紫锥菊和黄芪活性成分缓解IBD雏鸡免疫抑制性的研究

为探讨紫锥菊、黄芪对感染传染性法氏囊病(IBD)雏鸡免疫的影响,给14日龄雏鸡灌服不同浓度紫锥菊、黄芪合剂(按3∶1比例混匀),其有效成分为菊苣酸和黄芪多糖,连续灌服7 d,21日龄时给雏鸡接种传染性法氏囊病病毒(IBDV)。结果表明,应用紫锥菊、黄芪后可缓解IBDV造成法氏囊的病理损伤,增加免疫器官指数,在攻毒20 d后差异明显;用药组中球蛋白含量在攻毒后11 d升高明显,可以缓解免疫抑制,进而调节机体免疫机能,增强机体的防御功能,有利于该病的防治。     

紫锥菊、黄芪对感染IBDV雏鸡胸腺、小肠中CD4+、CD8+T淋巴细胞动态分布的影响

将14日龄雏鸡随机分为3组,A组灌服1 mL的紫锥萄、黄芪合荆,B、C组灌服生理盐水,连续灌服7 d.21日龄时A、B组雏鸡接种传染性法氏囊病病毒(IBDV),用免疫组化法观察雏鸡胸腺、小肠中CD4+、CD8+T淋巴细胞动态分布的变化.结果表明,用药组和攻毒对照组相比较,CD4+T淋巴细胞差异显著(P<0.05),但是CD8+T淋巴细胞差异不显著(P>0.05),与空白对照组相比CD4+淋巴细胞显著增多.胸腺、小肠中24日龄时CD4+、CD8+T细胞数量较其他日龄差异显著(P<0.05).总试验期胸腺中CD4+、CD8+含量是所测总数的60%.表明紫锥菊、黄芪对机体免疫有显著增强作用,以胸腺中CD4+、CD8+含量多于小肠,能显著降低IBDV对机体造成的损伤.     

紫锥菊复合物对雏鸡人工感染传染性法氏囊病病毒的效果观察

本试验将240只海兰褐雏鸡随机分为8组,每组30只,分别为紫锥菊复合物高剂量组、中剂量组、低剂量组、中药对照组、西药对照组、疫苗对照组、阴性对照组、健康对照组,采用紫锥菊复合物,将试验鸡人工感染传染性法氏囊病病毒（IBDV）强毒,观察紫锥菊复合物对雏鸡的保护作用。结果表明：紫锥菊复合物可以减弱IBDV强毒对雏鸡免疫器官的损害,对传染性法氏囊病强毒感染雏鸡具有明显的保护作用。     

紫锥菊、黄芪对感染IBDV雏鸡胸腺、小肠中CD4~＋、CD8~＋ T淋巴细胞动态分布的影响

将14日龄雏鸡随机分为3组,A组灌服1 mL的紫锥菊、黄芪合剂,B、C组灌服生理盐水,连续灌服7 d。21日龄时A、B组雏鸡接种传染性法氏囊病病毒（IBDV）,用免疫组化法观察雏鸡胸腺、小肠中CD4＋、CD8＋T淋巴细胞动态分布的变化。结果表明,用药组和攻毒对照组相比较,CD4＋T淋巴细胞差异显著（P〈0.05）,但是CD8＋T淋巴细胞差异不显著（P〉0.05）,与空白对照组相比CD4＋淋巴细胞显著增多。胸腺、小肠中24日龄时CD4＋、CD8＋T细胞数量较其他日龄差异显著（P〈0.05）。总试验期胸腺中CD4＋、CD8＋含量是所测总数的60%。表明紫锥菊、黄芪对机体免疫有显著增强作用,以胸腺中CD4＋、CD8＋含量多于小肠,能显著降低IBDV对机体造成的损伤。     

