育雏期与育成期火鸡的饲养管理

1育雏期雏火鸡饲养密度为:1周龄30只/平方米,2周龄20只/平方米,3~6周龄10只/平方米,7~8周龄7只/平方米。10日龄前,育雏舍温度要保持在20℃以上,育雏器内的温度应达到35~38℃。以后随着日龄增加,逐渐下调温度。在实际生产中,要记录育雏舍内不同部位的温度,观察火鸡群的精神状态和活动表现,并根据气候、昼夜及火鸡群情况及时调整。为便     

一起猪弓形体病的教训

我省湘西自治州某集约化养猪场 ,年出栏 80 0 0头商品猪生产规模。现在饲养长×大杂种母猪 40 0余头 ,杜洛克公猪 1 5头 ,自 1 998年投产以来生产经营运转基本正常 ,为我省湘西贫困地区发展瘦肉型猪生产起到示范作用 ,深受当地政府和群众的好评。1　发病经过　在 2 0 0 1年 8月 2 7日至 9月 2 0日相继发生妊娠母猪 1 0余头减食、停食现象 ,随后又出现流产。当时气温 3 1℃～ 3 5℃、舍温 3 6℃～ 3 8℃ ,有时下午舍温达3 9℃。由于猪场建在山坡北边 ,猪舍之间距离狭窄 (仅5～ 6米 ) ,猪舍通风不良。因此当时我们认为热应激所致 ,虽然采取了…     

火鸡新城疫的诊断

在自然情况下,鸡和火鸡均可患新城疫。火鸡新城疫国内尚未见报道。我们于1985年11月在北京观察到一起火鸡新城疫,现报告如下。一、发病经过北京郊区某县火鸡场,饲养30～80日龄贝蒂纳火鸡共6群,6500只;110日龄以上火鸡3群,共5100只。各群用铁丝网隔开,中间有约一米宽空隙,种有树木。该场周围为砖墙所围,场内没有饲养其它禽类。     

火鸡新城疫的诊断

广州地区某饲养专业户于1988年开始饲养火鸡,自繁自养,从未作过任何疫苗接种,自配饲料,采用平养,并每天上、下午各一次将火鸡赶到农田、草地上放牧。至发病时共养有火鸡101只,其中龄期在1年左右的有23只,3～5个月龄的78只。在3～5个月龄火鸡群中个别出现精神沉郁、食欲不振、头和双翅下垂、不愿走动、驱赶后走路蹒跚、     

饲养父母代后备青年火鸡

<正> 有了好的种火鸡才能有好的雏火鸡。饲养1只父母代母火鸡就要饲养4只雏火鸡,在地面散养时,养2只母火鸡就要饲养4—5只公火鸡, 120日龄的后备青年火鸡应用120％的后备群母火鸡,而公火鸡不应少于200％。例如:饲养1000只后备青年火鸡就要按下列计算方式。     

英国布特火鸡生长发育规律研究

近些年来 ,我国相继从国外引进一些火鸡新品种 ,英国布特 (BUT)火鸡便是其中之一 ,有关布特火鸡引入我国后的生长发育规律的研究尚未有报道。本文是在对布特火鸡的体尺、体重及耗料量等方面实测的基础上进行分析探讨 ,为布特火鸡在我国的引进开发提供生长发育规律及饲料转化等方面的可资借鉴的数据。1　试材与方法1 1　试材的选择　本次研究的试材是由丹东职业技术学院布特火鸡繁育基地饲养的商品代火鸡 1 0 2 0只。1 2　饲养管理　采取网上平养 ,红外线灯与地上火墙结合取暖。 1周龄温度为 3 5℃ ,以后每周下降 2℃ ,至 7周龄时降至室…     

圈养鹅循环出栏技术探讨

<正>1选择优良鹅种选体型大、生长快、耐粗饲的鹅种。雏鹅保温饲养刚出壳的仔鹅,要进行温室饲养,室内温度为1～2日龄32℃;3～7日龄28℃,以后22℃～26℃。气温高时育雏气温高时育雏10天,气温低时育雏20天。温室的饲养密度为每平方米8～12只。饲喂室要     

