雏鹅感染烟曲霉鉴定与病理组织学观察

为确定荣昌3个养鹅场雏鹅感染的真菌种类,本研究采集病死雏鹅肺脏病变组织样本进行病原分离,对分离的真菌进行了形态学鉴定和ITS2序列PCR扩增及测序分析。结果显示:分离的真菌菌落颜色、菌丝结构、孢子无性繁殖方式均符合烟曲霉的特征,ITS2序列与GenBank的烟曲霉AF454113、AF454114、AY660923菌株同源性均为100%。分离菌株雏鹅回归试验显示,感染雏鹅气囊有真菌结节,肺泡壁增厚,毛细血管淤血,支气管管腔有脓性纤维蛋白或粘液,肝细胞变性坏死,淋巴细胞浸润等病变。肺脏主要表现为非典型肺炎,肝脏主要表现为实质性肝炎。本研究为临床诊断曲霉病提供了实验依据。     

雏鹅沙门氏杆菌病的诊治

齐市某个体养鹅户于１９９７年６月购进雏鹅１２００只,于３日龄时注射小鹅瘟疫苗,于２３日龄时突然发病,３日内共死亡１４０只,死亡率为１１．７％。速用青霉素饮水,结果不理想,后经我们诊治,疫情很快得以控制。１临床症状病鹅表现精神不振,食欲减少或废绝。排出...     

雏鹅沙门氏杆菌与葡萄球菌混合感染的诊治

大庆市萨尔图区一饲养户刘某，5月2日进雏鹅5000只。从进雏的第3天雏鹅开始发病，当天死亡13只，第2天死亡增至80多只，自第3天起每天死亡都在100只以上，到5月15日发病10天，共死亡雏鹅2300多只，死亡近一半，经济损失惨重。现将诊治情况报道如下。     

肉鸭场雏鸭沙门菌感染的诊治

沙门菌种类繁多,目前已发现2500多个血清型,且不断有新的血清型发现.它们主要寄生于人类及各种温血动物肠道,引起人和动物发生沙门杆菌病.鸭沙门菌能引起2周内雏鸭急性死亡,尤其是败血症病例,给养殖场带来巨大的经济损失.2010年10月宜城市多家肉鸭场发生雏鸭沙门菌病,死亡率高,危害当地养鸭业,报告如下.     

雏鹅小鹅瘟与沙门氏杆菌混合感染的诊治

随着养鹅业的快速发展，鹅病也随之增多，并常呈几种病混合感染。下面介绍1例小鹅瘟与沙门氏杆菌混合感染的病例。     

一例雏鹅法氏囊病并发沙门菌的诊治

1病情介绍2012年5月份,牡丹江市郊区李某从外地购进鹅雏1 000余只,1日龄时注射了小鹅瘟卵黄抗体,8日龄时接种了小鹅瘟疫苗。18日龄时个别雏鹅出现腹泻症状。禽主在兽药店买了青霉素和链霉素进行全群饮水,连用2 d后下痢症状稍微好转,但有10多只雏鹅死亡,继续用药效果不明显。就诊时已有30余只雏鹅死亡。     

雏鹅沙门氏杆菌病的诊治

我县某个体养鹅户于2005年5月购进雏鹅1 200只,3日龄时注射小鹅瘟疫苗,23日龄时突然发病,3日内共死亡140只,死亡率为11.7%.速用盐酸恩诺沙星饮水,但治疗效果不理想,后经我站诊治,疫情很快得以控制.现将此次发病的诊疗情况介绍如下.     

鹅沙门菌病的诊断与防治

2011年1月18日吉林省农安的一养鹅户养鹅1 000只,发病100只,死亡20只,临床表现为下痢、结膜炎和消瘦。经本人流行病学调查、临床症状、病理剖检、实验室诊断确诊为鹅沙门菌病,报告如下。1流行病学调查病鹅和病愈带菌鹅虽无明显的临床症状,但能长期带菌,在饲养管理不良等因素的影响下,能促使     

鼠伤寒沙门菌人工感染鹅的病理组织学观察

为研究鼠伤寒沙门菌感染鹅的病理组织学变化,采取肌肉注射鼠伤寒沙门菌的方法,人工感染58日龄健康鹅,对试验鹅进行病理剖检,并采取心脏、肺脏、肝脏、脾脏、肾脏、脑、胰腺和肠道病料制作病理切片,观察病理组织学变化。结果可见,受感染鹅18 h内开始出现死亡,死亡率达66.7%;主要病理变化为皮下、心肌、肝脏、脾脏、肠道、脑膜等多组织器官多处充血、出血,肝脏实质肿胀,表面可见大量大小不一的雪花状坏死灶,胆囊、脾脏肿大;病理组织学变化为心脏、肝脏、脾脏、肺脏、肠道等多组织器官的细胞变性、坏死,大量红细胞及炎性细胞浸润。研究结果表明,鼠伤寒沙门菌感染鹅,致病性强、死亡率高,感染鹅可出现全身多组织器官充血、出血与组织细胞变性、坏死的急性败血症。     

