鸡滑液囊支原体病理模型的建立及感染途径探索

为了探究鸡滑液囊支原体感染途径及抗体产生情况,试验采用人工复制病理模型的方法,分别通过呼吸道、消化道和皮下途径将滑液囊支原体感染6周龄幼鸡,感染后每天记录鸡的肛温,观察鸡的临床症状,每隔3 d采血1次,检测滑液囊支原体抗体,感染后第18天剖检试验鸡,观察病变,同时进行菌落培养。结果表明:感染第12天时,呼吸道组和皮下组鸡出现抗体阳性血清;至第15天时,鸡体温普遍升高,呼吸道组感染的鸡出现典型的临床症状,并且剖检后脾脏肿大,关节液渗出较多,在关节液与脾脏中分离出菌株,感染滑液囊支原体鸡的血清抗体检测结果均为阳性。说明本试验成功建立病理模型,鸡滑液囊支原体主要通过呼吸道进行传播,感染后第12天鸡产生抗体,通过消化道和皮下感染的鸡也引起一定的感染反应,但无明显临床症状。     

产蛋鸡实验性卵巢炎—腹膜炎的病理学研究

产蛋鸡经静脉、腹腔、肌肉、皮下、气囊、气管、口服、口服与气管内联合以及泄殖腔等９种途径实验感染鸡源致病性大肠杆菌,证明鸡大肠杆菌病主要经呼吸道感染,引起以嗜异性粒细胞渗出和浸润为主的急性炎症,经泄殖腔感染不成功;经静脉和腹腔接种其粗制内毒素则可引起急性死亡,以出血性坏死和弥散性血管内凝血为特征。电镜观察发现,经改良马丁肉汤３７℃培养７２ｈ,感染菌菌毛生长良好,并有大量大肠杆菌粘附和克隆在鸡胚气管粘膜上皮细胞纤毛表面,而３７℃２４ｈ的相同培养物中却几乎没有菌毛表达和细菌粘附。本研究结果表明,鸡源致病性大肠杆菌借助其菌毛经呼吸道入侵,在局部生长繁殖,病菌本身及其裂解释放的内毒素对产蛋高峰期的鸡卵巢有强致病作用,引起卵巢炎、卵黄性腹膜炎以及化脓和坏死。     

种鸡葡萄球菌病病因浅析

鸡葡萄球菌病是由金黄色葡萄球菌引起鸡的一种细菌性传染病，是禽类几个主要细菌性传染病之一。葡萄球菌广泛分布在自然界中，大多数为正常菌群，但具有潜在的致病性，如金黄色葡萄球菌可感染不同日龄的鸡群，引起化脓性或坏疽性皮炎、化脓性关节炎、腱鞘炎、脐炎等，还可以导致菌血症、败血症及内脏器官的严重感染，引起鸡只大量死亡。     

鸡葡萄球菌病

1892年Lucet证明葡萄球菌是一种鹅关节炎的病原后,在世界许多国家相继出现了禽类葡萄球菌感染的报道。Volkman(1929)从患脐炎的小鸡和小火鸡,Hale等(1931)从关节受感染的野鸡,Povar等(1947)从患心内膜炎病鸡,Carnaghan(1966)从患脊椎炎的病鸡中均分离出葡萄球菌。禽葡萄球菌病分布于世界各地。     

上海宠物犬弓形虫病流行情况调查

犬弓形虫病分布于世界各地，感染范围很大，可呈先天性感染或获得性感染。以犬的弓形虫滋养体进行静脉、腹腔、皮下和口内等不同途径的感染犬，均可引起发病。Lainson（1956）在犬静脉接种后3小时至5天，肠内感染第7天，发现虫血病。Chamkerlain等（1953）经静脉和肠腔途径感染5只1．5—2岁的怀孕犬，在怀孕的第30—52天观察到，5只母犬新生的28只小犬，有23只发生流产或早产，并在母犬的乳汁和子宫内也证明有弓形虫。     