中西结合治疗萨索鸡大肠杆菌和球虫混合感染

1发病情况 2006年7月21日，固原市彭阳县白阳镇中庄村黄某引进法国萨索鸡1200只，经30天的舍饲育雏和6天的过度阶段饲养后，于8月27日开始散养（放牧），9月1日鸡群出现排白色稀粪或红色血粪。畜主用硫酸庆大霉素、诺氟沙星、盐酸氯苯胍治疗，效果不佳，每天死亡5—20只，至9月27日就诊共发病680只，死亡216只。     

2004年南丰蜜桔生产的"四不利"和"四注意"

20 0 4年制约江西省南丰县1 7万hm2 南丰蜜桔生产有四大不利因素,如何面对?应采取积极应对措施,做到四个注意。1　“四不利”1 1　桔园遭受特大旱灾　从2 0 0 3年7月起南丰县久旱无雨。7月1—31日,仅7月7日出现了一次雷阵雨,其余30天都保持在中午34℃以上的晴朗高温天气。8月份除4、5、12、15、2 1日等5天经用人工降雨曾降下少量雨水外,其余2 6天早晚气温保持32～33℃、中午35～37℃以上。9月份仅4天有雨,雨量很少,10月份仅3天有雨,11月份降雨日也是3天、12月份降雨日4天。7月1日至12月31日,降雨日仅2 0天,干旱无雨天气达16 4天,晴天数是雨…     

饲喂山胖头鱼所引起的火鸡组织滴虫病

我场饲养青铜火鸡15周龄雏210只,分两群舍饲,鸡舍为砖墙水泥地面,于8月10日在饲料中拌入切碎的山胖头鱼,以代替鱼粉,喂饲其中一群青铜火鸡,饲后14天全群减食30%左右,继之出现硫黄色稀便,被毛蓬乱,双翅下垂,缩头呆立一隅,头部皮肤发绀,体温42℃,临死前体温降至38℃,全群发病率为60%,于9月5日死亡三只。剖检见肝脏肿大,边缘钝厚,肝表面有指甲大小界线清楚的灰黄色变性区,盲肠明显增粗,肠壁厚达0.5cm,盲肠粘膜     

Enhancement of enteropathogenic Escherichia coli pathogenicity in young turkeys by concurrent turkey coronavirus infection

In a previous study, turkey coronavirus (TCV) and enteropathogenic Escherichia coli (EPEC) were shown to synergistically interact in young turkeys coinfected with these agents. In that study, inapparent or mild disease was observed in turkeys inoculated with only TCV or EPEC, whereas severe growth depression and high mortality were observed in dually inoculated turkeys. The purpose of the present study was to further evaluate the pathogenesis of combined TCV/EPEC infection in young turkeys and determine the role of these agents in the observed synergistic interaction. Experiments were conducted to determine 1) effect of EPEC dose, with and without concurrent TCV infection, and 2) effect of TCV exposure, before and after EPEC exposure, on development of clinical disease. Additionally, the effect of combined infection on TCV and EPEC shedding was determined. No clinical sign of disease and no attaching and effacing (AE) lesions characteristic of EPEC were observed in turkeys inoculated with only EPEC isolate R98/5, even when turkeys were inoculated with 10(10) colony forming units (CFU) EPEC (high dose exposure). Only mild growth depression was observed in turkeys inoculated with only TCV; however, turkeys inoculated with both TCV and 10(4) CFU EPEC (low dose exposure) developed severe disease characterized by high mortality, marked growth depression, and AE lesions. Inoculation of turkeys with TCV 7 days prior to EPEC inoculation produced more severe disease (numerically greater mortality, significantly lower survival probability [P < 0.05], increased frequency of AE lesions) than that observed in turkeys inoculated with EPEC prior to TCV or simultaneously inoculated with these agents. Coinfection of turkeys with TCV and EPEC resulted in significantly increased (P < 0.05) shedding of EPEC, but not TCV, in intestinal contents of turkeys. These findings indicate that TCV infection predisposes young turkeys to secondary EPEC infection and potentiates the expression of EPEC pathogenicity in young turkeys.     

