共查询到20条相似文献，搜索用时 31 毫秒
1.
2.
3.
The Escherichia coli type III secretion system 2 (ETT2) is found in most pathogenic E. coli strains. Although many ETT2 gene clusters carry multiple genetic mutations or deletions, ETT2 is known to be involved in bacterial virulence. To date, no studies have been conducted on the role of ETT2 in the virulence of avian pathogenic Escherichia coli (APEC), which harbours ETT2. Thus, we deleted the ETT2 of APEC strain and evaluated the phenotypes and pathogenicities of the mutant. The results showed that deletion of ETT2 had no effect on APEC growth, but significantly promoted biofilm formation. In addition, as compared to the wild-type （WT） strain, the ETT2 deletion significantly promoted adherence to and invasion of DF-1 chicken fibroblasts and facilitated survival in the sera of specific-pathogen-free chickens. Analysis of the role of ETT2 in animal infection models demonstrated that the distribution of viable bacteria in the blood and organs of chicks infected with the ΔETT2 was significantly higher than those infected with WT. The results of RNA sequencing indicated that multiple genes involved in biofilm formation, lipopolysaccharide components, fimbrial genes and virulence effector proteins are regulated by ETT2. Collectively, these results implicated ETT2 is involved in the biofilm formation and pathogenicity of APEC. 相似文献
4.
Zhu C Feng S Sperandio V Yang Z Thate TE Kaper JB Boedeker EC 《Veterinary microbiology》2007,125(3-4):313-322
Attaching and effacing (A/E) organisms, such as rabbit enteropathogenic Escherichia coli (EPEC), human EPEC or enterohemorrhagic E. coli (EHEC) share attaching and effacing phenotype and LEE pathogenicity island responsible for A/E. The present study was undertaken to investigate the impact of the LuxS quorum sensing (QS) signaling system in vitro and in vivo pathogenicity of A/E organisms using rabbit EPEC (rEPEC) strain E22 (O103:H2). Analysis of the bioluminescence indicated abolished production of the QS signal AI-2 by luxS mutant (E22DeltaluxS). Strain E22Deltalux also exhibited impaired expression of several normally secreted proteins and reduced adherence to cultured HeLa cells. Complementation of the intact luxS gene to E22DeltaluxS restored secreted protein expression comparable to the WT type but not adherence to HeLa cells. In experimentally infected rabbits, the isogenic luxS mutant induced clinical illness and intimate adherence to the intestinal mucosa, albeit to a less extent, comparable to that seen with the parent virulent strain. It is worth noting that reduced fecal bacterial shedding, mucosal adherence and improved cumulative weight gain were seen for the mutant strain complemented with luxS when compared to the WT. It appears that the luxS gene is not essential for in vivo pathogenicity by rEPEC where exogenous QS signals are present in the gut. The impact of AI-2 provided by multicopy plasmid on bacterial virulence is discussed. 相似文献
5.
猪链球菌2型srtA基因缺失菌株的构建及生物学特性 总被引：1，自引：0，他引：1
扩增了srtA基因的上、下游同源臂P1和P2及其全长序列,利用温度敏感型"自杀性"质粒pSET4s构建了重组质粒pSET4s-P1-P2,并将该质粒电转化入野生菌株SS2(SC21)中,通过抗生素和温度双重筛选,得到srtA基因缺失菌株,命名SC211.同时,将srtA基因定向插入穿梭质粒pAT18,构建穿梭质粒pAT18-srtA,并将该质粒电转入srtA基因缺失菌株SC211中,通过抗生素筛选,得到质粒介导的srtA基因互补菌株SC212.通过PCR、South-ern blotting等对缺失突变菌株和互补菌株进行了鉴定.对基因缺失突变菌株和回复菌株传代培养遗传稳定性试验结果显示,缺失突变菌株和互补菌株能够稳定遗传.比较了基因缺失突变菌株、互补菌株及野生菌株的生长特性、溶血活性、细胞粘附特性,结果表明,3个菌株的生长速度、溶血活性没有明显差异.基因缺失后SS2对Hep2细胞的粘附能力明显下降,只有野毒菌株的49%,互补菌株粘附能力几乎达到野毒菌株的水平,是野毒菌株的89%.CD1小鼠毒力试验结果显示,srtA基因缺失株SC211的LD_(50)(4.93×10~7)约为野毒菌株SC21的LD_(50)(8.21×10~6)的6倍,质粒介导的互补菌株SC212的LD_(50)(1.43×10~7)是野生菌株SC21的1.7倍,接近野毒菌株的水平,说明srtA基因缺失后SS2毒力显著下降. 相似文献
6.
