黄羽肉鸡实验性感染火鸡组织滴虫后体内虫体的动态分布

为研究火鸡组织滴虫感染黄羽肉鸡后在其体内的动态分布,本研究将JSYZ-A株虫体通过泄殖腔感染15日龄苏禽黄羽肉鸡,在感染后1d^34d内,每3d迫杀5只感染鸡,采集其不同组织脏器样品,并对样品进行PCR检测。结果显示,火鸡组织滴虫主要靶器官为肝脏和盲肠。感染后4d,感染鸡肝脏和盲肠中检测到虫体特异性基因,感染后13d和16d虫体检出率即达到100%,之后检出率逐渐降低,一直持续到感染后34d还能检测到虫体特异性基因。感染后10d^22d从鸡十二指肠、直肠和脾脏能够检测到虫体特异性基因。感染后13d^19d从鸡腺胃和空肠、心脏均检测到虫体特异性基因。感染后19d从鸡肺脏检测到虫体特异性基因,并且呈现一过性感染。感染鸡的胰腺、脑、肾脏和睾丸组织在整个实验过程中并未检测到虫体DNA。上述结果为临床火鸡组织滴虫致病机理的研究、诊断奠定了基础。     

笼养AA商品肉鸡感染滴虫病的体会

组织滴虫病又名盲肠肝炎或黑头病,是鸡或火鸡的一种原虫病。由火鸡组织滴虫寄生于盲肠和肝脏引起,以肝脏坏死和盲肠溃疡为特征,也发生于野雉,孔雀和鹌鹑等鸟类。该病多发生于15~60 d的小鸡,传播途径多数人认为是盲肠异刺线虫、蠕虫卵为媒。健康鸡采食异刺线虫虫卵,鸡食入病鸡排出的虫体可感染。     

鸡组织滴虫病及其防治

鸡组织滴虫病又称盲肠肝炎,是鸡的一种急性寄生原虫病,其病原为火鸡组织滴虫。虫体寄生于鸡的盲肠和肝脏内,一部分虫体可随鸡粪排出体外,由于虫体对外界环境抗抵力不强,大多数虫体排出后很快死亡,感染鸡的机会不多。但当病鸡同时有鸡异刺钱虫寄生时,     

禽类组织滴虫病有效防治方法

组织滴虫病又称盲肠肝炎或黑头病,是鸡、火鸡、鹧鸪的寄生原虫病,其他禽类有时也可感染。主要特征是盲肠发炎和肝表面有扣状坏死灶。鸡经常感染,但很少出现症状。1病原病原是火鸡组织滴虫。寄生在家禽的盲肠和肝脏内,在盲肠寄生的虫体呈变形虫样,有一细鞭毛,能作节律性钟摆状运动;在肝或肠壁中寄生的虫体,单个或成堆存在,呈圆形或卵圆形,无鞭毛。部分虫体可随着肠内容物排出体外,这种原虫对外界环境的抵抗力不强,迅即死亡。当病鸡同时有鸡异刺线虫寄生时,组织滴虫就侵入异刺线虫,并转入异刺线虫卵内,随卵排出鸡的体外,由于有虫卵保护,故能长…     

鸡组织滴虫病的防治

鸡组织滴虫病又称鸡盲肠肝炎、鸡黑头病,是由变形鞭毛虫科的黑头组织滴虫寄生于鸡和火鸡的盲肠、肝脏所引起的一种原虫病。主要特征是盲肠发炎,肝脏有扣状坏死性溃疡病灶。雏鸡、雏火鸡最易感染,成年鸡、火鸡感染时多为隐性经过。其他禽如野鸡、孔雀、珍珠鸡及鹌鹑等也时有发生     

鸡组织滴虫病的中西医结合疗法

鸡组织滴虫病又名盲肠肝炎或黑头病,是鸡和火鸡的原虫病,由火鸡组织滴虫寄生于盲肠和肝脏引起,以肝的坏死和盲肠溃疡为特征,也发生于野雉、孔雀和鹌鹑等鸟类. 鸡组织滴虫病由于症状的不典型性经常被养殖户忽视,而且很容易和球虫病混淆,希望引起养殖户的注意,不要盲目用药,现将诊治方法介绍如下. 1 病原学 组织滴虫病的病原为火鸡组织滴虫,为多样性虫体,大小不一. 火鸡组织滴虫的生活史与异刺线虫和存在于鸡场土壤中的几种蚯蚓密切相关联. 鸡盲肠内同时寄生着组织滴虫和异刺线虫,组织滴虫可钻人异刺线虫体内,在其卵巢中繁殖,异刺线虫卵可随鸡粪排到外界,成为重要的感染源,土壤中的蚯蚓吞食异刺线虫卵后,组织滴虫可随虫卵进入蚯蚓体内.当鸡采食这种蚯蚓后,便可感染组织滴虫病.     

