临床分离非O1/O139群霍乱弧菌毒力及耐药特征分析

目的 了解临床分离的非O1/O139群霍乱弧菌毒力及耐药特征。方法 收集2014-2015年北京友谊医院4-10月肠道门诊分离到的非O1/O139群霍乱弧菌,采用微量肉汤稀释法检测霍乱弧菌对15种抗生素的耐药性;PCR检测霍乱弧菌的毒力相关基因。结果 35株非O1/O139群霍乱弧菌对复方新诺明的耐药率(40.0%)最高,其次是氯霉素(28.5%)和磺胺异恶唑(22.6%),对阿莫西林/克拉维酸、头孢曲松、头孢西丁、头孢吡肟及亚胺培南完全敏感。毒力基因检测显示所有菌株均携带hlyA和ompU,hapA(97.1%)、rtxA(91.4%)、Ⅵ型分泌系统T6SS(94.3%~97.1%)、Ⅲ型分泌系统T3SS(80.0%~85.7%)和nanH(62.9%)阳性率较高;主要的毒力基因型为hlyA-rtxA-hapA-ompU-nanH-vasA-vasK-vasH-vcsC-vcsV-vcsN-vspD(40.0%)。结论 临床分离非O1/O139群霍乱弧菌毒力基因多样化,对抗菌药物耐药性较高,需加强腹泻病例中非O1/O139群霍乱弧菌的毒力及耐药监测。     

2018-2021年湖南省人源非O1/非O139群霍乱弧菌药物敏感性及基因组特征

目的 了解2018—2021年间湖南省从病例分离到的非O1/非O139群霍乱弧菌的药物敏感性及基因组特征。方法 选取2018—2021年间湖南省腹泻病例肠道标本分离的非O1/非O139群霍乱弧菌分离株4株和非腹泻病例血液标本分离的非O1/非O139群霍乱弧菌分离株3株,进行药物敏感性测试以及基因组序列测定,分析其药物敏感性及基因组特征。结果 3株血液样品分离株对氨苄西林、诺氟沙星、头孢曲松、美罗培南、米诺环素、复方磺胺甲恶唑、庆大霉素、头孢噻肟、萘啶酸、环丙沙星全部敏感,1株对四环素中介,1株对氯霉素耐药;4株粪便样品分离株对诺氟沙星、头孢曲松、美罗培南、米诺环素、复方磺胺甲恶唑、庆大霉素、头孢噻肟全部敏感,1株对四环素、氯霉素中介,1株对氯霉素耐药,2株对氨苄西林、环丙沙星、萘啶酸耐药;其中1株对氨苄西林、萘啶酸、环丙沙星二重耐药;1株对氨苄西林、萘啶酸、环丙沙星、氯霉素多重耐药。7株非O1/非O139群霍乱弧菌的基因组序列表现出明显的多样性,但是部分菌株在核心基因组和泛基因组都高度相似。基因组序列中均未检出ctxAB基因、VPI-1和VSPII基因组岛。分离自粪便的菌株携带耐药基因...     

1株非O1群非O139群霍乱弧菌的错误鉴定和原因分析

<正>霍乱弧菌(Vibrio cholerae)是弧菌科弧菌属中具有相似生化性状、相同鞭毛抗原、不同菌体抗原的弧菌的统称,按照菌体脂多糖抗原的不同,已分离出200余个血清群[1],除O1群和O139群的产毒株会导致霍乱的大流行外,其他非O1群非O139群霍乱弧菌亦可引起感染性腹泻、败血症等[2]。本研究从我院收治的1例腹泻患者粪便标本中分离培养到1株非O1群非O139群霍乱弧菌,然而布鲁克基质辅助激光解吸电离飞行时间质谱(Bruker BioT yperTMMALDI-TOF MS)仪却错误鉴定为易北河弧菌(Vibrio albensis)。报道如下。     

浙江省非O1、非O139群霍乱弧菌快速检测与毒力基因研究

目的 建立一种快速检测非O1、非O139群霍乱弧菌方法,并对浙江省部分地区海水产品中非O1、非O139 群霍乱弧菌及其携带毒力基因开展快速检测.方法 采用三糖斜面、氧化酶实验、粘丝实验、无盐胨水等简单生化进行初筛,对全部结果阳性的菌株用聚合酶链反应(PCR)方法检测霍乱弧菌外膜蛋白OmpW以及毒力基因ctxA、hl...     

