been reported worldwide. Toxigenic V. cholerae is a well-known etiological agent of cholera, responsible for acute dehydrating watery diarrhea. Outbreaks occur in an epidemic seasonal pattern, particularly in countries with poverty and poor sanitation. Strains of NOVC are usually not involved in causing the epidemic or pandemic outbreaks seen with potential strains of V. cholerae serogroup O1 and O139. However, they can still cause severe sporadic cases of intestinal as well as extraintestinal infections. In this study, we investigated a case of extraintestinal infections associated with the NOVC serogroup isolated from a deep closed wound abscess. The isolate was screened for the presence of three major virulence genes, toxR, ctxA, and tcpA. The strain tested positive for the toxR gene encoding the regulatory protein and cholera toxin (ctx) gene and tested negative for the toxin-coregulated pilus (TCP) gene, which is essential for the colonization of the human intestine, causing the severe diarrheal disease cholera. To the best of our knowledge, this is the first case of extraintestinal infection caused by toxigenic Vibrio cholerae non-O1/non-O139 in a hospitalized patient in Saudi Arabia.

Background and objectives: The vaginal microbiome plays a critical role in reproductive health through Lactobacillus-dominated communities that maintain acidic pH and suppress pathogens. Disruptive hygiene practices, such as douching and certain feminine products, may negatively affect this balance. Limited data exist on vaginal microbiome awareness and related behaviors among women in Saudi Arabia. This study aimed to assess women’s knowledge of the human and vaginal microbiome and examine associated hygiene practices. Materials and methods: A cross-sectional online survey was conducted between November 2024 and February 2025 among women aged ≥ 18 years residing in Saudi Arabia. A total of N = 1,040 participants were recruited using convenience and snowball sampling through social media platforms. The questionnaire assessed sociodemographic characteristics, microbiome knowledge, and vaginal hygiene practices. Associations were examined using multivariable linear regression, and results are reported with 95% confidence intervals (CIs). Results: Participants demonstrated moderate general microbiome knowledge but limited understanding of the vaginal microbiome. Only 20.67% correctly identified Lactobacillus as the dominant genus in a healthy vaginal ecosystem. Higher knowledge scores were observed among women with higher education and those working in healthcare. Use of internal vaginal washes was significantly associated with lower vaginal microbiome knowledge (β = − 0.30, 95% CI: − 0.58 to − 0.01, p = 0.0403). Other feminine product use showed no significant associations with knowledge levels. Conclusions: Substantial gaps exist in vaginal microbiome awareness among Saudi women, accompanied by frequent use of potentially disruptive hygiene practices. Targeted health education and culturally appropriate interventions are needed to promote microbiota-supportive behaviors and improve reproductive health outcomes.

Background/Objectives: Asthma affects millions of patients worldwide and impacts their quality of life, particularly among children. Colonisation or an imbalance within natural resident microbiota may drive inflammatory responses in asthma; antibiotic resistance genes (ARGs) have also been investigated in asthma microbiome studies. However, research on the association between airway microbiota and ARGs remains limited. Therefore, we elucidated functional-level characterisation at the level of ARGs, virulence factors, and active pathways among a paediatric asthma cohort relative to a healthy control. Methods: Overall, 29 children with asthma and 20 control subjects were enrolled, and 3 swabs (2 nasal and 1 oropharyngeal) were obtained from each participant. Genomic DNA was extracted and sent for shotgun sequencing, after which bioinformatic analysis was conducted to remove human reads and analyse the microbiota pattern in the samples. The abundance of antibiotic resistance genes was evaluated along with the distribution of virulence genetic markers. Functional investigation of the most prevalent metabolic pathways was also performed. Results: Upper airway microbiome functional capacity varied by anatomical location, with oropharyngeal communities exhibiting greater metabolic breadth than nasal communities, suggesting the sample source to be the dominant factor shaping gene content, pathway profiles, and community structure. Asthma-related functional differences were modest, and no biological pathways remained significant following false discovery rate correction. Enrichment of antimicrobial resistance genes was observed, particularly those conferring resistance to β-lactams, macrolides, and tetracyclines. Conclusions: Different anatomical niches exhibit differential activities, and further exploration in this direction could aid in the development of diagnostic and therapeutic biomarkers for asthma.