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1.
《畜牧与兽医》2014,(9):84-86
在基础日粮中添加0.5100 mg/kg亚硒酸钠,连续14 d饲喂雏鹅,观察硒中毒的临床表现、病理剖检变化和组织学变化,同时测定主要组织中硒的含量。结果表明,随着日粮中硒浓度的增加,雏鹅出现以采食减少、体重增重缓慢、呼吸困难甚至死亡的急、慢性中毒症状,以胃肠道出血及心、肝、脾、肾等器官变性、坏死及出血为主的病理剖检变化,以及以心、肝、脾、肾、胸肌等器官实质细胞变性、坏死及组织内充血、出血与炎性细胞浸润为特征的组织学变化。而组织中硒含量一般随着日粮硒浓度的增加而增加。  相似文献   

2.
雏鸡实验性硒中毒的病理组织学研究   总被引:2,自引:0,他引:2  
对10日龄雏鸡实验性急性硒中毒的病理组织学变化进行了详细研究。结果表明,随着给药剂量增加,雏鸡出现急性中毒症状,病理剖检变化以胃肠道出血及心、肝、肾等器官变性、坏死及出血为主;病理组织学变化以肝、心、肾、肺、脑等器官实质细胞变性、坏死及组织内充血、出血与炎性细胞浸润为特征;超微病理变化表现为肝细胞、心肌细胞及肾小管上皮细胞核形不规则,染色体分布不均匀,线粒体肿胀、空泡化,内质网扩张。  相似文献   

3.
亚硒酸钠在低硒雏鸡体内组织药动学的研究   总被引:1,自引:1,他引:0  
低硒雏鸡按单剂量0.526mg/kgBW口服亚硒酸钠后在不同时间点采集肝、肾、胰、心、肺、脾、十二指肠和胸肌,用荧光分光光度法测定组织硒浓度。应用微机MCPKP药动学程序自动拟合组织硒浓度-时间数据并求药动学参数。结果显示,心、肺、十二指肠符合一定开放模型,肝、肾、脾、胰符合二室开放摸型,肌肉符合吸收滞后二室开放模型。吸收以肝、十二指肠为最快,肾、胰、心、肺、脾依次减慢,肌肉吸收最慢,并有一个滞后期。组织中硒的消除均较缓慢。  相似文献   

4.
低硒雏鸡口服亚硒酸钠后,对不同时间血液(清)、肝、肾、胰、心、脾硒浓度及谷胱甘肽过氧化物酶活性的动态变化规律测定。结果发现随着硒浓度的变化,酶活性也发生相应变化,但192h后肾、脾酶活性出现第2次升高而其硒浓度仍降低。值得注意的是酶活性的变化总滞后于硒浓度的变化  相似文献   

5.
应用光镜和电镜技术研究了人工感染雏番鸭细小病毒病死鸭的心、肝、脾、肺、肾、胰、法氏囊和大脑等8种器官的显微结构和发病鸭的心、肝、脾、肺、肾、胰等6种器官的超微结构变化。结果如下:1.显微结构变化主要表现为:各器官的血管扩张、充血,以肺脏尤为严重,并见少量淋巴单核细胞浸润,同时心、肝、肾、胰和大脑均呈现不同程度的变性;而免疫器官脾、法氏囊则主要表现为淋巴细胞数量减少。2.超微结构变化主要表现为:(1)各实质细胞内线粒体肿胀,嵴变少而或崩解,内质网减少,脂滴增多,部分细胞水肿坏死;(2)血管内皮均有不同程度的脂滴增多,水肿以至脱落;(3)吞噬能力加强,表现为细胞内次级溶酶体增多,吞噬细胞数量增加,其胞浆内含大量的吞噬体。  相似文献   

6.
新生羔羊腹泻症患羔的心、肝、脾、肺、肾、皱胃、小肠、淋巴结等内脏器官的病理形态学变化主要表现为程度不同的细胞变性、坏死;骨骼肌、心肌、肺、肝、脾、肾、小肠等组织器官的血管周围结缔组织均可见纤维素样坏死。  相似文献   

