B亚型禽偏肺病毒对SPF鸡的致病性

利用分离的1株B亚型禽偏肺病毒,采用静脉注射和点眼滴鼻两种途径接种SPF鸡,并在接种同时免疫新城疫弱毒疫苗。在攻毒后3、6、9、12、15d,每组随机抽取3只翅下采血,检测血液生化指标,利用血凝和血凝抑制试验检测新城疫HI抗体效价;利用流式细胞术分析外周血CD40／CD8比值,ELISA试剂盒测定血清中IL-2、IFN7的含量;同时观察静脉注射组和点眼滴鼻组鸡的临床症状、剖检病变和病理组织学变化。结果表明,攻毒后9～15d,静脉注射组和点眼滴鼻组外周血CD4＋/CD8＋比值和血清II-2、IFN-γ的含量均显著低于对照组（P〈0．05）,而静脉注射组与点眼滴鼻组间无显著差异（P〉0．05）;静脉注射组和点眼滴鼻组的免疫器官指数低于对照组,但各组间差异不显著（P〉0．05）;各组间新城疫HI抗体水平无显著差异（P〉0．05）;血液生化指标仪谷丙转氨酶（ALT）和谷草转氨酶（AST）在攻毒后显著升高（P〈0．05）,其他指标在各组间无显著差异（P〉0．05）;静脉注射组和点眼滴鼻组在感染后3～10d出现轻微临床症状;病理组织学检测结果显示,静脉注射组和点眼滴鼻组的呼吸道和肝脏病变最明显。综上所述,B亚型禽偏肺病毒感染SPF鸡后,在一段时间内抑制机体细胞免疫,导致免疫机能下降,并引起轻微的组织病变;B亚型禽偏肺病毒通过两种不同的攻毒途径对SPF鸡的致病性无显著差异。     

Avian metapneumovirus subtype A in China and subtypes A and B in Nigeria

In order to detect and characterize avian metapneumovirus, organs or swabs were collected from 697 chicken and 110 turkeys from commercial farms in Southwestern Nigeria and from 107 chickens from live bird markets in Southeastern China. In Nigeria, 15% and 6% of the chicken and turkey samples, respectively, and 39% of the chicken samples from China, were positive for aMPV genome by PCR. The sequence of a 400 nt fragment of the attachment protein gene (G gene) revealed the presence of aMPV subtype A in both Nigeria and Southeastern China. Essentially identical subtype A viruses were found in both countries and were also previously reported from Brazil and the United Kingdom, suggesting a link between these countries or a common source of this subtype. In Nigeria, subtype B was also found, which may be a reflection of chicken importations from most major poultry-producing countries in Europe and Asia. In order to justify countermeasures, further studies are warranted to better understand the metapneumoviruses and their impact on poultry production.     

1株B亚型禽偏肺病毒的分离与鉴定

从山东省多个地区的商品肉鸡养殖场采集64份疑似病料,通过RT-PCR方法检测出37份禽偏肺病毒阳性病料,以此作为病毒分离材料接种SPF鸡胚,盲传至第7代时鸡胚生长明显迟滞。取阳性尿囊液在CEF中培养,呈现禽偏肺病毒典型细胞病变(CPE):细胞变圆、悬浮,有合胞体形成。将分离株接种于Vero细胞及DF-1细胞均出现类似病变。对分离株F基因进行测序,并与GenBank中发表的部分代表序列比较。结果显示,与B亚型禽偏肺病毒的核苷酸同源性最高,为97.4%⁹9.3%;与A亚型禽偏肺病毒核苷酸同源性较低,为77.4%99.3%;与A亚型禽偏肺病毒核苷酸同源性较低,为77.4%⁷8.1%;而与C亚型禽偏肺病毒核苷酸同源性最低,为69.5%78.1%;而与C亚型禽偏肺病毒核苷酸同源性最低,为69.5%⁶9.7%。基因分型显示分离株为B亚型禽偏肺病毒,将该毒株命名为禽偏肺病毒SDWF株。     

1株B亚型禽偏肺病毒的分离与鉴定

从山东省多个地区的商品肉鸡养殖场采集64份疑似病料,通过RT—PCR方法检测出37份禽偏肺病毒阳性病料,以此作为病毒分离材料接种SPF鸡胚,盲传至第7代时鸡胚生长明显迟滞。取阳性尿囊液在CEF中培养,呈现禽偏肺病毒典型细胞病变（CPE）：细胞变圆、悬浮,有合胞体形成。将分离株接种于Veto细胞及DF-1细胞均出现类似病变。对分离株F基因进行测序,并与GenBank中发表的部分代表序列比较。结果显示,与B亚型禽偏肺病毒的核苷酸同源性最高,为97．4％～99．3％;与A亚型禽偏肺病毒核苷酸同源性较低,为77．4％～78．1％;而与C亚型禽偏肺病毒核苷酸同源性最低,为69．5％～69．7％。基因分型显示分离株为B亚型禽偏肺病毒,将该毒株命名为禽偏肺病毒SDWF株。     