紫锥菊、黄芪提取物对鸡传染性法氏囊病疫苗免疫调节作用和生产性能的影响

为了探讨紫锥菊和黄芪的免疫调节作用,以1日龄罗斯308肉鸡作为试验材料,用传染性法氏囊病(IBD)疫苗进行免疫,以紫锥菊提取物单剂,黄芪提取物单剂,以及紫锥菊和黄芪合剂3种组方,分别以3种剂量在6日龄连续给雏鸡口服7 d,在13、20、27、34、41日龄采血检测外周血中鸡传染性法氏囊病毒(IBDV)抗体,IL-2含量,并测定肉鸡生产性能.结果表明,应用紫锥菊提取物能明显提高外周血中IBDV抗体和IL-2含量,提高试验鸡料肉比.说明紫锥菊提取物具有明显的免疫促进作用,改善生产性能作用,其中0.5%为最佳剂量.用两种提取物相配伍后(0.5% 0.25%)同样提高其机体免疫水平,显示出两种物质的协同作用和增强作用.     

鸡传染性贫血病毒感染对雏鸡免疫系统的影响 Ⅰ.T、B淋巴细胞增殖反应的变化

1日龄雏鸡感染鸡传染性贫血病毒（CIAV）后,胸腺和脾脏T淋巴细胞增殖反应分别于14d和7～21d明显减弱（P相似文献   

米糠多糖对免疫抑制鸡脾脏和法氏囊细胞周期和抗细胞凋亡作用

为探讨米糠多糖(RBS)对免疫抑制鸡免疫调节作用的机理,作者采用流式细胞术检测了健康雏鸡、环磷酰胺(CTX)和传染性法氏囊病毒(IBDV)诱导的免疫抑制雏鸡在给予RBS[剂量150 mg/(kg·d)]和不给予RBS情况下脾脏和法氏囊细胞的DNA含量、细胞周期及细胞凋亡率.结果显示:(1)CTX+RBS组雏鸡脾脏S期细胞比例和PI值显著高于CTX组(P<0.05),该2组鸡的法氏囊细胞周期没有显著差异(P>0.05).(2)IBDV+RBS组雏鸡脾脏S期、G2期细胞比例和PI值、法氏囊的S期细胞和PI值均高于IBDV组(P<0.05);(3)CTX+RBS组和IBDV+RBS组雏鸡脾脏和法氏囊细胞的凋亡率分别低于CTX组和IBDV组(P<0.05).结果表明:RBS能够促进CTX处理鸡脾脏细胞和IBDV感染鸡脾脏和法氏囊细胞DNA复制,对CTX和IBDV诱导鸡的脾脏和法氏囊细胞凋亡过程均有一定的拮抗作用.     

紫锥菊黄芪对传染性囊病疫苗免疫雏鸡淋巴细胞亚群和肿瘤坏死因子含量的影响

为探讨紫锥菊、黄芪提取物提高雏鸡免疫力的效果,本试验选用紫锥菊、黄芪、紫黄(紫锥菊黄芪)合剂3种组方分别以不同的3种剂量给6日龄雏鸡连续口服7 d,13日龄进行腔上囊疫苗免疫,在20,27,34日龄时ELISA方法检测血清中TNF-α的含量;在13,20,27日龄时流式细胞仪检测外周血中CD4+、CD8+含量并计算CD4+/CD8+比值.结果表明,紫锥菊对外周血CD4+/CD8+ T淋巴细胞亚群的比例以及血清TNF-α的含量均有一定的提高,说明紫锥菊提取物针对IBD疫苗具有明显的免疫促进作用,是一种效果极为明显的免疫增强剂.     

雏鸡感染新城疫病毒后机体抗氧化功能的变化

用新城疫病毒(NDV)LD强毒株以肌肉注射方式感染21日龄麻鸡,于感染后1 d、2 d、3 d、4 d、5 d采取脑、心脏、肺脏、脾脏、法氏囊等组织,分光度法测定其超氧化物歧化酶(SOD)的活性和脂质过氧化物丙二醛-(MDA)的含量.结果显示,NDV感染组雏鸡的各组织中SOD活性在人工感染后2 d显著低于对照组(p<0.05);雏鸡心脏、肺脏、脾脏、法氏囊MDA含量在人工感染后2 d显著高于对照组(P<0.05),脑组织MDA含量在人工感染后3 d显著高于对照组(p<0.05).     

