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1.
为了解猪伪狂犬病病毒(PRV)变异株R13139株对猪的致病性情况,本试验将PRV R13139株和PRV经典强毒株SC株均以10~6 TCID_(50)剂量经滴鼻途径接种6和9周龄健康仔猪各3头,空白对照组鼻腔接种生理盐水,通过攻毒后两个年龄段猪的临床症状表现、眼观病例变化、显微病理变化、抗体产生情况及病毒在体内部分情况评定两毒株对猪的致病力差异。结果显示,SC株对6和9周龄猪的致死率分别为66.7%(2/3)和100.0%(3/3),而R13139株对6和9周龄猪的致死率分别为33.3%(1/3)和66.7%(2/3),表明R13139株对猪的致死性弱于SC株,但R13139株引起两个年龄段猪发病时间比SC株早,同时间段的体温升高幅度更高,神经发症状更严重;眼观病理变化发现,R13139株引起的发病猪肝脏坏死现象比SC株更明显,而心脏、肺脏、脾脏、膀胱和脑的病理变化差异不明显;显微病理结果显示,R13139株对病猪的扁桃体、肺脏、肝脏和三叉神经节等组织造成的病理损伤明显强于SC株;PCR结果显示,R13139株在濒死猪扁桃体、脾脏、肺脏、三叉神经节和淋巴节(腹股沟、肠系膜和颌下)等组织脏器中分布比SC株更广泛;应用ELISA检测攻毒猪抗体发现,R13139株诱导PRV-gB抗体产生的时间比SC株早1d。本研究结果可为揭示中国伪狂犬病重新流行的原因及进一步开展防控技术研究提供科学依据。  相似文献   

2.
为了解广东省猪伪狂犬病病毒(pseudorabies virus,PRV)野毒株的基因变异及遗传演化的情况,本试验对广东佛山疑似暴发伪狂犬病的猪场采集的病料(脑、肺脏、扁桃体、肝脏、脾脏)进行了PCR鉴定,初步鉴定为PRV毒株后,将阳性病料接种非洲绿猴肾细胞(Vero),进行毒株传代培养,对分离毒株进行PCR检测及小鼠感染试验,证实该病毒为PRV,并命名为PRV FS-2015株;并对该毒株进行细胞病变观察、病毒TCID50测定、毒株gC和TK基因扩增及序列分析。结果显示,PRV FS-2015株TCID50为10-7.5/0.1 mL。PRV FS-2015株的gC和TK基因序列与国内外PRV参考毒株进行同源性比对分析发现,其核苷酸序列同源性分别为95.8%~100.0%和99.4%~100.0%,氨基酸同源性分别为92.3%~100.0%和98.7%~100.0%。遗传进化分析表明,PRV FS-2015株与国内近几年分离的PRV变异株GY、ZJ01、HB1201、HN1201、JS2012、BJ/YT和BP属于同一分支,同源性较高,亲缘关系更近;但与PRV经典株Kaplan、Becker、NIA3、Kolchis、Bartha、Yangsan、Min-A、SS和SL株的同源性较低,基因变异较大,表明PRV FS-2015毒株属于近几年流行的变异株。本研究结果可为广东省伪狂犬病的防控工作和疫苗株的选择提供科学依据。  相似文献   

3.
为确诊广东某猪场母猪流产发病原因,本研究收集该猪场流产死胎的脑、淋巴结、肺脏混合液,进行PCR鉴定、病毒分离培养、半数组织培养感染剂量(tissue culture infective dose,TCID50)测定、猪伪狂犬病病毒(pseudorabies virus,PRV)重要功能基因(gB、gC、gD、gE)序列测定和进化分析及动物回归试验。结果显示,病料混合液为PRV阳性,接种Vero细胞传至第3代即出现稳定的细胞病变(CPE),第5代TCID50达到10-6.8/0.1 mL,PRV gB、gC、gD、gE基因序列测定、同源性及进化树分析显示为,PRV中国变异株,命名为LC株。动物试验显示,LC株对12周龄猪具有一定致病性,可形成PRV典型临床症状及病理变化。本研究分离到一株PRV流行毒株,推测当前使用疫苗Bartha-K61株尚无法完全控制新毒株的流行。  相似文献   