同时感染雏鹅的两种血清型沙门菌分离鉴定及遗传进化分析

为了解鹅源沙门菌的病原学特性,本研究从一发病雏鹅体内分离到2株细菌,根据培养特性、染色镜检、生化试验、PCR检测及血清学分型结果鉴定,分离菌分别为鼠伤寒沙门菌与印第安纳沙门菌。药敏试验表明,2个沙门菌分离株均为多重耐药菌株,其中鼠伤寒沙门菌耐3种药物(耐药率16.7%),而印第安纳沙门菌耐12种药物(耐药率66.7%);2个分离株均对头孢曲松钠、呋喃唑酮、多粘菌素B及链霉素表现高度敏感。对分离菌株16S r DNA基因进行扩增测序后,与Gen Bank登录的22株不同血清型沙门菌序列进行比较,构建系统进化树,结果显示:2个分离菌株具有较高同源性,与大多数泛嗜性血清型亲缘性较近,而与鸡沙门菌感染密切相关的血清型亲缘性相距较远。本研究为鹅沙门菌病的流行病学调查积累了数据,也为临床防控提供了试验依据。     

Histopathological changes in myxosomosis in rainbow trout

Rainbow trout, caught in a pond 25, 45 and 48 days from releasing, were studied for histopathological changes. Protozoan activity destroys the basal matter of the hypertrophic cartilage. The chondral tissue around plasmodium reacts by showing an increased basophilia and by chondrocytal reaction. The plasmodia tend to spread spherically, but the spreading is prevented by compact bone, connective tissue, or hardened cartilage with flattened chondrocytes. One host can bear one plasmodium or more plasmodia, up to the possibility of a generalized process. The host organism reacts to the destructive changes caused by the protozoan by letting its connective tissue cells grow into the cavities produced by the protozoan, into the plasmodia of the protozoan and into the destruction line; thus the protozoan is separated from the nutrition base. The connective tissue enters the lesion via a hole in compact bone or via a fissure between bone and cartilage. Circulation and blood elements were not found to be present in the penetrating connective tissue. The bone tissue reacts to the presence of the protozoan by thickening the periosteum. Mature spores in the lesions by the protozoan are reduced with host age.     

Histopathological changes in green muscle disease of turkeys

In this study, results of histopathological investigations of meat samples collected from turkeys with macroscopically recognized green muscle disease were compared with those obtained from turkeys without macroscopic signs of this syndrome. The histopathological lesions were assessed based upon the self-designed 7-grade scale of the intensity of changes. The greatest intensity of the histopathological alterations were found in the smaller pectoral muscle collected from turkeys in which macroscopical signs of the green muscle disease were observed. Similar changes were also found in the greater pectoral muscle, however, they were less intense than those determined in the smaller pectoral muscle.     

雏番鸭暴发小鹅瘟的诊疗

小鹅瘟是雏鹅的一种急性或亚急性败血症,以发生渗出性肠炎为主要病理变化。病原为细小病毒科,细小病毒属的鹅细小病毒,本病主要侵害4～20日龄鹅,具有传染快而病死率高,番鸭也易发生感染。2007年4月邳州市某养殖户饲养的雏番鸭暴发了小鹅瘟,现将诊疗情况报告如下：     

Histopathological changes in sheep experimentally infected with Babesia ovis

Histopathological study was made of 12 Merino sheep - five splenectomized and seven intact - experimentally infected with Babesia ovis. Non-purulent encephalitis; initially exudative and subsequently interstitial pneumonia; pericarditis, myocarditis and haemorrhagic endocarditis; centrilobular necrotic hepatitis; hyperplasia of the lymphoreticular system; necrosis and vascular changes in adrenal glands were observed. The kidney was the most severely affected organ, exhibiting acute tubular necrosis typical of kidney shock syndrome. The lesions observed were suggestive of hypovolemic shock culminating in haemorrhagic diathesis owing to consumptive coagulopathy. Additionally, the massive release of catabolites from lysis and necrosis apparently produced endotoxic shock.     

小鹅瘟病毒贵州株的分离与鉴定

采用鹅胚接种、动物感染、电镜观察及病原核酸与结构蛋白分析等方法对贵州省某养殖场疑似小鹅瘟病例进行了病原的分离与鉴定.结果:该病例组织病料可使鹅胚呈现特征性病变,雏鹅人工感染后能表现出与自然感染病例相似的症状;电镜下病毒粒子直径为20～25 nm,无囊膜,具有典型细小病毒特征;经1%琼脂糖凝胶电泳,病毒核酸扩增片段约为5100 bp;经SDS-PAGE发现,病毒结构蛋白由3条多肽组成,即VP1、VP2、VP3,分子量依次为88、68、57 ku.实验成功分离得到了一株贵州小鹅瘟病毒流行毒株.     

Morphologic changes following intraarticular inoculation of Mycoplasma bovis in calves

Intraarticular inoculation of Mycoplasma bovis into the joints of six-week-old calves caused severe arthritis in five inoculates and mild arthritis in a sixth. Intraarticular inoculation of killed M. bovis did not cause arthritis. Arthritic calves had fever, joint swelling, lameness, neutrophilia, and intercurrent pneumonia from which M. bovis could not be recovered. Gross lesions were massive fibrinosuppurative synovitis and tenosynovitis, erosion of cartilage, and its replacement by polypoid granulation tissue. Histologic lesions were extensive ulceration of synovial membranes, leukocytic infiltration of the subsynovium, congestion, hyperemia, and thrombosis of the subsynovial vessels. Cartilage erosion was accompanied by chronic osteomyelitis and formation of pannus tissue. The presence of thrombi and platelet aggregates suggests that the inflammatory process in the synovium may arise from the interaction of M. bovis with the vasculature and the coagulation process of the host.