Biofilms are structured microbial communities that adhere to biotic and abiotic surfaces embedded in an autonomous extracellular matrix. These structures contribute to persistent infections, especially in patients with indwelling medical devices, due to their resistance to antimicrobial agents; they have evolved to evade host immune responses. Despite advances in antimicrobial therapies, biofilm-associated infections remain a major challenge in clinical infectious diseases. This perspective explores the underlying mechanisms of biofilm resilience and immune evasion, emphasizing the limitations of conventional treatments and the need to develop pre-emptive measures that focus on preventing biofilm formation rather than implementing a treatment. This work discusses emerging strategies, such as quorum-sensing inhibition, hormonal modulation, matrix-degrading enzymes, anti-adhesive surface modifications, and nanotechnology-based drug delivery, that offer promising avenues to disrupt biofilm formation and maturation. Also offers a shift from the paradigm, looking into proactive prevention rather than treatment, emphasizing clinical translation, scalability, and biocompatibility. Embedding these strategies into routine care could significantly reduce healthcare-associated infections, improve patient outcomes, and mitigate the development of antimicrobial resistance. Our analysis highlights biofilm prevention as a critical frontier in the future of infectious disease management.

Contamination of seafood products with multi-drug-resistant (MDR) bacteria is considered to be a potential source for the spread of MDR bacteria in communities. However, little is known about the extent of the contamination of seafood, in particular shrimp, with MDR bacteria in Saudi Arabia. In this study, imported frozen shrimp in retail markets were examined for the antimicrobial susceptibility patterns of Escherichia coli. Escherichia coli was isolated from 40 frozen shrimp samples; a total of 25 and 15 shrimp samples were imported from China and Vietnam, respectively. Of the 40 examined frozen shrimp samples, 30 tested positive for E. coli, resulting in an overall isolation rate of 75%, with a total of 180 isolates being identified. The largest number of positive samples for E. coli isolates (n = 140) were found in 22 out of 25 samples from frozen shrimp imported from China. Additionally, eight out of 15 samples from frozen shrimp imported from Vietnam were positive for E. coli, leading to the recovery of 40 isolates. Overall, the susceptibilities among E. coli isolates were observed against 99.4% for amikacin, augmentin and kanamycin, 95% for cefoxitin and 92.7% for ceftazidime and nitrofurantoin. High percentage of the isolates exhibited resistance to cephalothin (174/180, 96.6%), ampicillin (167/180, 92.7%), Cephalexin (163/180. 90.5%), piperacillin (156/180, 86.6%), ceftriaxone (123/180, 68.3%), nalidixic acid (95/180, 52.7%), trimethoprim sulphamethoxazole (90/180, 50%), and tetracycline (88/180, 48.8%). Additionally, the MDR (resistant to ≥3 different class of antimicrobials) rate among E. coli isolates was 94.4% (170/180). A relatively high intermediate resistance of 60% (108/180) was exhibited for aztreonam. Notably, E. coli showed 71 different antibiotic resistance patterns with the multiple antibiotic resistant (MAR) index ranging from 0.04 to 0.66 and 89.4% of E. coli isolates recorded very significant MAR indexes above the range of 0.2. In this study, we recorded highest antimicrobial co-resistance patterns of 162 (90%) isolates between cephalothin and ampicillin, followed by 158 (87.7%) isolates between cephalothin and cephalexin. Furthermore, and interestingly, the segregation of antimicrobial resistance patterns based on the source of country origin of frozen shrimp revealed few inter-country resistant patterns found interconnecting and this influenced 44 (24.4%) isolates overlapping between isolates origin from frozen shrimp imported from China and Vietnam. This study documents the antimicrobial resistance in E. coli isolated from imported frozen shrimp and the presence of MDR E. coli in shrimp consuming communities, which may pose a risk to public health and the transfer of resistant bacteria to the food chain and environment.

Background: Urinary tract infection (UTI) caused by V. cholerae is rare and less common. V. cholerae is a Gram-negative bacterium motile using single polar flagellum and, originally, is a waterborne microbe found in aquatic and estuarine environments. Toxigenic V. cholerae is well-known as a causative agent of acute and excessive watery diarrhea after ingesting food and water contaminated with this bacterium. Case Presentation: A 27-year-old male patient presented to the emergency department on 17th July 2021 with burning micturition, normal vital signs, and no fever, vomiting, or diarrhea. In 2017, the patient complained of short stature and vitamin D deficiency. He was on human growth hormone from January 2018 till October 2019. The diagnosis was V. cholerae Non-O1/non-O139 urinary tract infection (UTI). Considering a urinary tract infection, empirical treatment with Lornoxicam and Ciprofloxacin was initiated, while the result of urine culture was still pending. The patient was discharged on the same day and without any complications. Conclusion: V. cholerae non-O1/non-O139 is primarily a marine inhabitant and is associated with sporadic cases resulting in cholera-like diarrhea after consumption of contaminated seafood and exposure to seawater. Extraintestinal infection associated with this bacterium should no longer be ignored as this change in the behavior of cholera bacteria mechanism of pathogenicity might be related to some associated virulence genes.

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.

Colorectal cancer (CRC) is a major cause of cancer-related morbidity and mortality worldwide, and dysregulation of phosphoinositides signaling pathways plays a critical role in its pathogenesis. The involvement of Set Binding Factor 1 (SBF1; MTMR5), a pseudophosphatase of the myotubularin family in CRC, remains unexplored. This study compiled experimental and bioinformatics approaches to investigate the expression and potential relevance of SBF1 in CRC. Immunohistochemical analysis was performed on CRC tissue specimens and corresponding normal adjacent tissues (NAT), with estimation of SBF1 staining followed by statistical comparison. In parallel, bioinformatics assessed gene ontology and protein-protein interactions, and open CRC datasets were analyzed to assess SBF1 alterations, expression profiles, and survival associations. The results demonstrated a significant overexpression of SBF1 in CRC tissues compared with NAT. Bioinformatics revealed SBF1 as a partner within a functional network enriched in phosphoinositide metabolism. Bioinformatics identified SBF1 genetic alterations in approximately 5% of cases, and survival analysis indicated that wild-type SBF1 could be an unfavorable prognostic marker, as reflected by hazard assessment. Collectively, these findings provided the first experimental evidence that SBF1 is overexpressed in CRC and suggest that it may represent an unrecognized component of phosphoinositide related pathways involved in colorectal tumorigenesis.