Cefoxitin Sodium

The multidrug-resistant clone identified as Escherichia coli sequence type 131 (E. coli ST131) has spread worldwide. The current study is one of the first comprehensive investigations to ascertain the prevalence of ST131 and molecularly characterize the ST131-O25b and ST131-O16 subgroups causing bloodstream infections in Iran.

To this end, 119 consecutive, non-repetitive E. coli clinical strains were isolated from blood samples of patients with septicemia in different hospital wards for one year in Tehran. The isolates were provided by the laboratories of tertiary hospitals affiliated with Tehran University of Medical Sciences. The disk diffusion method was used to investigate the sensitivity of bacteria to antibiotics. All phylogroup B2 isolates were screened for E. coli ST131 status using a triplex PCR assay that combines the identification of ST131-O25b and -O16 clades. The seven putative virulence factor genes (kpmstII, fimH, afa A, iroN, Sat, ibeA, and ompT) and resistance genes (bla_CTX-M-15, bla_OXA-48, and bla_CMY) were detected by PCR in E. coli ST131 isolates.

The highest incidence of antibiotic resistance among 74/119 (62.18%) extended-spectrum β-lactamases-producing E. coli isolates was observed, respectively, against Nalidixic acid (82%), and Aztreonam (75%), followed by Ciprofloxacin (70%). Twenty out of 74 ESBL-producing E. coli isolates were found to be ST131 (27%), with 13 (65%) ST131-O25b and 7 (35%) ST131-O16 clades, respectively. The ST131-O16 isolates had a higher prevalence of resistance to Ceftriaxone, Amikacin, Aztreonam, and Cefepime than the -O25b ones. Concerning virulence capacity, our findings demonstrated that kpmstII, fimH, and ompT genes were found in 85%, 65%, and 30% of ST131 isolates, respectively. Our results reinforce the surveillance of E. coli ST131 clone dissemination as a major drug-resistant pathogen and an important new public health threat in Iran. Accumulation of multiple virulence factors, ESBL carriage, and identified antimicrobial resistance patterns of ST131-O25b and ST131-O16 clones indicate a necessity to develop strategies to control the spread of these isolates in both community and hospital settings.

The zoonotic pathogen S. Infantis is of emerging importance, making detection in poultry critical. Phenotypic changes, which are significant for standardized control programs via EN/ISO 6579-1:2017, could lead to pathogens remaining undetected, increasing the risk of food-borne outbreaks. This study investigates an S. Infantis strain with both normal growth (NCP) and atypical H₂S-negative colony variant (ACV) from an Austrian broiler farm. NCP and ACV underwent comprehensive analyses, including stability tests, electron microscopy, whole-genome sequencing, transcriptomics, and proteomics. Our findings demonstrate a stable atypical colony variant exhibiting acquired resistance against cefoxitin in ACV. Genomic analysis identified 9 single nucleotide polymorphisms (SNPs) and two deletions, affecting genes involved in porphyrin and sulfur metabolism. Key factors were a mutation disrupting cysG, which is essential for siroheme biosynthesis and a vital cofactor in sulfur metabolism, and a stop codon in menD (2-oxoglutarate decarboxylase), crucial for small colony variant appearance. Consequently, we hypothesize that these mutations lead to a deficiency in siroheme, as well as anaerobic sulfur respiration altogether resulting in the H₂S-negative phenotype. Functional network analysis highlighted compensatory upregulation of alternative metabolic pathways, including nitrate metabolism, propanoate metabolism and mixed-acid fermentation, which may aid ACV's persistence and adaptation under anaerobic conditions. Reduced flagellin expression suggests a mechanism for immune evasion. These genetic and metabolic adaptations likely respond to environmental stressors, such as oxidative stress from disinfectants or antimicrobial pressure, leading to the emergence of the H₂S-negative phenotype. Consequently, this study provides insights into the genetic and biochemical adaptations of an atypical S. Infantis variant.