畜禽葡萄球菌病的诊断及防治

葡萄球菌病通常称为葡萄球菌感染,是由葡萄球菌引起的人和动物多种疾病的总称。葡萄球菌常引起皮肤的化脓性炎症,也可引起菌血症、败血症和各内脏器官的严重感染。除鸡、     

猪链球菌Ⅱ 型五种感染途径感染猪模型的比较

为研究猪链球菌2型感染猪的发病进程,选择24头28日龄杜长大败血波氏杆菌阳性猪,分别采用皮下、肌肉、静脉、鼻腔、胸腔5种途径感染实验猪,猪链球菌2型山东株剂量为60亿CFU,同时设立生理盐水对照组,试验期为30 d。观察感染猪的临床症状和病理变化,并对各脏器进行细菌记数。结果表明,除鼻腔外的4种感染模式均复制出了猪链球菌2型的感染症状,细菌计数结果印证了感染模型。细菌计数结果提示血液、肺脏组织及脑是猪链球菌2型易增殖部位,肺脏可能是呼吸道传播模式致全身性感染的中转站(上呼吸道-肺脏-全身性感染),所有致死猪均出现菌血症。     

肉鸡皮炎型金黄色葡萄球菌病的诊治

鸡葡萄球菌病是危害养鸡业较大的一种条件性传染病,山东省莒南县某养鸡场近两年来陆续发生一种以蓝翅、翅膀和胸腹部脱毛、皮下浮肿为主要特征的疾病,经临床诊断、病理剖检和实验室细菌检查,诊断为鸡金黄色葡萄球菌感染.报告如下.     

禽葡萄球菌病诊断

禽葡萄球菌病四季均可发生,但在高温高湿和气候多变季节多发,可在某些地区引起地方性流行。涉及的禽种包括鸡、鸭、鹅、天鹅。火鸡、鹌鹤等,可发生于任何年龄的禽类,但以雏禽较为敏感。该病30－70日龄的鸡多发,也有孵化后期鸡胚感染金黄色葡萄球菌而致死的报道。有资料报道,纯种鸡比杂种鸡的易感性强,肉鸡比蛋鸡的易感性强,群发病率、死亡率变化很大,分别为2．4％－74％和2．1％一万％。该病可与某些传染病混合感染,或继发或诱发,如大肠杆菌病、新城疫、马立克病等。感染途径为创伤、消化道和呼吸道。该病为一种条件性疾病。引起…     

马立克氏病二价苗胚胎免疫的现场应用效果

马立克氏病二价苗胚胎免疫的现场应用效果马立克氏病．（ＭＤ）是鸡的一种淋巴增生性疾病。可使养鸡业遭受严重的经济损失。疫苗接种是一种有效的防制方法。传统的免疫是通过给出壳鸡作肠道外途径（皮下、肌肉内和腹腔内）的接种。近年来，由于早期感染的不断增多，寻找一...     

Staphylococcosis of turkeys. 1. Portal of entry and tissue colonization

Staphylococcus aureus and various coagulase-negative staphylococci were isolated from turkeys with staphylococcosis. Virulent S. aureus adhered well (averaged more than 100 bacteria per tissue cell) in vitro to cells from tissues of the respiratory tract but did not adhere well (averaged fewer than 12 bacteria per tissue cell) to cells from tissues of the alimentary tract. Some avirulent coagulase-negative staphylococci also adhered well to cells from the respiratory tissues. Lungs and livers of turkeys became colonized with virulent S. aureus following experimental aerosol exposure. Tracheas, livers, and hock joints of some market-age turkeys were naturally colonized with S. aureus and various species of coagulase-negative staphylococci.     

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.     

Newcastle disease virus pathogenesis in the respiratory tract of local or systemic immunized chickens.

Establishment of selective immunity, local or systemic, made it possible to evaluate the pathogenesis of Newcastle disease virus (NDV) in the respiratory tract of chickens that were previously immunized with beta-propiolactone-inactivated antigen. NDV was inoculated intranasally or intramuscularly to chickens in different states of immunity (local or systemic). Humoral antibodies protected chickens against intranasal as well as intramuscular infection. Local antibodies, on the other hand, conferred immunity only against intranasal challenge. The respiratory tract supported multiplication of the virus, producing a self-limited subclinical infection. Replication of the virus in this system was negligible, playing only a minor role in the pathogenesis of the disease.     

