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1.
A temperature-sensitive (Ts) mutant strain of Ornithobacterium rhinotracheale (ORT) was developed after exposure of the wild-type organism to N-methyl-N'-nitro-N-nitrosoguanidine. The Ts mutant strain grew at 31 C but had its growth inhibited at 41 C unlike wild-type parent strain. The Ts mutant and parent strains were characterized. Morphologic and biochemical properties of wild-type and mutant strains did not show any differences. The strains were also characterized by polymerase chain reaction (PCR)-based fingerprinting methods. Results showed similar patterns in repetitive sequences by repetitive PCR (enterobacterial repetitive intergenic consensus, highly conserved repeated DNA elements present in Streptococcus pneumoniae (BOX), repetitive extragenic palindromic, and Salmonella enteritidis repetitive element primers); however, random amplified polymorphic DNA fingerprinting was able to differentiate mutant and parent strains showing a unique pattern for each of the ORT strains. The rationale for the use of a Ts strain as a vaccine is based on the ability of the mutant to colonize the upper respiratory tract but not the lower respiratory tract and systemic system of the birds, where the wild-type strain causes severe lesions. In a preliminary evaluation, Ts strain of ORT was recovered from tracheas and choanae of Ts-treated turkeys for 13 days postadministration of the strain either in drinking water or by oculonasal instillation. Humoral immune response was detected in Ts-vaccinated but not in control group birds after 3 wk postadministration. Results suggest that Ts strain of ORT has promising potential use as a live vaccine for ORT.  相似文献   

2.
Invasion of Salmonella into intestinal epithelial cells is believed to be essential for the pathogenesis of Salmonella infections. Invasion is mediated by genes located on the Salmonella pathogenicity Island I (SPI-1), which are needed for assembling a type three secretion system, that mediates injection of bacterial proteins into the cytosol of epithelial cells, resulting in cytoskeletal rearrangements and as a consequence invasion. HilA is the key regulator of the Salmonella Pathogenicity Island I. To assess the role of hilA in colonization of gut and internal organs in poultry, animals were infected with 10(8) CFU of a delta hilA mutant of S. Enteritidis and its parent strain at day of hatch. Very low numbers of delta hilA mutant strain were able to colonize the internal organs shortly after infection, but they were not eliminated from internal organs at 4 weeks post-infection. At that time, the colonization level of the wild type bacteria in internal organs was decreased to the same low level compared with delta hilA mutant strain bacteria. Shedding of the delta hilA mutant strain and colonization of the caeca was seriously decreased relative to the parent strain starting from Day 5 post-infection. At 4 weeks post-infection, the delta hilA mutant strain was more or less eliminated from the chicken gut, while the parent strain was still shed to a high level and colonized the caeca to a high extent (more than 10(7) CFU/g). It is concluded that hilA is involved in long-term shedding and colonization of S. Enteritidis in the chicken caeca.  相似文献   

3.
为探究内化素inlA/inlB/inlC基因对单增李斯特菌(Listeria monocytogenes,Lm)生物学特性的影响,本研究采用融合PCR方法构建Lm681 inlC基因缺失突变体,并构建pKSV7-△inlC穿梭载体,将其转化Lm681-△inlAB感受态细胞,利用温度(42℃)和氯霉素(10μg/mL)抗性双重压力来实现同源重组,筛选同源重组子进行鉴定并研究其部分生物学特性。结果显示,PCR和测序结果证实成功构建了3基因缺失株(Lm681-△inlABC),且缺失株的生长特性与野生株相比无明显差异,溶血特性与野生株保持一致;小鼠感染试验显示,野生株Lm681、Lm681-△inlAB和Lm681-△inlABC对小鼠的致死率分别为80%(8/10)、60%(6/10)和40%(4/10),对小鼠的LD50分别为4.36×10~4、1.35×10~6和2.95×10~7 CFU,且Lm681-△inlABC在肝脏、脾脏及脑组织中的定植能力极显著低于野生株(P<0.01)。研究结果表明,inlA/inlB/inlC基因对Lm致病性发挥具有一定的作用,为深入研究inlX基因介导Lm入侵宿主细胞过程中的作用机制提供了科学依据。  相似文献   

