CLINDAMYCIN-INDUCED ENTEROCOLITIS IN HAMSTERS
CLINDAMYCIN-INDUCED ENTEROCOLITIS IN HAMSTERS
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DOI：
10.1093/infdis/137.4.464
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发表时间：
1978-01-01
影响因子：
6.4
通讯作者：
ABRAMS, GD
中科院分区：
文献类型：
--
作者：
LUSK, RH;FEKETY, R;ABRAMS, GD
通过口服或胃肠外给予克林霉素（剂量与人类治疗中使用的剂量相当），在仓鼠中诱导致死性小肠结肠炎。肠道病变的组织学特征为急性炎症反应伴假膜形成，与人类过敏性结肠炎中观察到的病变相似。定量粪便培养结果显示，100 mg/kg克林霉素激发后，结肠炎动物中消化链球菌和棒状杆菌的数量减少，而大肠埃希菌、粪链球菌、克林霉素耐药梭菌和艰难梭菌的数量增加。肠道病变内未观察到细菌。未从患有结肠炎的仓鼠中分离出病毒。虽然该综合征的发病机制尚未完全确定，但证据与该疾病由梭菌毒素引起的假设一致，并且克林霉素对肠道植物群的影响增强了肠道内微生物产生这些毒素。
A lethal enterocolitis was induced in hamsters by oral or parenteral administration of clindamycin in amounts comparable to those used in humans treatment. 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.