Pseudomonas aeruginosa (P. aeruginosa) is a major opportunistic pathogen associated with nosocomial infections. The intrinsic resistance of P. aeruginosa to many antibiotics and the ability of P. aeruginosa to rapidly acquire resistance make the management of infections difficult. This study aimed to evaluate the antibiotic resistance profiles and inducible beta-lactamase (ibl) synthesis in P. aeruginosa strains isolated from hospitalized patients at the Azerbaijan Medical Faculty Hospital. This study included 125 samples including 44 sputum samples from pneumonia patients, 44 urine samples from individuals with urinary tract infections, and 41 postoperative samples encompassing pus, drainage, and abscess contents derived from surgical site infections. P. aeruginosa was isolated by conventional culture methods and drug susceptibility and ibl synthesis were investigated by disc diffusion. Fisher's exact test compared the ibl synthesis of P. aeruginosa strains isolated from different infection sources. Statistical significance was accepted as 0.05 (p≤0.05). Of 26 P. aeruginosa, 19 (73.1%) were resistant to ceftazidime, 20 (76.9%) to cefepime, 20 (76.9%) to piperacillin and 23 (88.4%) to aztreonam, while 19 (73.1%) were susceptible to imipenem, 19 (73.1%) to amikacin, 23 (76.9%) to piperacillin and 23 (88.4%) to colistin. In addition, the ibl synthesis (+) P. aeruginosa strains isolated from pneumonia patients (77.8%) were marginally significantly higher than those isolated from urinary tract infections (25.0%) (p=0.057). Our results reveal high rates of antibiotic resistance among P. aeruginosa strains isolated from patients in our hospital, particularly against several key antibiotics. We recommend larger studies involving multiple centers and various sample types.

Klebsiella pneumoniae which is a causative agent of nosocomial infections, is protected from phagocytosis and the lethal effect of serum bactericidal proteins owing to its capsular polysaccharides (CPS). The important leading problem in treating infections caused by this bacterium that successfully develops antimicrobial resistance, especially via mobile genetic elements, is that it acquires beta-lactamase genes, which are responsible for the resistance against beta-lactam antibiotics. Due to the increase in studies targeting capsular polysaccharides in developing strategies for vaccination and treatment, we aimed to investigate the possible relationship of the capsular genotypes of K.pneumoniae isolates obtained from various clinical specimens with antibiotic susceptibility and beta-lactamase genes. In K.pneumoniae clinical isolates; K1, K2, K5, K20, K54 and K57, which are known as hypervirulent capsular types, were investigated by polymerase chain reaction (PCR) method. In isolates whose capsular genotypes were determined, antibiotic susceptibility was examined by Kirby-Bauer disc diffusion method. Colistin resistance was investigated by the broth microdilution method. Carbapenem resistance was confirmed with the carbapenem inactivation test. The beta-lactamase genes blaCTX-M1, blaCTX-M2, blaCTX-M9, blaCTX-M8/25, blaKPC, blaNDM-1, and blaOXA-48-like were investigated by using PCR. Of the 38 K.pneumoniae isolates whose capsular genotypes were determined, 15 (39.5%), 12 (31.6%), seven (18.4%), two (5.3%), one (2.6%) and one (2.6%) were K5-CPS, K2-CPS, K20-CPS, K1-CPS, K54-CPS and K57-CPS genotypes, respectively. blaOXA-48-like, blaNDM-1, and blaCTX-M1 were detected in 68.4, 10.5, and 7.9%, whereas coexistence of blaOXA-48-like with blaNDM-1, and blaOXA-48-like with blaCTX-M1 were determined in 7.9, and 5.3% of the isolates, respectively. The relationship of the blaCTX-M1 gene, detected only in three K20-CPS isolates, was found to be statistically significant with this genotype. In addition, of the blaNDM-1-positive four isolates, three were K5-CPS, and one was K2-CPS, while blaOXA-48-like was similarly detected mostly in K5-CPS and K2-CPS (10 and 9 isolates, respectively). Except for the two isolates that were resistant to colistin, one K1-CPS and the other K5-CPS, the highest resistance was detected against cefotaxime (36/38) and the lowest resistance was detected against gentamicin (23/38) as a result of antibiotic susceptibility tests. The resistance relationship of K5-CPS isolates with amoxicillin/clavulanate, piperacillin/tazobactam, cefoxitin and ertapenem and the susceptibility relationship of K20-CPs isolates with amoxicillin/clavulanate, piperacillin/tazobactam, imipenem, tetracycline and trimethoprim/sulfamethoxazole were found as statistically significant. Our study is the first to investigate the relationship between K.pneumoniae capsular genotypes and beta-lactamase genes in Turkey. As a result, it is believed that this research will contribute to the determination of vaccine and treatment options by providing data to wider and regional studies that will examine other capsule genotypes and antibiotic resistance genes to clarify the importance of the capsule in virulence.

This study evaluated changes in motor nerve conduction velocity (MNCV) over a four-week follow-up period in non-diabetic and diabetic rats exposed to systemic rotenone and investigated the potential modulatory effect of pulsed magnetic field (PMF) application. Eight experimental groups were included: control (C), control+PMF (C+PMF), control+rotenone (C+ROT), control+rotenone+PMF (C+ROT+PMF), diabetes mellitus (DM), diabetes mellitus+PMF (DM+PMF), diabetes mellitus+rotenone (DM+ROT), and diabetes mellitus+rotenone+PMF (DM+ROT+PMF). The final analysis included 80 rats, with 10 animals in each group. MNCV was measured at study baseline and at the end of weeks 1, 2, 3, and 4. Rotenone-treated animals were also monitored qualitatively for Parkinsonian-like motor signs. Rotenone exposure was associated with a progressive reduction in MNCV. Compared with the C group, MNCV was significantly lower in the C+ROT group from week 1 through week 4. Similarly, MNCV was significantly lower in the DM+ROT group than in the DM group during weeks 2–4. MNCV was significantly higher in the C+PMF group than in the C group at week 4 and in the DM+PMF group than in the DM group during weeks 2–4. No significant differences were detected between the C+ROT and C+ROT+PMF groups or between the DM+ROT and DM+ROT+PMF groups at any measurement time. Overall, systemic rotenone exposure was associated with impaired peripheral motor nerve conduction in both non-diabetic and diabetic rats. The applied PMF protocol was associated with time-dependent changes in MNCV under non-rotenone conditions but did not significantly attenuate rotenone-associated impairment in peripheral motor nerve conduction.