Zhang X, McDaniel A D, Wolf L E, Keusch G T, Waldor M K, Acheson D W
Division of Geographic Medicine and Infectious Diseases, Tupper Research Institute, New England Medical Center, Boston, MA 02111, USA.
J Infect Dis. 2000 Feb;181(2):664-70. doi: 10.1086/315239.
Shiga toxin-producing Escherichia coli (STEC) cause significant disease; treatment is supportive and antibiotic use is controversial. Ciprofloxacin but not fosfomycin causes Shiga toxin-encoding bacteriophage induction and enhanced Shiga toxin (Stx) production from E. coli O157:H7 in vitro. The potential clinical relevance of this was examined in mice colonized with E. coli O157:H7 and given either ciprofloxacin or fosfomycin. Both antibiotics caused a reduction in fecal STEC. However, animals treated with ciprofloxacin had a marked increase in free fecal Stx, associated with death in two-thirds of the mice, whereas fosfomycin did not. Experiments that used a kanamycin-marked Stx2 prophage demonstrated that ciprofloxacin, but not fosfomycin, caused enhanced intraintestinal transfer of Stx2 prophage from one E. coli to another. These observations suggest that treatment of human STEC infection with bacteriophage-inducing antibiotics, such as fluoroquinolones, may have significant adverse clinical consequences and that fluoroquinolone antibiotics may enhance the movement of virulence factors in vivo.
产志贺毒素大肠杆菌（STEC）可引发严重疾病；治疗以支持性治疗为主，抗生素的使用存在争议。环丙沙星而非磷霉素可在体外诱导产志贺毒素的噬菌体，并增强大肠杆菌O157:H7的志贺毒素（Stx）产生。在定殖有大肠杆菌O157:H7并给予环丙沙星或磷霉素的小鼠中研究了这一现象的潜在临床相关性。两种抗生素均使粪便中的STEC数量减少。然而，接受环丙沙星治疗的动物粪便中游离Stx显著增加，三分之二的小鼠死亡，而磷霉素则未出现这种情况。使用卡那霉素标记的Stx2原噬菌体进行的实验表明，环丙沙星而非磷霉素可导致Stx2原噬菌体在肠道内从一株大肠杆菌向另一株大肠杆菌的转移增强。这些观察结果表明，用诱导噬菌体的抗生素（如氟喹诺酮类）治疗人类STEC感染可能会产生严重的不良临床后果，并且氟喹诺酮类抗生素可能会增强体内毒力因子的移动。