4.
Chickens were immunized orally with 10(9)cfu of the temperature-sensitive (T(s)) mutant E/1/3 of Salmonella enteritidis at 1, 2, 3 and 7 days of age. The animals were challenged with wild-type strains of Salmonella of different serotypes 7 or 14 days following immunization. Chickens receiving multiple oral doses of the vaccine strain showed no signs of disease. Immunized animals shed the vaccine strain for at least 2 weeks after the last inoculation; on the other hand, colonization by the attenuated mutant of internal organs such as spleen and liver was limited. Early exposure of the immunized animals to the virulent bacteria resulted in a reduced cecal colonization by the pathogen. Visceral invasion by the wild-type strain of S. enteritidis or S. gallinarum was drastically diminished in birds challenged 14 days after immunization. Significant differences in the number of these Salmonella were found in the cecal contents, spleen and liver of immunized birds compared with the control animals. In addition, cecal colonization by the virulent strain was reduced in birds challenged with S. typhimurium. These results demonstrate that immunization of newly hatched chickens with live attenuated T(s) mutant E/1/3 of S. enteritidis is safe and reduces Salmonella shedding.  相似文献   

5.
Campylobacter jejuni, a common commensal in chickens, is one of the leading causes of bacterial gastroenteritis in humans worldwide. The aims of this investigation were twofold. First, we sought to determine whether mutations in the C. jejuni ciaB and pldA virulence-associated genes impaired the organism's ability to colonize chickens. Second, we sought to determine if inoculation of chicks with C. jejuni mutants could confer protection from subsequent challenge with the C. jejuni wild-type strain. The C. jejuni ciaB gene encodes a secreted protein necessary for the maximal invasion of C. jejuni into cultured epithelial cells, and the pldA gene encodes a protein with phospholipase activity. Also included in this study were two additional C. jejuni mutants, one harboring a mutation in cadF and the other in dnaJ, with which we have previously performed colonization studies. In contrast to results with the parental C. jejuni strain, viable organisms were not recovered from any of the chicks inoculated with the C. jejuni mutants. To determine if chicks inoculated with the C. jejuni mutants become resistant to colonization by the C. jejuni parental strain upon subsequent challenge, chicks were inoculated either intraperitoneally (i.p.) or both orally and i.p. with the C. jejuni mutants. Inoculated birds were then orally challenged with the parental strain. Inoculation with the C. jejuni mutants did not provide protection from subsequent challenge with the wild-type strain. In addition, neither the C. jejuni parental nor the mutant strains caused any apparent morbidity or mortality of the chicks. We conclude that mutations in genes cadF, dnaJ, pldA, and ciaB impair the ability of C. jejuni to colonize the cecum, that chicks tolerate massive inoculation with these mutant strains, and that such inoculations do not provide biologically significant protection against colonization by the parental strain.  相似文献   

6.
The present study was conducted to study the impact of the virulence factors invC and sseD of the two type III secretion systems of Salmonella enterica serovar Typhimurium (S. Typhimurium) on the pathogenesis of the porcine S. Typhimurium DT104 infection. For this purpose, two S. Typhimurium mutant strains with a disrupted invC gene of the Salmonella pathogenicity island 1 or with a disrupted sseD gene of the Salmonella pathogenicity island 2 have been studied in experimental infection of pigs. Twenty-two 7-week-old male hybrid pigs were either infected with one of the mutants or the wild-type S. Typhimurium DT104 strain. Each group was examined for clinical signs, Salmonella shedding rate and the specific antibody response. Survival and replication were evaluated by qualitative and quantitative determination of the colonization rate. The humoral and cellular immune responses were examined using isotype-specific ELISA and quantitative real-time PCR of IL-2, IL-4, IL-10, IL-12 and IFN-gamma. The results proved that both mutants had a lower virulence (with marked differences between both mutants) than the wild-type and that both virulence factors have importance in porcine salmonellosis. Only pigs infected with the wild-type S. Typhimurium DT104 exhibited typical clinical symptoms of salmonellosis like anorexia, vomiting, disturbed demeanour, fever and diarrhoea. Deletion of the invC gene resulted in a significantly reduced colonization rate. Interestingly, the mRNA expression of both type-1 and type-2 cytokines were significantly decreased in pigs infected with either the invC-mutant and the sseD-mutant strain.  相似文献   