为了探讨猪链球菌2型(Streptococcus suis serotype 2,SS2)的Ⅲ型溶血素是否具有溶血活性以及Ⅲ型溶血素在SS2致病过程中的作用,本研究利用同源重组基因敲除法成功构建了SS205ZY的Ⅲ型溶血素(slyrp)基因缺失突变菌株△slyrp及双基因缺失突变菌株△sly/△slyrp,并比较了野生菌株和基因缺失突变菌株的溶血能力以及对小鼠的致病力.结果表明,slyrp基因敲除后可导致SS2裂解红细胞的能力有所下降,而双基因缺失突变菌株△sly/△slyrp的溶血能力完全丧失;slyrp基因敲除后对小鼠的致病力没有影响.结果提示猪链球菌2型Ⅲ型溶血素具有一定的溶血能力,该Ⅲ型溶血素在SS2感染过程中,对溶血素(sly)起协同作用,不是SS2主要的毒力相关基因. 相似文献
7.
为研究dnaJ基因序列与细菌致病力的关系,本研究构建了dnaJ基因缺失株和互补株,并对其致病性进行验证。参照GenBank中无乳链球菌GD201008-001（登录号：NC_018646）目的基因序列分别设计引物,PCR克隆dnaJ基因上、下游同源臂基因序列,通过融合PCR将两个片段连接到一起,构建dnaJ基因上、下游同源臂融合片段,PCR克隆含有启动子序列的dnaJ基因。将dnaJ基因上、下游同源臂融合片段和含有启动子序列的dnaJ基因分别连接链球菌-大肠杆菌穿梭质粒pSET4s和pSET2,电转化GD201008-001感受态细胞,构建dnaJ基因缺失株ΔdnaJ和互补株CΔdnaJ。通过分析ΔdnaJ和CΔdnaJ的遗传稳定性与形态学变化对dnaJ上、下游基因转录的影响,以及生长速率和斑马鱼攻毒试验评价dnaJ基因对无乳链球菌毒力的影响。经PCR鉴定和测序证明,ΔdnaJ和CΔdnaJ构建成功;与野生株GD201008-001相比,ΔdnaJ和CΔdnaJ在细菌染色形态上均无明显差异,但ΔdnaJ在液体培养基中的生长速度明显减缓;dnaJ基因的缺失未对相邻基因的转录造成影响;ΔdnaJ对斑马鱼的毒力明显下降,对斑马鱼的LD50为5.68×104 CFU,约是野生株的241倍。dnaJ基因对无乳链球菌的毒力有显著影响,本试验结果为进一步探究无乳链球菌dnaJ基因的功能提供了参考依据。 相似文献
8.
试验旨在研究抗菌肽Temprine-La（S）（T-La（S））、Temprine-La（FS）（T-La（FS））、RGD-T-La（S）和RGD-T-La（FS）对2型猪链球菌（SS2）生物被膜形成的抑制作用。通过结晶紫染色法（CV）检测SS2生物被膜形成能力；微量稀释法测定抗菌肽对SS2生物被膜的最小生物被膜抑菌浓度（MBIC）和最小生物被膜杀菌浓度（MBEC）；结晶紫染色法和扫描电镜（SEM）检测抗菌肽对SS2生物被膜形成的影响；XTT法检测抗菌肽对SS2生物被膜代谢活性的影响；苯酚硫酸法检测抗菌肽对SS2生物被膜胞外多糖含量的影响；建立猪链球菌-斑马鱼感染模型，HE染色法观察T-La（FS）对斑马鱼脑组织病理变化的影响；实时荧光定量PCR法分析抗菌肽对SS2生物被膜相关基因及对斑马鱼炎性细胞因子基因转录水平的影响。结果显示，SS2具有良好的生物被膜形成能力；T-La（S）、RGD-T-La（S）、T-La（FS）和RGD-T-La（FS）对SS2生物被膜的MBIC分别为31.3、15.6、7.8和15.6 μg/mL；MBEC分别为62.6、31.2、15.6和31.2 μg/mL；结晶紫染色结果表明，抗菌肽对SS2生物被膜的形成有抑制作用；扫描电镜结果显示，抗菌肽使SS2生物被膜中的细菌数量和生物被膜的形态发生明显变化，细胞外基质大量减少；XTT法结果显示，抗菌肽可显著降低SS2生物被膜的代谢活性；苯酚硫酸法结果显示，抗菌肽能有效抑制SS2生物被膜合成胞外多糖；实时荧光定量PCR结果表明，抗菌肽作用后降低了SS2生物被膜基因的转录水平；T-La（FS）作用后TLR2、MyD88及促炎性细胞因子基因的转录水平显著或极显著降低（P<0.05；P<0.01），抗炎性细胞因子基因的转录水平显著或极显著升高（P<0.05；P<0.01）。抗菌肽主要通过影响生物被膜相关基因转录水平和阻断胞外多糖的合成与分泌来抑制SS2生物被膜的形成，其中T-La（FS）可能通过抑制TLR2信号通路中TLR2和MyD88分子表达，抑制炎性细胞因子的释放，减轻脑膜炎的炎性反应。 相似文献
9.