非O1/O139群霍乱弧菌:流行、致病因子和耐药

非O1/O139群霍乱弧菌引起的腹泻在许多发展中国家都有发生,其流行涉及到多个血清群。在有些地方,非O1/O139群霍乱弧菌腹泻的发病率甚至超过了O1/O139群霍乱弧菌腹泻的发病率。非O1/O139群霍乱弧菌的致病因子多种多样,肠毒素、蛋白酶、溶血素和三型分泌系统等被认为是重要的致病因子,但其致病机制非常复杂,至今仍然不完全清楚。随着抗生素使用的增加,出现了许多耐药甚至多重耐药菌株。本研究从非O1/O139群霍乱弧菌腹泻的流行情况、致病因子以及耐药方面加以综述。     

肝硬化患者血液及腹水中检出3株非O1非O139群霍乱弧菌

<正>霍乱弧菌是烈性肠道传染病——霍乱的病原菌,目前有155个血清群。自1817年以来,已发生7次世界性的霍乱大流行,均由霍乱弧菌的O1群引起[1]。非O1非O139群霍乱弧菌(non-O1non-O139 Vibrio choleraev,NOVC)虽尚未引起世界性流行,但也可引起人类腹泻及肠道外感染,如伤口感染、败血症等,国内、外已有关于从血液中分离出NOVC的报道。2012年7月河池市人民医     

一起引起食物中毒的非O1群霍乱弧菌实验室鉴定

目的 查明引发浙江省宁波市某服饰公司食物中毒事件的病原菌.方法 对采集到可疑食品和肛拭等标本参照GB/T4789-2003标准进行细菌的分离、鉴定及血清学分型;参照霍乱防治手册检测菌株的CT毒力基因.结果 6份患者大便标本与14份轻微腹泻患者或腹部不适者大便标本中检出非O1群霍乱弧菌O29血清型9株,其中腹泻患者标本检出6株,轻微腹泻患者中检出3株,检出率为45.0%.未检出志贺菌、副溶血性弧菌、致病性大肠杆菌、O1群和O139霍乱弧菌、金黄色葡萄球菌等致病菌,剩余食物未检出志贺菌、副溶血性弧菌、致病性大肠杆菌、O1群和O139霍乱弧菌、金黄色葡萄球菌等致病菌.结论 此次食物中毒为非O1群霍乱弧菌O29血清型所致.     

非O1群霍乱弧菌的鉴定及耐药性分析

对本院1999年6～9月在肠道门诊检出的20株非O1群霍乱弧菌进行生化鉴定、血清学分群和药敏试验.根据1998年美国NCCLS药敏法规中新增的霍乱弧菌抗生素选择规定和判别标准[2],所选用抗生素已能满足临床治疗的需要.药敏结果提示: 抗O/129的非O1群霍乱弧菌对抗生素的敏感性比O/129敏感的非O1群霍乱弧菌有明显下降.     

