一起绵羊痘病例分析

<正>1临诊症状2019年3月,吉林省长春郊区某绵羊养殖户所养羊只出现精神沉郁、呼吸困难、食欲下降、发热、眼睑水肿和流涎等临床症状。在病羊的口、唇可见有痘状结节,并在口腔黏膜能够看到明显的溃疡灶,其尾根及会阴等部位可见明显的红色丘疹结节。2 病理剖检对病死羊只进行病理剖检,发现胸腔有少量积液,肺脏表面有较多突起的黄豆样大小的颜色为灰白色的痘状结节;肝脏表面及边缘部位有坏死灶。肾脏肿胀并可见大量灰白色坏死灶。瘤胃浆膜层分布     

一例奶牛曲霉菌病的诊断

本文通过临床病史、尸体剖检、组织病理学、血液涂片以及肺脏触片方法综合诊断了1例病死奶牛曲霉菌病。病牛表现为喜卧、精神沉郁、体温升高。尸体剖检可见下颌淋巴结肿大,心外膜、心内膜出血,肺脏尖叶实变、肺脏表面可见大小不等脓肿结节,真胃胃壁可见出血性坏死灶、真胃黏膜弥散分布小溃疡灶。组织病理学可见肺组织内大小不等霉菌性结节,结节内分布大量曲霉菌菌丝,真胃肌层以及黏膜下层表现为坏死性变化、坏死灶内可见曲霉菌丝。血涂片以及肺脏触片可见血液和肺组织内中性粒细胞增多。综合判断本病例为饲喂发霉玉米引起奶牛的曲霉菌病,因此应加强奶牛的饲养管理,减少曲霉菌病的发生。     

产蛋鸡溃疡性肠炎的诊治

<正> 1 发病情况山西省太原市某鸡场饲养海兰褐商品蛋鸡700只,45周龄时个别鸡只出现了死亡,整个鸡群精神较好,采食量无明显下降,看不到明显症状,只有个别鸡只嗉囊充盈,伴有白色水样下痢,胸肌萎缩,最后极度消瘦而死亡。此病表现为散发,病程较长,共死亡32只,死亡率为4.8%。2 剖检病变剖检病死鸡只,眼观病变大致相同,可见嗉囊充盈,肌胃中充满食物。肝脏肿大呈浅土黄色,肝脏表面有大小不一的黄白色坏死斑点;脾脏肿大呈紫黑色;十二指肠肠壁增厚,在浆膜面和黏膜面均可见出血点和出血斑,并与周边组织界限明显;空肠和回肠黏膜上有散在的枣核状溃疡灶,溃疡深达肌层,上覆一层伪膜。盲肠扁桃体坏死、脱落,直肠黏膜有密集的粟粒状突出于表面的出血溃疡;其他内脏器官无明显肉眼可见病变。     

生猪宰后内脏检验和常见病判定

1胃、肠、脾的检查一般在开膛后把胃肠拉出腹腔外检查。首先视检胃肠黏膜及肠系膜,检查胃肠表面有无细颈囊尾蚴,然后用手提起盲肠头,检查回、盲、结肠黏膜有无出血、充血、溃疡、糜烂、水肿、坏死灶、痈肿。剖检肠系膜淋巴结,注意有无肠炭疽及结核。检查脾脏时,用左手提取脾脏,视形态、大小、色泽,观察脾头、脾尾边缘有无坏死、梗死和出血,触检其弹性和硬度,判断其性质(坚硬、柔软、脆弱)及有无病灶。必要时剥离网膜,剖检脾门淋巴结和脾髓。常见病的判定:①猪瘟:肠系膜淋巴结外观色泽呈红色或暗红色,形似黑枣,剖检可见切面呈大理石样。慢性…     

鹧鸪念珠菌病的诊断报告

新沂市某养殖户饲养鹧鸪300多只,自2003年9月1日190日龄以来,陆续出现死亡,每天死亡2～5只,根据临床症状、剖检变化、实验室检查,确认为念珠菌病,现将诊断情况报告如下:一.临诊症状发病初期可见口腔、咽部有白色斑点,继而扩大为黄白色干酪样伪膜,呼出臭气或酒糟气味。有的发生软嗉症、嗉囊充满气体,软而无收缩力,拉绿色稀粪,发病后2～3天或1周左右死亡。二.剖检变化剖检病死鹧鸪,可见口腔、食道有干酪样伪膜和溃疡。嗉囊内容物有酸臭味,粘膜增厚,有一层灰白色斑块状伪膜,易剥落,伪膜下可见坏死。有的腺胃粘膜增厚。出血和溃疡;肠道有卡他性…     

