重症急性胰腺炎细菌和真菌的分布状况研究

Investigation of distribution of bacteria and fungi in severe acute pancreatitis

目的探讨重症急性胰腺炎（SAP）患者细菌和真菌在不同部位的分布情况。方法前瞻性分析2000年1月至2008年12月收治的符合人选标准的205例SAP患者的一般资料，计算患者发病4周内的胰腺坏死组织、体液和中心静脉导管的细菌、真菌培养感染率。每周对体液、胰腺坏死组织（脓液或腹腔内渗液）进行两次细菌和真菌培养；中心静脉导管留置2周时拔除行细菌和真菌培养；对高热患者（T≥39℃）的血液进行细菌和真菌培养。观察发病28d内SAP患者细菌、真菌在不同部位以及整体构成比。结果共检出病原菌937株，革兰阴性菌菌株数量多于革兰阳性菌和真菌（P〈0．05），后两者感染率接近。坏死组织（55．2％）、胆汁（55．4％）、血液（68．1％）和中心静脉导管（44．4％）内革兰阴性菌感染率分别高于革兰阳性菌（30．2％、33．9％、23．4％、38．9％）和真菌（14．6％、10．7％、8．5％、16．7％）（P〈0．05）；尿液内真菌感染率（59．6％）高于革兰阴性菌（24．0％）和革兰阳性菌（16．3％）（P〈0．05）；痰液内革兰阴性菌感染率（53．2％）高于真菌（27．1％）和革兰阳性菌（19．7％）（P〈0．05）。坏死组织、胆汁、血液、中心静脉导管和痰液内非发酵菌（铜绿假单胞菌、鲍曼不动杆菌、嗜麦芽窄食假单胞菌）的感染率高于肺炎克雷伯菌、大肠埃希菌和阴沟肠杆菌（P〈0．01）；而尿液内发酵菌（大肠埃希菌、肺炎克雷伯菌）感染率高于非发酵菌（铜绿假单胞菌、鲍曼不动杆菌）（P〈0．01）。坏死组织和痰液内金黄色葡萄球菌、表皮葡萄球菌和溶血葡萄球菌感染率高于粪肠球菌和屎肠球菌（P〈0．05）；而胆汁和尿内屎肠球菌感染率显著高于其他革兰阳性球菌（P〈0．05）；血液内革兰阳性球菌之间差异无统计学意义，但中心静脉导管内的表皮葡萄球菌感染率显著升高（P〈0．05）。坏死组织、胆汁、尿液和痰液内假丝酵母菌感染率显著高于丝状菌（P〈0．05）。体液微生物培养感染率高峰在发病后2—3周。结论不同部位革兰阴性菌、革兰阳性菌和真菌以及三者内部的构成比各异，三者感染高峰在发病后2—3周。

Objective To investigate the spectrum of bacteria and fungi in different sites in severe acute panereatitis（SAP）. Methods The prospective study was performed in 205 patients with SAP treated from January 2000 to December 2008. The Infection rate of bacteria and fungi was observed prospectively in pancreatic necrosis and（or） pus form abdomen,body fluids and deep vein catheter in SAP. Body fluids and pancreatic necrosis were cultured twice a week. Central venous catheter was cultured when it had been placed for two weeks. Blood was cultured for bacteria and fungi when body temperature was more than 39℃. Constituent ratio of bacteria and fungi was observed in different sites and in all sites within 28 days after onset of SAP. Results There were 937 pathogens, among which infection rates of gram-negative bacteria was higher than gram-positive bacteria and fungi （ P 〈 0. 05 ）, the infection rates of gain-positive bacteria and fungi were similar. Infection rates of gram-negative bacteria in pancreatic necrosis （55.2%） , bile （55.4%）, blood （68. 1% ） and central venous catheter （44.4%） were increased significantly （P 〈 0. 05 ） compared with gramositive bacteria and （ 30. 2%, 33.9% , 23.4% , 2;8. 9% ） and fungi （ 14. 6%, 10. 7% , 8.5% , 16. 7% ）;however,infection rate of fungi （59. 6% ） was increased significantly（P 〈0. 05） compared with gram-nadtive bacteria（24. 0% ） and gram-positive bacteria（ 16. 3 % ） in urine;infection rate of gram-negative bacteria （53.2%） was significantly higher （P 〈 0. 05 ） than that of fungi （27.1% ） and gram-positive bacteria （ 19.7% ） in sputum. Infection rate of non-zymogenic bacteria （ Pseudomonas aeruginosa, Acinetobacter baumannii and Stenotrphomonas mahophilia） in gram-negative bacteria in pancreatic necrosis, bile, blood, central venous catheter and sputum was significantly higher than that of zymogenic bacteria （Klebsiella pneumoniae,Escherichia coli and Enterobaeter cloacae） （P 〈 0. 01 ）;infection rate of zymogenic bacteria （ Klebsiella pneumoniae, Escherichia coli ） was higher significantly （ P 〈 0. 01 ） than that of non-zymogenic bacteria （Pseudomonas aeruginosa, Acinetobacter baumannii ）. Infection rate of staphylococcus aureus, Staphylococcus epidermidis and Staphylococcus haemolyticus was significantly higher（ P 〈 0. 05 ） than that of Enterococcus faecalis and Enterococcus faecium in pancreatic necrosis and sputum; but infection rate of Enterococcus faecium in bile and urine was significantly higher than other gram-posotive bacteria（P 〈 0. 05）. There was not difference among gram-positive bacteria; however, infection rate of Staphylococcus epidermidis in central venous catheter was increased significantly （ P 〈 0. 05 ）. Infection rate of candida mycoderma in pancreatic necrosis, bile, urine and sputum was significantly higher than that of trichobacteria （P 〈 0.05 ）. The peak of infection rate of microbes in body fluid was within 2 to 3 weeks. Conclusions Constituent ratio in gram-negative, gram-positive bacteria and fungi as well as their species in different sites is diverse. The peak of infection rate of microbes is 2 to 3 weeks after onset of the disease.