4.
《畜牧与兽医》2014,(10):11-14
2011年以来,我国多个省份伪狂犬病免疫猪群相继暴发伪狂犬病疫情。为了探明伪狂犬病毒(PRV)流行毒株是否存在抗原变异,本研究从3个规模猪场3种PRV商品疫苗免疫的健康猪群中采集30份血清,经检测PRV gB ELISA抗体均为阳性,gE ELISA抗体均为阴性。采用PRV新流行毒株ZJ-01株和传统的LA毒株分别进行血清中和抗体测定,结果显示,3个毒株活疫苗免疫血清与ZJ-01株中和抗体效价明显低于其与LA株中和抗体效价。同时,ZJ-01株抗血清与ZJ-01株和LA株的中和抗体效价相似,其变异系数R值为0.2790.413,证明PRV分离毒株ZJ-01抗原性发生明显变异。本研究为伪狂犬病的防控提供了重要依据。  相似文献   

5.
为评估猪伪狂犬病病毒(Pseudorabies virus,PRV)灭活疫苗(HN1201-ΔgE株)免疫后对PRV流行毒株和经典毒株的保护效果,本研究对试验猪分别免疫PRV灭活疫苗(HN1201-ΔgE株)和PRV活疫苗(Bartha-K61),免疫后第0、7、10、14、17、21、24和28天采血测定PRV gB抗体,并分别使用PRV流行毒株HN1201株和经典毒株闽A株测定免疫后第0、7、14、21和28天血清的中和抗体水平,于免疫后第28天分别使用HN1201株和闽A株攻毒并观察,之后测定体温,测定攻毒后第7和14天PRV gE抗体,及攻毒后0~8 d的排毒情况。结果显示,HN1201-ΔgE免疫组较Bartha-K61免疫组gB抗体和中和抗体产生早,且抗体水平较高。两个免疫组试验猪在攻毒后虽然均无明显临床症状,且免疫组织化学检测(IHC)组织中的病毒抗原均为阴性,但HN1201-ΔgE免疫组试验猪脏器未见任何病理损伤,Bartha-K61免疫组试验猪部分脏器具有病理损伤。与未免疫对照组相比,2个免疫组试验猪在HN1201株和闽A株攻毒后,gE抗体转阳时间晚且排毒率低,HN1201-ΔgE免疫组gE抗体水平整体均低于Bartha-K61免疫组,攻毒后排毒检测中,Bartha-K61免疫组于2个毒株攻毒后第3~5天可检测到排毒,而HN1201-ΔgE免疫组全程未检测到排毒。研究结果表明,灭活疫苗(HN1201-ΔgE株)对PRV流行毒株和经典毒株均可提供完全保护。  相似文献   

6.
一株猪伪狂犬病病毒变异株的分离鉴定   总被引:3,自引:2,他引:1  
为了解广东省猪伪狂犬病病毒(pseudorabies virus,PRV)野毒株的基因变异及遗传演化的情况,本试验对广东佛山疑似暴发伪狂犬病的猪场采集的病料(脑、肺脏、扁桃体、肝脏、脾脏)进行了PCR鉴定,初步鉴定为PRV毒株后,将阳性病料接种非洲绿猴肾细胞(Vero),进行毒株传代培养,对分离毒株进行PCR检测及小鼠感染试验,证实该病毒为PRV,并命名为PRV FS-2015株;并对该毒株进行细胞病变观察、病毒TCID50测定、毒株gC和TK基因扩增及序列分析。结果显示,PRV FS-2015株TCID50为10-7.5/0.1mL。PRV FS-2015株的gC和TK基因序列与国内外PRV参考毒株进行同源性比对分析发现,其核苷酸序列同源性分别为95.8%~100.0%和99.4%~100.0%,氨基酸同源性分别为92.3%~100.0%和98.7%~100.0%。遗传进化分析表明,PRV FS-2015株与国内近几年分离的PRV变异株GY、ZJ01、HB1201、HN1201、JS2012、BJ/YT和BP属于同一分支,同源性较高,亲缘关系更近;但与PRV经典株Kaplan、Becker、NIA3、Kolchis、Bartha、Yangsan、Min-A、SS和SL株的同源性较低,基因变异较大,表明PRV FS-2015毒株属于近几年流行的变异株。本研究结果可为广东省伪狂犬病的防控工作和疫苗株的选择提供科学依据。  相似文献   