试验旨在研究抗菌肽Temprine-La(S)(T-La(S))、Temprine-La(FS)(T-La(FS))、RGD-T-La(S)和RGD-T-La(FS)对2型猪链球菌(SS2)生物被膜形成的抑制作用。通过结晶紫染色法(CV)检测SS2生物被膜形成能力;微量稀释法测定抗菌肽对SS2生物被膜的最小生物被膜抑菌浓度(MBIC)和最小生物被膜杀菌浓度(MBEC);结晶紫染色法和扫描电镜(SEM)检测抗菌肽对SS2生物被膜形成的影响;XTT法检测抗菌肽对SS2生物被膜代谢活性的影响;苯酚硫酸法检测抗菌肽对SS2生物被膜胞外多糖含量的影响;建立猪链球菌-斑马鱼感染模型,HE染色法观察T-La(FS)对斑马鱼脑组织病理变化的影响;实时荧光定量PCR法分析抗菌肽对SS2生物被膜相关基因及对斑马鱼炎性细胞因子基因转录水平的影响。结果显示,SS2具有良好的生物被膜形成能力;T-La(S)、RGD-T-La(S)、T-La(FS)和RGD-T-La(FS)对SS2生物被膜的MBIC分别为31.3、15.6、7.8和15.6μg/mL;MBEC分别为62.6、31.2、15.6和31.2μg/mL;结晶紫染色结果表明,抗菌肽对SS2生物被膜的形成有抑制作用;扫描电镜结果显示,抗菌肽使SS2生物被膜中的细菌数量和生物被膜的形态发生明显变化,细胞外基质大量减少;XTT法结果显示,抗菌肽可显著降低SS2生物被膜的代谢活性;苯酚硫酸法结果显示,抗菌肽能有效抑制SS2生物被膜合成胞外多糖;实时荧光定量PCR结果表明,抗菌肽作用后降低了SS2生物被膜基因的转录水平;T-La(FS)作用后TLR2、MyD88及促炎性细胞因子基因的转录水平显著或极显著降低(P<0.05;P<0.01),抗炎性细胞因子基因的转录水平显著或极显著升高(P<0.05;P<0.01)。抗菌肽主要通过影响生物被膜相关基因转录水平和阻断胞外多糖的合成与分泌来抑制SS2生物被膜的形成,其中T-La(FS)可能通过抑制TLR2信号通路中TLR2和MyD88分子表达,抑制炎性细胞因子的释放,减轻脑膜炎的炎性反应。 相似文献
10.
Salmonella living in biofilms are more resistant to chemical and physical stresses. However, information regarding the regulation of genes involved in biofilm formation for Salmonella enterica serovar Pullorum remains limited. In this study, eight mutants with knockout of genes ompR, rpoS, rfaG, rfbH, rhlE, metE, spiA, or steB from the Salmonella enterica serovar Pullorum strain S6702 were constructed. Phenotypic analysis revealed that all mutants were similar to the wild-type strain in growth rate. Only the ompR mutant showed a complete loss of production ofcurli and biofilm formation. The other mutants showed a modified production of curli and cellulose with less effect related to biofilm formation. The results of animal experiments indicated that the deletion of genes ompR, spiA, rfaG, or metE in wild-type strains contributed to attenuation of virulence in 1-day-old chickens. This study may bring new insights into novel vaccines or therapeutic interventions against Salmonella enterica serovar Pullorum infections. 相似文献
11.
