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鸭坦布苏病毒对雏鸭免疫系统的影响 总被引：1，自引：0，他引：1
《中国兽医学报》2017,(2):211-217
为研究鸭坦布苏病毒(DTMUV)对雏鸭免疫系统的影响,本试验对5日龄雏鸭静脉接种DTMUV,并于接种后不同时间取雏鸭脾脏、胸腺、法氏囊进行组织病理学、抗原和凋亡检测。结果显示,DTMUV感染雏鸭的脾脏、胸腺、法氏囊均严重受损。接种DTMUV后4d,脾脏淋巴细胞减少,胸腺可见严重细胞崩解和大面积坏死区域,法氏囊滤泡轻度萎缩;接种后6d免疫器官病变最为严重,其中胸腺静脉严重栓塞,淋巴细胞变性坏死,空泡化也更加严重;接种后8d免疫器官病变均有所减轻,至16d,免疫器官结构基本恢复正常。通过免疫组织化学方法在感染雏鸭的脾脏、胸腺、法氏囊中均检测到DTMUV抗原;细胞凋亡试验显示DTMUV能够显著引起脾淋巴细胞凋亡。综上所述,DTMUV可严重损伤雏鸭免疫器官,且这种损伤常发生于感染早期,并于感染后8d出现好转。 相似文献
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本文报导了鸡传染性氏囊吉九地方株的分离与鉴定，该病毒株与英国ＪＡＮ－７８号ＩＢＤ血清做琼脂扩散沉淀试验，在判定时间内呈现沉淀线，该病毒株使传氏鸡法氏囊萎缩，粘膜出血，滤泡间结缔组织疏松水肿，异染性细胞浸润，淋巴滤泡内的淋巴细胞坏死，用荧光抗体染色，接种鸡的法氏囊淋巴滤泡内呈现荧光细胞。该病毒株接种敏感鸡，首次在接种鸡胸腺中的淋巴细胞的胞浆内观察到病毒包涵体和病毒颗粒，病毒颗粒为六角形，无囊膜，以结 相似文献
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本文探讨番鸭呼肠孤病毒强弱毒株对番鸭免疫器官超微结构的影响。强毒株感染番鸭显微结构变化表现为:各器官不同程度变性、细胞溶解坏死及血管扩张充血,病灶区及血管周围淋巴单核细胞明显浸润;免疫器官脾、胸腺和法氏囊淋巴细胞变性坏死,数量明显减少。脾脏淋巴细胞坏死,数量减少,网状结缔组织显露。而弱毒疫苗株接种后番鸭胸腺、法氏囊、脾脏组织学形态与健康对照鸭一致,均未发现在显微结构上的损伤。表明番鸭呼肠孤病毒强毒严重损伤免疫器官,而弱毒不仅失去对雏番鸭的致病性,而且也失去了损伤免疫器官和免疫抑制能力。 相似文献
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《畜牧兽医学报》2016,(2)
禽网状内皮组织增生病(RE)是禽类的一种重要免疫抑制性疾病,目前对其造成免疫抑制的机制尚不十分清楚。本研究对实验室分离的一株REV流行毒株(HLJR0901株)感染1日龄SPF鸡后对感染鸡免疫器官和免疫功能造成的影响进行研究。结果表明,1日龄SPF鸡感染REV后出现生长迟缓,法氏囊、胸腺萎缩,脾肿大的症状。感染鸡出现法氏囊滤泡淋巴细胞大量坏死减少,间质结缔组织增生;胸腺出血,胸腺小体增多;脾小结明显萎缩,淋巴细胞减少等病理变化。荧光定量PCR检测发现,病毒在感染鸡法氏囊、胸腺和脾内均有分布,且持续存在。SPF鸡感染REV后出现严重的免疫抑制,使AIV灭活疫苗和NDV弱毒疫苗的免疫效果显著下降。本研究为阐明REV的免疫抑制机制提供了重要的实验数据。 相似文献
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高致病力传染性法氏囊病野毒致弱株回传SPF鸡致病性的研究 总被引：1，自引：0，他引：1
vvIBDV致弱株经4周龄SPF鸡传代培养过程中,对接种鸡的法氏囊、胸腺、脾脏、盲肠扁桃体等免疫器官进行病理组织学检查,并分析主要免疫器官指数.发现随传代次数的增加,法氏囊和胸腺萎缩及脾脏肿大的程度逐渐加重;法氏囊、胸腺、脾脏和盲肠扁桃体内淋巴细胞崩解、坏死及脾脏内网状巨噬细胞增生的程度逐渐加深.试验结果表明,在传代过程中vvIBDV致弱株的毒力又逐渐恢复. 相似文献
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探讨番鸭呼肠孤病毒强毒株和弱毒株在番鸭免疫器官中的分布和排毒的差异。结果显示强毒株在感染后1d就可在脾脏、法氏囊、胸腺检出病毒RNA,高峰期为攻毒后7～14d;直到感染后35d,在免疫器官中不能检测到病毒RNA。接种强毒株后7d开始向外界排毒,而14d后停止向外界排毒。雏鸭免疫弱毒疫苗后3d,即可在脾、胸腺、法氏囊中检出病毒RNA;高峰期为攻毒后7～14d,免疫后21d免疫器官中的检测逐渐降低,直到感染后28d,在免疫器官中不能检测到病毒RNA。表明番鸭接种活疫苗后7d开始向外界排毒,而11d后停止向外界排毒。 相似文献
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鸡感染J亚群禽白血病病毒的免疫抑制机理 总被引：16，自引：4，他引：16
通过人工接种建立了雏鸡感染J亚群禽白血病病毒（ALV-J）后发生免疫抑制的病理模型。对免疫抑制的机理进行了初步研究。结果表明：ALV-J感染早期可诱导胸腺、法氏囊的淋巴细胞凋亡，这种早期的淋巴细胞凋亡是胸腺和法氏囊萎缩的重要原因之一。病理组织学动态观察表明。ALV-J主要引起骨髓的髓系细胞灶状或弥漫性增生，病变导致骨髓机能受损，使机体免疫机能下降。是引起免疫抑制的根本原因。病毒感染组免疫器官均发生了严重的实质萎缩性病变．这种病变的发生除与骨髓的病变及淋巴细胞凋亡有关外。还与中后期淋巴细胞的坏死有关．从而导致严重的免疫抑制。ALV-J感染可引起免疫器官及部分内脏器官中嗜酸性粒细胞样的瘤细胞浸润增生，这可以作为病毒感染早期的病理诊断指标。 相似文献
