肉鸡腺胃炎研究进展

随着近年来肉鸡养殖业的集约化、规模化、智能化的发展,肉鸡腺胃炎大范围暴发的风险增加,作为一种最常见的由传染性或非传染性因素导致的肉鸡腺胃体炎症,其传播途径繁多、临床表现复杂、治疗难度大、传播速度快,疫病出现后难以在短时间内进行有效控制,在造成鸡场重大经济损失的同时,由于抗生素类药物的使用,严重威胁着人类公共卫生安全。因此,开展肉鸡腺胃炎的研究具有重大意义,本文针对腺胃炎症,从发病原因、传染性因素、非传染性因素、临床症状、病理变化5方面展开阐述,并提出两种因素导致该病的防治措施,以期为该病的防治工作提供科学的理论依据。     

一例肉鸡腺胃炎的诊治

肉鸡腺胃炎属于一种多病因疾病,腺胃是肉鸡主要的消化功能器官之一,当出现病变时,饲料不能被完全消化吸收利用,影响机体生长。山东省东营市某养殖场发生一例肉鸡腺胃炎,经过诊治,病情得到控制。     

鸡腺胃炎非传染性致病因素研究进展

鸡腺胃炎给养鸡业造成了严重的经济损失。本文概述了鸡腺胃炎的临床症状和病理变化,分析了诱发该病的非传染性因素,提出了相应的防控思路,有助于对该病的防治提供参考。     

肉鸡腹水征的致病因素与防制对策

肉鸡腹水征又称肉鸡腹水综合征。本病发生于快速生长的肉仔鸡,最早发病于3日龄,死淘率很高。病多发于炎热夏季或寒冷冬季。临诊表现是腹部膨大,两腿叉开,行动不便。剖检见腹腔内聚积大量黄褐色腹水,液体中混有纤维素团块或絮状物;右心室扩张肥大,质地松软,壁薄;肝淤血肿胀,边缘变厚易破;肺部瘀血水肿,压之有液体溢出等病变。本病与猝死征、腿病一起被称为世界肉鸡养殖业的三大严重的非传染性新病。     

肉鸡腺胃炎之我见

肉鸡腺胃炎是一种以腺胃肿胀,粘膜出血、溃疡为病理特征的疾病。引起本病的病原或病因较复杂,截止目前还没有定论。目前本病呈现发病日龄提前,采食量低下,鸡群大小不均匀,细长条状饲料便,临床上很难治愈,尤其是贻误治疗最佳时机造成后期细菌病毒混合感染,给养殖户带来巨大的经济损失。     

肉鸡腺胃炎诊疗经验总结

(一)流行情况肉鸡腺胃炎发病日龄一般在10～20天,采食量低于正常的1/3或更多,大群拉饲料颜色粪便,鸡群中体重不达标的鸡占比增大,死亡率5‰左右,解剖病死鸡腺胃肿胀,腺胃壁出血,肌胃角质层干裂、易剥离,肠道肿胀,死亡鸡只黏膜脱落,胸腺、法氏囊、脾脏萎缩,肾脏轻微肿胀。发现该病后,养殖场技术人员一般都投服很多药物,但收效甚微。(二)防制措施1.预防腺胃炎应该从雏鸡开始。造成肉鸡腺胃炎的最主要原     

FB，对肉鸡免痉系统的影响

家禽日粮中的植物源性饲料容易受到霉菌毒素的污染，大量采食后可导致病理综合征，引起霉菌毒素中毒，造成严重的经济损失，霉菌毒素种类繁多，其中，烟曲霉毒素(Fumonisin)B1(FB1)是一种最近发现的由一些镰刀菌产生的霉菌毒素。已经证实，这种霉菌毒素与马脑白质软化病和猪肺水肿有关，对小鼠有致癌作用，并与人的食道癌有关。对于家禽，可以引起食欲废绝、生长不良、血清化学值改变和器官发生病变，虽然对FB。的毒性影响已经有了比较充分的认识。     

肉鸡传染性腺胃炎的诊治

近几年,在我国一些养殖密集地区出现的一种以发病鸡群生长受阻、鸡只大小及体重参差不齐、采食量低,生长不良、消瘦、衰竭死亡,粪便过料以及腺胃肿大似球状,腺胃黏膜溃疡、脱落、肌胃糜烂有出血为主要特征的疾病。临床统称为“传染性腺胃炎”。本病的发生、流行给养殖业及临床防治带来了新的挑战。     

