دانلود رایگان مقاله بررسی خصوصیات فنوتیپی انتروکوک مقاوم به وانکومایسین در خوک

Abstract

The presence and characteristics were investigated of vancomycin-resistant enterococci (VRE) in pigs in Thailand. A total of 179 rectal swabs were collected aseptically from suckling pigs, fattening pigs and breeding sows on four commercial farms located in Central Thailand. VRE with minimum inhibitory concentrations ranging from 8 μg/mL to 16 μg/mL were detected in 43 of 179 pigs (an overall prevalence rate of 24%). VRE carriers were identified in 12 of 61 (19.7%) suckling pigs, 15 of 60 (25%) fattening pigs and 16 of 58 (27.6%) breeding sows, respectively. Enterococcus gallinarum was the most prevalent species for VRE in all age groups, followed by the detection of Enterococcus casseliflavus. All of the isolates were susceptible to teicoplanin. A large proportion of VRE isolates showed resistance to tetracycline (86.5%), erythromycin (61.5%), ampicillin (53.8%), chloramphenicol (34.6%) and ciprofloxacin (32.7%). Resistance to ampicillin was more prevalent in E. gallinarum isolates than in E. casseliflavus isolates. The results of this study indicate that VRE isolates of pigs are of the VanC phenotype and commonly exhibit multiple drug resistance. Different antimicrobial susceptibility is present between VanC species, while E. gallinarum is less susceptible than E. casseliflavus.

Discussion

Vancomycin resistance in enterococci can be acquired or can be intrinsic. Two main types of acquired vancomycin resistance, VanA and VanB, have been described (Courvalin, 2005). The VanA phenotype is characterized by high-level (MIC,  64 mg/mL), transferable resistance to both vancomycin and teicoplanin, while variable levels of resistance to vancomycin and susceptibility to teicoplanin are the characteristics of the VanB phenotype. The VanB phenotype is also considered to be transferable. The VanC phenotype appears to be an intrinsic property of E. gallinarum and E. casseliflavus and is a low level of vancomycin resistance (Courvalin, 2005). VanA, VanB and VanC phenotypes are mediated by vanA, vanB and vanC gene clusters, respectively. Since Van phenotypes are different in their transferability and susceptibility, the status of the Van type in clinical settings and more broadly is important epidemiologic data for VRE control