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给２８日龄伊莎雏鸡人工接种新城疫病毒后，应用常规病理学检验、细胞化学和免疫组化技术对免疫器官的病理学变化作了研究。接毒１２ｈ，法氏囊滤泡的髓质、胸腺小叶的髓质、脾白髓、盲肠扁桃体的淋巴小结及弥散淋巴组织的部分淋巴细胞和网状细胞首先出现核浓缩、胞浆固缩等坏死变化。接毒１～３ｄ（潜伏期），骨髓、法氏囊滤泡、胸腺小叶、脾白髓和红髓、盲肠扁桃体粘膜层及弥散淋巴组织的淋巴细胞、巨噬细胞和网状细胞发生核浓缩、碎裂、胞浆固缩，强嗜酸性等坏死变化。接毒４～６ｄ死亡病例，这些免疫器官的淋巴组织散在呈蜂窝状空泡结构坏死灶（法氏囊为滤泡坏死），进一步崩解成无结构嗜酸性颗粒状物质。这些坏死变化可作为雏鸡新城疫诊断的根据。 相似文献
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传染性法氏囊病病毒超强毒感染SPF鸡免疫器官中CD4+和CD8+T淋巴细胞动态分布 总被引：1，自引：0，他引：1
利用免疫组织化学染色对传染性法氏囊病病毒（IBDV）超强毒LX株感染SPF鸡免疫器官中CD4^ 和CD8^ T淋巴细胞的动态分布进行了研究。超强毒LX株接种2周龄SPF雏鸡，在其法氏囊、脾脏、胸腺、盲肠扁桃体、骨髓和哈氏腺中均可检出IBDV抗原的存在和CD4^ 与CD8^ T淋巴细胞的数量改变。在法氏囊中，CD4^ 淋巴细胞主要存在于淋巴滤泡间隙和滤泡皮质，而CD8^ T淋巴细胞则丰在于整个淋巴滤泡和滤泡间隙，并且CD8^ T淋巴细胞数量明显多于CD4^ T淋巴细胞，在接种后14d仍未见CD4^ 和CD8^ T淋巴细胞数量减少。脾脏中CD4^ T淋巴细胞主要存在于外周小动脉淋巴鞘或散在，而CD8^ T淋巴细胞则多存在于外周小动脉淋巴鞘和红髓。接种后胸腺中CD4^ 和CD8^ T淋巴细胞在皮质中减少，但在髓质增多，尤其是CD8^ T淋巴细胞数明显多于CD4^＋T淋巴细胞。盲肠扁桃体中CD4^ 和CD8^ T淋巴细胞主要存在于发生中心，尤其是CD8^ T淋巴细胞数比CD4^ T淋巴细胞明显多。骨髓和哈氏腺中也可见CD4^ 和CD8^ T淋巴细胞，而且CD8^ T淋巴细胞更多。在这些淋巴器官中，病毒损伤部位出现CD4^ 和CD8^ T淋巴细胞的迁入聚集，表明T淋巴细胞可能参与IBDV超强毒的免疫致病过程。 相似文献
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传染性法氏囊病病毒变异株的致病性 总被引：6，自引：1，他引：5
传染性法氏囊病病毒变异ＧＣ９０２株可引起１０日龄ＳＰＦ鸡胚肝脏坏死和脾脏明显肿大及较高的死亡率。接种２周龄ＳＰＦ雏鸡,同时设标准Ｉ型强毒ＣＪ８０１株和标准变异株强毒１０８４Ａ株接种对照,该毒株接种后第３天才出现法氏囊粘膜浆膜出血、个别黄化、质硬等病变,且于第４天法氏囊明显萎缩变小,至接种后２０天法氏囊仍严重萎缩;接种后第２天引起脾脏显著肿大,于第１２天时大小恢复正常。试验结果表明,该ＧＣ９０２株对ＳＰＦ雏鸡的致病性与标准变异株基本一致,仅有一定的差异,但明显不同于标准Ｉ型强毒株的致病性。 相似文献
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The pathogenesis of 4 isolates of turkey-origin reovirus (NC/SEP-R44/03, NC/98, TX/98, and NC/85) and 1 chicken-origin reovirus (1733) was examined by infecting specific pathogen free (SPF) poults. These turkey-origin reovirus (TRV) isolates were collected from turkey flocks experiencing poult enteritis and are genetically distinct from previously reported avian reoviruses. Microscopic examination of the tissues collected from the TRV-infected poults revealed different degrees of bursal atrophy characterized by lymphoid depletion and increased fibroplasia between the bursal follicles. To understand the relationship between virus spread and replication, and the induction of lesions, immunohistochemical staining (IHC) for viral antigen, in situ hybridization (ISH) for the detection of viral RNA, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay for the detection of apoptosis in affected tissues was performed. Both IHC and ISH revealed viral antigen and RNA in the surface epithelial cells of the bursa, in