旨在研究鼠伤寒沙门菌ABC转运膜蛋白SapC在沙门菌致病机制中的功能。本研究利用λ-Red重组技术构建了鼠伤寒沙门菌sapC基因缺失突变株SMΔsapC,对其进行生长特性、酸性应激试验、多黏菌素B敏感性试验、生物被膜检测、胞内存活和小鼠体内毒力试验。结果显示,基因缺失株SMΔsapC与亲本菌株和互补菌株相比,其生长速度无明显差异;在酸应激条件下,SMΔsapC存活率显著低于亲本菌株;sapC基因缺失降低了鼠伤寒沙门菌生物被膜的形成能力;同时,SMΔsapC基因缺失株在鼠源巨噬细胞内的增殖能力和小鼠体内的毒力显著低于亲本菌株。研究表明,sapC基因影响鼠伤寒沙门菌的抗酸能力、生物被膜形成能力,从而影响沙门菌在体内外的毒力。本研究为进一步阐释鼠伤寒沙门菌的致病机制奠定了基础。 相似文献
12.
试验旨在研究aroA基因对肠炎沙门菌生物学特性及毒力的影响。利用λ-Red同源重组技术，将从田间分离的禽源肠炎沙门菌的aroA基因进行敲除，经连续传代检测缺失株遗传稳定性，并通过细菌生长曲线、对不同生化反应管的利用情况、生物膜形成能力、对环境应激的抵抗能力及对1日龄雏鸡的毒力比较野生株和基因缺失株之间的差异。结果显示，试验成功构建缺失株，连续传30代未发现目的基因回复突变；在相同培养条件下，缺失株与野生株在相同时间进入对数生长期和稳定期，但缺失株生长速率低于亲本株；缺失株较野生株生化特性未发生改变；缺失株的生物膜形成能力及对酸、碱、高渗和热应激的抵抗能力均显著低于野生株（P<0.05）；1日龄雏鸡分别滴口接种缺失株和野生株，观察14 d，野生株组鸡全部死亡，而缺失株组无死亡。综上所述，本试验成功构建并获得了具有良好遗传稳定性的肠炎沙门菌aroA基因缺失株，缺失株生化特性和体外生长趋势未发生明显改变，但生物膜形成能力、对环境应激抵抗能力及毒力均明显下降。本研究为进一步研究肠炎沙门菌aroA基因缺失株的免疫原性奠定了基础。 相似文献
13.
Superoxide dismutase (SOD) is a virulence factor of certain pathogenic bacteria by diminishing the effect of oxidative burst of phagocytic cells. Earlier reports indicated the presence of manganese-cofactored SOD in Streptococcus suis type 2 (SS2). However, the biological role of SOD and its coding sequence in SS2 has not yet been characterized. The SSU1356-ORF of a clinical SS2 strain ZJ081101 encodes a protein of 201 amino acids with 81-88% identity to SodA of other Streptococcus spp. A sod deletion mutant (Δsod) from the clinical strain was constructed. SOD activity was absent in the cell extract from the Δsod mutant, but present in that from the wild-type or the sod-complemented (CΔsod) strain. The Δsod mutant was more susceptible to oxidative stresses induced by hydrogen peroxide or paraquat. Survival of the sod deletion mutant in RAW264.7 macrophages was only half of that of the wild-type strain. Deletion of sod significantly attenuated virulence of SS2 to mice. Effects of such genetic deletion were complementable using the strain CΔsod. The co-inoculation experiment in mice revealed that the Δsod mutant was far more easily cleared from the body than the wild-type strain as shown by about 3-log reduction of its infection potential in blood and tissues. In summary, we reveal an important role of SOD in pathogenesis of S. suis type 2, most probably by scavenging reactive oxygen species from macrophages. 相似文献
14.
