How to Cite
Abstract
Treatment of bacteria with antibiotics is known to cause persistence. In this persistence state, the cells that survived ceased to grow and became resistant to antibiotics. The mechanism of such protection however, was never elucidated. Utilizing isogenic E. coli strains CP78 and CP79 pretreated with 9 μ g/mL of kanamyin for 1 hour in M9 minimal media, we invistigated whether or not ppGpp synthase I (RelA) in E. coli CP78 pretreated with an inhibitory amount of kanamycin are responsible in eliciting cross-protection against subsequent lethal antibiotic insults the different antibiotics Tetracyclin and Ampicilin. RelA was found to be important in the viability of the cells during the kanamycin pretreatment and the subsequent lethal antibiotic treatments: CP78 and CP79 strains both started with similar turbidity and cell counts prior to the kanamycin treatment; after 1 hour treatment the CP78 strain was found to have 28% more cells that survived the pretreatment compared to the CP79 strain. After the secondary lethal antibiotic treatments, the RelA carrying strain CP78 was found to be at least 3 times or more resistant to tetracycline or ampicillin killing compared to its isogenic strain, CP79 strain, which carries a relA mutation. We conclude that the presence of RelA could provide short-term (1.5 hours) protection against antibiotics such as kanamycin, and that relA in conjunction with a pretreatment of inhibitory level of kanamycin was able to provide short-term protection (2.5 hours) against subsequent lethal levels of antibiotic insults from different classes of antibiotics.