烟曲霉菌感染对雏鸡免疫器官指数及新城疫抗体水平的影响

为了研究烟曲霉菌感染对雏鸡免疫器官指数及新城疫抗体水平的影响,试验选取40只14日龄海兰褐公鸡,随机分成2组,每组20只,试验组用霉菌孢子攻毒3 d,对照组不攻毒,所有试验鸡均按常规模式进行饲养和防疫,并于攻毒后第5天从试验组和对照组中各选10只鸡进行免疫器官指数的测定和血清中新城疫病毒抗体效价测定。结果表明:试验组雏鸡体重降低,法氏囊、胸腺重及法氏囊指数、胸腺指数均低于对照组且差异显著(P0.05);脾脏重和脾脏指数与对照组相比差异不显著(P0.05);试验组雏鸡新城疫血清抗体效价低于对照组,且差异显著(P0.05)。说明烟曲霉菌感染能造成雏鸡免疫抑制,导致免疫器官萎缩、变小,使免疫机能下降,影响疫苗免疫效果。     

In ovo vaccination of specific-pathogen-free chickens with vaccines containing multiple agents.

We used in ovo technology to protect chickens against multiple diseases by inoculating vaccines containing mixtures of live viral agents. A single in ovo injection of a vaccine containing serotypes 1, 2, and 3 of Marek's disease virus (MDV), a vaccine strain of serotype 1 infectious bursal disease virus (IBDV), and recombinant fowl pox vaccine with HN and F genes of Newcastle disease virus (rFP-NDV) induced protection against virulent MDV, IBDV, Newcastle disease virus, and fowl poxvirus. The multiple-agent vaccine induced specific antibodies against the viral agents present in the mixture and did not adversely affect the survival of hatched chickens. Inoculation of a vaccine containing serotypes 1, 2, and 3 of MDV and IBDV did not affect hatchability of eggs, although the addition of rFP-NDV to the mixture reduced hatchability by 23%-26%. In ovo vaccination with a vaccine containing MDV and IBDV vaccine viruses did not exacerbate the inhibitory effect of individual viral agents on humoral and cellular immune competence.     

Protective immunity against infectious bursal disease virus in chickens in the absence of virus-specific antibodies

The role of cell-mediated immunity (CMI) in pathogenesis of infectious bursal disease virus (IBDV) was investigated. One-day-old specific pathogen-free chickens were treated with 3mg of cyclophosphamide (Cy) per chicken for 4 consecutive days and, 3 weeks later, infected with the IBDV-IM strain. Chickens were examined for: (a) mitogenic response of splenocytes to ConA, as an indicator of T-cell functions in vitro, (b) antibody against IBDV by ELISA, (c) IBDV genome in various tissues by RT-PCR and (d) immunological memory. At the time of IBDV infection, Cy-treated chickens had depleted bursal tissue (an avian primary B-cell lymphoid organ), severely compromised antibody-producing ability, but normal T-cell response to ConA. In primary infection, no detectable antibody against IBDV antigen in Cy-treated, IBDV-infected chickens was observed up to 28 days post-infection (PI), while IBDV genome was detected by RT-PCR in spleen, thymus, liver and blood until 10 days PI. Like intact control chickens infected with IBDV, Cy-treated, IBDV-infected chickens suppressed splenocytes responses to ConA from 5 to 10 days PI, suggesting that intact control as well as Cy-treated chickens responded similarly to IBDV infection in the early phase. Following re-infection with IBDV, no detectable secondary antibody response to IBDV as well as IBDV genome in tissues were observed in Cy-treated chickens, while intact control chickens developed vigorous secondary antibody response. Similar to intact control chickens infected with IBDV, Cy-treated chickens after second infection with IBDV did not suppress splenocyte response to ConA. These results suggested that in the absence of detectable anti-IBDV antibodies, protection of Cy-treated chickens from IBDV infection may occur via immunological memory mediated by CMI. We concluded that under normal conditions, IBDV induces a protective antibody response, however, in the absence of antibody, CMI alone is adequate in protecting birds against virulent IBDV.     