Edwardsiella tarda is a Gram-negative broad-host-range pathogen that causes hemorrhagic septicemia in many commercially important fish species. Its ability to adapt to and thrive in diverse environments outside and inside of its hosts prompts us to investigate the roles of the previously identified 33 putative two-component signal transduction systems (TCSs) in E. tarda. In this work, we successfully constructed deletion mutations in each of the response regulator genes, suggesting that none of the TCSs are essential for cell viability in E. tarda. The mutants were further examined for roles in biofilm formation, antibiotic resistance, stress response, expression and secretion of proteins involved in either the type III secretion system (T3SS) or type VI secretion system (T6SS), as well as virulence. Through these assays, we identified four regulators of biofilm development, two regulators of antibiotic resistance, and four regulators involved in stress responses. We found that two regulators, EsrB and PhoP, are essential for the pathogenicity of E. tarda and further demonstrated that these two regulators have codependent and independent contributions to E. tarda virulence. Mutation of EsrB resulted in the complete loss of both the T3SS and T6SS proteins, while PhoP partially regulated the expression of T3SS and T6SS genes through EsrB, and was essential for resistance to antimicrobial peptides. This work suggested that these two response regulators are involved in the regulation of the complex virulence network of this bacterium and merit as candidate genes for live attenuated vaccine construction. 相似文献
15.
Jing Tu Fengying Lu Shuang Miao Xintao Ni Pan Jiang Hui Yu Linlin Xing Shengqing Yu Chan Ding Qinghai Hu 《Veterinary microbiology》2014,168(2-4):395-402
Riemerella anatipestifer causes epizootic infectious disease in poultry and serious economic losses especially to the duck industry. However, little is known regarding the molecular basis of its pathogenesis. The ability to acquire iron under low-iron conditions is related to the virulence of a variety of bacterial pathogens. In this study, a sip (Riean_1281) deletion mutant CH3Δsip was constructed and characterized for iron-limited growth, biofilm formation, and pathogenicity to ducklings. Results showed that siderophore-interacting protein (SIP) was involved in iron utilization and the sip deletion significantly reduced biofilm formation and adherence to and invasion of Vero cells. In addition, the sip gene was absent in 1 of 24 (4.17%) virulent strains and 2 of 3 (66.7%) avirulent strains of R. anatipestifer, and the sip gene from six R. anatipestifer strains, which belong to serotypes 1, 2, and 10, respectively, shared 100% amino acid identities to those of R. anatipestifer strains DSM15868 and RA-GD. These results suggested that siderophore-mediated iron acquisition may be an important iron-uptake pathway in R. anatipestifer. Animal experiments indicated that the median lethal dose of the CH3Δsip mutant in ducklings was about 35-fold higher than that of the wild-type CH3 strain. Thus, our results demonstrated that R. anatipestifer SIP was involved in iron acquisition and necessary for its optimal virulence. 相似文献
16.
Jinquan Li Chen Tan Yang Zhou Shulin Fu Linlin Hu Jin Hu Huanchun Chen Weicheng Bei 《Veterinary microbiology》2011
Two-component regulatory systems (TCSs) are widely distributed among bacteria and enable the organisms to make coordinated changes in gene expression in response to a variety of environmental stimuli. In this work, we constructed a mutant strain of the TCS CiaRH and measured its virulence in vitro and in vivo. Compared with the wild type strain, the mutant strain exhibited a significant decrease in adherence to epithelial cells Hep-2 and PIEC. Furthermore, the deletion of CiaRH not only enhanced the bactericidal activity of RAW264.7 macrophage against Streptococcus suis 2, but also increased blood clearance of S. suis 2 in vivo. More importantly, the mutant was attenuated in vivo in CD1 mice and pigs, with reduced mortality, morbidity and impaired bacterial growth observed in specific organs. These results suggest that the CiaRH is required for S. suis 2 virulence. 相似文献
17.
Duan Q Zhou M Zhu X Bao W Wu S Ruan X Zhang W Yang Y Zhu J Zhu G 《Veterinary microbiology》2012,160(1-2):132-140
Bacterial flagella contribute to pathogen virulence; however, the role of flagella in the pathogenesis of F18ab E. coli-mediated swine edema disease (ED) is not currently known. We therefore evaluated the role of flagella in F18ab E. coli adhesion, invasion, biofilm formation, and IL-8 production using an in vitro cell infection model approach with gene-deletion mutant and complemented bacterial strains. We demonstrated that the flagellin-deficient fliC mutant had a marked decrease in the ability to adhere to and invade porcine epithelial IPEC-J2 cells. Surprisingly, there was no difference in adhesion between the F18 fimbriae-deficient ΔfedA mutant and its parent strain. In addition, both the ΔfedA and double ΔfliCΔfedA mutants exhibited an increased ability to invade IPEC-J2 cells compared to the wild-type strain, although this may be due to increased expression of other adhesins following the loss of F18ab fimbriae and flagella. Compared to the wild-type strain, the ΔfliC mutant showed significantly reduced ability to form biofilm, whereas the ΔfedA mutant increased biofilm formation. Although ΔfliC, ΔfedA, and ΔfliCΔfedA mutants had a reduced ability to stimulate IL-8 production from infected Caco-2 cells, the ΔfliC mutant impaired this ability to a greater extent than the ΔfedA mutant. The results from this study clearly demonstrate that flagella are required for efficient F18ab E. coli adhesion, invasion, biofilm formation, and IL-8 production in vitro. 相似文献
18.
