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Background and Aim: Selection and dissemination of plasmid-encoded extended-spectrum β-lactamase (ESBL) among Enterobacteriaceae confers resistance to beta-lactam antibiotics. The purpose of this study was to determine the prevalence and molecular characteristics of ESBL-producing organisms isolated from dairy cattle with a uterine infection. Materials and Methods: Bacterial isolates (n=62) were characterized by biochemical test for genus and species determination. Antimicrobial susceptibility tests were performed by Kirby–Bauer disk diffusion method using panel of antibiotics for initial screening of ESBL organism. Phenotypic confirmation of ESBL-suspected strains was done by combination disk method and double-disk method. Multiplex polymerase chain reaction (PCR) was carried out for phylogrouping of Escherichia coli isolates as well as for genotyping ESBL genes. Enterobacterial repetitive intergenic consensus-PCR method was used for genotypic characterization of isolates. Results: Antibiotic susceptibility profile of E. coli (n=40) isolates showed high rates of resistance for ampicillin (95.0%), cefpodoxime (97.5%), cefotaxime (87.5%), and ceftriaxone (70%). However, low rates of resistance were observed for cefoxitin (25%), amoxicillin/clavulanic acid (20%), ceftazidime (17.5%), gentamicin (10%), and ertapenem (7.5%). A total of 39/40 E. coli isolates were confirmed as ESBL with Epsilometer test as well as the genotypic method and 28 (70%) of them were multidrug-resistant. Genotype blaCTX-M was observed as a predominant beta-lactamase type with the preponderance of CTX-M Group 1. The following combinations were observed: blaTEM + blaCTX-M in 15 (36.2%) isolates, blaTEM / blaSHV in 8 (5.2%) isolates, and blaCTX-M / blaSHV in 6 (5.2%) isolates. The phylogenetic grouping of E. coli strains revealed the highest prevalence for B1 (22.0%) followed by A (20%). Conclusion: This report shows a high frequency of ESBL E. coli from cattle with postpartum uterine infections. These isolates showed reduced susceptibility to common antibiotics used for the treatment of uterine infections greater affecting the therapeutic outcome.

Inhibition of Notch signaling in macrophages is known to reduce inflammation, however, its role in regulating vascular hyporeactivity in sepsis is unknown. Thus we aimed to evaluate the effect of sepsis on vascular Notch signaling. Polymicrobial sepsis was induced by caecal ligation and puncture (CLP) in mice. mRNA expressions of Notch receptors (Notch1,3) and ligands (Jag1, Dll4), and downstream effector genes (Hey1, MLCK, MYPT1) were assessed by RT-qPCR. Protein level of activated Notch (NICD) was assessed by Western blot and immuno-histochemistry. Isometric tension in isolated aortic rings was measured by wire myography.CLP down-regulated aortic expression of Notch3, Jag1 and Dll4 as compared to control mice. Additionally, the protein level of NICD was found to be lesser in aortic tissue sections from CLP mice. Expression of Hey1 and MLCK were attenuated whereas MYPT1 expression was increased in septic mouse aorta. DAPT pretreatment did not improve CLP-induced vascular hyporeactivity to NA, CaCl2 and high K+ (80 mM), rather significantly attenuated the aortic response to these vasoconstrictors in control mice. Treatment with 1400 W reversed attenuated Notch3 (but not Jag1 and MLCK) expression in septic mouse aorta. In conclusion, sepsis significantly attenuated the Notch (especially Notch3) signaling in mouse aorta along with reduction in contractile gene expression and vasoconstriction response. Further, iNOS/NO pathway was involved in sepsis-induced down-regulation of Notch3 receptor. Thus systemic inhibition of Notch signaling during sepsis may have serious impact on sepsis-induced vascular hyporeactivity.

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