鸡肾型传染性支气管炎病毒分离及鉴定

某鸡场暴发主要以侵害鸡肾脏的疾病,引起肾脏肿大、苍白,肾小管和输尿管有白色尿酸盐沉积,伴有下痢。产蛋鸡产蛋下降,雏鸡的死亡率达25%～90%。从感染鸡分离到1株疑为鸡肾型传染性支气管炎病毒,接种鸡胚,鸡胚出现侏儒化、卷曲等特征性病变。     

鸡肾型传染性支气管炎病毒分离及鉴定

青岛地区暴发了侵害鸡肾脏的疾病,引起肾脏肿大、苍白,肾小管和输尿管有白色尿酸盐沉积,伴有下痢.产蛋鸡产蛋量下降,雏鸡的死亡率达25%～90%.从感染鸡分离到1株疑为鸡肾型传染性支气管炎病毒,接种鸡胚,鸡胚出现侏儒化、卷曲等特征性病变,暂定名为NIBV_AH111.     

鸡肾型传支病毒RZ株的分离及鉴定

从某一疑似鸡肾型传染性支气管炎发病鸡场的病死鸡的肾、肝组织中分离到一株病毒，经鸡胚连续传代和动物回归实验，初步确定该病毒为鸡肾型传染性支气管炎病毒，命名为IBV-RZ株。     

鸡贤型传染性支气管炎病毒分离及鉴定

某鸡场暴发主要以侵害鸡肾脏的疾病，引起肾脏肿大、苍白，肾小管和输尿管有白色尿酸盐沉积，伴有下痢。产蛋鸡产蛋下降，雏鸡的死亡率达25%～90%。从感染鸡分离到1株疑为鸡肾型传染性支气管炎病毒，接种鸡胚，鸡胚出现侏儒化、卷曲等特征性病变。     

鸡肾型传染性支气管炎的防制

1病原 鸡传染性支气管炎病毒属于冠状病毒科冠病毒属,有囊膜,单股正链RNA病毒.传染性支气管炎病毒能在10～11日龄的鸡胚中生长,用自然毒辣初次接种鸡胚,多数鸡胚存活,但随继代次数的增加,对鸡胚的毒力增强,到第10代时,可在接种后的第9天引起80%的鸡胚肾细胞、鸡肾细胞和鸡胚肝细胞上生长,经多次传代(6～10)后,可引起较明显的细胞病变;表现为胞浆融合,形成合胞体及细胞死亡.     

鸡肾型IBV JL株的分离和鉴定

研究通过电镜形态学观察、理化特性测定、致鸡胚矮小化试验、血凝试验、NDV毒株干扰试验、中和试验和致病力试验,分离、鉴定出1株鸡肾型传染性支气管炎病毒当地毒株(IBV JL株),为下一步进行鸡肾型传染性支气管炎疫苗制备的研究提供了毒种.     

山东地区鸡肾型传染性支气管炎病毒的分离鉴定及防治

山东临沂地区某鸡场25日龄鸡群发病,临床表现为气管啰音、咳嗽、打喷嚏,剖检肾脏有大量尿酸盐沉积,疑似感染鸡肾型传染性支气管炎。为了探究发病鸡群的病因,试验选取120只该场疑似鸡肾型传染性气管炎病毒致死的病死鸡,进行剖检,取肾、肺和气管等组织器官经过无菌处理后,分离得到若干株病毒,通过临床检查、病毒分离、血凝试验、鸡胚传代试验等方法鉴定。试验表明,所得结果与鸡肾型传染性支气管病毒的临床特征和特性基本一致,说明引起该鸡群发病的病原为鸡肾型传染性支气管炎病毒。     

鸡肾型传染性支气管炎病毒的分离鉴定

通过鸡胚接种盲传,从重庆某地疑似鸡肾型传染性支气管炎的发病鸡群中,分离到一株病毒,该病毒能导致鸡胚出现侏儒胚。用本病毒对10日龄雏鸡做回归实验,可使试验鸡出现典型的花斑肾。试验应用反转录-聚合酶链式反应(RT—PCR)技术扩增出了该病毒的特异性基因M和N,从分子学角度进一步证实了引起鸡群死亡的病毒为鸡传染性支气管炎病毒。     