7.
伪狂犬病病毒gE/gB PCR鉴别方法的建立及其应用   总被引:5,自引:0,他引:5  
为了检测伪狂犬病病毒(PRV)潜伏感染及确定病毒潜伏的主要部位,建立了能鉴别PRV野毒株和gE基因缺失疫苗株gE/gB的PCR诊断方法。结果表明,所建立的PCR特异性强、敏感性高、稳定性好,能用于病毒潜伏感染的检测;同时还确定PRV潜伏感染的主要部位是三叉神经节、扁桃体、嗅球、脑干、脑桥和咽黏膜。  相似文献   

8.
为了解广西近年猪伪狂犬病(PR)流行情况及猪伪狂犬病病毒(PRV)流行株gBgETK基因的遗传变异特点,于2013-2018年采集广西各地区疑似PR发病猪靶组织714份,进行PRV的PCR检测及病毒分离鉴定,并运用DNAStar、MEGA 6.0等生物学软件对分离毒株gBgETK基因进行遗传变异分析。结果显示:样品检测阳性率为24.5%(175/714),共分离获得PRV流行株38株。受检猪群普遍存在PRV感染,经典毒株及变异毒株并存,而且以变异毒株为主。广西流行株不同亚群PRV在gBgETK基因上均存在相同的氨基酸变异特点,与国内变异株亲缘关系较近。推测广西流行株存在两种不同重组变异形式产生的PRV重组毒株,分别为疫苗株gB基因和变异株gE基因重组产生的重组毒株,以及经典株的TK基因被疫苗株(HB98)的TK基因替换而产生的重组毒株。近年广西受检猪场较普遍存在PRV感染,而且PRV流行株以变异毒株为主,可能存在两种不同重组变异形式产生的重组毒株,猪场需重视及实施针对性PR免疫防控计划。  相似文献   

9.
伪狂犬病毒在潜伏感染猪体内的组织分布   总被引:2,自引:0,他引:2  
潜伏感染是猪伪狂犬病防治和净化工作中的重要障碍之一。本研究用伪狂犬病毒(PRV)gG-/LacZ+标记毒株感染经过PRV灭活疫苗免疫的PRV阴性仔猪,建立了猪伪狂犬病毒潜伏感染动物模型,再用地塞米松激活PRV在猪体内的潜伏感染。运用免疫组织化学SABC染色法研究了PRV在潜伏感染猪和潜伏感染激活猪体内部分组织的分布情况。结果显示,阳性细胞主要分布在神经系统的大脑、小脑、脑干、三叉神经和视神经以及非神经系统的扁桃体、肺和肾等部位。阳性细胞数量随着攻毒后时间的发展呈现减少的趋势,而注射地塞米松后,阳性细胞数量在上述组织中显著增加。  相似文献   

10.
2015年山东省烟台市某免疫伪狂犬病疫苗Bartha-K61猪场暴发疑似伪狂犬病疫情,临床表现为妊娠母猪繁殖障碍,仔猪神经症状。脑组织病料样品接种BHK21细胞,分离获得1株伪狂犬病病毒(PRV),命名为PRV-YT株。该病毒株gE基因与JS-2012、HN1201和ZJ01株序列同源性为99.4%~99.8%,且位于同一遗传进化分支。选择70日龄PRV阴性健康猪接种PRV-YT株,发病率和死亡率均达100%(5/5),均表现严重脑组织、肝脏与肺脏损伤,表明PRV-YT株为猪伪狂犬病病毒变异强毒株。本研究为制定猪伪狂犬病防控方案提供了重要基础。  相似文献   

11.
The avirulent Bartha's K strain of pseudorabies virus (PRV) was used to vaccinate 8 pigs at 10 weeks of age by the intransal route (experiment 1). On postvaccination days (PVD) 63 and 91, pigs were treated with corticosteroids. Viral shedding could not be detected. Explant cultures of trigeminal ganglia and tonsils did not produce virus. Four pigs with maternal antibody were vaccinated intranasally with Bartha's (attenuated) K strain of PRV at 10 weeks of age and were challenge exposed with a virulent strain of PRV on PVD 63 (experiment 2). Corticosteroid treatment, starting on postchallenge exposure day 70 (PVD 133) resulted in viral shedding in 1 of 4 pigs. In another pig of these 4, a 2nd corticosteroid treatment was required to trigger reactivation. In both pigs, sufficient reactivated virus was excreted to infect susceptible sentinel pigs. Restriction endonuclease analysis indicated that viruses isolated from the 2 pigs after challenge exposure and corticosteroid treatment were indistinguishable from the virulent virus. Evidence was not obtained for simultaneous excretion of vaccinal and virulent virus. Of 4 pigs without maternal antibody vaccinated twice with 1 of 2 inactivated PRV vaccines, challenge exposed on PVD 84, and treated with corticosteroids on postchallenge exposure day 63 (PVD 147), 1 was latently infected, as evidenced by the shedding of PRV (experiment 3). However, its sentinel pig remained noninfected.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

