Lusk R H, Fekety R, Silva J, Browne R A, Ringler D H, Abrams G D
J Infect Dis. 1978 Apr;137(4):464-75. doi: 10.1093/infdis/137.4.464.
A lethal enterocolitis was induced in hamsters by oral or parenteral administration of clindamycin in amounts comparable to those used in treatment of humans. The intestinal lesions were characterized histologically as an acute inflammatory reaction with pseudomembrane formation and resembled the lesions seen in humans with antibiotic-induced colitis. Results of quantitative stool cultures showed the numbers of Peptostreptococcus and Corynebacterium decreased in animals with colitis after challenge with 100 mg of clindamycin/kg, while numbers of Escherichia coli, Streptococcus faecalis, and clindamycin-resistant Clostridium sordellii and Clostridium difficile increased. Bacteria were not seen within the intestinal lesions. Viruses were not isolated from hamsters with colitis. Although the pathogenesis of this syndrome is not completely established, the evidence is consistent with the hypothesis that the disease is caused by clostridial toxins and that the production of these toxins by organisms within the intestines is enhanced by the effects of clindamycin upon the bowel flora.
通过口服或肠胃外给予仓鼠与用于人类治疗量相当的克林霉素,诱发了致死性小肠结肠炎。肠道病变的组织学特征为伴有假膜形成的急性炎症反应,类似于人类抗生素诱导性结肠炎所见的病变。定量粪便培养结果显示,用100mg克林霉素/千克攻击后,患有结肠炎的动物中消化链球菌和棒状杆菌数量减少,而大肠杆菌、粪链球菌以及耐克林霉素的索氏梭菌和艰难梭菌数量增加。在肠道病变内未见到细菌。未从患有结肠炎的仓鼠中分离出病毒。尽管该综合征的发病机制尚未完全明确,但证据与该疾病由梭菌毒素引起且克林霉素对肠道菌群的作用增强了肠道内微生物产生这些毒素的假说一致。