鸡肾型传染性支气管炎病毒的分离鉴定

从安徽省巢湖地区鸡群中出现的以肾肿大为主要特征的呼吸道疾病的病例中分离到1株病毒,易感雏鸡,病死鸡出现肾肿大、苍白呈花斑状、大量尿酸盐沉积;鸡胚连续盲传至第5代时开始出现死亡和侏儒胚.电镜观察可见80～120nm的病毒颗粒.分离病毒在鸡胚上可干扰新城疫病毒clone-30株的增殖.上述试验证实所分离的病毒为鸡肾型传染性支气管炎病毒,暂定名为NIBV-AH99.     

鸡马立克氏病的诊断及防制

鸡马立克氏病是鸡常见的病毒性传染病,又称鸡麻痹症,对养鸡业危害很大,可造成重大损失. 1 病原 该病毒能在鸡胚绒毛尿囊膜上产生典型的痘斑,卵黄囊接种较好.能在鸡肾细胞、鸡胚成纤维细胞和鸭胚成纤维细胞上生长产生痘斑. 完整病毒的抵抗力较强,在粪便和垫料中的病毒,室温下可存活4～6个月.细胞结合病毒在4℃可存活2星期,在37℃存活18小时,在50℃存活30分钟,60℃只能存活1分钟.     

鸡传染性支气管炎病毒LH2/01/10的分离鉴定

2001年在我国黑龙江省某鸡场疑似鸡传染性支气管炎的发病鸡群中，分离到一株病毒，将该病毒接种10日龄SPF鸡胚，取72h的尿囊液进行电镜观察并用1％胰酶处理，结果发现尿囊液中存在典型的冠状病毒，用胰酶处理过的尿囊液能凝集SPF鸡的红细胞，初步鉴定为鸡的传染性支气管炎病毒。将该病毒尿囊液再次接种10日龄SPF’鸡胚，通过病毒对鸡胚的致病作用、病毒超微形态特征以及病毒凝集鸡红细胞的特性等对该毒株进行研究，结果表明：经胰酶处理后的病毒尿囊液可凝集鸡红细胞。鸡胚的第二代病毒尿囊液(命名为LH2,／01／10)分别接种1日龄和15日龄的SPF鸡，发现对不同日龄的鸡表现不同的致病性，对1日龄接种鸡和同笼饲养的同居对照鸡致病力高，发病率为11／11，致死率分别为4／6和2／5；15日龄接种和同居感染鸡发病率为9／9，致死率分别为1／5和1／4。实验应用反转录一聚合酶链式反应技术对LH2／01／10的膜蛋白基因进行扩增、克隆和序列测定，结果表明该基因具有IBVM基因的共有分子特征．与IBV标准株M41的M基因核苷酸的同源性为90％，氨基酸的同源性为91％。这从分子水平进一步证实引起鸡群死亡的病毒为鸡传染性支气管炎病毒。     

Adenovirus infection associated with respiratory disease in commercial chickens

The lesions and etiologic agents associated with 13 outbreaks of respiratory disease in commercial chickens were investigated. Adenoviruses were isolated from tracheal and lung tissues of affected chickens in all 13 outbreaks. Escherichia coli was isolated from the lung of an occasional bird. The tracheal specimens were consistently negative for Bordetella avium, but E. coli and occasionally Staphylococcus aureus were isolated. There was also serological evidence in one outbreak, and pathological evidence in another, of a concurrent infectious bursal disease virus (IBDV) infection of chickens affected with the disease. Gross and microscopic alterations in the tracheas and lungs of affected chickens were similar in all outbreaks and consisted of catarrhal tracheitis and occasionally multifocal pneumonia with mononuclear cell infiltrates. Hepatitis and splenitis with heterophil infiltrates occasionally were seen in birds with coliform septicemia. The tracheal and lung lesions in the present investigation were considered primarily of adenovirus etiology, complicated by secondary bacterial infection.     

