The COVID-19 pandemic has led to significant changes in healthcare practices, including increased antibiotic usage. This study aimed to investigate the impact of the pandemic on the prevalence of extended-spectrum β-lactamase (ESBL) production and carbapenem resistance among key bacterial species causing urinary tract infections (UTIs). Conducted at King Fahad Medical City in Riyadh from January 2018 to December 2022, the study analyzed urine samples from 9697 UTI patients. Patients were categorized into ‘pre-COVID-19’ and ‘during COVID-19’ groups. Bacterial isolates were identified, and antimicrobial susceptibility testing was performed following guidelines. ESBL production was detected using the Double-Disc Synergy Test. Escherichia coli and Klebsiella pneumoniae were the main pathogens. During the pandemic, ESBL production decreased in E. coli by 1.9% and in K. pneumoniae by 6.0%. Carbapenem resistance also declined, with E. coli displaying a 1.2% reduction and K. pneumoniae and Pseudomonas aeruginosa displaying 10.7% and 7.9% reductions, respectively. Notably, logistic regression analysis revealed that the odds of ESBL presence were 10% lower during the COVID-19 pandemic (OR 0.91; 95% CI 0.83–0.99; p = 0.040), and there was a significant reduction in the odds of carbapenem resistance (OR 0.43; 95% CI 0.37–0.51; p < 0.001). This study reveals a significant decrease in ESBL production and carbapenem resistance among UTI pathogens during the COVID-19 pandemic, hinting at the impact of modified antibiotic and healthcare approaches. It emphasizes the need for persistent antimicrobial resistance surveillance and policy adaptation to address resistance challenges, offering key directions for future public health actions.

Background: One of the most prevalent bacterial infections in children is urinary tract infection (UTI), which has become a major concern with increasing resistance of the pathogens to the routinely used antimicrobial agents. The aim of the study is to determine the antimicrobial susceptibility patterns of pediatric UTI-causing pathogens, including ESBL-producing bacteria, in Saudi Arabia. Methods: This cross-sectional retrospective study was conducted to ascertain the frequency of isolation and the antimicrobial resistance pattern of uropathogens among children aged 0–15 years. The data from the urine cultures was collected during 2019–2020 at the King Fahad Medical City, a major tertiary hospital in Riyadh, Saudi Arabia. A total of 1022 urine samples from patients diagnosed with urinary tract infections (UTIs) were collected for this study. Microbial species present in the samples were cultured and identified using standard biochemical techniques. To assess the resistance of these strains to antimicrobial drugs, an in vitro method was employed, and the criteria set by the Clinical Laboratory Standard Institute (CLSI) were followed. In addition, a double-disc synergy test was conducted to identify strains of E. coli that produce extended-spectrum beta-lactamase (ESBL). Results: The predominant pathogens were E. coli (58.6%), followed by Klebsiella sp. (23.9%). E. coli isolates were more sensitive to meropenem and ertapenem in 99.2% of cases, followed by amikacin (99%). Klebsiella sp. were sensitive to amikacin in 97.1% of cases, followed by meropenem and ertapenem (92.2% in both). The highest sensitivities of antimicrobials toward ESBL were for meropenem and ertapenem (100% in both), followed by amikacin (99%). Conclusions: Our study recommends using local antibiotic sensitivity data for empirical UTI treatment. Amikacin, ertapenem, and meropenem are effective intravenous options. Cephalosporin, cefuroxime, amoxicillin/clavulanic acid, and nitrofurantoin are suitable oral choices. No significant changes in antimicrobial susceptibility were observed during the COVID-19 pandemic. Further research is needed to assess potential pandemic-related alterations.

Background: Whole-genome sequencing is one of the best ways to investigate resistance mechanisms of clinical isolates as well as to detect and identify circulating multi-drug-resistant (MDR) clones or sub-clones in a given hospital setting. Methods: Here, we sequenced 37 isolates of Acinetobacter baumannii, 10 Klebsiella pneumoniae, and 5 Pseudomonas aeruginosa collected from the biobank of the hospital setting of the King Fahad Medical City. Complete phenotypic analyses were performed, including MALDI-TOF identification and antibiotic susceptibility testing. After the genome assembly of raw data, exhaustive genomic analysis was conducted including full resistome determination, genomic SNP (gSNP) analysis, and comparative genomics. Results: Almost all isolates were highly resistant to all tested antibiotics, including carbapenems and colistin. Resistome analysis revealed many antibiotic resistance genes, including those with resistance to β-lactams, aminoglycosides, macrolides, tetracyclines, sulfamids, quinolones, and phenicols. In A. baumannii isolates, the endemic carbapenemase bla_OXA-23 gene was detected in 36 of the 37 isolates. Non-synonymous mutations in pmrB were detected in almost all of the isolates and likely mediated colistin resistance. Interestingly, while classical analyses, such as MLST, revealed the predominance of an ST2 clone in A. baumannii isolates, the genomic analysis revealed the presence of five circulating sub-clones and identified several isolate transmissions between patients. In the 10 K. pneumoniae isolates, several resistance genes were identified, and the observed carbapenem resistance was likely mediated by overexpression of the detected extended-spectrum-β-lactamase (ESBL) genes associated with low membrane permeability as few carbapenemase genes were detected with just bla_OXA-48 in three isolates. Colistin resistance was mediated either by non-synonymous mutations in the MgrB regulator, PmrA, PmrB, and PhoQ proteins or the presence of the MCR-1 protein. Here, gSNP analysis also revealed the existence of bacterial clones and cases of isolate transmissions between patients. The five analyzed P. aeruginosa isolates were highly resistant to all tested antibiotics, including carbapenems mediated by loss or truncated OprD porin, and colistin resistance was associated with mutations in the genes encoding the PmrA, PmrB, or PhoQ proteins. Conclusion: We demonstrate here the usefulness of whole-genome sequencing to exhaustively investigate the dissemination of MDR isolates at the sub-clone level. Thus, we suggest implementing such an approach to monitor the emergence and spread of new clones or sub-clones, which classical molecular analyses cannot detect. Moreover, we recommend increasing the surveillance of the endemic and problematic colistin resistance mcr-1 gene to avoid extensive dissemination.