7.
试验旨在探究ClpS基因在布鲁氏菌中的作用,分析比较ClpS基因突变对布鲁氏菌毒力的影响。利用同源重组技术,构建布鲁氏菌ClpS基因突变株,通过检测细菌生长曲线、细菌LPS合成能力及其在巨噬细胞内的存活能力和小鼠模型中的毒力,比较亲本株2308和突变株ΔClpS两者之间的差异。结果显示,在相同的培养条件下,亲本株2308和突变株ΔClpS的细菌浓度无明显差异,且两者提取的LPS银染结果基本一致,表明ClpS基因突变不影响布鲁氏菌生长速度,不影响细菌LPS合成;在细胞感染模型中,突变株ΔClpS在感染后72 h的胞内存活能力极显著低于亲本株2308（P<0.01）;小鼠感染试验显示,在感染后1周,亲本株2308感染组和突变株ΔClpS感染组小鼠脾脏重量及细菌含量无显著差异,但在感染后4周,突变株ΔClpS感染组的小鼠脾脏细菌含量为103.93 CFU/g脾脏,显著低于亲本株2308（106.68 CFU/g脾脏,P<0.01）,且突变株ΔClpS感染组的小鼠脾脏肿胀程度极显著低于亲本株2308（P<0.01）。综上所述,布鲁氏菌ClpS基因突变不影响细菌生长速度及细菌LPS合成能力,但ClpS基因突变可降低布鲁氏菌在小鼠脾脏内的定殖能力。  相似文献   

8.
The present study aimed to determine the role of ClpS gene,and to analyse the impact of ClpS mutation on the virulence of Brucella.A ClpS gene mutant strain,named ΔClpS was constructed by homologous recombination technology.The bacterial growth kinetics,the LPS synthesis ability and the survival ability of bacterial within macrophages as well as the virulence in mouse model were measured.In addition,the difference between parent strain 2308 and the mutant strain ΔClpS were compared.The results showed that under the same culture conditions,no difference in bacterial concentration was observed between 2308 and ΔClpS strains.The silver staining examination showed that the expression level of LPS extracted from two strains were similar,indicating ClpS gene mutation did not alter the growth rate and LPS synthesis ability of Brucella. In the cell infection assay,the survival ability of ΔClpS strain in cells was extremely significantly lower than that of 2308 strain at 72 h after infection (P<0.01).The results of mouse infection experiment showed that in the first week after infection,no significant difference in spleen weight and bacterial concentration between 2308 and ΔClpS strains infected mice was observed.However,at 4 weeks after infection,the bacterial concentration in spleen of ΔClpS infected mice was 103.93 CFU/g spleen,which was significantly lower than that of 2308 strain (106.68 CFU/g spleen,P<0.01).The spleen weight of ΔClpS infected mice was also remarkably lower than that of 2308 strain (P<0.01).In summary,the results suggested that the ClpS gene of Brucella did not play a role in Brucella growth rate and ability of LPS synthesis,whereas ClpS gene mutation decreased the ability of Brucella colonization in mouse spleen.  相似文献   

9.
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   

10.
Two Bordetella bronchiseptica mutants, lacking the adenylate cyclase (Cya) or both Cya and pertactin (Prn), were compared with their parental strain NL1013 in their abilities to colonize the nose of neonate piglets and to induce local and systemic antibody responses against filamentous hemagglutinin (FHA) after intranasal (i.n.) inoculation. The number of bacteria recovered and the duration of infection in the nasal secretions were greater for the wild-type parent strain than for the Cya-deficient mutant, indicating that Cya plays an important role during B. bronchiseptica colonization of the nasal cavity. The double mutant did not colonize the nasal cavity and was less able to adhere to epithelial cells in vitro than the other two strains, supporting the hypothesis that Prn plays a major role in cell adhesion. In piglets inoculated with the wild type strain, anti-FHA IgM was found in the nasal secretions one week after inoculation, followed two weeks later by anti-FHA IgA; their presence was concomitant with decreases in bacterial counts. Anti-FHA IgG appeared at six weeks after infection in the serum. In contrast, i.n. inoculation with either mutant failed to induce a nasal secretory antibody response but did induce an earlier and higher IgM response in the serum than inoculation with the wild type strain. However, only the Cya-deficient mutant was able to prime the piglets for the development of a secondary nasal IgM and serum IgG response to FHA after intranasal inoculation with the wild type B. bronchiseptica.  相似文献   