7.
对送检的9只家兔进行病理解剖,对心血、肝、脾及肠系膜淋巴结进行细菌分离培养,并选取心、肝、脾、肺等组织按常规病理制片进行病理组织学检查,应用免疫组化染色(ABC法)检测肝细胞内兔病毒性出血症病毒(RHDV)抗原,结果证实此次家兔自然暴发的传染病即是兔病毒性出血症(RHD)。其临床主要表现为最急性型及急性型,病理变化特点以全身微循环障碍为主;DIC形成,以实质器官淤血、水肿、出血、变性、坏死为主要特点,其中以肝、肾、脾等器官病变较重,尤其肝脏的病变具有特征性。综合病理学检测结果,确定此次家兔暴发的是RHD。  相似文献   

8.
番鸭呼肠孤病毒病雏番鸭实质器官的超微结构   总被引:2,自引:0,他引:2  
对人工感染番鸭呼肠孤病毒发病雏番鸭的心、肝、肺、肾、脾脏、胸腺、法氏囊等7种实质器官的超微结构进行了观察。电镜下发现:心、肝、肺、肾等实质器官出现不同程度的细胞变性、水肿以及局灶性溶解坏死;各器官血管内皮细胞脂滴增多、水肿以至坏死脱落.通透性增加;浆细胞、淋巴细胞和吞噬细胞呈散在或灶性浸润于坏死区和实质细胞间。免疫器官脾脏、胸腺和法氏囊中的部分淋巴细胞、浆细胞坏死和不同程度凋亡,且细胞溶解坏死形成大小不一的坏死灶并被大量增生的吞噬细胞所吞噬,淋巴细胞数量明显减少。上述结果提示,番鸭呼肠孤病毒能导致番鸭免疫抑制。  相似文献   

9.
给7日龄樱桃谷鸭饲喂含黄曲霉毒素AFB,的饲料,分别于采食AFB1后第12、24、48、72、96、120、144、168、192h各剖杀2只雏鸭,观察病理变化并采取组织病料,制作石蜡切片观察组织病理学变化和超薄切片观察超微结构变化。眼观病变为气囊有黄色纤维性物质渗出,肝、肾肿大,质地变脆。组织病理学变化为胆管增生,肝细胞空泡变性及后期极度肿胀;肾小管上皮细胞颗粒变性和散在凝固性坏死;脾红髓淤血,脾窦扩张;大脑膜水肿扩张,脑实质毛细血管扩张;心肌纤维、十二指肠腺上皮细胞、胰腺细胞颗粒变性。超微结构变化为肝细胞中空泡大量聚集导致细胞核变形,肾上皮细胞线粒体肿胀变形,大脑神经细胞髓鞘溶解及胰腺细胞酶原颗粒减少。表明,AFB,对雏鸭心、肝、脾、肺、肾、脑、十二指肠、胰腺等均有明显病理损害,以肝的病变最为严重和典型。  相似文献   

10.
用兔出血症病毒西藏株人工感染3月龄家兔,在接种后8h的病理变化主要表现为肝、肾,心等实质细胞变性,坏死,内皮细胞肿胀以及其它器官充血,淤血等变化。在接种后16h全身各器官均呈现一定程度的坏死,出血以及透明血栓形成等变化。濒死期表现为全身各组织器官均受到严重损害,实质细胞广泛坏死,微血管有大量透明血栓形成,以及出血,水肿,炎性细胞浸润等特征性的败血症变化。  相似文献   

11.
将人工感染弓形虫兔于濒死期(3~46d不等)扑杀,取其心、肝、脾、肺和肾五种脏器组织,作了病理形态学观察。主要结果如下:肝、心、脾组织中有周边无炎性反应的凝固性坏死;肝组织中还有网状细胞增生形成的结节;肺脏表现为肺泡隔炎等,这些特征性病变与其他动物弓形虫病变基本相同。同时观察到在肝窦状隙、小叶间动、静脉、肺泡壁毛细血管、肺支气管动脉、心肌纤维间毛细血管和脾静脉窦内均有血栓形成,同时伴?坏死性血栓性血管炎;各脏器的动脉管壁呈现不同程度的玻璃样变,以及由血栓形成所致其周围组织的病变。另外,应用PAS、PTAH、Weigert-Gram等染色方法显示组织切片中的弓形虫,比H.E染色更易于观察。  相似文献   