浙江省丽水市首起非O1群霍乱弧菌食物中毒分子生物学溯源分析

目的 利用分子生物技术了解引起食物中毒的非O1群霍乱弧菌携带毒力基因情况及耐药性特征.方法 对检出的非O1群霍乱弧菌菌株进行耐药性分析,同时采用聚合酶链反应(PCR)方法进行霍乱弧菌肠毒素基因(Ctx)、小带联结毒素基因(Zot)、辅助霍乱肠毒素(Ace)基因的检测,并参照美国CDC PulseNet的统一方法进行脉冲场凝胶电泳(PFGE)分型并作同源性分析.结果 从8例患者和8份食品标本中分离到7株非O1群霍乱弧菌,未检出Ctx、Zot、Ace等毒素基因,检出溶血素,Dienes试验和脉冲场凝胶电泳图谱显示病人分离株和剩余食物检出株同源.经耐药性分析,菌株除对复方新诺明、氨苄西林100%耐药外,对其余抗生素均较敏感.结论 通过实验证实本次食物中毒是由聚餐者共同食用冷菜凤爪所致,流行病学追溯从患者共同食用冷菜和海产品中非O1群霍乱弧菌毒力基因、耐药性和脉冲场凝胶电泳分析为同源菌株.     

广州市一起非O1/O139群霍乱弧菌食物中毒分离株的病原特征分析

目的 了解2014年广州市某工厂发生的一起非O1/O139群霍乱弧菌食物中毒分离株的耐药特性及分子特征。方法 对分离到的6株非O1/O139群分离株进行生化鉴定、血清学鉴定、药物敏感性实验、毒力相关基因检测和脉冲场凝胶电泳（PFGE）分子分型分析。结果 6株分离株经生化鉴定、血清学鉴定为非O1/O139群。药物敏感性分析显示,6株分离株均对氨苄西林、头孢克肟、头孢拉定、阿米卡星、妥布霉素、庆大霉素和多粘菌素B耐药,对诺氟沙星、环丙沙星、复方新诺明、呋喃唑酮、四环素、吡哌酸、红霉素和氯霉素敏感。毒力基因聚合酶链反应检测结果显示,所有菌株均携带毒力表达调控基因（toxR）和溶血素基因（hlyA）,未检出霍乱肠毒素基因（ctxA）、毒力协同调节菌毛基因（tcpA）和肠毒素基因（ST）;5株病例分离株和1株冷柜内壁分离株经限制性内切酶NotⅠ消化后的PFGE图谱为同一型别。结论 此次食物中毒的病原体为非O1/O139群霍乱弧菌,具有共同的遗传特征,菌株出现了多重耐药,提示应加强该类菌株的监测,防止大范围扩散或暴发流行。     

Spontaneous bacterial empyema due to non-O1, non-O139 Vibrio cholerae in a cirrhotic patient with hepatocellular carcinoma

Vibrio cholerae is known as a common etiology of epidemic diarrheal disease and rarely causes extra-intestinal infections. In this report, we described a cirrhotic patient with hepatocellular carcinoma who developed spontaneous bacterial empyema due to non-O1, non-O139 V. cholerae. The patient was successfully treated with antimicrobial agents and percutaneous drainage.     

O1 and non-O1 Vibrio cholerae bacteremia produced by hemolytic strains

Vibrio cholerae are Gram-negative bacteria capable of producing serious infections. They are differentiated into O1 and non-O1 serogroups, depending on their ability to agglutinate with specific antiserum. In contrast to non-O1 V. cholerae, which are more prone to invading the bloodstream, V. cholerae O1 is rarely the cause of bacteremia. We describe 2 cases of O and non-O1 V. cholerae bacteremia in patients with hepatitis C virus cirrhosis. We postulate that the hemolytic properties of the isolates contributed to their virulence in immunocompromised hosts.     

致血流感染非O1群非O139群霍乱弧菌的鉴定及毒力基因检测

目的对襄阳市中心医院分离1株疑似霍乱弧菌进行鉴定及药物敏感性试验,并检测其主要毒力基因。方法利用MicroScan WalkAway 40鉴定仪进行生化鉴定及药物敏感性试验,玻片凝集法确定其血清型别,应用PCR及测序技术分析其16SrRNA基因;PCR检测其6个毒力基因。结果经鉴定,该株疑似霍乱菌株为非O1群非O139群霍乱弧菌,经16SrRNA分析与美国国家生物技术信息中心数据库中霍乱弧菌相似性达100%。药敏试验结果显示该菌对氨苄西林、氯霉素、甲氧苄啶-磺胺甲（口恶）唑、四环素均敏感,毒力基因检测rtxC和toxR阳性,tcpAET、ctxA、hlyA、tcpACL阴性。结论该株疑似霍乱弧菌为非O1群非O139群霍乱弧菌,其致病与rtxC、toxR毒力基因有关。     