放养小公鸡盲肠肝炎的诊疗

鸡盲肠肝炎是由组织滴虫属的火鸡组织滴虫寄生于鸡的盲肠和肝脏而引起的一种原虫病,该病原主要侵害肝和盲肠,因发病后期出现血液循环障碍,头部颜色发紫,因而又称黑头病。本病呈世界性分布,在加拿大、法国、英国、美国、意大利等一些主要火鸡饲养国,非常普遍。     

鸡盲肠肝炎病与鸡线虫病混合感染的防治

鸡盲肠肝炎又叫鸡黑头病,是由组织滴虫引起的感染鸡、火鸡、珍珠鸡、孔雀、野鸡等的一种急性原虫病,鸡黑头病主要侵害4~6周龄的鸡,主要表现为肝脏圆形坏死、盲肠栓塞、发病后期鸡头黑紫等特征,温暖潮湿季节多发,夏末秋初最易感染。鸡的线虫病是指寄生在鸡的腺胃、肌胃和肠道的一类线虫所引起的寄生虫病的总称。以腺胃卡他性炎或溃疡、肌胃黏膜出血性炎症和肠道黏膜出血性炎症为特征。     

一例鸡组织滴虫病的诊治

鸡组织滴虫病又名盲肠肝炎、黑头病,是由单毛滴虫科组织滴虫属的火鸡组织滴虫寄生于禽类盲肠和肝脏中引起的原虫病.     

鸡组织滴虫病的诊断与综合防治

鸡组织滴虫病由火鸡组织滴虫寄生于盲肠和肝脏引起,以肝坏死和盲肠溃疡为特征。由于鸡组织滴虫病症状不典型常被养殖户忽视,导致家禽生长发育迟缓,产蛋量下降,给畜牧业生产造成经济损失。1病原病原为火鸡组织滴虫,为多样性虫体。火鸡组织滴虫的生活史与异刺线虫和存在于鸡场土壤中的蚯蚓关系密切。鸡盲肠内同时寄生着组织滴虫和异刺线虫,组织滴虫可钻入异刺线虫体内,在其卵巢中繁殖,异刺线虫卵可随鸡粪排到外界,土壤中的蚯蚓吞食异刺线虫卵后，组织滴虫可随虫卵进入蚯蚓体内。当鸡食入这种蚯蚓后便可感染组织滴虫病。     

Systemic spindle-cell proliferative disease in broiler chickens

The major organs and tissues of 24 broiler chickens (70 or 71 days old) suspected of spindle-cell proliferative disease (SPD) because of showing the tumorous lesions distributed throughout the body at meat inspection were collected for histopathological and immunohistochemical examination. Macroscopically, liver, spleen and cecal tonsil showed severe enlargement and white nodules or plaques were observed in the liver, spleen, kidney, intestine and bone marrow of the femur. All chickens were diagnosed with SPD based on the histopathological examination. The lesions of SPD were observed in the liver, spleen, kidney, heart, lung, pancreas, proventriculus, gizzard, duodenum, jejunum, ileum, rectum, cecal tonsil, bursa of Fabricius, bone marrow of the femur and skin. Hemangioma was observed in the lung of 1 bird. Eight 1-day-old specific pathogen-free chicks were inoculated intraperitoneally with 0.25 ml of a 20% homogenate of the affected spleens of three naturally occurring cases. One inoculated bird, necropsied at 10 weeks of age, macroscopically had a white nodule in the kidney and histopathologically had spindle-cell proliferative lesions, a pattern similar to that seen in the naturally occurring cases, in the liver, spleen, kidney, heart, lung, pancreas, proventriculus, duodenum, cecal tonsil and bone marrow of the femur, and was diagnosed with SPD. Immunohistochemically, significant positive reactions with a rabbit antiserum against avian leukosis virus antigens were detected in all spindle cells in the proliferative lesions of all examined SPD cases and in tumor cells of the hemangioma of a field case.     