12.
Sixteen 20 day old pigs, devoid of neutralizing antibody to pseudorabies virus (PRV), were divided into two groups of eight, and the animals of each group were housed in a separate unit. In each group 6 pigs were inoculated intranasally with the thymidine kinase (TK) mutant (Group 1) or the field strain of PRV (Group 2), each pig receiving an inoculum of 4 ml. The remaining 2 pigs in each group served as uninoculated controls. The only clinical sign observed in the pigs of Group 1 was a transient febrile reaction, in the case of six pigs inoculated with the TK mutant of PRV, whereas no signs of disease were seen in the uninoculated controls. The virus was isolated from the 6 infected pigs of the group only on post infection day (PID) 2, whereas it was never isolated from the controls. By contrast, the pigs of Group 2, had a severe clinical response and one, among those that were inoculated with the field strain of the PRV, died on PID 9. Virus was consistently isolated from all pigs of Group 2, inoculated and control. On PID 30 all pigs, i.e. the 8 of Group 1 and 7 of the Group 2 which survived to the infection, were subjected to dexamethasone (DMS) treatment. After DMS treatment virus was never isolated from the nasal swabbings obtained from the pigs of Group 1, whereas it was consistently isolated from pigs of Group 2. After 30 d from the start of DMS treatment the pigs were killed and several tissues were collected from each pig for virus detection, by isolation in tissue culture and by PCR analysis. At necropsy no lesions were found in pigs of Group 1, whereas acute pneumonia and gliosis in the trigeminal ganglia were observed in pigs of Group 2. Virus was never isolated from any of the tissues taken from pigs of both, Group 1 and Group 2, nevertheless sequences of PRV were detected by PCR analysis in the trigeminal ganglia of the pigs of both Groups.  相似文献   

13.
The aim of this study was to investigate the effects of a porcine reproductive and respiratory syndrome virus (PRRSV) infection on the development of the immune response after pseudorabies virus (PRV) vaccination in pigs. Pigs were intranasally inoculated with the European PRRSV strain, Lelystad virus ter Huurne, and were vaccinated intramuscularly with PRV 2 weeks later (LV-PRV group). Control pigs were vaccinated with PRV only (PRV group). Eight weeks after PRV vaccination, pigs from both groups were challenged intranasally with wild-type PRV. We measured the lymphoproliferative, and the cytolytic responses to PRV of peripheral blood mononuclear cells (PBMC), isolated from blood samples. In addition, serum samples were examined for antibodies against PRV and LV. One week after PRV vaccination, PBMC proliferated abundantly to PRV in both groups. However, in the LV-PRV group the lymphoproliferative response declined after 1 week, whereas, in the PRV group, the lymphoproliferative response was high for 3 weeks and declined thereafter (P<0.05). After challenge, the lymphoproliferative response was 1 week earlier and was consistently and significantly higher in the PRV group than in the LV-PRV group. The PRV-specific killing was higher at 3 weeks after PRV vaccination and 5 weeks after PRV challenge 19+/-3 and 24+/-6%, respectively, in the PRV group, compared to 7+/-4 and 6+/-9%, respectively, in the LV-PRV group (P<0.05). However, later after vaccination and challenge the cytolytic response was identical in both groups. The antibody titre against PRV developed equally in both groups. After challenge, no PRV virus was isolated from both groups. From these results we conclude that, although PRRSV infection did cause changes in the time course of the T-lymphocyte response after PRV vaccination, PRRSV infection did not inhibit the development of vaccine-induced protection after PRV.  相似文献   

