الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 244 |  |  |
| | | from | 244 | | |
Abstract
This study was carried out over a period of 24 months, from October 2018 to October 2020 aiming to identify S. aureus isolates collected from Surgical Departments of TUHs by MALDI-TOF MS, compare their antibiotic susceptibility by conventional disc diffusion method and VITEK 2 system, determine the existence of different levels of vancomycin resistance among S. aureus isolates and detect mecA, vanA and vanB genes by conventional PCR assay. A total of 200 patients with HAIs were enrolled in this study. The majority of those patients (72.5%) were ≥ 40 years. The patients included 55.6% males and 44.4% females. This study was carried out on 200 samples including 70 surgical wound swabs, 45 infected burn swabs, 30 urine samples, 45 endotracheal aspirates as well as10 sputum samples. All samples were subjected to bacteriological examination. Isolation and identification of S. aureus were done by conventional cultural methods. Confirming identification of S. aureus was performed by MALDI-TOF MS. Antimicrobial sensitivity were done by disc diffusion method and VITEK 2 system. Vancomycin susceptibility was assessed by vancomycin E-test and vancomycin screen agar. Conventional PCR was done to detect the prevalence of mecA, van A and van B genes in the isolated S. aureus. The present study revealed Gram-negative bacteria were responsible for 63.2% of HAIs and Gram-positive bacteria prevalence was 32.5%. S. aureus was responsible for 27% of HAIs. In this study, out of 60 Gram-positive isolates, 50 (83.3%) were S. aureus by conventional methods. MALDI-TOF MS (VITEK MS model) system identified 49/50 of these S. aureus isolates with 98% accurate genus‐ and species‐level identifications. Regarding antibiotic susceptibility, it was found that the highest resistance rate was detected to penicillin. The most active compounds against these isolates were linezolid and tigecycline. S. aureus isolates showed resistance to erythromycin and gentamicin (54%, each), ciprofloxacin and ofloxacin (46%, each), tetracycline (44%), doxycycline (42%), trimethoprim-sulfamethoxazole (40%) and clindamycin (34%). In this study, the results of AST conducted by VITEK 2 were quite similar to the results obtained by disc diffusion method. VITEK 2 reported all isolates (100%) were sensitive to teicoplanin and tigecycline. The VITEK 2 system showed 100% agreement with the D-zone test for the detection of ICR in S. aureus isolates. The prevalence of MRSA in the present study was 70% according to both cefoxitin disc diffusion and VITEK 2 MICs for oxacillin and cefoxitin. Conventional PCR detected mecA gene in 68% of S. aureus isolates. Out of 35 phenotypically diagnosed MRSA isolates, 34 isolates were positive for mecA gene (97.1%). Vancomycin susceptibility was assessed by 3 methods; VITEK 2, E-test and vancomycin screen agar. In VITEK 2 system, all S. aureus isolates were sensitive to vancomycin. By E-test, VISA represented 8% of S. aureus isolates. Additionally, 3 isolates were query hVISA (MIC =3μg/ml). There were 9/50 isolates grew on vancomycin screen agar including 3 (6%) VSSA isolates and 3 (6%) isolates with MICs 3 μg/ml. Three isolates out of 4 VISA isolates detected by E-test, grew on vancomycin screen agar with 75% sensitivity in detection of VISA isolates. So, the prevalence of SA-RVS in the present study was 20% between staphylococcal isolates. Of notice, no VRSA isolates were detected in this study and none of these isolates could demonstrate the presence of vanA and or vanB genes.