浅析肉鸡肌胃炎和腺胃炎综合征

1现状按近期行情,每只肉鸡可赚6～7元,而实际上有的养殖户只能赚到3～4元,甚至还有相当一部分养殖户赔钱。这是什么原因造成的?通过调查我们发现这些养殖户所养肉鸡有以下几点共同之处。(1)从8~9日龄左右开始出现料便,腹泻,粪便发稀,鸡冠萎缩,极个别瘫痪,开始出现大小差异,使用肠炎肠毒药物治疗无明显效果,伤亡率不高。     

肉鸡腺胃炎的原因分析及诊治

近期许多地区的鸡群出现了以采食量低,生长不良、消瘦、整齐度差,粪便过料等外观症状以及腺胃肿大如球状,腺胃黏膜溃疡、脱落、肌胃糜烂为主要特征的流行病,发病鸡群病死率可达30%～50%,     

Effect of pelleted feed on the incidence of gizzard erosion and black vomit in broilers

Mash and pellet broiler feeds were compared for effectiveness. During an 8-week study, pelleted diets were associated with significantly higher mortality and poorer growth, accompanied by black vomit, gizzard erosion, and condemnations due to septicemia.     

肉鸡传染性腺胃炎诱发肌胃炎的机理探析

为了探索出肉鸡患传染性腺胃炎时诱发肌胃炎的发病机理,本试验通过对发病肉鸡腺胃、肌胃组织形态学的观察,酸度对肌胃类角质膜重量的影响研究,发现肉鸡患传染性腺胃炎时,腺胃固有层复管泡状腺的腺上皮细胞以立方形为主,使腺胃分泌胃酸功能增强,引起胃液中酸度增高,加速了肌胃类角质膜的溶解;肌胃腺导管中的黏液凝固,堵塞导管,使肌胃腺分泌物不能及时运转到肌胃黏膜表面,同时,肌胃腺上皮细胞变性、坏死,出现核裂解、核浓缩、核溶解,使肌胃腺上皮细胞的分泌功能降低,减少了黏液的分泌量,引起肌胃类角质膜生成障碍。在肌胃类角质膜溶解增快、形成障碍的情况下,引起肌胃类角质膜溃疡、糜烂,严重的引起肌胃上皮溃疡,甚至肌胃穿孔。     

鸡发生传染性腺胃炎后炎症因子的变化

为了阐明鸡传染性腺胃炎(chickens infectious proventriculitis,CIP)的发病规律,研究了该病的病变特点和机体内炎症因子的变化规律。对于不同日龄的自然发病肉杂鸡分别进行腺胃肉眼病变计分,发现患病鸡在第21天时分值最高,病变最典型。采用ELISA对21日龄鸡血清中炎症因子和SIgA的含量进行检测。结果显示,与对照组相比,患病鸡IL-1分泌量增加,但差异不显著;IL-6、IL-8、TNF-ɑ的分泌量分别达到76.933 7±7.233 4 ng/L、62.206 3±7.869 3 ng/L和134.598 8±18.649 7,显著高于对照组(P<0.05)。SIgA分泌量为19.187 5±1.976 8 ng/L,明显高于对照组,差异极显著(P<0.01)。这些变化表明,机体发生了全身性或局灶性炎症,也表明机体产生了显著的免疫应答,并且有助于该病的辅助诊断。     

肉鸡肌胃角质膜炎的诊治

鸡肌胃角质膜糜烂是由多种致病因素引起的肌胃角质膜糜烂、溃疡的一种消化道疾病，是一种胃溃疡、出血性的非传染性疾病，主要发生于10～25日龄的肉仔鸡，其次为蛋雏鸡。临床特征为食欲减少、精神沉郁、贫血、消瘦。     

Adenoviral gizzard erosion in commercial broiler chickens

Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.     

Pathogenicity by parenteral injection of fowl adenovirus isolated from gizzard erosion and resistance to reinfection in adenoviral gizzard erosion in chickens

The pathogenicity of a serotype-1 fowl adenovirus (FAV-99ZH), which causes adenoviral gizzard erosion by oral inoculation in chickens, was investigated in specific pathogen-free white leghorn chickens. In trial 1, 14 chickens were inoculated intravenously with the virus at 21 days of age and euthanatized for necropsy within 1-14 days of inoculation. Gizzard erosion was grossly observed from day 7 postinoculation (PI), and histologically, FAV-99ZH antigen-positive, basophilic intranuclear inclusion bodies were seen in the gizzard lesions from day 7 to 11 PI. Necrotizing pancreatitis, and cholecystitis and cholangitis associated with the inclusions were observed from day 3 to 14 PI (pancreatitis) and from day 5 to 9 PI (cholecystitis and cholangitis), respectively. The inclusions were also observed in the epithelial cells of the cecal tonsils from day 3 to 5 PI. The virus was recovered from samples of the lesions. It was revealed that FAV-99ZH causes not only gizzard erosion but also pancreatitis, cholecystitis, and cholangitis by intravenous inoculation in chickens. In trial 2, 10 chickens were inoculated orally with the virus twice, at 13 and 36 days of age, and euthanatized for necropsy within 4-17 days after reinfection. Macroscopically, focal gizzard lesions were observed; however, neither necrosis nor inclusions were observed by microscopy. Moreover, FAV was not recovered from the gizzard or rectum of any of the chickens at necropsy. This suggests that the gizzard lesions occurred as a result of the primary infection, and that the chickens were able to resist reinfection.     

