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1.
实验性鸡大肠杆菌病的超微动态病理变化   总被引:1,自引:0,他引:1  
10~ 12日龄 SPF鸡 180只 ,随机分为 4组 ,分别气管内注射致病性大肠杆菌 O18分离株 (大肠杆菌接种组 )、低致病性禽流感病毒 (mildly pathogenic avian influenza virus,MPAIV) H9N2株 (MPAIV接种组 )、先接种 MPAIV再接种大肠杆菌 (混合接种组 ) ,并设健康对照组 ,分别于接种后不同时间 ,取气管、肺、气囊、胸腺、法氏囊、脾、肝和肾组织 ,制作超薄切片 ,电镜观察。结果表明 ,MPAIV与大肠杆菌混合接种组比大肠杆菌接种组出现病变的时间早、恢复慢 ;在大肠杆菌接种组 ,接种后 3h气囊上皮和间质细胞中都可见典型的大肠杆菌 ;在混合接种组 ,接种后 3h,气囊间质细胞的吞噬泡中可见多个 MPAIV粒子。由此认为 ,MPAIV可使鸡大肠杆菌病严重化 ,大肠杆菌对 MPAIV的入侵和在鸡体内的复制可能有促进作用。  相似文献   

2.
实验性鸡大肠杆菌病试验鸡细菌的动态分布   总被引:3,自引:1,他引:2  
用致病性大肠杆菌O18分离株和或低致病性禽流感病毒(mildly pathogenic avian influenza virus,MPAIV)接种10-12日龄SPF鸡,细菌接种后1-96小时鸡鸡的血液、气管、肺、脾、肝和肾进行细菌学检查,发现大肠杆菌接种组、MPAIV与大肠杆菌混合接种组的气管、肺在整个试验过程均分离到细菌,血液、脾、肝、肾中细菌数随接种时间延长而减少,直至消失,MPAV与大肠杆菌混合接种组比大肠杆菌接种组从气管、肺中分离到细菌的频率更高,数量更多,表明气管、肺是鸡大肠杆菌定居的场所,MPAIV可延长细菌在气管、肺中定居的时间。  相似文献   

3.
SPF鸡经不同顺序、不同时间间隔人工感染MPAIV和E.coli 173株(04)后,对试验鸡的病死率和针对大肠杆菌不同抗原体液免疫应答水平等进行研究。结果表明:各混合感染组试验鸡病死率明显高于单独接种组,且以先接种MPAIV再接种E.coli组死亡率最高;各混合感染组试验鸡针对E.coli OMPs和LPS的抗体水平低于单独感染E.coli组,其中又以先接种MPAIV再接种E.coli组为最低,提示MPAIV和E.coli间存在协同致病作用,这种协同机理可能与因MPAIV的感染导致一定程度的免疫抑制并进而促进了E.coli在体内的定居与繁殖有关。  相似文献   

4.
以 2× 1 0 5EID50 的低致病性禽流感病毒 ( mildly pathogenic avian influenza virus,MPAIV)、2× 1 0 6 EID50 新城疫病毒 L asota株( Newcastle disease virus Lasota strain,NDVL asota)气管内注射 1 0日龄 SPF鸡 ,2 4h后 ,同剂量、同法重复感染一次 ;48h后 ,分别气管内注射较低致病性禽病原性大肠杆菌 1 2 0( O1 8)和 1 73( O2 6 )株 ,2× 1 0 7CFU/羽 ,2 4h后同剂量、同法重复攻毒一次 ,连续观察 1 0d。结果 :MPAIV单独感染组死亡率为 53% ;NDV Lasota株单独攻毒组未见死亡 ;大肠杆菌 1 2 0株单独攻毒组死亡率为 40 % ,1 73株单独攻毒组死亡率为 7% ;MPAIV与大肠杆菌1 2 0株联合攻毒组的死亡率为 87% ,NDV L a-sota株与 1 2 0株联合攻毒组的死亡率为 40 % ;MPAIV与大肠杆菌 1 73株联合攻毒组的死亡率为 80 % ,NDV Lasota株与 1 73株联合攻毒组的死亡率为 2 0 %。  相似文献   