Potential of low pathogenicity avian influenza viruses of wild bird origin to establish experimental infections in turkeys and chickens

The potential of low pathogenicity (LP) avian influenza virus (AIV) isolates of wild bird origin to establish infection in commercial turkeys and broiler chickens was studied. Isolates, representing subtypes H5N1, H7N3, H6N2, and H3N6, were recovered in 2005 and 2006 from waterfowl and shorebirds in the Delmarva Peninsula region of the east coast of the United States. The LP AIV isolates were not pathogenic for 2-wk-old meat-type turkeys and broiler chickens. No mortality, clinical signs, or gross lesions were observed following intratracheal and conjunctival sac routes of exposures with 10(6.0) EID50 (embryo infectious dose) per bird. Isolates resulting in an established infection based on virus isolation were: A/mallard/Maryland/1159/ 2006 (H5N1) in the upper respiratory tract of turkeys; A/mallard/Delaware/418/2005 (H7N3) in the upper respiratory and intestinal tracts of turkeys and chickens; and A/shorebird-environment/Delaware/251/2005 (H3N6) in the upper respiratory and intestinal tracts of chickens. Infections were also confirmed by production of AIV-specific serum antibodies detected by hemagglutination inhibition.     

The pathology and pathogenesis of Salmonella stanley infection in experimental chicks

Experimental infection with Salmonella stanley was produced by oral, intravenous and intramuscular routes in day-old chicks. The earliest evidence of the presence of the organisms was in duodenal mucosa six hours after oral infection. Following oral infection the organisms were detected in the duodenum from six hours to five days, in the caecum from 12 hours to nine days, liver, spleen and blood from 24 hours to seven days. The resistance to infection was found to be significant after 10 days old, but not up to six days old. The work confirmed that the survival time of birds given S stanley by the intravenous or intramuscular routes was inversely proportional to the dose up to a maximum beyond which the survival time was not further decreased by dose increase. The presence of S stanley in tissues and blood was detected by isolation and by the fluorescent antibody technique.     

Different infection routes of avian influenza A (H5N1) virus in mice

The continuing outbreaks of avian influenza A H5N1 virus infection in Asia and Africa have caused worldwide concern because of the high mortality rates in poultry, suggesting its potential to become a pandemic influenza virus in humans. The transmission route of the virus among either the same species or different species is not yet clear. Broilers and BABL/c mice were inoculated with the H5N1 strain of influenza A virus isolated from birds. The animals were inoculated with 0.1 mL 10^6.83 TCID₅₀ of H5N1 virus oronasally, intraperitoneally and using eye drops. The viruses were examined by virological and pathological assays. In addition, to detect horizontal transmission, in each group, healthy chicks and mice were mixed with those infected. Viruses were detected in homogenates of the heart, liver, spleen, kidney and blood of the infected mice and chickens. Virus antigen was not detected in the spleen, kidney or gastrointestinal tract, but detected by Plaque Forming Unit (PFU) assay in the brain, liver and lung without degenerative change in these organs (in the group inoculated using eye drops. The detection results for mice inoculated using eye drops suggest that this virus might have a different tissue tropism from other influenza viruses mainly restricted to the respiratory tract in mice. All chicken samples tested positive for the virus, regardless of the method of inoculation. Avian influenza A H5N1 viruses are highly pathogenic to chickens, but its virulence in other animals is not yet known. To sum up, the results suggest that the virus replicates not only in different animal species but also through different routes of infection. In addition, the virus was detection not only in the respiratory tract but also in multiple extra‐respiratory tissues. This study demonstrates that H5N1 virus infection in mice can cause systemic disease and spread through potentially novel routes within and between mammalian hosts.     

