Fordtran John S
Division of Gastroenterology, Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas 75246, USA.
Proc (Bayl Univ Med Cent). 2006 Jan;19(1):3-12. doi: 10.1080/08998280.2006.11928114.
Clostridium difficile colitis is a major complication of antibiotic therapy. Antibiotics cause a reduction in bacteria that normally reside in the colon. If an antibiotic-treated patient ingests C. difficile bacteria, this organism may proliferate in the colon because it is resistant to most antibiotics and because it does not have to compete with the normal bacteria for nutrients. If the C. difficile organism has the gene for toxin production, the toxin can produce a colitis. In addition to antibiotics, other proposed risk factors for development of C. difficile colitis include advanced age, contact with infected patients and with their health care providers, impaired immune function, suppression of gastric acid secretion by a proton pump inhibitor, and postpyloric tube feeding. Many of the risk factors become simultaneously focused on patients admitted to the hospital. The incidence of C. difficile disease has been rising, and strains have become more virulent. In some forms of the disease, the patient doesn't have diarrhea, and in such patients C. difficile can be deadly but difficult to diagnose. The standard treatment, with metronidazole or vancomycin, fails to work in up to 25% of patients with the fulminant form of colitis. Since C. difficile causes only 20% of cases of antibiotic-associated diarrhea, a specific test is needed to diagnose this organism. Toxigenic cultureis highly specific but not available at most institutions. The tests that are available--enzyme-linked immunosorbent assay and fecal cytotoxicity assay--have high false-negative rates, even in patients with severe clinical disease, creating a diagnostic dilemma. The only proven way to reduce the risk of C. difficile disease is implementation of an antibiotic management program in conjunction with enhanced infection control procedures.
艰难梭菌结肠炎是抗生素治疗的主要并发症。抗生素会导致正常存在于结肠中的细菌数量减少。如果接受抗生素治疗的患者摄入艰难梭菌，这种微生物可能会在结肠中增殖，因为它对大多数抗生素具有抗性，并且无需与正常细菌竞争营养物质。如果艰难梭菌具有产生毒素的基因，毒素就会引发结肠炎。除了抗生素外，其他被认为与艰难梭菌结肠炎发生相关的风险因素包括高龄、与感染患者及其医护人员接触、免疫功能受损、质子泵抑制剂抑制胃酸分泌以及幽门后管饲。许多风险因素同时集中在住院患者身上。艰难梭菌疾病的发病率一直在上升，菌株的毒性也变得更强。在某些形式的疾病中，患者没有腹泻症状，在这类患者中，艰难梭菌可能是致命的，但却难以诊断。标准治疗方法，即使用甲硝唑或万古霉素，在高达25%的暴发性结肠炎患者中不起作用。由于艰难梭菌仅导致20%的抗生素相关性腹泻病例，因此需要进行特定检测来诊断这种微生物。产毒培养具有高度特异性，但大多数机构无法进行。现有的检测方法——酶联免疫吸附测定和粪便细胞毒性测定——即使在患有严重临床疾病的患者中也有很高的假阴性率，这造成了诊断上的困境。降低艰难梭菌疾病风险的唯一经证实的方法是实施抗生素管理计划并加强感染控制措施。