11.
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12.
Three swine commercial farms with high mortality rates in nursery pigs due to Streptococcus suis serotype 2 were studied. Brain samples from diseased animals were collected for a period of 6 to 10 mo and used to isolate the strain that was responsible for the mortality (virulent strain) in each farm. Tonsil swabs from piglets at 5, 10 and 15 d were taken to assess both total colonization and colonization by the virulent strain. The effect of sow vaccination against S. suis on colonization was evaluated in 1 of the farms. All suspect tonsil isolates were identified biochemically and then tested against serotype 2. The genomic patterns of serotype 2 isolates were compared to that of the virulent strain using Rep-PCR. Results showed that total colonization by S. suis occurred very early in the pigs' life, with most animals being colonized by weaning age. Prevalence of colonization by serotype 2 strains was much lower than total colonization. After comparing serotype 2 isolates with the virulent strains, only 1 tonsillar isolate had the same genomic pattern as the virulent strain and it belonged to a 4-week-old weaned pig. The genomic pattern of the virulent strain was not found in any tonsillar isolate from 15-day-old or younger pigs. Although limited by sample size, sow vaccination against S. suis increased total colonization at the same time significantly decreasing colonization by serotype 2 strains. Even though most pigs are colonized early in age by S. suis, colonization by the virulent strain is of low prevalence and delayed in time. This could constitute a risk factor for developing the disease later in time, because animals would be colonized when maternal immunity is no longer present, allowing the organism to become systemic.  相似文献   

13.
The diseases caused by pathogenic Escherichia coli constitute a major economic loss to the poultry industry. The development of a live oral E. coli vaccine to prevent or reduce diseases in poultry had been the objective of our work. Four spontaneous streptomycin-dependent (str-dependent) mutants were generated from a virulent avian strain that contains a mutation in the fur region of the chromosome. Genetic analysis of the mutants indicated that the str-dependent phenotype was due to a base change of C --> T at base 272 in the rpsL gene. The mutants were tested for attenuation using the day-old chick model. Day-old birds, in groups of 20, were either challenged with 10(6) colony-forming units (CFU) of the str-dependent mutant, the parent strain (containing the fur mutation), or the wild-type strain without the fur mutation. The parent strain and the wild-type strain were highly virulent, and 80% or more of the birds died. None of the birds challenged with the str-dependent mutants died, indicating attenuation of the mutants. The protective effect of the mutant as a live vaccine against the challenge with 10(6) CFU of the wild-type strain EC317 was investigated. Vaccination by both aerosol (day 1) and oral (days 14 and 28) routes using 10(8) CFU of the str-dependent mutant (EC1598) had no effect on the occurrence of cellulitis in the birds. Two vaccinations given as aerosol on day 1 and given orally on day 14 also had no significant effect on the occurrence of systemic lesions. Three immunizations on days 1, 14, and 28 resulted in a significant reduction in the number of birds with systemic lesions. Antibody titers prior to challenge were not predictive of outcome of challenge.  相似文献   

14.
Salmonella enterica serotype Gallinarum (S. Gallinarum) is the causative agent of fowl typhoid (FT) in chickens. FT is a severe systemic disease of chickens causing heavy economic losses to the poultry industry through mortality, reduced egg production and culling of precious breeding stocks. In this study, a metC (encoding cystathionine beta lyase) mutant was produced from a virulent strain of S. Gallinarum by Mini-Tn5 insertional inactivation. The mutant was significantly attenuated in virulence for 1-day-old White Leghorn chickens. Inactivation of metC resulted in 10(4)-fold increase in the LD50 when compared with the wild type parent. The metC mutant showed an in vivo competitiveness defect in the challenged chickens and significantly lower (P < 0.01) bacterial burden in the reticuloendothelial organs when compared with the wild-type parent. These results indicate that metC gene is important for virulence of S. Gallinarum in chickens.  相似文献   

