目的：了解2007年浙江省衢州地区产志贺毒素大肠埃希菌O157：H7在动物中的分布情况及其耐药性、PFGE分型及毒力基因携带状况。方法：按全国O157：H7监测方案于5～10月份肠道传染病高发季节，在衢州地区采集各种动物粪便／肛拭，用免疫...目的：了解2007年浙江省衢州地区产志贺毒素大肠埃希菌O157：H7在动物中的分布情况及其耐药性、PFGE分型及毒力基因携带状况。方法：按全国O157：H7监测方案于5～10月份肠道传染病高发季节，在衢州地区采集各种动物粪便／肛拭，用免疫磁珠富集后进行O157：H7分离培养、鉴定，可疑菌株以PCR法检测O、H抗原及志贺样毒素（SLT1和SLT2）、粘附抹平因子（eaeA）及溶血素（hly）4种毒力基因。用脉冲场凝胶电泳（pulse field gel electrophoresis，PFGE）方法进行同源性分析，同时选择14种抗生素进行药敏试验，分析分离所得菌株的耐药状况。结果：共监测动物粪便标本300份，分离得产志贺毒素大肠埃希菌O157：H7菌株16株，分离率为5．33％。16株O157：H7菌株，毒力基因Hly、eaeA、SLT2均阳性，SLT1均阴性。脉冲场凝胶电泳分型显示，16株O157：H7菌株可分2个PFGE基因型，型间差异较小。耐药性分析显示这些菌株对红霉素、利福平的耐药率最高，达100．0％，对其他受试抗生素均敏感。结论：该地区动物中产志贺毒素大肠埃希菌O157：H7带菌率较高，所分离菌株主要携带SLT2基因，因此推测该地区存在发生产志贺毒素大肠埃希菌O157：H7感染暴发或流行的潜在危险，需增加对动物源性O157：H7的监测力度。展开更多
Shiga toxin producing Escherichia coli (STEC) are noninvasive enteric pathogens that may cause hemorrhagic colitis (HC) and diarrhea-associated hemolytic uremic syndrome (D+HUS). We hypothesized that development of D+...Shiga toxin producing Escherichia coli (STEC) are noninvasive enteric pathogens that may cause hemorrhagic colitis (HC) and diarrhea-associated hemolytic uremic syndrome (D+HUS). We hypothesized that development of D+HUS is associated with increased serum procalcitonin (PCT) levels. PCT was measured by an immunoluminometric assay in 113 patients. Concentrations of PCT were different in normal controls,disease control groups (rotavirus enteritis,HC due to non-STEC pathogens,chronic renal failure),and children with uncomplicated O157:H7HC or D+HUS. Children with D+HUS showed higher PCT levels than those with uncomplicated O157:H7 HC,and increased concentrations were noted in cases requiring peritoneal dialysis. Severely increased concentrations were observed in children with D+HUS on d 5 or 6 after the onset of enteritis,whereas serial measurements in those with uncomplicated O157:H7 HC remained within the normal range throughout the first week of illness. PCT was correlated with serum concentrations of lipopolysaccharide (LPS)-binding protein and serum levels of alanine aminotransferase. Using two separate sets of real-time PCR primers,we were unable to detect elevated PCT mRNA transcripts in nonadherent undifferentiated (monocytic) or differentiated (macrophage-like) THP-1 cells stimulated with purified Shiga toxin-1 and/or LPS. Our data show that serum levels of PCT are associated with the severity of illness in children with D+HUS. Further studies are needed to determine the role of PCT in the pathogenesis of thrombotic microangiopathy associated to childhood D+HUS.展开更多
文摘目的：了解2007年浙江省衢州地区产志贺毒素大肠埃希菌O157：H7在动物中的分布情况及其耐药性、PFGE分型及毒力基因携带状况。方法：按全国O157：H7监测方案于5～10月份肠道传染病高发季节，在衢州地区采集各种动物粪便／肛拭，用免疫磁珠富集后进行O157：H7分离培养、鉴定，可疑菌株以PCR法检测O、H抗原及志贺样毒素（SLT1和SLT2）、粘附抹平因子（eaeA）及溶血素（hly）4种毒力基因。用脉冲场凝胶电泳（pulse field gel electrophoresis，PFGE）方法进行同源性分析，同时选择14种抗生素进行药敏试验，分析分离所得菌株的耐药状况。结果：共监测动物粪便标本300份，分离得产志贺毒素大肠埃希菌O157：H7菌株16株，分离率为5．33％。16株O157：H7菌株，毒力基因Hly、eaeA、SLT2均阳性，SLT1均阴性。脉冲场凝胶电泳分型显示，16株O157：H7菌株可分2个PFGE基因型，型间差异较小。耐药性分析显示这些菌株对红霉素、利福平的耐药率最高，达100．0％，对其他受试抗生素均敏感。结论：该地区动物中产志贺毒素大肠埃希菌O157：H7带菌率较高，所分离菌株主要携带SLT2基因，因此推测该地区存在发生产志贺毒素大肠埃希菌O157：H7感染暴发或流行的潜在危险，需增加对动物源性O157：H7的监测力度。
文摘Shiga toxin producing Escherichia coli (STEC) are noninvasive enteric pathogens that may cause hemorrhagic colitis (HC) and diarrhea-associated hemolytic uremic syndrome (D+HUS). We hypothesized that development of D+HUS is associated with increased serum procalcitonin (PCT) levels. PCT was measured by an immunoluminometric assay in 113 patients. Concentrations of PCT were different in normal controls,disease control groups (rotavirus enteritis,HC due to non-STEC pathogens,chronic renal failure),and children with uncomplicated O157:H7HC or D+HUS. Children with D+HUS showed higher PCT levels than those with uncomplicated O157:H7 HC,and increased concentrations were noted in cases requiring peritoneal dialysis. Severely increased concentrations were observed in children with D+HUS on d 5 or 6 after the onset of enteritis,whereas serial measurements in those with uncomplicated O157:H7 HC remained within the normal range throughout the first week of illness. PCT was correlated with serum concentrations of lipopolysaccharide (LPS)-binding protein and serum levels of alanine aminotransferase. Using two separate sets of real-time PCR primers,we were unable to detect elevated PCT mRNA transcripts in nonadherent undifferentiated (monocytic) or differentiated (macrophage-like) THP-1 cells stimulated with purified Shiga toxin-1 and/or LPS. Our data show that serum levels of PCT are associated with the severity of illness in children with D+HUS. Further studies are needed to determine the role of PCT in the pathogenesis of thrombotic microangiopathy associated to childhood D+HUS.