Avian paramyxovirus type I infection in pigeons: clinical observations

An outbreak of a neurological disease in pigeons caused by avian paramyxovirus type I occurred in the New York metropolitan area in 1984. It was characterized clinically by head tremors, paresis of the wings and legs, ataxia, torticollis, and loose droppings. Clinical pathologic evaluation revealed anemia and elevated plasma transaminase enzymes. Mortality was virtually 100% in juvenile pigeons, whereas the adults generally experienced much lower morbidity and mortality.     

Avian paramyxovirus type 1 infection in pigeons: recent changes in clinical observations

Since its first appearance in 1984, avian paramyxovirus type 1 has remained an enzootic disease in racing pigeons on Long Island, New York. The clinical presentation of the disease in the autumn of 1987 suggests a decrease in the severity and incidence of neurological signs, with the chief complaint being watery droppings accompanied by poor racing performance. Diagnosis is based upon serology, using hemagglutination-inhibition tests with Newcastle disease or paramyxovirus type 1 virus.     

B亚型禽偏肺病毒逆转录套式PCR检测方法的建立与应用

根据GenBank发布的B亚型禽偏肺病毒Fusion(F)基因的保守序列设计2对引物,建立了一种适用于B亚型禽偏肺病毒的逆转录套式PCR检测方法.采用该方法对B亚型禽偏肺病毒山东分离株进行检测,可以特异性地扩增出415 bp的目的片段.此方法具有高度特异性和敏感性,以H9亚型禽流感病毒、新城疫病毒、传染性支气管炎病毒、传染性喉气管炎病毒作为模板进行扩增,结果均为阴性.经检测,该方法第1次PCR扩增的敏感性为102 copies/μL,第2次扩增的敏感性为102 copies/μL,第2次扩增敏感性比第1次高105倍.应用本方法对采自山东省不同地区的64份可疑临床病料进行检测,最终从64份疑似病料中检测出37份为阳性.结果表明,所建立的套式PCR检测方法具有特异、敏感、实用等优点,为B亚型禽偏肺病毒的快速诊断以及深入研究奠定了基础.     

Kinetic disposition, systemic bioavailability and tissue distribution of apramycin in broiler chickens

Apramycin was administered to chickens orally, intramuscularly and intravenously to determine blood concentration, kinetic behaviour, bioavailability and tissue residues. Single doses of apramycin at the rate of 75 mg kg⁻¹ body weight were given to broiler chickens by intracrop, i.m. and i.v. routes. The highest serum concentrations of apramycin were reached 0·20 and 0·76 hours after the oral and i.m. doses with an absorption half-life () of 0·10 and 0·19 hours and an elimination half life () of 1·22 and 2·31 hours respectively. The systemic bioavailability was 2·0 and 58 per cent after intracrop and i.m. administration, respectively, indicating poor absorption of the drug when given orally.Following i.v. injection, the kinetics of apramycin was described by a two-compartment open model with a () of 1·5 hours, () of 2·1 hours, V_d(ss) (volume of distribution) of 4·82 litre kg⁻¹ and C1_(B) (total body clearance) of 1·88 litre kg⁻¹ hour⁻¹. The serum protein-binding of apramycin was 26 per cent.The highest tissue concentrations of apramycin were present in the kidneys and liver. No apramycin residues were detected in tissues after six hours except in the liver and kidneys following intracrop dosing and kidneys following i.m. administration.     

Metabolic behaviour and tissue distribution of nalidixic acid in chickens

The metabolic behaviour and tissue distribution of nalidixic acid in normal and E. coli infected chickens were carried out using spectrofluorimetric and microbiological techniques following a single and multiple oral administration of 25 mg/kg b. wt. The obtained results revealed that free nalidixic acid (free NA) is the major fraction of the total drug concentration in serum, liver and kidneys. The free active nalidixic acid was in a higher concentration than hydroxynalidixic acid (free HNA) and both conjugates of NA and HNA following single and multiple oral administration. The obtained results showed that nalidixic acid was highly distributed in all tissues in normal and E. coli infected chickens, with the highest concentrations in kidneys, liver and heart and lowest concentrations in brain, muscles and intestine following oral administration of 25 mg/kg b. wt. twice daily for 5 successive days. Spectrofluorimetic technique was more sensitive for nalidixic acid determination than microbiological method. Nalidixic acid revealed longer withdrawal time in diseased chickens than in normal chickens.     