15.
Attenuated derivatives (delta cya delta crp mutants) of an O2 and an O78 avian septicemic Escherichia coli strain were used to immunize broiler chickens by spray to determine the safety, immunogenicity, and efficacy of the derivatives in single- and double-dose regimens. In the safety and immunogenicity studies, groups of 10 chickens were vaccinated by spray (droplet size approximately 20 microm) with the parent E. coli, the mutant organisms, or phosphate-buffered saline (PBS) at 14 days of age and euthanatised 21 days later. There was no deaths or gross pathologic finding in any of the chickens immunized with the vaccine strains. Compared with the levels in chickens exposed to PBS, there were significantly higher levels of immunoglobulin (Ig) G antibody in serum and air sac washings and of IgA antibody in air sac washings in response to the virulent parent strains than to the vaccine strains. In efficacy studies, chickens were immunized with the O2 or the O78 vaccine strain or PBS at day 14 and with the O2 vaccine strain or PBS at days 10 and 14 and challenged with the parent strain 10 days after the last vaccination. There was no significant difference in local IgA and IgG and serum IgG responses between vaccinated and control groups. Chickens vaccinated with the O2 strain, but not the O78 strain, had significantly lower air sac lesion scores compared with those of the unvaccinated groups in both single- and double-dose regimens. We conclude that the mutant O2 strain provided moderate protection against airsacculitis.  相似文献   

16.
本研究旨在阐明鸭疫里默氏杆菌RA-LZ01株GE296_RS01450基因介导其对重金属离子产生耐受性的作用。构建RA-LZ01株的GE296_RS01450基因缺失株Δ1450和回复株cΔ1450,测定菌株的生长曲线、抗菌素对菌株的最小抑菌浓度（MIC）、菌株对重金属离子的耐受程度以及GE296_RS01450基因在特异性重金属离子刺激下的转录水平。结果显示,与亲本株相比,缺失株的生长能力以及11类抗菌素对缺失株的MIC值均无明显变化;与亲本株和回复株相比,缺失株对重金属离子Ni、Mn和Co的敏感性显著上升,并且在Ni、Mn刺激下,GE296_RS01450基因的转录水平显著上调。上述结果表明,GE296_RS01450基因不参与亲本株的生长及菌株对抗菌素的耐药性,可介导菌株对Ni、Mn和Co产生耐受性。GE296_RS01450基因属于GE296_RS01445-GE296_RS01450-GE296_RS01455 RND外排泵,编码外膜蛋白,我们将其命名为RopM。  相似文献   

17.
兔肠致病性大肠杆菌(rEPEC)菌株RDEC-1的基因组中lifA基因与LEE(Locus for enterocyte effacement)致病岛相毗邻.本试验通过DNA序列分析、基因打靶技术、细胞因子检测以及动物试验,分析lifA基因完整核苷酸序列及其生物学功能.结果表明,RDEC-1的lifA基因的核苷酸序列与人肠致病性大肠杆菌的完全相同;ifA基因具有降低家兔外周血单核细胞IL-2表达的作用.与野生型菌株RDEC-1相比,被定点敲除lifA基因的RDEC-1突变株(RDEC-1△lifA)口服接种家兔后,排菌量明显降低.利用野生型RDEC-1和RDEC-1△lifA基因缺失菌株同时口服接种家兔,从粪便中分离细菌,结果显示野生型RDEC-1是优势菌,而RDEC-1△lifA基因缺失菌数量极少.RDEC-1△lifA基因缺失菌株和野生型RDEC-1都能引起特征性家兔肠道上皮的黏附与细胞脱落病变(A/Elesion).表明rEPEC的lifA基因在免疫调节和细菌的肠道定居中起重要作用,这为研究lifA基因的生物学功能提供了直接证据.  相似文献   