Different routes of inoculation impact infectivity and pathogenesis of H5N1 high pathogenicity avian influenza virus infection in chickens and domestic ducks

The H5N1 type A influenza viruses classified as Qinghai-like virus (clade 2.2) are a unique lineage of type A influenza viruses with the capacity to produce significant disease and mortality in gallinaceous and anseriform birds, including domestic and wild ducks. The objective of this study was to determine the susceptibility and pathogenesis of chickens and domestic ducks to A/Whooper Swan/Mongolia/224/05 (H5N1) high pathogenicity avian influenza (HPAI) virus when administered through respiratory or alimentary routes of exposure. The chickens and ducks were more susceptible to the H5N1 HPAI virus, as evidenced by low infectious and lethal viral doses, when exposed by intranasal as compared to alimentary routes of inoculation (intragastric or oral-fed infected chicken meat). In the alimentary exposure pathogenesis study, pathologic changes included hemorrhage, necrosis, and inflammation in association with virus detection. These changes were generally observed in most of the visceral organs of chickens, between 2 and 4 days postinoculation (DPI), and are similar to lesions and virus localization seen in birds in natural cases or in experimental studies using the intranasal route. Alimentary exposure to the virus caused systemic infection in the ducks, characterized by moderate lymphocytic encephalitis, necrotized hepatitis, and pancreatitis with a corresponding demonstration of virus within the lesions. In both chickens and ducks with alimentary exposure, lesions, virus, or both were first demonstrated in the upper alimentary tract on 1 DPI, suggesting that the alimentary tract was the initial site affected upon consumption of infected meat or on gavage of virus in liquid medium. However, as demonstrated in the infectivity study in chickens, alimentary infection required higher exposure doses to produce infection as compared to intranasal exposure in chickens. These data suggest that upper respiratory exposure to H5N1 HPAI virus in birds is more likely to result in virus infection and transmission than will consumption of infected meat, unless the latter contains high doses of virus, as found in cannibalized infected carcasses.     

Kidney lesions associated with mortality in chickens inoculated with waterfowl influenza viruses

Seventy-six type A influenza viruses recovered from waterfowl in Wisconsin, California, South Dakota, Florida, Texas, Alabama, and Nebraska were tested for virulence in chickens. The challenge to chickens was intravenous inoculation of first-, second-, or third-egg-passage virus. Each of the virus strains was tested separately in three or four chickens. Eighteen of the 76 viruses caused the death of one or more chickens following inoculation. Postmortem lesions were similar in all dead birds. In decreasing order of frequency, gross lesions included: swollen kidneys evident as accentuated lobular patterns, urates in the pericardial sac, and urates on the surface of the liver. Microscopic lesions present in kidneys were consistent with visceral gout. Mortality was associated with inoculations having higher concentrations of infectious virus. These results indicate that the influenza A viruses circulating in duck populations may include strains potentially pathogenic for chickens.     

Studies on gross footpad lesions of chickens infected with avian reoviruses via the footpad route.

Avian reoviruses grew well in the footpad of chickens inoculated with the viruses via the footpad route, resulting in gross footpad lesions of swelling. The gross footpad lesions induced under some different conditions were investigated for 14 days by two methods. In method A, the lesions were observed grossly and graded as lesion scores 0 to 4. In method B, they were expressed as a swelling index assessed by relative thickness of an inoculated footpad to uninoculated. Both methods are successful, and similar results were obtained. Gross footpad lesions were produced in all chickens aged 9 to 310 days, and the younger were the birds at infection, the earlier and severer were the lesions observed. The lesions began to appear late when the virus titer inoculated was low. It has been elucidated that severity of the lesions depends on virus strains, not on the sexes of chickens.     