Pharmacokinetic profile and tissue distribution of monensin in broiler chickens

1. The pharmacokinetics of monensin, including half‐life, apparent volume of distribution, total body clearance, systemic bio‐availability and tissue residues were determined in broiler chickens. The drug was given by intracrop and intravenous routes in a single dose of 40 mg/kg body weight.

2. Following intravenous injection the kinetic disposition of monensin followed a two compartments open model with absorption half life of 0.59 h, volume of distribution of 4.11 I/kg and total body clearance of 28.36 ml/kg/min. The highest serum concentrations of monensin were reached 0.5 h after intracrop dosage with an absorption half‐life of 0.27 h and an elimination half life of 2.11 h. The systemic bioavailability was 65.1% after intracorp administration. Serum protein‐binding tendency of monensin calculated in vitro was 22.8%.

3. Monensin concentrations in the serum and tissues of chickens after a single intracrop dose of pure monensin (40 mg/kg body weight) were higher than those after feeding a supplemented monensin pre‐mix (120 mg/kg) for 2 weeks. Monensin residues were detected in tested body tissues, collected 2, 4, 6 and 8 h after oral administration. The highest conentration was found in the liver. In addition, monensin residues were detected only in liver, kidney and fat 24 h after the last oral dose. No monensin residues could be detected in tissues after 48 h, except in liver which cleared completely by 72 h.     

Isolation of ureaplasmas from poultry and experimental infection in chickens

Ureaplasmas were isolated from the oropharynxes of 47 of 247 (19 per cent) Leghorn chickens (Gallus gallus domesticus) and from five Japanese bantams but none was isolated from the oropharynx or cloaca of other poultry comprising 10 Japanese game, 75 common quails (Coturnix coturnix japonica), 17 turkeys (Meleagris gallopavo) and 10 guinea fowls (Numida galeata). In apparently healthy chickens, ureaplasmas were found at various sites, including the conjunctiva, nasal cavity, oropharynx, upper and lower tracheas, but not from the air sac, lungs, yolk, oviduct, urine or cloaca. All the isolates were antigenically similar but had no serological relation to those isolated from man, monkey, cattle, goat, sheep, dog and cat. In chickens experimentally infected with an avian ureaplasma, the organisms infected the oropharynx and nasal cavity but none of the birds inoculated demonstrated any clinical signs or macroscopic lesions.     

Avian paramyxovirus type 1 infection of racing pigeons: 5. Continued spread in 1984

The neurotropic disease of pigeons caused by a variant avian paramyxovirus type 1 virus was confirmed in 866 lofts in Great Britain during 1984, in comparison with 192 lofts during July to December 1983. The 1984 outbreaks were spread over 48 counties in England and Wales and three regions in Scotland. The main methods of spread of disease in the 1984 outbreaks appeared to be similar to 1983 with 574 of 866 probably resulting from contact with infected birds at, or travelling to, races or shows. In 791 of 866 (92.5 per cent) outbreaks in 1984 disease was seen only in unvaccinated birds. A further 61 (7 per cent) occurred in inadequately vaccinated birds or birds vaccinated after clinical signs appeared.     

佛山市存栏禽群H5亚型禽流感抗体效价连续监测结果初报

佛山市从2005年1月至2006年9月,对规模养殖和散养两类养禽场的禽群,开展了H5亚型禽流感抗体效价连续监测.监测结果表明:禽群H5亚型禽流感抗体效价总体合格率较高,但合格率有较明显的季节性波动,且规模场和散养禽场之间存在一定的差异.     

Avian leukosis virus infection and congenital transmission in lines of chickens resisting selection for reduced shedding

Two lines (D and E) of three breeder lines of chickens that had resisted selection for reduced avian leukosis virus (ALV) congenital transmission on the breeder's premises did not resist the same selection procedures (tests for gs-antigen in albumen) under laboratory conditions. The incidence of ALV congenital transmission in the remaining third line (F) was spontaneously reduced from 13% to 0.9%. Environmental ALV exposure of uninfected chicks after hatching induced 7-10% of the progeny from lines E and F to become congenital transmitters but had negligible effects on line D. Neither errors in identifying dams nor horizontal transmission leading to congenital transmission were great enough to explain the lack of improvements in the three lines on the breeder's premises. Conditions of environmental exposure on the breeder's farm seem most likely to account for the resistance to reduced shedding. These findings suggest that the effectiveness of testing and selection procedures used to reduce ALV may be greatly influenced by the environment.