复方中药对蛋雏鸡感染IBDV后免疫器官的形态学影响

２００只３０日龄健康海兰蛋雏鸡随机分为四组,每组５０只。Ａ组饲料中添加复方中药,接种ＩＢＤＶ;Ｂ组饲料中添加中药,接种ＩＢＤＶ;Ｃ组不添加中药,接种ＩＢＤＶ;Ｄ组不作任何处理为对照组。在接种后７ｄ剖检、取材作石蜡切片,观察鸡免疫器官的形态学变化。结果表明,传染性ＩＢＤ野毒可使鸡免疫器官发育不良,主要导致法氏囊的淋巴细胞变性坏死,抑制免疫活性细胞的生成,导致免疫抑制;中药促进免疫器官发育及免疫活性细胞生成,提高免疫活性,调节免疫抑制,使免疫器官的组织结构保持或恢复正常水平;复方中药抗ＩＢＤＶ感染的效果优于中药。     

Experimental inoculation of avian polyomavirus in chemically and virally immunosuppressed chickens.

The purpose of this series of experiments was to determine the effect of various types of immunosuppressive treatments (cyclophosphamide, infectious bursal disease virus [IBDV], chicken anemia virus [CAV], and combination infection with IBDV and CAV) on susceptibility of chickens to challenge with avian polyomavirus. In the first experiment, chickens were chemically bursectomized with intraperitoneal injections of cyclophosphamide; in the second study, chickens were orally inoculated with IBDV; in the third study, birds were intramuscularly inoculated with CAV; and in the final study, birds were inoculated with both IBDV and CAV. In all experiments, chickens were challenged with 10(4.7) tissue culture infective doses of polyomavirus intraperitoneally. Only chemically bursectomized chickens developed lesions similar to those found in the naturally occurring multisystemic fatal form of polyomavirus infection seen in psittacine nestlings, including hepatic necrosis and large pale intranuclear inclusions.     

INTERACTION BETWEEN INFECTIOUS BURSAL DISEASE VIRUS AND NEWCASTLE DISEASE VIRUS IN CHICKENS

The Australian strain of infectious bursal disease virus (IBDV), 002/73, affected the response of chickens to Newcastle disease virus (NDV). The titre of serum antibodies to NDV in chickens infected with IBDV was significantly lower than that of birds infected with NDV alone. It also appeared that IBDV affected NDV excretion from chickens as NDV was more frequently isolated from chickens infected with IBDV, IBDV infection did not alter the pathogenicity of NDV in chickens. This Australian strain of IBDV therefore appeared to be immunodepressive in one-day-old chickens.     

Embryo vaccination with infectious bursal disease virus alone or in combination with Marek's disease vaccine

Studies with specific-pathogen-free chickens revealed that chicks hatching from eggs inoculated at the 18th day of embryonation with infectious bursal disease (IBD) vaccine viruses of low virulence (isolates TC-IBDV and BVM-IBDV) developed antibody against IBD virus (IBDV) and resisted challenge with virulent IBDV at 3 weeks of age or older. Embryo vaccination did not adversely affect hatchability of chicks or survival of hatched chicks. Chicks embryonally vaccinated with TC-IBDV had transient histologic lesions in the bursa of Fabricius at hatch. Similar but milder lesions were also noted in chickens that received TC-IBDV at hatch. The level of protection following embryo vaccination with TC-IBDV and BVM-IBDV was similar to that following vaccination with the same vaccines at hatch. Vaccine viruses of moderate virulence (isolates BV-IBDV and 2512-IBDV) were not suitable as vaccines in embryos lacking maternal antibody to IBDV, because the vaccinated chicks developed acute IBD after hatch. Isolate 2512-IBDV was not pathogenic for embryos bearing maternal antibody to IBDV. Maternal antibody against IBDV interfered with efficacy of embryo vaccination with BVM-IBDV but not with 2512-IBDV. Embryo vaccination with a mixture of vaccines against IBD and Marek's disease resulted in protection of hatched chicks against challenge with virulent IBDV and Marek's disease virus.     