14.
Twenty 6-week-old specific pathogen-free pigs were divided into four groups. On day 0 of the experiment, PRRSV-PRV (n = 6) and PRRSV (n = 4) groups were intranasally inoculated with porcine reproductive and respiratory syndrome virus (PRRSV) (10(5.6) TCID50). On day 7, the PRRSV-PRV and PRV (n = 6) groups were intranasally inoculated with pseudorabies virus (PRV) (10(3.6) TCID50). Control pigs (n = 4) were kept as uninoculated negative controls. Half of the pigs in each group were euthanized and necropsied on day 14 or 21. Clinical signs such as depression and anorexia were observed in the PRRSV-PRV and PRV groups after inoculation with PRV. Although febrile response was observed after virus inoculations, the duration of that response was prolonged in the PRRSV-PRV group compared with the other groups. The lungs in the PRRSV-PRV group failed to collapse and were mottled or diffusely tan and red, whereas the lungs of the pigs in the other groups were grossly normal. Histopathologically, interstitial pneumonia was present in all PRRSV-inoculated pigs, but the pneumonic lesions were more severe in the PRRSV-PRV group. Mean PRRSV titres of tonsil and lung in the PRRSV-PRV group were significantly (P < 0.05) higher than that in the PRRSV group on day 21. These results indicate that dual infection with PRRSV and PRV increased clinical signs and pneumonic lesions in pigs infected with both viruses, as compared to pigs infected with PRRSV or PRV only, at least in the present experimental conditions.  相似文献   

15.
To study the antibody response to glycoprotein I (gI) of pseudorabies virus (PRV) in maternally immune pigs, 3 groups of 6 pigs were given low doses of the mildly virulent Sterksel strain of PRV at 3 and 11 weeks of age. Group A consisted of seronegative pigs; groups B and C consisted of pigs with maternal antibodies deficient of antibodies to gI. At 3 weeks of age, 3 pigs of each group were inoculated intranasally with 10(2.5) plaque-forming units (groups A and B), or with 10(3.5) plaque-forming units (group C) of PRV. The 3 other pigs in each group were contact-exposed to the inoculated pigs. In group A, 4 of 6 pigs shed virus and all developed antibodies to gI of PRV and produced PRV-specific IgM and virus-neutralizing antibodies. In groups B and C, 10 pigs shed virus and all developed low and inconsistent titers of gI antibodies, whereas only 3 pigs produced PRV-IgM antibodies with low titers. Thus, after PRV infection of pigs with high concentrations of maternal antibodies deficient of gI antibodies, the antibody responses to PRV were severely inhibited. The pigs were reinoculated with 10(3) plaque-forming units of the same virus 8 weeks after the first inoculation. The pigs in group A did not respond at all, as they were immune. The pigs in groups B and C shed considerable amounts of virus. Three pigs had a clear secondary antibody response to gI, whereas the others developed an early to normal antibody response to gI. None of the pigs mounted a secondary neutralizing antibody response to PRV.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

16.
A mutant of pseudorabies virus (PRV) deficient in thymidine kinase (TK-) activity was isolated and characterized. The mutant grew well in cell culture and did not revert to the thymidine kinase-positive phenotype. The PRV-TK- was not virulent when inoculated intranasally into 3-to 4-week-old pigs and could not be reactivated from the ganglia of these pigs by explantation and cocultivation with susceptible cells several weeks after virus inoculation. Pigs that had been exposed to PRV-TK- were immune to challenge exposure with a virulent strain of PRV. Furthermore, the challenge virus was not recovered from the ganglia of most of these pigs, indicating that colonization of the ganglia by a super-infecting virulent PRV strain was considerably reduced by vaccination.  相似文献   

17.
Evaluation in swine of a subunit vaccine against pseudorabies   总被引:2,自引:0,他引:2  
A subunit vaccine against pseudorabies virus (PRV) was prepared by treating a mixture of pelleted virions and infected cells with the nonionic detergent Nonidet P-40 and emulsifying the extracted proteins incomplete Freund's adjuvant. Three 7-week-old pigs without antibodies against PRV were given 2 IM doses of this vaccine 3 weeks apart. Thirty days after the 2nd vaccination, 10(6) median tissue culture infective doses (TCID50) of a virulent strain of PRV were administered intranasally. Tonsillar and nasal swabs were collected daily between 2 and 10 days after challenge exposure. The pigs vaccinated with the subunit vaccine were not found to shed virulent PRV. Two groups of five 7-week-old pigs vaccinated with commercially available vaccines, either live-modified or inactivated virus, and subsequently exposed to 10(6) TCID50 of virulent PRV, shed virulent virus for up to 8 days. The subunit vaccine induced significantly higher virus-neutralizing antibody titers than either the live-modified or inactivated virus vaccine.  相似文献   