5.
禽大肠杆菌内毒素对蛋鸡致病作用的病理学研究   总被引:1,自引:0,他引:1  
将鸡源致病性大肠杆菌悬液反复冻融,提取粗制细菌内毒素,以静脉注射和腥腔注射途径接种于产蛋鸡,结果证明,鸡大肠杆菌内毒素可引起产蛋鸡急性死亡,病理变化以出血性坏死和弥散性血管内凝血为特征。  相似文献   

6.
将鸡源致病性大肠杆菌悬液反复冻融,提取粗制细菌内毒素.以静脉注射和腹腔注射途径接种于产蛋鸡。结果证明,鸡大肠杆菌内毒素可引起产蛋鸡急性死亡,病理变化以出血性坏死和弥散性血管内凝血为特征.  相似文献   

7.
几种病毒与禽病原性大肠杆菌的人工联合感染   总被引:6,自引:0,他引:6  
以2种剂量的低致病性禽流感病毒(lowly pathogenic avian influenza virus,LPAIV),传染性支气管炎病毒(infectious bronchitis virus,IBV)疫苗株H120和H52,新城疫病毒(Newcastle disese viurs,NDV)Lasota株分别于气管内注射10日龄易感鸡,2d后,气管注射禽病原性大肠杆菌O37株(O78),连续观察5d,结果,除LPAIV单独感染组有6.25%的死亡率外,其余各病毒单独接种组均健活;大肠杆菌O37株单独接种组的死亡率为62.50%,较高剂量的LPAIV,IBV H120和H52,NDV Lasota株与大肠杆菌O37株有效强的协同致病作用,死亡率分别达到81.25%,100.00%,93.75%和87.50%,而较低剂量的上述病毒则无明显的协同作用,IBV,NDV疫苗株与大肠杆菌联合接种组的多数死亡鸡病程推迟。  相似文献   

8.
鸡毒支原体是导致禽多病因气囊炎的重要病原之一,经常与禽致病性大肠杆菌混合感染,严重威胁养禽业的健康发展。此外,饲料中的霉菌毒素是一大类由真菌、霉菌的产生的二级代谢产物,给人类和动物健康带来严重的风险。为了探究霉菌毒素与鸡毒支原体及禽致病性大肠杆菌混合感染的相关性,以浓度为1×1010CCU/mL鸡毒支原体S6标准菌株接种7日龄麻黄鸡,6天后接种1×107CFU/mL禽致病性大肠埃希氏杆菌O78株,并在试验期间饲喂含8 mg/kg呕吐毒素饲料。试验结果表明,雏鸡感染鸡毒支原体和禽致病性大肠杆菌后,不会导致呼吸道感染的相关临床症状出现;在感染上述病原的基础上,饲喂呕吐毒素会导致鸡毒支原体的抗体水平显著下降,血液中鸡毒支原体的检出率明显升高。该研究评价了呕吐毒素的免疫抑制能力,且证实雏鸡多病因气囊炎的发生可能需其他致病因子。  相似文献   

9.
<正>1鸡细菌性疾病1.1大肠杆菌病导致鸡大肠杆菌病的病原为致病性大肠杆菌,该菌广泛分布于自然界中,同时也是鸡肠道正常菌群组成部分。在鸡免疫力低下、发生应激或感染其他病原后,致病性大肠杆菌会迅速增殖,分泌毒素,造成鸡发病。鸡大肠杆菌病的潜伏期因鸡的抵抗力、感染菌株毒力和饲养管理水平等的不同,从数小时至3 d不等。1.1.1临床症状和病理变化致病性大肠杆菌感染部位不同、  相似文献   