macrophages in the interstitium of the bursa and, to lesser degree, in splenic red pulp macrophages and intestinal epithelial cells. Increased apoptosis of bursal lymphocytes and macrophages was observed at 2 and 5 days postinoculation. No lesions were found in tissues from poults inoculated with the virulent chicken-origin strain, however viral antigen was detected in the bursa and the intestine. Although all TRVs studied displayed similar tissue tropism, there were substantial differences in the severity of the lesions produced. Poults inoculated with NC/SEP-R44/03 or NC/98 had moderate to severe bursal atrophy, whereas poults inoculated with TX/98 or NC/85 presented a mild to moderate bursal lymphoid depletion. The lymphoid depletion observed in the bursa appears to be the effect of an indirectly induced apoptosis and would most likely result in immune dysfunction in poults infected with TRV. 相似文献
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对28日龄无特定病原(SPF)鸡通过点眼、滴鼻方式人工感染了传染性法氏囊病病毒(IBDV)超强毒株GX;自感染第2天至第9天,每天用免疫胶体金试纸膜和琼脂扩散试验(AGP)两种方法检测九种组织(法氏囊、脾脏、胸腺、肾脏、肝脏、盲肠、扁桃体、肺脏、心脏、直肠内容物)的病毒含量变化,初步探索出传染性法氏囊病病毒在鸡体内各组织的侵染性变化规律。 相似文献
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OBJECTIVE: To examine effects of virus exposure on embryonic lymphoid organ structure, apoptosis, and lymphoid cell subpopulations. ANIMALS: Eggs of specific pathogen free (SPF) White Leghorn chickens at embryonation day (ED) 17. PROCEDURES: Eggs were inoculated with 2,000 plaque-forming units (PFU) of serotype 1 herpesvirus (Marek's disease virus [MDV 1]), 2,000 PFU of herpesvirus of turkeys (MDV 3), or 1,000 embryo infectious doses (EID50) of infectious bursal disease virus (IBDV). On post-inoculation days (PID) 3 and 5, lymphoid organ to body weight ratios were determined, and bursa of Fabricius, thymus, and spleen were evaluated for lesions and apoptosis. Proportions of lymphoid cell subpopulations of PID-3 chicken embryos and 7- to 10-day-old chicks were quantitated by flow cytometry. RESULTS: Lymphoid organ weights were similar in virus-free, MDV1, and IBDV groups. Embryos inoculated with 2,000 PFU MDV 3/egg had lower bursal weights than virus-free controls. In a repeated trial, MDV 3 (1,000 PFU to 4,000 PFU) did not reduce bursal weights among groups. Histologic changes were seen in bursae after MDV 1 and IBDV inoculation. Apoptosis was greater in bursae of MDV 1-infected embryos than controls. Lymphoid cell subpopulations were