12.
以SD大鼠为研究对象,采用一次性灌胃给药法进行米尔贝肟的急性毒性试验,研究了试验大鼠对米尔贝肟的毒性反应和病理变化.结果显示,米尔贝肟对SD大鼠具有雄雌差异性,半数致死量(LD50)分别为2002、1131 mg/kg·BW.大鼠急性中毒4h后,出现明显的临床症状,主要表现为共济失调、立毛、精神委靡、呼吸困难、食欲减退,且呈明显的量效关系.组织病理学变化主要为肝脏中央静脉淤血,肝索排列紊乱,肝细胞颗粒变性;肺淤血;肾小管上皮细胞和消化道黏膜上皮颗粒变性、坏死;脾脏淤血;大脑皮层血管炎症细胞浸润,边缘空泡化.根据WHO外源性急性毒性分级标准,米尔贝肟属低毒化学物.米尔贝肟急性中毒后会广泛损害大鼠肝、肺、肾和肠等多种组织器官,甚至引起这些组织器官的变性坏死,并可对神经组织造成一定的损伤.  相似文献   

13.
Dried Nerium oleander leaves at single lethal dose of 110 mg/kg body weight were administered orally to six native male sheep. Clinical signs of toxicosis in sheep began to appear about 30 min after receiving the oleander and included decrease of the heart rate followed by cardiac pauses and tachyarrhythmias; ruminal atony, mild to moderate tympany, abdominal pain, polyuria and polakiuria. Electrocardiography revealed bradycardia, atrio-ventricular blocks, depression of S-T segments, ventricular premature beats and tachycardia, and ventricular fibrillation. Five sheep died within 4-12 h and one survived. At necropsy there were varying degrees of haemorrhages in different organs and gastroenteritis. Histopathological examination of tissue sections revealed myocardial degeneration and necrosis, degeneration and focal necrosis of hepatocytes, necrosis of tubular epithelium in kidneys, oedema in the lungs, and ischemic changes in the cerebrum.  相似文献   

14.
旨在对甘肃某羊场小尾寒羊疑似绵羊痘进行确诊,并深入探讨其病理变化特点。对临诊疑似患绵羊痘的小尾寒羊进行了羊痘间接ELISA抗体检测和PCR检测确诊,并对6只病羊进行病理剖检、病理组织学和超微结构研究。结果如下:羊痘间接ELISA抗体检测显示6例病羊样品均为阳性;同时,对2例病羊样品进行PCR检测,均扩增出绵羊痘病毒(SPV)585 bp的目的基因片段,表明本次小尾寒羊所患疫病为绵羊痘。病理剖检显示,病羊皮肤无毛或少毛处充血,局部有红斑和坏死,尾部常有感染化脓形成溃疡;消化道黏膜,尤其舌和瘤胃黏膜有大小不等痘疹与坏死病灶,局部甚至形成糜烂或溃疡。肺膈叶以及肝、脾等常有痘疹和坏死病灶。病理组织学观察显示,肺痘疹病灶主要呈现渗出-增生结节和坏死-增生结节变化,病灶内血管、细支气管等周围常有大量绵羊痘细胞,胞质内有嗜酸性包涵体;病变消化道黏膜局部,上皮细胞程度不等增生、水泡变性,固有层及黏膜下层充血、水肿,有大量绵羊痘细胞,其细胞质内包涵体明显。肝、脾、肾也有程度不等坏死-增生结节变化。肺超微结构观察显示,肺泡上皮细胞肿大,细胞核浓缩、染色质聚集,线粒体程度不等肿胀、嵴断裂、空泡化,可见细胞质内包涵体。研究证明,除局部皮肤病变外,消化道黏膜和肺等实质器官的痘疹病变是患绵羊痘小尾寒羊具代表性的病理变化,尤其痘疹病灶中大量绵羊痘细胞的出现具有证病性意义。  相似文献   