18.
This study characterizes the clinical response and colonization pattern of caesarean-derived, colostrum-deprived swine exposed to a delta cya/delta crp mutant (chi 4233) of S. typhimurium and challenged with the wild-type parent strain. chi 4233 was mildly virulent in swine and induced transient fever and soft stools. Chi 4233 colonized the ileum, cecum, liver, spleen, tonsils, and mandibular and ileocolic lymph nodes of swine in a manner similar to the parental wild-type, but the numbers of S. typhimurium (chi 4233) in the ileum were 100- to 1000-fold less than those of pigs exposed to the parental wild-type. Pigs exposed to chi 4233 21 days before parental wild-type challenge demonstrated a milder clinical response to challenge than did pigs that did not receive chi 4233. The wild-type populations in the ilea of chi 4233-exposed pigs after challenge were 100- to 10,000-fold less than those in pigs not receiving chi 4233. The liver, spleen, and ileocolic lymph nodes were cleared of wild-type S. typhimurium more quickly after challenge in chi 4233-exposed pigs. The populations of chi 4233 in the ilea of exposed pigs after wild-type challenge were also less than would have been expected in unchallenged pigs. Thus, exposure of swine to a delta cya/delta crp mutant of S. typhimurium modulated the subsequent response to parental wild-type challenge and reduced carrier populations of wild-type S. typhimurium in infected swine.  相似文献   

19.
Several studies suggest that the expression of F1 fimbriae could be involved in the virulence of Escherichia coli for chickens. F1 fimbriae display multivalent properties such as adhesion to epithelia or interaction with the immune system that imply specific interactions between the adhesin FimH and different cell receptors. We constructed a delta fimH mutant of the avian pathogenic E. coli MT78 and evaluated its in vivo colonization and pathogenicity, as compared to that of the parent strain. The generated mutant PA68 was unable to adhere in vitro to chicken epithelial pharyngeal or tracheal cells; mutant bacteria were mostly afimbriated although a minority of them displayed altered piliation phenotypes. Two inoculation routes were used to compare the ability of MT78 and PA68 to colonize the respiratory tract and to induce colibacillosis in chickens. In the first model, 2-wk-old axenic chickens were inoculated intratracheally with one or both E. coli strains, after primary infection with infectious bronchitis virus. In the second model, 3-wk-old specific-pathogen-free chickens were inoculated via the caudal thoracic air sac. After intratracheal inoculation, the delta fimH mutant was found to be a better colonizer than MT78 in the trachea of inoculated chickens. Furthermore, when both strains were inoculated simultaneously, the delta fimH mutant constituted 98% of the bacterial population in the trachea at day 7 postinoculation. Irrespective to the inoculation route, MT78 and PA68 showed similar abilities to induce macroscopic lesions in chickens, to provoke bacteremia, and to colonize the internal organs. However, 4 days after intra-air sac inoculation, bacterial counts of the mutant were lower in the spleen and liver than those of MT78. Our results show that FimH is not required for colonization of the trachea of axenic chickens by E. coli and that it is not a major determinant of bacterial pathogenicity. On the contrary, the lack of expression of FimH seems to favor the in vivo colonization of the trachea of chickens by E. coli.  相似文献   

20.
CpxR是细菌中Cpx双组分系统（two component system,TCS）的反应调控蛋白,通过调控靶基因的转录表达,在细菌细胞膜稳定及毒力方面发挥作用。本研究旨在探究TCS CpxR对禽致病性大肠杆菌（avian pathogenic Escherichia coli,APEC）基本生物学特性、抗血清杀菌能力及致病性的影响。利用Red同源重组系统及互补质粒构建cpxR基因缺失株、互补株,然后比较分析野生株、基因缺失株与互补株的生长曲线、运动性、生物被膜形成能力、药物敏感性、抗血清杀菌能力、动物致病性的差异。结果显示：cpxR基因缺失株与野生株、互补株的生长速度和运动性能无明显差异,且缺失cpxR基因不影响APEC的生物被膜形成能力。然而,缺失CpxR导致APEC对阿米卡星和卡那霉素耐药性降低。血清杀菌试验结果显示,CpxR有助于APEC的抗血清杀菌能力。动物感染试验结果显示,野生株、cpxR基因缺失株和互补株对雏鸭的半数致死量（LD50）分别为7.50×105、7.50×106、1.33×106 CFU,表明CpxR缺失显著降低APEC的毒力。综上表明,TCS CpxR在APEC耐药性、抗血清杀菌能力及毒力方面发挥作用,为阐明APEC的环境适应性、生存能力及致病机制提供参考。  相似文献   

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