10.
为分离鉴定鸡传染性支气管炎病毒(IBV)及其致病性,本研究通过病料鸡胚接种和鸡胚尿囊液的RT-PCR检测,从四川某养鸡场的发病鸡群中分离出一株IBV.其S1基因测序分析表明,该病毒分离株属于台湾基因Ⅰ型(TWⅠ)IBV,命名为SCTW株,这是中国大陆地区首次分离的TWⅠ型IBV.将该分离株与禽源致病性大肠杆菌(E.coli)分别或混合感染15日龄白羽肉鸡以鉴定其致病性,结果显示:SCTW分离株具有较强的致病性;而且E.coli的混合感染可明显增加SCTW的发病率和病死率,使其组织病理变化更加严重.因此,加强IBV的流行病学调查,做好E.coli的防治,对鸡传染性支气管炎(IB)的防制有重要的意义.  相似文献   

11.
This study determined optimal conditions for experimental reproduction of colibacillosis by aerosol administration of avian pathogenic Escherichia coli to 2-to-4-wk-old broiler chickens. The basic model for reproducing disease was intranasal administration of approximately 10(4) mean embryo infectious dose of infectious bronchitis virus (IBV) followed by aerosol administration of an 02 or an 078 strain of E. coli in a Horsfall unit (100 ml of a suspension of 10(9) colony-forming units/ml over 40 min). Scores were assigned to groups of infected chickens on the basis of deaths; frequency and severity of lesions in the air sacs, liver and heart; and recovery of the challenge E. coli 6 days post-E. coli infection. An interval of 4 days between the IBV and E. coli challenges was best whether the chickens received the IBV at 8 or 20 days of age. Typically, 50%-80% of the chickens developed airsacculitis and 0 to 29% of the chickens developed pericarditis or perihepatitis, with little or no mortality. Escherichia coli alone resulted in no deaths and 0 to 20% airsacculitis, but these percentages increased to 0 to 5% and 52%-60% when the E. coli aerosol was administered through a cone-shaped chamber. Administration of IBV alone failed to induce lesions. Recovery of the challenge E. coli from chickens did not correlate well with lesions. On the basis of these data, administration of IBV to 20-day-old chickens followed 4 days later by exposure to an avian pathogenic E. coli reproduces avian colibacillosis with the low mortality, high percentage of airsacculitis, and low percentage of septicemic lesions characteristic of the conditions seen in the natural disease.  相似文献   

12.
Escherichia coli numbers and histopathological changes were studied in the respiratory tract of line 151 chickens intranasally inoculated with infectious bronchitis virus (IBV) and/or virulent E. coli; this line is highly susceptible to IBV. Chickens inoculated with IBV alone showed increased numbers of E. coli in the trachea and had tracheitis, airsacculitis, and bronchiolitis. One of 17 chickens inoculated with IBV alone died with fibrinopurulent serositis. Chickens inoculated with IBV and E. coli had more severe and persistent respiratory lesions than those inoculated with IBV alone. E. coli was isolated from tracheas of chickens inoculated with IBV and E. coli more frequently than from chickens inoculated with IBV alone. In this group, 14 of 27 chickens died with tracheal plugs or with fibrinopurulent serositis. There was neither increased numbers of E. coli nor significant lesions in the respiratory tract of the group inoculated with E. coli alone. These results suggest that IBV may facilitate E. coli invasion into the lower respiratory tract of the chicken.  相似文献   

13.
In chickens inoculated into the heart with a sodium chloride extract of Escherichia coli strain (serotype O2) isolated from a chicken with colibacillosis, characteristic hemorrhages into the anterior chamber of the eyes (hyphema) were found. Significant lesions were limited to the eyes. Cyclophosphamide-treated chickens were more sensitive to the extract than untreated chickens and hyphema was usually seen in association with hemorrhages of the iris. These activities were not reduced by heating the extract at 60 degrees C for one hour or by trypsin digestion. Chickens inoculated into the heart with commercial lipopolysaccharides of E. coli (serotypes O111:B4 and O55:B5) and Salmonella typhimurium showed similar lesions in the eyes as the chickens inoculated with the sodium chloride extract. These findings suggest that the endotoxin may induce hyphema in chickens.  相似文献   