10种疾病可致猪猝死

1猪瘟 最急性型病猪发病很急。突然死亡。尸体剖检可见脏器上有程度不同的出血斑点,淋巴结肿大,肾脏皮质部有数量不等的小出血点,脾脏有紫黑色出血性梗死。典型特征是回盲瓣有纽扣状轮层样溃疡。     

10种疾病可致猪猝死

(1)最急性型猪瘟发病很急,突然死亡.尸体剖检可见脏器上有程度不同的出血斑点,淋巴结肿大,肾脏皮质部有数量不等的小出血点,脾脏有紫黑色出血性梗死.典型特征是回盲瓣有纽扣状轮层样溃疡.     

鸡排血性稀便疾病的鉴别诊断

1肠炎类疾病 溃疡性肠炎幼禽比成禽更易感,4～12周龄的鸡发病较多.病鸡精神萎顿,蹙头缩颈,羽毛蓬松,翅膀下垂,食欲减退.消瘦,下痢,粪便褐色带血.剖检病死鸡可闻到腹腔有恶臭气味.肝脏有淡黄色坏死小区或白色坏死灶.急性患鸡小肠出血,慢性者小肠后段黏膜有黄白色坏死灶、伪膜、深陷溃疡,溃疡边缘凸起火山口状,肠内充满暗红色血样渗出物,并混有黏膜碎片和气体,严重者肠穿孔,引起纤维素性腹膜炎、肠粘连.脾脏肿大、充血、出血.     

一起肉牛运输应激综合征的病例报告

江西某牛场从吉林引进67头周岁左右的肉牛,该批牛于购进第5天陆续发病,发病的肉牛有38头,发病率57%,其中,死亡8头、病死率12%,临床主要表现呼吸困难、喘气,部分病牛严重腹泻或关节肿胀,剖检可见肺脏呈纤维素性胸膜肺炎,少数牛肺出现化脓性或干酪样坏死灶,真胃和小肠可见溃疡灶,镜检可见两端着色的杆状菌,血琼脂平板培养可见露珠样小菌落,表明与巴氏杆菌感染有关。对该起肉牛运输应激综合征发病和诊断情况进行报道,以期为临床实践提供参考。     

鸭瘟及其防制

鸭瘟是由鸭瘟病毒引起的急性传染病。临床特征为体温升高、两脚发软无力、下痢、流泪和部分病鸭头颈部肿大。剖检特征是食道黏膜小点出血,并有灰黄色假膜或溃疡灶,泄殖腔黏膜充血、出血、水肿和坏死,肝有不规则的大小不等的坏死灶及出血点。本病传播迅速,发病率和死亡率都很高。1病原（1）鸭瘟病毒分类上属于疱诊病毒属,核酸类型为DNA,具有囊膜,近似球形,其大小在91～181nm。     

Chemical deicer poisoning was suspected as a cause of the 2005-2006 wintertime mortality of small wild birds in Hokkaido

Many small wild birds died in the 2005-2006 wintertime in Hokkaido. Thirteen birds were pathologically examined and it was attempted to detect West Nile and influenza viruses from their organs. Consecutive pathological changes were fresh hemorrhage and acute circulatory failure. Viral detections were negative. Selective occurrence in wintertime, literature review and the results of pathological and virological examinations suggested chemical deicer poisoning as the cause of wild bird death. Chicks treated orally with deicer showed acute death and their pathological changes were similar to those of the wild birds. Because the chicks showed significant elevation of plasma Na concentration, plasma electrolyte analysis of the affected wild birds might be crucial to confirm our tentative diagnosis.     

Deaths in yellow-eyed penguins (Megadyptes antipodes) on the Otago Peninsula during the summer of 1990

About 150 rare, adult, yellow-eyed penguins died over a short period during the summer of 1989-1990 on the Otago Peninsula. These were from a total mainland population estimated at 240 breeding pairs. Penguin chicks and non-breeding birds were not affected, but there were indications of shortages in feed supply for birds that bred successfully. Thirteen dead penguins were examined. In ten birds, the cause of death was not established. Although it was commonly found that adult birds had little or no food in their gut, none were considered to have starved to death. No consistent pathological lesions were found, nor were any viruses, Chlamydia or significant bacteria recovered from selected tissues. Toxicology tests ruled out poisoning by copper, zinc, iron, lead, arsenic, selenium, cadmium, mercury, organophosphates, organochlorines, polychlorinated biphenyls, hexachlorobenzene or the toxins of Clostridium perfringens, Clostridium botulinum and dinoflagellates. The problem did not recur during the following summer.     