New carbenicillin-hydrolyzing beta-lactamase (CARB-7) from Vibrio cholerae non-O1, non-O139 strains encoded by the VCR region of the V. cholerae genome

In a previous study, an analysis of 77 ampicillin-nonsusceptible (resistant plus intermediate categories) strains of Vibrio cholerae non-O1, non-O139, isolated from aquatic environment and diarrheal stool, showed that all of them produced a beta-lactamase with a pI of 5.4. Hybridization or amplification by PCR with a probe for bla(TEM) or primers for bla(CARB) gene families was negative. In this work, an environmental ampicillin-resistant strain from this sample, ME11762, isolated from a waterway in the west region of Argentina, was studied. The nucleotide sequence of the structural gene of the beta-lactamase was determined by bidirectional sequencing of a Sau3AI fragment belonging to this isolate. The gene encodes a new 288-amino-acid protein, designated CARB-7, that shares 88.5% homology with the CARB-6 enzyme; an overall 83.2% homology with PSE-4, PSE-1, CARB-3, and the Proteus mirabilis N29 enzymes; and 79% homology with CARB-4 enzyme. The gene for this beta-lactamase could not be transferred to Escherichia coli by conjugation. The nucleotide sequence of the flanking regions of the bla(CARB-7) gene showed the occurrence of three 123-bp V. cholerae repeated sequences, all of which were found outside the predicted open reading frame. The upstream fragment of the bla(CARB-7) gene shared 93% identity with a locus situated inside V. cholerae's chromosome 2. These results strongly suggest the chromosomal location of the bla(CARB-7) gene, making this the first communication of a beta-lactamase gene located on the VCR island of the V. cholerae genome.     

Territorial waters of the Baltic Sea as a source of infections caused by Vibrio cholerae non-O1, non-O139: report of 3 hospitalized cases

A fatal infection with temporal relation to 2 other febrile infections caused by Vibrio cholerae non-O1, non-O139 (NCV) occurred in Finland in 2003. All infections were associated with contact with seawater. The patient who died had also eaten home-salted whitefish, tested positive for NCV, preceding his symptoms. All patients had compromising factors, and all strains were distinguishable by pulsed-field gel electrophoresis and negative for the ctx gene. These 3 cases illustrate that, despite being uncommon in Finland, NCVs can cause clinically significant and even fatal infections.     

Experimental non-O group 1 Vibrio cholerae gastroenteritis in humans.

In this study, 27 volunteers received one of three non-O group 1 Vibrio cholerae strains in doses as high as 10(9) CFU. Only one strain (strain C) caused diarrhea: this strain was able to colonize the gastrointestinal tract, and produced a heat-stable enterotoxin (NAG-ST). Diarrhea was not seen with a strain (strain A) that colonized the intestine but did not produce NAG-ST, nor with a strain (strain B) that produced NAG-ST but did not colonize. Persons receiving strain C had diarrhea and abdominal cramps. Diarrheal stool volumes ranged from 154 to 5,397 ml; stool samples from the patient having 5,397 ml of diarrhea were tested and found to contain NAG-ST. The median incubation period for illness was 10 h. There was a suggestion that occurrence of diarrhea was dependent on inoculum size. Immune responses to homologous outer membrane proteins, lipopolysaccharide, and whole-cell lysates were demonstrable with all three strains. Our data demonstrate that V. cholerae of O groups other than 1 are able to cause severe diarrheal disease. However, not all strains are pathogenic for humans: virulence of strain C may be dependent on its ability both to colonize the intestine and to produce a toxin such as NAG-ST.