18.
Twenty 6‐week‐old specific pathogen‐free pigs were divided into four groups. On day 0 of the experiment, PRRSV–PRV (n = 6) and PRRSV (n = 4) groups were intranasally inoculated with porcine reproductive and respiratory syndrome virus (PRRSV) (105.6 TCID50). On day 7, the PRRSV–PRV and PRV (n = 6) groups were intranasally inoculated with pseudorabies virus (PRV) (103.6 TCID50). Control pigs (n = 4) were kept as uninoculated negative controls. Half of the pigs in each group were euthanized and necropsied on day 14 or 21. Clinical signs such as depression and anorexia were observed in the PRRSV–PRV and PRV groups after inoculation with PRV. Although febrile response was observed after virus inoculations, the duration of that response was prolonged in the PRRSV–PRV group compared with the other groups. The lungs in the PRRSV–PRV group failed to collapse and were mottled or diffusely tan and red, whereas the lungs of the pigs in the other groups were grossly normal. Histopathologically, interstitial pneumonia was present in all PRRSV‐inoculated pigs, but the pneumonic lesions were more severe in the PRRSV–PRV group. Mean PRRSV titres of tonsil and lung in the PRRSV–PRV group were significantly (P < 0.05) higher than that in the PRRSV group on day 21. These results indicate that dual infection with PRRSV and PRV increased clinical signs and pneumonic lesions in pigs infected with both viruses, as compared to pigs infected with PRRSV or PRV only, at least in the present experimental conditions.  相似文献   

19.
Ara-T-resistant strain of pseudorabies virus (PRV) was inoculated intranasally into six 2-week-old gnotobiotic pigs. Five inoculated pigs were sneezing and coughing. In pigs 1 to 4 killed on postinoculation days (PID) 3, 5, 7, and 9, respectively, PRV antigen was detected in respiratory epithelial cells, and pigs had severe pneumonitis. In pigs 5 and 6 killed on PID 11 and 13, respectively, PRV antigen was localized in macrophages in alveoli and necrotizing nodules. Immunoglobulin-containing cells (IgG, IgM, and IgA) were detected first in pneumonic lesions in pig 4 killed on PID 9. Detection of immunoglobulin-containing cells was coincident with pulmonary inflammation and regeneration of pneumonic lesions. The number of IgG-containing cells was greater than that of IgM- and IgA-containing cells. Corresponding to transient viral multiplication, IgG-, IgM-, and IgA-containing cells were demonstrated first in lymphatic tissues in pig 1 killed on PID 3 and their number was 5 to 10 times more than those in control pigs 7 and 8. Seemingly, PRV replication in lymphatic tissues stimulated the proliferative response of specific immunoglobulin-producing cells, and the appearance of immunoglobulin-containing cells in the lungs was associated with clearance of PRV and regeneration of pneumonic lesions.  相似文献   

20.
Pigs (9 [+/- 1] weeks old) were inoculated with Streptococcus suis type 2, pseudorabies virus (PRV), or both. For each pig of groups A, B, and C the inoculum of S suis was 10(9) colony-forming units. For each pig of groups A, B, and D the inoculum of PRV was 5 x 10(3) TCID50 of either PRV strain 4892 (group A, n = 9) or PRV isolate B (group B, n = 9). The PRV strain 4892 is a highly virulent strain; isolate B causes mild clinical signs of infection in inoculated pigs. Group-C pigs (n = 9) were given S suis alone, and group-D pigs (n = 3) were inoculated only with PRV isolate B. Clinical signs of infection and development of lesions were readily seen in pigs of groups A, B, and C. Duration and severity of clinical signs of disease and lesions were reduced in pigs of group C, compared with those of the other 2 groups. Lesions, such as polyarthritis and fibrinous pericarditis, were more abundant and acute in the groups of pigs given mixed challenge exposure, compared with pigs inoculated exclusively with S suis type 2 (group C). The group of pigs inoculated with PRV isolate B alone did not manifest clinical signs of disease or lesions. Average daily gain for group-C pigs was higher, compared with that of other groups; the difference was statistically significant at P less than 0.02 and P less than 0.05 for groups B and D, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

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