大肠杆菌Ⅲ型分泌系统2（Escherichia coli type III secretion system 2，ETT2）参与禽致病性大肠杆菌（avian pathogenic Escherichia coli，APEC）的致病作用。本研究旨在探究ETT2结构基因epaPQR对禽致病性大肠杆菌的生物学特性及致病作用的影响，为进一步阐明ETT2的致病机制提供依据。基于CRISPR-Cas9基因编辑技术，构建epaPQR基因缺失株和回复株，通过生长曲线测定、运动性和生物被膜形成能力等试验，分析epaPQR基因对APEC生物学特性的影响；通过血清杀菌与组织载菌量等试验分析epaPQR基因对APEC致病性的影响。结果表明，成功构建ETT2结构基因epaPQR基因缺失株和回复株，epaPQR基因缺失后，其生长能力和生物被膜形成能力并没有显著改变（P>0.05）；但epaPQR基因缺失后，其运动能力显著降低（P<0.05），在透射电镜下观察到缺失株鞭毛数量明显减少，通过荧光定量PCR发现，鞭毛T3SS结构基因及鞭毛输出蛋白基因的转录水平均显著下调（P<0.05）。epaPQR基因缺失后其抗血清杀菌能力显著增强（P<0.05），缺失株AE81ΔepaPQR在雏鸡体内不同器官的定殖能力显著降低。结果说明，ETT2结构基因epaPQR参与调控APEC的鞭毛形成，影响APEC抗血清杀菌能力以及在体内组织器官的定殖能力，表明epaPQR在APEC致病过程中发挥重要作用，本研究为深入探究ETT2功能和APEC致病机制提供参考。 相似文献
19.
生物被膜是导致细菌产生耐药性的主要原因之一,本文通过探究Ⅲ型分泌系统2（ETT2）转录调节因子YqeI对禽致病性大肠杆菌生物被膜形成的影响及其影响机制,为探究ETT2对禽致病性大肠杆菌致病机制的影响提供研究基础。利用Red同源重组的方法构建yqeI基因缺失株,并通过检测野生株与缺失株生物被膜形成能力、结合转录组学测序及荧光定量检测生物被膜基因表达量等,探究转录调节因子YqeI对禽致病性大肠杆菌生物被膜形成能力的影响。结果显示成功构建了yqeI基因缺失株,且yqeI的缺失并不影响生长曲线,但生物被膜形成能力显著下降,且相关生物被膜基因转录量显著下调。禽致病性大肠杆菌ETT2转录调节因子YqeI显著影响了禽致病性大肠杆菌生物被膜形成能力,为从ETT2及yqeI的角度发掘潜在的调控网络提供依据。 相似文献
20.
副溶血性弧菌（Vibrio parahaemolyticus）是海洋环境中常见的食源性致病茵。本研究从对虾中分离出1株细菌SHJLA,在TCBS和弧菌显色培养基上分别显示典型的蓝绿色和紫红色的菌落,且其生理生化特性具有典型副溶血弧菌的特性。以SHJLA菌株的基因组为模板。检测副溶血弧菌种特异性基因（tlh、toxR、groEL）均为阳性,gyrB基因序列分析表明SHJLA与副溶血弧茵的亲缘关系最近,同源性达98％～100％;检测副溶血弧菌主要毒力相关基因tdh和T3SS2（VopC2和vcrD2）均为阳性。该菌的神奈川溶血实验为阳性,对小鼠的半数致死量（LD50）为4．8×10^8 cfu／mL。结合SHJLA菌株的形态、生理生化、种特异性基因的检测、gyrB基因序列分析、毒力相关基因的检测以及小鼠半数致死量的测定结果,确定SHJLA是一株携带毒力基因的副溶血弧菌。 相似文献