鹅的鸭疫里氏杆菌和大肠杆菌混合感染

鸭疫里氏杆菌(Riemerella anatipestifer, RA)可引起家鸭、火鸡和多种禽类的急性或慢性传染病,主要致2～3周龄小鸭的传染性浆膜炎.环境条件差或并发感染可加重死亡,给养鸭业造成极大的损失.一般来说,除鸭外,火鸡、鹅、雉鸡、鹌鹑以及鸡亦可感染发病,但少见.     

Acute fibrinopurulent blepharitis and conjunctivitis associated with Staphylococcus hyicus, Escherichia coli, and Streptococcus sp. in chickens and turkeys

Multiple outbreaks of acute severe fibrinopurulent lesions of the eyelids occurred in chickens and turkeys. Lesions began as tiny foci of epidermal necrosis and ulceration and spread to involve the entire eyelid. Scabs overlying the epidermis contained large gram-positive cocci; lesser numbers of small cocci and gram-negative bacilli were in more superficial areas. Staphylococcus hyicus was isolated from birds in all stages of the disease. Escherichia coli and Streptococcus sp. were isolated only during severe stages; no anaerobic bacterial pathogens were isolated. Vasculitis and perivascular lymphocytic infiltrates in deep layers of the dermis suggested that a staphylococcal toxin may have been involved. The disease was not reproduced by scarifying S. hyicus onto the eyelids or by intravenous inoculation of retrovirus-infected chickens.     

Effects of Bordetella avium infection on the pulmonary clearance of Escherichia coli in turkeys

Thirty-six 1-day-old turkeys were inoculated intranasally with Bordetella avium (BA) strain 838. Noninoculated hatchmates (n = 36) were housed separately. At 2 and 4 weeks of age, 15 inoculated (BA+) and 15 noninoculated (BA-) turkeys were exposed to an aerosol of virulent Escherichia coli. The remaining six BA+ turkeys and six BA- turkeys were used as controls (ie, not exposed to E coli). Turkeys were necropsied on postaerosolization days 0 (immediately after aerosolization), 1, 3, 5, and 7. Lung and tracheal specimens were collected from each turkey for bacterial quantitation and histologic examination. A 1-ml blood sample was collected for detection of bacteremia. Numbers of E coli in lung specimens from 2- and 4-week-old turkeys were not significantly different between BA+ and BA- groups (pooled data over time); however, numbers of E coli isolated from tracheal specimens were significantly greater in BA+ turkeys than those in BA- turkeys. Although the incidence of pulmonary abcesses and E coli bacteremia was greater in 2-week-old turkeys than in 4-week-old turkeys, the incidence was not different between BA+ and BA- turkeys. At both ages, air sacculitis developed more often and was more severe in BA+ turkeys than in BA- turkeys. Hyperplastic bronchus-associated lymphoid tissue was found more often in BA+ turkeys than in BA- turkeys and appeared to be the first site of heterophil infiltration after E coli aerosolization.     

Experimental infection of turkeys with avian pneumovirus and either Newcastle disease virus or Escherichia coli

Avian pneumoviruses (APVs) are RNA viruses responsible for upper respiratory disease in poultry. Experimental infections are typically less severe than those observed in field cases. Previous studies with APV and Escherichia coli suggest this discrepancy is due to secondary agents. Field observations indicate APV infections are more severe with concurrent infection by Newcastle disease virus (NDV). In the current study, we examined the role of lentogenic NDV in the APV disease process. Two-week-old commercial turkey poults were infected with the Colorado strain of APV. Three days later, these poults received an additional inoculation of either NDV or E. coli. Dual infection of APV with either NDV or E. coli resulted in increased morbidity rates, with poults receiving APV/NDV having the highest morbidity rates and displaying lesions of swollen infraorbital sinuses. These lesions were not present in the single APV, NDV, or E coli groups. These results demonstrate that coinfection with APV and NDV can result in clinical signs and lesions similar to those in field outbreaks of APV.     