14.
The aetiologic agent of avian colibacillosis is Escherichia coli. Colibacillosis is a disease that causes mortality and production performance problems in chickens which results in economic losses for the poultry industry. It will be increasingly important for scientists to identify novel solutions that can be implemented which will provide poultry producers with a tool to manage this economically important disease. The purpose of this investigation was to determine whether lipopolysaccharide (LPS) could be used as a positive control to evaluate novel chemistries for immunopotentiator activity in battery or floor-pen avian colibacillosis models in chickens. In the battery study, subcutaneous administration of LPS to one-day-old broiler cockerels caused a significant reduction (P < 0.003) in all parameters of colibacillosis evaluated, i.e. mean air sac lesion scores, per cent air sac lesions, E. coli re-isolation and per cent mortality. However, in the floor-pen study, subcutaneous administration to one-day-old broiler chicks resulted in a numerical, but not statistically significant reduction (P < 0.1) in mortality associated with colibacillosis. These data indicate that LPS can be used as a positive control to evaluate the efficacy of immunopotentiator drug candidates in avian colibacillosis models.  相似文献   

15.
The clinical and microbial efficacy of antimicrobial treatments of avian colibacillosis was studied, using an experimental model on chickens previously inoculated with multiresistant commensal Escherichia coli strains. One E. coli with pMG252 plasmid containing bla(FOX5) and qnrA1 genes and another E. coli with pMG298 plasmid containing bla(CTX-M15) and qnrB1 genes were first orally inoculated to chickens Both isolates were also resistant to chloramphenicol, sulphamethoxazole, trimethoprim, streptomycin, gentamicin, kanamycin, and tetracycline. The birds were then experimentally infected with an avian pathogenic E. coli (APEC), via the air sac. Treatments (oxytetracycline (OTC), trimethoprim-sulfadimethoxin (SXT), amoxicillin (AMX) or enrofloxacin (ENR) were then offered at the therapeutic doses. Symptoms, lesions in dead or sacrificed birds, and isolation and characterization of APEC from internal organs were studied. Results showed that OTC, SXT or ENR treatments could control the pathology. AMX worsened the disease, possibly due to endotoxin shock. All APEC re-isolated from internal organs showed the same antimicrobial susceptibility as the APEC inoculated strain, except for one APEC isolate from an infected OTC-treated bird, which acquired tetracycline resistance only, and one APEC isolate recovered from the air sacs of a chicken in the infected SXT-treated group, which acquired the pMG252 plasmid and became multi-resistant. Thus three antimicrobials could control the disease but the experimental model enabled, to our knowledge, the first observation of plasmid transfer from a bacterium of the intestinal tract to a pathogenic isolate from the respiratory tract.  相似文献   

16.
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   

17.
The interactive effects of Eimeria tenella and Escherichia coli infection in chickens were investigated. Specific pathogen free chickens inoculated orally with E tenella and challenged four days later with E coli via the air sac showed more severe acute septicaemic lesions and subacute serositis than chickens given E coli alone. Moreover, caecal lesions induced by E tenella were more severe in chickens given both E tenella and E coli than in those given E tenella alone. In contrast, oral inoculation of E coli did not result in acute septicaemic lesions or subacute serositis and had no effect on the severity of the caecal lesions caused by E tenella.  相似文献   

18.
The objective of this study was to characterize virulence factors of Escherichia coli isolates from broilers with simultaneous occurrence of cellulitis and other colibacillosis lesions. Thirty flocks were sampled and 237 birds with cellulitis were examined. Eighty-two (34.6%) of 237 birds condemned for cellulitis had gross lesions in the heart, air sacs, joints, or liver. In 58 chickens, E. coli was isolated from both the cellulitis and other lesions of colibacillosis, and 18.9% of the E. coli isolates from the 2 types of lesions belonged to the same O group. Escherichia coli of serogroups O78, O1, and O2 predominated. Isolates of the same serogroup that were derived from different lesions in the same birds had similar patterns of biotype, aerobactin production, serum sensitivity profile, antibiotic sensitivity, and K1 capsule production. Escherichia coli derived from cellulitis lesions produced virulence factors similar to those found in E. coli isolated from other colibacillosis lesions in poultry.  相似文献   

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