Response of B congenic chickens to infection with infectious bursal disease virus.

Six congenic lines of chickens that differ from the parental inbred line RPRL-15I5 for genes in the major histocompatibility (B) complex were used to study the influence of the B haplotypes on the response of chickens to infection with virulent infectious bursal disease virus (IBDV) at 1 day or 4 weeks of age, and on the antibody response to vaccination with live or inactivated oil-emulsion (OE) IBDV vaccines at 7 weeks of age. IBDV-induced immunodepression and lesions in the bursa, spleen, and thymus in chickens infected with virus at 1 day of age were of the same degree of severity, regardless of line of chickens used. The response of blood cells to the mitogens phytohemagglutinin-M and concanavalin A was elevated in chickens infected with IBDV at 1 day of age. In an experiment conducted to study the effect of the B haplotype on IBDV infection in 4-week-old chickens, B congenic line C-12 (B12B12) showed the highest susceptibility to clinical IBD, with mortality of 79%. No detectable difference in the serological response to vaccination with live or OE IBDV vaccines was noted among chickens of various congenic lines. We conclude that the B haplotypes may influence IBDV-induced mortality, but not immunodepression or severity of lesions in lymphoid organs, or the antibody response to live or OE IBDV vaccines.     

Humoral and cell-mediated immune responses in chickens with infectious bursal disease

Primary and secondary immune responses to Newcastle disease virus (NDV) was evaluated in chickens infected with infectious bursal disease virus (IBDV) at one and 28 days of age. The geometric mean primary hemagglutination-inhibition antibody titers (GMT) of chickens infected with IBDV at one day of age was significantly lower (P less than or equal to 0.01) than those infected at 28 days of age. Infection with IBDV had no influence on secondary immune response to NDV. The effect of IBDV infection at one day of age on the cell-mediated immunity of chickens was evaluated by skin allograft acceptance or survival time. There was no significant difference between the percentage of grafts accepted in IBDV infected and noninfected control chickens. However, the mean graft survival time in the IBDV infected chickens was significantly longer (P less than or equal to 0.05) than those in the control group. This suggested a suppression of cell-mediated immunity due to IBDV infection.     

A study of the epidemiology of infectious bursal disease in poultry in Queensland, 1976–1979

The epidemiology of infectious bursal disease (IBD) was studied by serology and sometimes by visual examination of the bursa of Fabricius in poultry flocks in Queensland during 1976–1979.
Ten flocks, each of approximately 30,000 meat breeding chickens, were surveyed. All chickens had maternally-derived antibody against IBD virus (IBDV) at hatching and active antibody was not detected while the chickens were brooded on rearing farms. When distributed to breeding farms, 7 of the flocks developed antibody when 11 to 25 weeks of age. The remaining 3 flocks were vaccinated by infection of 10% of the birds and within 4 weeks more than 80% of the chickens had developed precipitating antibody to IBDV.
Blood samples of 20 to 30 broiler chickens were collected at slaughter (7 to 9 weeks of age) from each of 312 broiler flocks raised on 37 contract farms. While the samples from 21 flocks were without detectable antibody to IBDV, all serum samples for 263 flocks contained antibody. The ratio of bursal weight to bodyweight was significantly lower in birds from 144 flocks having antibody to IBDV than in birds from 10 flocks that were without detectable antibody. In sequential studies, IBDV antibody became demonstrable in 27 of 30 flocks when the chickens were one to 6 weeks of age and was accompanied by bursal atrophy.
Serological investigation of 4 flocks of layer breeding chickens on a multi-age farm at approximately monthly intervals resulted in antibody to IBDV being detected at every examination.
Serological tests and bursal examinations were carried out weekly in 2 flocks each of 4000 layer chickens between one and 20 weeks of age. Serum antibody developed in one flock at 4 weeks of age and in the other at 17 weeks of age. In both flocks, bursal atrophy occurred concurrently with the development of antibody.