Traci P A, Duncan C L
Appl Microbiol. 1974 Nov;28(5):815-21. doi: 10.1128/am.28.5.815-821.1974.
Several observations have been made in regard to cold shock lethality of Clostridium perfringens: (i) loss of viability was not consequence of exposure of the cells to air; (ii) stationary-phase cells were much more resistant to cold shock at 4 C than exponential-phase cells; (iii) at 4 C 96% of an initial population of exponential-phase cells was killed upon cold shock and 95% of the remaining population was killed within 90 min of continued exposure at 4 C; (iv) the minimal temperature differential for detectable cold shock lethality was between 17 and 23 C, and the maximum beyond which lethality was not appreciably increased was between 28 and 33 C. Up to 75% of viable cold-shocked cells were injured, as demonstrated by cold shocking late exponential-phase cells at 10 C and using differential plating procedure for recovery. Repair of injury was temperature dependent, and occurred in a complex medium and 0.1% peptone but not water. Nalidixic acid, chloramphenicol, and rifampin did not inhibit repair of injury.
关于产气荚膜梭菌的冷休克致死性,已有多项观察结果:(i) 细胞活力丧失并非细胞暴露于空气中的结果;(ii) 稳定期细胞比指数期细胞对4℃的冷休克更具抗性;(iii) 在4℃时,指数期细胞初始群体的96%在冷休克后死亡,其余群体的95%在继续暴露于4℃的90分钟内死亡;(iv) 可检测到冷休克致死性的最小温度差在17至23℃之间,而致死率不再明显增加的最高温度在28至33℃之间。通过在10℃对指数期后期细胞进行冷休克并使用差异平板培养法进行复苏,结果表明高达75%的存活冷休克细胞受到损伤。损伤修复取决于温度,且发生在复杂培养基和0.1%蛋白胨中,而不是水中。萘啶酸、氯霉素和利福平不抑制损伤修复。