Exacerbation of Chlamydophila psittaci pathogenicity in turkeys superinfected by Escherichia coli

Both Chlamydophila psittaci and Escherichia coli infections are highly prevalent in Belgian turkeys and therefore they both might contribute to the respiratory disease complex observed in turkeys. C. psittaci can infect turkeys within the first week of age, even in the presence of maternal antibodies. However, the first C. psittaci outbreaks occur mostly at the age of 3 to 6 weeks, the period when also E. coli infections appear on the farms. Therefore, we examined in this study the pathogenicity of an E. coli superinfection on C. psittaci predisposed turkeys. Turkeys were infected with C. psittaci, E. coli or with C. psittaci followed by E. coli. Simulating the impact of an E. coli infection during the acute phase or the latent phase of a C. psittaci infection, turkeys received E. coli at 1 or 5 weeks post C. psittaci infection, respectively. E. coli superinfection during the acute phase of C. psittaci infection increased C. psittaci excretion and stimulated chlamydial replication in the respiratory tract resulting in exacerbated clinical disease. Interestingly, E. coli superinfection during the latent phase of C. psittaci infection induced chlamydial replication, leading to increased C. psittaci-specific antibody titres. In addition, chlamydial predisposition gave higher E. coli excretion compared with turkeys that had only been infected with E. coli. Overall, the present study clearly demonstrates the pathogenic interplay between C. psittaci and E. coli resulting in more severe respiratory disease.     

Colonization of Escherichia coli in young turkeys and chickens.

In order to investigate the possibility of pathogenic Escherichia coli penetrating the bloodstream via the intestinal mucosa in normal and stressed turkeys and chickens, birds were inoculated orally with the bacteria or exposed environmentally to it. Immediately after hatch, intestines contained a substantial number of coliform bacteria that increased with time. In orally infected turkeys, the pathogenic bacteria (nalidixic-acid-resistant O78) replaced 10%-50% of the native coliform flora but could not be isolated from the trachea or blood. Environmentally exposed groups exhibited pathogenic bacteria in intestines but not in blood. Stressing of exposed turkeys resulted in isolation of the pathogenic bacteria from blood and even spleen. In orally infected broiler chickens, stress resulted in bacteremia and mortality. Chickens that were exposed to pathogenic bacteria at a young age and showed no mortality or morbidity demonstrated no detrimental effects due to challenge with the same pathogenic bacteria later in life. Stress seems to cause penetration of the pathogenic bacteria into the bloodstream, which in turn can cause severe disease and mortality.     

Serum resistance and virulence of Escherichia coli isolated from turkeys

Twenty-five strains of Escherichia coli isolated from turkeys were characterized for their serum resistance and virulence. An in vitro bactericidal assay was used to determine the serum resistance of E coli. Virulence was determined by survival time after IV inoculation of each strain into 3-week-old turkeys. Serum-resistant E coli strains were generally found to be virulent for turkeys, whereas serum-sensitive E coli strains were avirulent. Of the 25 strains, 18 strains were placed in the 2 categories of serum-resistant/virulent and serum-sensitive/avirulent. Five strains were serum-resistant and avirulent, and 2 strains were serum-sensitive and virulent. Serum resistance appears to be an important determinant of virulence for E coli in turkeys; however, the requirement for other virulence factors, in addition to serum resistance, was suggested by the finding that 5 serum-resistant strains were avirulent in turkeys.     

High mortality and growth depression experimentally produced in young turkeys by dual infection with enteropathogenic Escherichia coli and turkey coronavirus

Six-day-old turkeys were inoculated with turkey coronavirus (TCV) and an enteropathogenic Escherichia coli (EPEC) (isolate R98/5) that were isolated from poult enteritis and mortality syndrome (PEMS)-affected turkeys. Turkeys inoculated with only R98/5 did not develop clinically apparent disease, and only mild disease and moderate growth depression were observed in turkeys inoculated with only TCV. Turkeys dually inoculated with TCV and R98/5 developed severe enteritis with high mortality (38/48, 79%) and marked growth depression. R98/5 infection resulted in attaching/effacing (AE) intestinal lesions characteristic of EPEC: adherence of bacterial microcolonies to intestinal epithelium with degeneration and necrosis of epithelium at sites of bacterial attachment. AE lesions were more extensive and were detected for a prolonged duration in dually inoculated turkeys compared with turkeys inoculated with only R98/5. An apparent synergistic effect in dually inoculated turkeys was indicated by increased mortality, enhanced growth depression, and enhanced AE lesion development. The results suggest that TCV promoted intestinal colonization by R98/5; however, R98/5 did not appear to alter TCV infection. The present study provides a possible etiologic explanation for PEMS.