Isosporoid coccidiosis in translocated cirl buntings (Emberiza cirlus)

Four of 17 cirl buntings (Emberiza cirlus) involved in a trial translocation in 2004 for conservation purposes died and were examined postmortem. Two of the cirl buntings showed intestinal and hepatic lesions, including necrotising enteritis, consistent with isosporoid coccidiosis, and a third had an intestinal infestation of isosporoid coccidia. Sporulated oocysts from faecal samples from the birds were identified as Isospora normanlevinei, a parasite previously detected in cirl bunting populations in continental Europe. In a subsequent translocation of 75 cirl buntings from Devon to Cornwall in 2006, each brood of birds was placed in strict quarantine at low stocking density, with improved hygienic precautions and detailed health surveillance, and each bird was treated prophylactically with toltrazuril in an attempt to control the disease but not eliminate the I normanlevinei parasites. Seventy-two of the 75 birds were successfully reared and released, and there were no apparent clinical or pathological signs of isosporoid coccidiosis in any bird. I normanlevinei was detected in the released population, an indication that it had been successfully conserved.     

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.     

不同来源高钙日粮对青年蛋鸡血清和肾脏线粒体自由基代谢的影响

以海蓝褐蛋鸡为试验对象,通过检测蛋鸡血清和肾脏线粒体自由基代谢的变化,研究不同来源高钙日粮对青年蛋鸡血清和肾脏线粒体自由基代谢的影响。选40日龄海蓝褐蛋鸡120羽,随机分成3组,每组40羽,分别饲喂正常钙日粮（以磷酸氢钙形式含钙0.9%,对照组）、石粉高钙日粮（含钙3.78%,试验组1）、磷酸氢钙高钙日粮（含钙3.78%,试验组2）,试验期65d。于试验65d,每组随机选取蛋鸡12羽,观察其病理学变化,并分离血清和肾脏线粒体,检测自由基代谢变化。结果显示：试验期间,高钙日粮组均出现青年蛋鸡的异常死亡。试验65d时,与正常对照组相比,石粉高钙组和磷酸氢钙高钙组的左肾重、右肾重、两侧肾总重及肾/体质量比均升高显著或极显著（P〈0.05或P〈0.01）,并导致肾脏出现不同程度的病理学损伤;高钙日粮组可导致蛋鸡血清及肾线粒体MDA、NO含量及XOD活性升高（P〈0.05或P〈0.01）,T-AOC、GSH-PX及SOD活性下降（P〈0.05或P〈0.01）;高钙组组间比较,石粉高钙组表现更严重的组织损伤,血清T-AOC活性降低,与磷酸氢钙高钙组比较差异显著（P〈0.05）。结果提示：高钙日粮可导致青年蛋鸡生长发育的缓慢,肾脏肿大,血清及肾线粒体的自由基生成增多及抗氧化功能的下降。     

Sudden death in turkeys with perirenal hemorrhage: pathological observations and possible pathogenesis of the disease.

A pathological study was conducted on 32 turkeys that died of sudden death with perirenal hemorrhage syndrome. Turkeys were selected from routine necropsy cases in a diagnostic laboratory. A higher incidence was observed in heavy tom turkeys. In addition to the characteristic gross lesions of perirenal hemorrhage, splenomegaly, and pulmonary congestion, turkeys in most cases had a hypertrophic cardiopathy. Microscopic lesions included moderate-to-marked acute passive congestion of all tissues examined (32/32), severe perirenal hemorrhage (32/32), and splenic lymphoid depletion (25/32). Changes in the thyroid follicular epithelium of most birds suggested an increased glandular activity. No lesions suggestive of arterial hypertension were observed. Adenoviral infection was detected in only four of 32 birds. Bacteriological cultures revealed no significant pathogen. Results suggest that sudden death in turkeys with perirenal hemorrhage is caused by an acute congestive heart failure consecutive to a hypertrophic cardiopathy. The perirenal hemorrhage would be a consequence of a severe passive congestion in kidneys.     

Efficacy of acyclovir against herpesvirus infection in Quaker parakeets.