Mortality of one-week-old chickens during naturally occurring Marek's disease virus infection

Marek's disease (MD) is a disease of chickens that occurs worldwide and has serious economic consequences. MD can present as one of several forms, with the most commonly occurring forms being the lymphoproliferative diseases. Under experimental conditions, an early mortality syndrome has been recognized following infection by some but not all strains of MD virus (MDV). This is the first report of a confirmed case of mortality due to naturally occurring MDV infection in 1-week-old, nonvaccinated, chickens. Necrotizing lesions were observed in the bursa of Fabricius, lung, duodenum, jejunum, and proventriculus, and large intranuclear inclusion bodies were a striking feature in tissues with lesions in all birds. Immunohistochemical staining for the pp38 protein of MDV revealed abundant pp38 antigen in the affected tissues, confirming the presence of MDV within the lesions. PCR yielded an amplicon with 97% homology to the meq gene of MDV. No evidence of co-infection by either of the immunosuppressive agents chicken anemia virus and infectious bursal disease virus was detected.     

Pulmonary congestion and edema (marble spleen disease) of chickens produced by group II avian adenovirus

"Marble spleen disease" of chickens was diagnosed in 22-week-old chickens. Total mortality was 8.9%. Deaths occurred over a period of 2 months. Gross lesions included pulmonary congestion, splenomegaly, hepatomegaly, and congestion of egg follicles. Microscopic lesions included pulmonary congestion and edema, and reticuloendothelial cell hyperplasia of the spleen with concurrent white-pulp necrosis and lymphocyte depletion. The pulmonary lesions were of sufficient intensity to have caused the death of fatally affected birds. Many of the hyperplastic reticuloendothelial cells contained basophilic intranuclear inclusions similar to those that characterize hemorrhagic enteritis of turkeys, marble spleen disease of pheasants, and adenovirus group II splenomegaly of chickens. These characteristic lesions, plus serologic identification of the causal virus, indicate that "marble spleen disease" caused by avian group II adenovirus was affecting the flock under study. This appears to be the first report of death of chickens due to pulmonary congestion and edema caused by spontaneous infection with avian group II adenovirus.     

一株鸡传染性贫血病毒对不同日龄SPF鸡的致病性研究

为评价鸡传染性贫血病毒AV1550株的致病性,取1日龄、7日龄和14日龄SPF鸡分别经胸部肌肉注射不同病毒含量的病毒液,同时设置正常对照,隔离饲养观察21日。感染后14日采血测定红细胞压积,21日统计死亡率、体重变化以及胸腺、骨髓、法氏囊病变情况并测定1日龄SPF鸡感染后不同组织中的病毒载量。结果表明,1日龄SPF鸡感染AV1550株后,表现出精神沉郁、增重减缓、贫血等明显的临床症状,死亡率为53.9%;死亡鸡或观察期结束时存活鸡剖检,可见胸腺萎缩,骨髓变成淡黄色;不同剂量感染后14日,均能引起红细胞压积显著下降;21日时,胸腺病毒载量最高,可达106.7copies/mg 。7日龄SPF鸡感染后,出现增重减缓,高感染剂量（100000EID50）出现贫血,部分鸡出现胸腺萎缩和骨髓病变,但病变率低于30%。14日龄SPF鸡感染后,不引起明显临床症状。研究证实,CAV对SPF鸡的致病性具有明显的日龄依赖性,红细胞压积降低、骨髓病变、胸腺萎缩以及胸腺病毒载量测定可作为评价CAV致病的指标。     

Comparative nephropathogenicity of infectious bronchitis virus in bursectomized and nonbursectomized chickens

A study was conducted to compare the responses of bursectomized (Bx) and nonbursectomized (non-Bx) specific-pathogen-free male chickens to Australian T strain of infectious bronchitis virus. Four chickens from each group were killed at 3, 5, 7, 14, 21, and 28 days after conjunctival inoculation of the virus. Clinical signs and gross and microscopic lesions were more severe in Bx than in non-Bx chickens. The non-Bx chickens had linear IgG deposits along the renal tubules. Virus-neutralizing titers were log10 2.74 to 4.33 for non-Bx chickens and less than log10 1.25 for the inoculated Bx and for broth-inoculated Bx and non-Bx chickens (controls). Early in the disease, renal lesions were of the same type in all infected chickens, but were more severe in Bx chickens. Later, nephritis was chronic and active in Bx chickens and was chronic in non-Bx chickens.