Epidemiology, pathology, and immunohistochemistry of layer hens naturally affected with H5N1 highly pathogenic avian influenza in Japan

Epidemiology, pathology, and immunohistochemistry were investigated in layer hens affected with H5N1 highly pathogenic avian influenza, which occurred for the first time in 79 years in Japan. The farm, which had a total of 34,640 chickens, experienced up to 43.3% mortality before the chickens were depopulated. Clinically, the affected chickens exhibited mortality without apparent clinical signs. Histologically, hepatocytic necrosis; necrosis of ellipsoids and follicles with fibrin in the spleen; necrosis with glial nodules in the brain stem, cerebrum, and cerebellum; necrosis of acinar cells in the pancreas; and necrosis of lymphoid tissues in intestinal lamina propria were seen. Occasionally, mild bronchiolitis, degeneration of smooth muscle fibers in the cecum, and mild tubulonephrosis were noted. Immunohistochemically, influenza virus antigens were detected often in the liver and spleen, heart, intestine, gizzard, proventriculus, and oviduct. In addition, antigens were seen also in the brain, kidney, pancreas, and ovary, but seldom in the lung and trachea. Virus antigen was mainly detected in the capillary endothelium and parenchymal cells. This suggests that virus excretion from the respiratory tract was not as prevalent as that from the digestive tract in the present cases.     

实用饲粮补锌对肉鸡组织锌、免疫器官及生产性能的影响

采用实用饲粮（玉米－多饼型,含锌３０ｍｇ／ｋｇ）,对狄高肉鸡（４～６周龄）分别补加锌４０和８０ｍｇ／ｋｇ,研究微量元素Ｚｎ对试鸡组织锌含量、免疫器官生长发育及生产性能的影响。结果表明饲粮缺锌（含Ｚｎ３０ｍｇ／ｋｇ）不影响鸡体重、饲料转化率和心、肝、肾、胰、肌胃、脑千克活体重（Ｐ＞０．０５）,但缺锌影响脾、胸腺、法氏囊、盲肠扁桃体、免疫器官及腺胃、小肠厚度、甲状腺生长发育（Ｐ＜０．０５或Ｐ＜０．０１）;饲粮补锌（４０、８０ｍｇ／ｋｇ）能改善免疫器官机能,增加胫骨、跗骨、趾骨、肝、胰、肾、心组织锌含量（Ｐ＜０．０５或Ｐ＜０．０１）;骨、肝、胰组织对饲粮锌缺乏较敏感,趾骨锌含量是标识鸡锌营养状况的灵敏指标。     

佳米驴β-防御素aBD-1组织表达

为检测aBD-1mRNA在佳米驴体内可能的表达器官,根据已知aBD-1cDNA的全长序列设计一对预计扩增产物为266bp的引物,以佳米驴舌背表面、食管、胃、十二指肠、空肠、回肠、盲肠、结肠、直肠、气管、胰腺、膀胱、子宫、心脏、肝脏、肺脏、肾脏、脾脏、淋巴结、卵巢组织中提取的总RNA为模板,采用反转录PCR（RT—PCR）技术检测佳米驴的上述器官内aBD-1mRNA的表达情况,同时以β-肌动蛋白（β-actin）基因作为内参。结果显示：aBD-1mRNA在佳米驴的舌、盲肠和结肠内有强的表达,在食管、胃、十二指肠、空肠、回肠、直肠、气管内有比较强的表达,在膀胱和子宫内有弱的表达,而在心脏、肝脏、脾脏、肺脏、肾脏、胰腺、淋巴结、卵巢等实质性器官组织内无表达。     

猪和绵羊组织器官乳酸脱氢酶同工酶酶谱比较

应用聚丙烯酰胺凝胶电泳法对猪和绵羊的心、肝、脾、肺、肾、胰、小肠７种组织器官及血清的乳酸脱氢酶同工酶酶谱进行比较研究，结果发现：①猪和绵羊各组织器官中ＬＤＨ同工酶共有５种区带，猪的ＬＤＨ３同工酶还可分为两条亚带；②猪和绵羊的肺、肾、小肠、胰、血清中ＬＤＨ区带数相同，其它组织器官各不相同；③猪和绵羊ＬＤＨ１同工酶的泳动速度最快，迁移率分别为５３．６４％、４１．８２％；ＬＤＨ５同工酶的泳动速度最慢，迁     