新城疫病毒GX-08流行株对鸡和鸭的致病性研究

选取新城疫病毒(Newcastle disease virus,NDV)GX-08株对26日龄雏鸡和20日龄雏番鸭进行人工感染试验,对体外细胞培养物进行致病性试验,并进行病理组织学观察。结果表明,以10^5.5EID₅₀的攻毒剂量对26日龄雏鸡和20日龄雏番鸭通过肌注接种,雏鸡的发病率和死亡率分别为100%和100%,雏番鸭的发病率和死亡率分别为70%和70%;通过点眼、滴鼻及口服接种,雏鸡的发病率和死亡率分别为80%和30%,雏番鸭的发病率和死亡率分别为20%和20%。感染鸡消化器官和部分呼吸器官病变严重,表现出典型的嗜内脏型NDV感染的病理变化特点;感染鸭则肝脏、脾脏和胰腺等实质器官病变明显,消化器官和部分呼吸器官病变较轻微。以200 TCID₅₀的剂量对单层鸡胚成纤维细胞(CEF)和鸭胚成纤维细胞(DEF)接种,结果CEF和DEF均于24 h左右开始出现病变,并分别于96和84 h左右细胞单层完全被破坏。与CEF相比,DEF接种病毒后,细胞坏死、裂解过程迅速,合胞体形成现象显著,合胞体的数量及合胞体平均含有的胞核数较多,病毒接种后培养物上清的HA效价峰值也较高,表明GX-08株均可致CEF和DEF病变,且对DEF有更强的细胞融合能力。     

网状内皮增殖病病毒(REV)感染SPF雏鸡后局部免疫组织抗体生成细胞的变化

对 SPF雏鸡人工感染 REV后局部免疫组织盲肠扁桃体和哈德氏腺的 Ig A、Ig G和 Ig M抗体生成细胞数量动态变化进行了检测。结果发现 ,REV感染 SPF雏鸡后 7～ 4 9天消化道局部免疫组织盲肠扁桃体和呼吸道相关局部免疫组织哈德氏腺的 Ig A、Ig G和 Ig M抗体生成细胞数量明显低于未感染对照雏鸡。表明雏鸡感染 REV后消化道局部组织盲肠扁桃体和呼吸道相关免疫组织哈德氏腺体液免疫机能均显著下降。     

Influence of E. coli infection on the disposition kinetic of nalidixic acid in broiler chickens.

The pharmacokinetic data of nalidixic acid were investigated in normal and E. coli infected chickens. The highest serum concentration were reached after 2 hours with t0.5 (ab) of (1.706 +/- 0.1 min in normal and 2.030 +/- 0.11 min in diseased) and (1.72 +/- 0.11 min in normal and 1.416 +/- 0.044 in diseased chickens) following oral and intramuscular administration, respectively. The elimination half-life t0.5 (beta) were (2.514 in normal and 2.35 hr in diseased) and (2.567 hr in normal and 2.672 hr in diseased) respectively. Following intravenous injection the kinetic of nalidixic acid followed two compartments open model with t0.5 of (6.27 and 9.15 hr), Vd (0.45 and 0.79 L/kg), Cltot (8.86 and 13.32 ml/kg/min) in normal and E. coli infected chickens, respectively. Administration of nalidixic acid twice daily for 5 successive days in a dose level of 25 mg/kg b. wt. by oral and intramuscular routes showed a cumulative behaviour.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

The age of the chicken at the time of infection with infectious avian encephalomyelitis virus (IAEV) and the route of the administration of the virus had a marked effect on the development of the clinical disease. Chickens given the virus by intramuscular, intraperitoneal and oral routes exhibited a decreased susceptibility to development of clinical disease with increasing age. Irrespective of age, chickens were consistently susceptible to intracerebral inoculation of IAEV. Chickens infected with the virus at 1-, 7- and 14-days of age developed lower neutralising antibody titres to IAEV than chickens infected at 21 and 28 days. A relationship between the ability to produce specific neutralising antibody to IAEV and susceptibility to the development of clinical disease is discussed.