We evaluated the efficacy of acyclovir against experimentally induced herpesvirus infection (Pacheco's parrot disease) in Quaker parakeets. Thirty-two of 40 birds were challenge-exposed with 0.1 ml of a suspension of herpesvirus (10(4) median cell culture infective doses [CCID50]) given IM. Treatment with acyclovir was started 24 hours later and was continued for 7 days. The birds were allotted to 5 groups of 8 birds each. There was a considerable difference in mortality between groups 1-5. Of 8 bird in each group, 6 died in group 1 (control), 1 died in group 2 (gavage), 3 died in group 3 (low dose, IM), 4 died in group 4 (high dose, IM), and none died in group 5 (contact controls). There was a significant (P = 0.023) difference in mortality between groups 1 and 2, thus the oral form of acyclovir administered by gavage was the most efficacious therapeutic regimen. Clinical signs and death occurred after discontinuation of acyclovir in groups 2 and 3, whereas the mean time of death for the control group was 6 days after challenge exposure. Herpesvirus was recovered by inoculation of chick embryo cell culture with pooled tissue suspensions from all birds that died. Histologic evidence of herpesvirus infection was found in most birds that died, with the control group having the most severe lesions. Surviving Quaker parakeets were transferred to cages with seronegative Quaker parakeets with no known exposure to herpesvirus. There have been no deaths attributable to herpesvirus infection in a period exceeding 2 years.     

Pathogenicity and antigenicity of avian nephritis isolates.

The G-4260, IR-N, M-6, and M-8 strains of avian nephritis virus (ANV) were inoculated orally into 1-day-old specific-pathogen-free chicks of the line PDL-1 for pathological and serological study. Five of 15 chicks inoculated with the G-4260 strain died with visceral urate depositions. One of 15 chicks each inoculated with the M-6 and M-8 strains died with nephrosis and visceral urate deposition, respectively. No chicks inoculated with the IR-N strain died. Mean body weights of ANV-inoculated chicks, except for the IR-N-inoculated chicks, at 14 days postinoculation (PI) were significantly lower than those of control chicks (P less than 0.01). However, interstitial nephritis was observed in all ANV-inoculated birds that were histopathologically examined at 14 days PI. In the serological study, the G-4260 and IR-N strains were classified as the same serotype, and the M-6 and M-8 strains were classified as a different serotype from the G-4260 and IR-N strains. These results indicate that there at least two serotypes of ANV and its strains differ in pathogenicity.     

An outbreak of avian malaria in captive yellowheads/mohua (Mohoua ochrocephala)

CASE HISTORY: Eight mohua, or yellowheads (Mohoua ochrocephala), were held in a large open aviary over the summer months of 2003-2004, following their capture for captive breeding purposes. Two birds died of transportation trauma shortly after arrival, one became ill and died a month later, and another four died within a 2-week period in February 2004. The eighth bird also became ill at this time but survived for a year following treatment with chloroquine and doxycycline. CLINICAL AND PATHOLOGICAL FINDINGS: The affected birds were depressed, lethargic and dyspnoeic. Necropsy of three birds showed a slightly pale and swollen liver and spleen. Impression smears of the liver of one bird revealed schizonts resembling Plasmodium spp. within the cytoplasm of many hepatocytes, which was confirmed histopathologically. Similar protozoal organisms were seen within splenic histiocytes and pulmonary endothelial cells of 5/6 birds. Electron microscopy identified these as protozoal schizonts containing merozoites of similar size and structure to those of Plasmodium spp. DIAGNOSIS: The birds were infected with a protozoal haemoparasite resembling Plasmodium spp.; asexual stages within hepatocytes and endothelial cells of the lung and spleen were typical of this organism. CONCLUSIONS AND CLINICAL RELEVANCE: The mohua captured from west Otago were highly susceptible to avian malaria as they came from an isolated population that was likely to be na?ve and have had no previous contact with this organism. The birds were probably infected by bites from mosquitoes feeding off local populations of blackbirds subsequently found to be infected with Plasmodium spp.     

Bone marrow hypoplasia and intestinal crypt cell necrosis associated with fenbendazole administration in five painted storks

Five painted storks were treated with fenbendazole for 5 days for internal parasitism. Four birds died following treatment. Profound heteropenia was a consistent finding in all samples evaluated; additionally, the 1 surviving bird had progressive anemia. Consistent necropsy findings in the 4 birds that died were small intestinal crypt cell necrosis and severe bone marrow depletion and necrosis. Fenbendazole has been associated with bone marrow hypoplasia and enteric damage in mammals and other species of birds. The dosages of fenbendazole used in birds are often substantially higher than those recommended for mammals, which may contribute to bone marrow hypoplasia and intestinal crypt cell necrosis associated with fenbendazole administration in birds.