Detection of Histomonas meleagridis DNA in different organs after natural and experimental infections of meat turkeys

Histomonas meleagridis infection of turkeys is usually accompanied by a severe disease with unspecific clinical symptoms but with distinct pathological lesions in the ceca and liver. In the literature some macro- and microscopic evidence of the spread of histomonads to the other organs has been provided. The aim of the present investigations was to use real-time polymerase chain reaction (PCR) to demonstrate the dissemination of H. meleagridis DNA to different organs after natural and experimental infection of meat turkeys. Samples from several organs were collected from a meat-turkey flock, which proved to be naturally infected with histomoniasis, and examined for histomonad DNA by real-time PCR. Histomonad DNA was detected in all investigated ceca, livers, spleens, kidneys, and pooled brain swabs. Additionally it was found in 75% of investigated samples from bursae of Fabricius, in 50% of investigated duodenums, and in 40% of investigated jejunum samples. After experimental intracloacal infection of 3-wk-old turkey poults with 147,500 histomonads, similar samples were collected from all turkeys that died. After a 3-wk observation period the surviving birds, as well as the noninfected control group, were euthanatized and samples were taken. During the entire experimental period, 10 birds out the 20 infected birds died. Histomonad DNA was detected in all investigated ceca, livers, lungs, and hearts (100%) and almost all kidneys (90%) and bursae of Fabricius (80%). On the other hand, only 30% of examined spleens and 10% of brain samples revealed positive results. Surviving infected birds were euthanatized and necropsied; histomonad DNA was found in one out of 10 livers but not in any ceca. Also, histomonad DNA could not be detected in examined cecal and lung samples from the noninfected control group.     

Progression of histomonosis in commercial chickens following experimental infection with an in vitro propagated clonal culture of Histomonas meleagridis

Four commercial strains of chickens, namely, ISA brown leghorn (ISA), TETRA-SL brown (TETRA-SL), Lohmann brown (LB), and Lohmann LSL (LSL), were infected with a well-defined clonal culture of Histomonas meleagridis (H. meleagridis/Turkey/Austria/2922-C6/04) to investigate their susceptibility to histomonosis. Each group included 16 chickens, which were housed under the same conditions in separate pens. All chickens were infected with 10(4) histomonads orally and intracloacally at 14 days of age. No mortality or clinical signs were observed during the experiment in all birds. Three birds of each chicken strain were euthanatized on days 4, 7, 10, 14, and 21 postinfection. Incidence of histomonosis on the basis of cecal lesions was found to be 64.00% in TETRA-SL, 62.50% in LB, 53.12% in LSL, and 43.75% in ISA chickens. Fewer lesions were noticed in livers than in ceca, with an incidence of 15.62% in TETRA-SL, 9.37% in LB, and 3.12% in ISA chickens. No liver lesions were found in the LSL chickens. Statistical analysis revealed that there was no significant difference (P > 0.05) in susceptibility to experimental H. meleagridis infection based on cecal and liver involvement. Polymerase chain reaction (PCR) and immunohistochemistry were found to be reliable tools to confirm the presence of histomonads and changes in the ceca. However, some negative PCR results were recorded from the livers despite the presence of macroscopic lesions. Additionally, DNA of H. meleagridis was detected by PCR in a few of the lungs, but immunohistochemistry was negative. Nucleic acid of the protozoan parasite was not detected in samples from kidney, brain, spleen, or bursa of Fabricius. Altogether, the high susceptibility of commercial chicken lines to histomonosis could be demonstrated and characterized by severe lesions in the ceca and insignificant involvement of the liver, approaching a maximum on days 7-14 postinfection.     

Invasion of avian encephalomyelitis virus from the gastrointestinal tract to the central nervous system in young chickens

Invasion sites of avian encephalomyelitis virus in the internal organs of orally infected chicks were determined by the immunofluorescent method. The invasion began when the epithelium tunica mucosae of the duodenum (together with the proventriculus, jejunum, or cecum in certain birds killed at postinoculation day 1) became test-positive. Viremia persisted for more than 5 days in the early stage of infection, then the pancreas was rapidly infected, followed by the liver, kidney, and spleen. Subsequently, the virus spread to the CNS. Rapid infection of the duodenum and pancreas was clearly observable.     

Pathologic study of specific-pathogen-free chicks and hens inoculated with adenovirus isolated from hydropericardium syndrome.

The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.