similar among all groups with the exception of CD8+ and IgM+ cells in spleens of IBDV-infected 10-day-old chicks. CONCLUSIONS AND CLINICAL RELEVANCE: Infection with pathogenic strains of MDV 1 and IBDV did not alter lymphocyte subpopulations in embryos or cause complete destruction of lymphoid organs. Changes in lymphoid cell subpopulations exposed as embryos to IBDV were seen only after hatching. 相似文献
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S S Cloud H S Lillehoj J K Rosenberger 《Veterinary immunology and immunopathology》1992,34(3-4):337-352
The potential effect of chicken anemia agent (CAA) alone or in combination with infectious bursal disease virus (IBDV) on the immune system of young chickens was determined by measuring alterations in hematocrit values, lymphoid organ-to-body weight ratios and lymphoid cell concentrations at 4, 7, 10, 14, 17, 21, 28 and 42 days post-inoculation (PI). Lymphocyte subpopulations were identified and counted by flow cytometry using cell suspensions stained with monoclonal antibodies (Mabs) for panlymphocytes (K55), cytotoxic T-cells (CTLA3), T-helper cells (CT3), Ia-expressing cells (P2M11) and macrophages (P7). Chicken anemia agent induced a substantial but transient decrease in hematocrit value, thymus-to-body weight ratio and bursa-to-body weight ratio between 7 and 21 days PI corresponding to a generalized lymphocytopenia in the thymus, bursa and spleen. However, cytotoxic T-cell, T-helper cell and Ia-expressing cell concentrations increased in the bone marrow of birds inoculated with CAA alone or in combination with IBDV during the same time period. T-helper-to-cytotoxic T-cell ratios increased in the thymus and spleen during severe lymphocytopenia, indicating a selective decrease in cytotoxic T-cells. T-helper-to-cytotoxic T-cells ratios increased in the bone marrow, indicating a selective increase in T-helper cell concentrations. The increase in Ia-expressing cells in the bone marrow may be a reflection of increased number of activated T-cells which express Ia antigen. Infectious bursal disease virus alone induced a persistent depression of Ia-expressing cells in the bursa and the spleen and no measurable change in the bone marrow lymphocyte subpopulations. Chickens inoculated simultaneously with CAA and IBDV experienced clinical signs observed in chickens inoculated with each virus separately with a prolonged acute phase prior to recovery or mortality. 相似文献