An outbreak of gizzard erosion and ulceration in chicks in Zambia

An outbreak of gizzard erosion and ulceration in broilers in Zambia is described. Approximately 100,000 chickens in the age group of 2-9 weeks were affected. Mortality ranged from 5 to 30%. In a majority of cases, crops, oesophaguses and gizzards were engorged with dark brown to black watery material. Lesions were mainly in the gizzard comprising erosions and ulcers. High levels of fish meal in the ration is indicated as a causative factor.     

Outbreaks of adenoviral gizzard erosion in slaughtered broiler chickens in Japan

Gizzard erosion in broiler chickens was investigated at 18 slaughterhouses in Japan. The condition was observed in 13 of them, and adenoviral gizzard erosion (AGE) was diagnosed histologically, immunohistochemically and virologically in the eroded gizzards from nine of these 13. The antigen-positive intranuclear inclusion body of group 1 fowl adenovirus was observed in the epithelial cells of the affected gizzards, and fowl adenoviruses were isolated from the lesions. In two of the slaughterhouses the total weights of the gizzards disposed of in three years were 3590 kg (0.40 per cent of the gizzards inspected) and 2880 kg (0.19 per cent). Sixteen of the 19 outbreaks of gizzard erosion on 15 farms that were confirmed in three of the slaughterhouses, including the previous two slaughterhouses, were diagnosed as AGE, and the condition was suspected in the other three outbreaks. Most of the adenoviruses isolated were identified as serotype-1 by PCR-restriction fragment length polymorphism. No apparent clinical signs were observed in any of the affected flocks.     

Quantity of virulent fowl adenovirus serotype 1 correlates with clinical signs,macroscopical and pathohistological lesions in gizzards following experimental induction of gizzard erosion in broilers

In the present study day-old specific-pathogen-free (SPF) and commercial broilers with maternally derived fowl adenovirus serotype 1 (FAdV-1) antibodies were orally infected with a European “pathogenic” FAdV-1, isolated from broilers showing signs of gizzard erosion. During the experiment, broilers were observed and weighed daily up to 17 days post infection (dpi). Clinically, both infected groups showed significant decrease of weight compared to respective negative control groups. Birds were examined by necropsy at 3, 7, 10, 14 and 17 dpi. Pathological changes in the gizzards were noticed in both experimentally infected groups from 7 dpi onwards. Macroscopically, erosion of the koilin layer and inflammation or ulceration of the gizzard mucosa were observed. Histologically, presence of FAdV-1 in intranuclear inclusion bodies of degenerated glandular epithelial cells was demonstrated by in-situ hybridization and inflammatory cell infiltration of the lamina propria, submucosa and muscle layer was detected. Tissue samples were investigated by a recently developed real-time PCR and the viral DNA load was calculated from gizzard, liver, spleen and cloacal swabs with the highest amounts of FAdV-1 DNA found in the gizzard. For the first time, successful reproduction of clinical signs in broilers as well as pathological lesions in the gizzard were achieved with a European FAdV-1 isolate displaying some genetic differences to so far reported virulent FAdV-1 from Japan. Furthermore, highest viral load in gizzards could be linked with macroscopical and histological lesions. Therefore, the conducted analyses provide important insights into the pathogenesis of adenoviral gizzard erosion.     

Epizootic outbreaks of gizzard erosion associated with adenovirus infection in chickens

Two outbreaks of gizzard erosion in slaughtered broiler chickens in Japan were examined pathologically and microbiologically. The prevalences of such lesions were 9%-11% and 4%-50% in the affected flocks. Affected chickens had no clinical signs. Group I fowl adenovirus (FAV) serotype 1 was isolated from gizzard lesions. Histologically, gizzard mucosa were necrotic. Intranuclear inclusion bodies were seen in the enlarged nuclei of degenerating epithelial cells of the gizzard. The keratinoid layer in the erosion was edematous and desquamated and contained degenerative cells. Moderate to marked inflammatory cell infiltration was observed in the lamina propria and perivascular connective tissue in the submucosa and muscle layer. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies within degenerating epithelial cells. Ultrastructurally, numerous viral particles were demonstrated in the inclusions.