15.
对90只11日龄鸭通过颈部皮下人工接种鸭疫里氏杆菌,分别在感染后12h、24h、36h、48h、60h、72h剖杀,观察其动态病理变化。结果表明,鸭在感染24h后就开始出现浆液纤维素性心包炎、肝周炎、气囊炎,并持续整个病理过程。组织学病变主要为肝脏、心脏、脾脏、气囊等表面增厚,有大量浆液纤维素性渗出物,其中有嗜中性粒细胞和单核细胞浸润;心肌细胞和肾小管上皮细胞颗粒变性,肝细胞脂肪变性和凝固性坏死,脾脏淋巴细胞减少,脑膜水肿充血。证实了鸭疫里氏杆菌主要侵害浆膜和肝脏,引起多发性浆膜炎和肝坏死。  相似文献   

16.
Porcine urinary tract epithelium responds to systemic infections with an increase in mucin secretion that has been called "mucinous degeneration." Here we describe similar changes in calyceal, pelvic, and ureteric urothelium in pig renal tracts 14 days after local embolism and cryoablation (four kidneys) or cryoablation alone (six kidneys). Large mucin-filled vacuoles surrounded by smaller cytoplasmic vesicles were present in the affected urothelium but were rare in calyceal urothelium of normal kidneys. These mucinous vacuolar changes were proportional to the extent of renal necrosis and could be important in the pathologic responses of xenotransplanted pig kidneys.  相似文献   

17.
Rabbit haemorrhagic disease (RHD) is caused by a calicivirus infection that kills most adult rabbits 24–72 h after viral inoculation. Two liver enzymes (AST, aspartate aminotransferase, and ALT, alanine aminotransferase) were monitored in blood samples of calicivirus-infected rabbits during the short course of RHD. Values of AST were used to differentiate three stages of hepatocellular degeneration in RHD: mild (up to 20-fold increase in AST), moderate (150–200-fold elevation of AST) and severe (more than 1000-fold elevation in AST). Liver samples of rabbits from these three biochemical stages of hepatocellular degeneration of RHD were studied by transmission electron microscopy to define the fine structure of the hepatocytes. In the mild hepatocellular degeneration there was proliferation (microvesiculation) of the smooth endoplasmic reticulum and swelling of mitochondria into spheroid bodies with loss of cristae. In moderate hepatocellular degeneration, vacuolization of cytoplasm and mitochondrial damage continued to be present, and there was also formation of autophagic vesicles. In the severe hepatocellular degeneration of RHD, the altered mitochondria also showed loss of density of their matrix; rupture of cytoplasmic vacuoles led to the formation of large vesicles. Marked depletion of liver glycogen was also found in this late stage of RHD. These data offer a correlation between biochemical and cytological features of the liver during the hepatocellular degeneration of RHD.  相似文献   

18.
Six dogs died after accidental ingestion of cottonseed bedding. No clinical signs of illness were observed prior to death. A full diagnostic workup was performed on one of these dogs. At necropsy, the lungs were congested and edematous, and the liver was firm, congested, and had a marked reticular pattern. There was also moderate ascites. Histopathologic examination revealed multifocal myocardial degeneration and necrosis, severe pulmonary edema, and chronic passive congestion of the lungs, heart, liver, and kidneys. Transmission electron microscopy of the myocardium revealed disruption of myofibrils, chromatin condensation, and disrupted and swollen mitochondria. The cottonseed bedding contained 1,600 mg/kg of free gossypol, a concentration considered toxic for monogastric animals. The stomach content revealed the presence of gossypol, thus confirming ingestion of cottonseed. Gossypol poisoning in dogs is extremely rare and has not yet been associated with cottonseed bedding. This first documented case of gossypol poisoning in a dog, caused by the ingestion of cottonseed bedding, demonstrates how specific toxicological analysis is crucial in reaching an accurate diagnosis.  相似文献   

19.
本研究选用2月龄比利时和大耳白肉用仔兔各30只,采用随机单位组法平均分为6组。饲养试验期90天,比较鹰嘴紫云英、沙打旺和苜蓿3种青草单喂和补精料对肉兔的饲喂效果和毒性反应。结果表明鹰嘴紫云英与沙打旺、苜蓿饲喂效果无显著差异,屠宰率高于沙打旺。育肥肉兔仍以补少量精料的饲喂效果为佳。 3种青草喂肉兔后经血液理化指标监测,屠体解剖,心、肝、肺、肾的病理剖解及组织学检查,结果证明:鹰嘴紫云英饲喂3~5月龄肉兔,无明显因中毒引起的任何变化,是安全的。  相似文献   

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