鸽Ⅰ型副粘病毒的分离与鉴定

从病死鸽脾脏分离到 1毒株 ,经电镜观察和HI试验、抗体检测 ,确定为鸽的Ⅰ型副粘病毒 ,生物学试验表明 ,该病毒属于强毒株 ,其致病指数分别为 :MDT =90h,ICPI=1 2 7,IVPI=1 30。将分离株经滴鼻接种于 1 5日龄非免疫肉乳鸽和 4周龄非免疫雏鸡 ,肉乳鸽发病后出现与自然发病鸽相同的症状和病变 ,但不引起鸡发病     

Characterization of a pigeon paramyxovirus (PPMV-1) isolated from chickens in South Africa

A paramyxovirus with a thermostability of 60 min (typical of velogenic viruses) and a mean death time of > 90 h (typical of lentogenic viruses) was isolated from layers near Mooi River, South Africa. Our results, based on comparative nucleotide sequence data indicated that the virus is pigeon paramyxovirus 1 (PPMV-1), a variant of Newcastle disease virus. The F0 cleavage site contains a 112RRKKRF117 motif, and the virus had 98% sequence identity with PPMV-1 strains from the Far East. PPMV-1 was last reported in South Africa during the 1980s, with this being the first report of PPMV-1 isolated from chickens in South Africa.     

Experimental infection of domestic pigeons with pigeon circovirus

Pigeon circovirus (PiCV) infection and young pigeon disease syndrome (YPDS), associated with high morbidity and mortality, have been recognized in young racing pigeons from large portions of Central Europe. There exist a number of data indicating that YPDS is a consequence of PiCV infection and subsequent immunosuppression. In order to prove PiCV to be one of the crucial factors of YPDS, an experimental infection with PiCV was performed under controlled conditions. Twenty-four domestic pigeons (Columba livia forma domestica) were divided into two groups with 12 pigeons each; an infection group and a control group. All birds were between their fourth to eighth week of life. Pigeons in the infection group were infected both intramuscularly and orally with PiCV purified from naturally infected birds, while pigeons in the control group received a placebo. To test a possible influence of the PiCV infection on the immune system, the animals in both groups were vaccinated simultaneously, on the same day, against PMV-1 (Lasovac plus, IDT, Dessau-Tornau, Germany). Weekly virologic testing showed a viraemic period, and excretion of the infection virus, in pigeons in the infection group. Replication of PiCV could be proved on the basis of histologic findings of multiglobular inclusion bodies, mainly observed in macrophages of the bursa of Fabricius. A PiCV, genetically distinct from the experimental virus, was detected in the control group by polymerase chain reaction (PCR) testing, but any histologic findings comparable to the infection group were absent. None of the pigeons revealed clinical signs of illness, or hints that immunosuppression had occurred, regardless of their group. The absence of stressful conditions, considered as a trigger for the development of YPDS, may be responsible for the failure of disease reproduction in our infection model.     

A comparative study of pigeons and chickens experimentally infected with PPMV-1 to determine antigenic relationships between PPMV-1 and NDV strains

To compare the pathogenicity of PPMV-1 in pigeons and chickens, both species of birds were experimentally infected with strain pi/CH/LHLJ/110822, which was isolated from a pigeon in China. The clinical signs, gross lesions, and histopathological changes were observed in pigeons inoculated with pi/CH/LHLJ/110822. The morbidity and mortality rates were 80% and 70% in pigeons, respectively, whereas there were no clinical signs or gross lesions in chickens inoculated with the same strain. The viral loads in tissue samples were detected by real-time RT-PCR, indicating that six tissue samples (i.e., kidney, lung, brain, trachea, Harderian glands, and proventriculus) had detectable viral RNA in all dead pigeons, and significant differences in viral loads between pigeons and chickens were observed in several tissue samples (i.e., Harderian glands, proventriculus, duodenum, pancreas, small intestine, and large intestine) on 3 days post-inoculation (dpi) and in brain tissue on 7 dpi. In general, viral loads in pigeons were higher than those in chickens, whereas antibody titers in pigeons were lower than those in chickens. These results showed differences in pathogenicity, efficiency of viral RNA replication, and humoral immunity, indicating different susceptibilities between the host species. Additionally, the cross hemagglutination inhibition assay and cross virus neutralization tests demonstrated that pi/CH/LHLJ/110822 antigenicity was different from those of strains La Sota and F48E9.     

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.     

Virological studies of paramyxovirus type 1 infection of pigeons

Over a period of three months in 1985, paramyxovirus type 1 infection was demonstrated for the first time in Canada, in six flocks of pigeons in Ontario, Alberta, and British Columbia. The paramyxovirus type 1 isolates did not cause clinical disease when serially passaged four times in four-to six-week-old chickens, and isolates were classified as lentogenic before and after such serial passage. Further cases of paramyxovirus type 1 clinical disease have not been reported since the last of these six outbreaks in August 1985.     

鸽Ⅰ型副黏病毒(S-1株)灭活疫苗免疫剂量研究

为了确定鸽Ⅰ型副黏病毒(pigeon paramyxovirus-Ⅰ,PPMV-Ⅰ)(S-1株)灭活疫苗的免疫剂量。本试验采用3批PPMV-Ⅰ(S-1株)灭活疫苗实验室制品以不同剂量肌肉注射免疫30日龄低抗体幼龄鸽(HI抗体≤2)和120日龄低抗体青年鸽(HI抗体≤2),分别在免疫后第14,28天对试验鸽进行攻毒,对试验鸽进行临床症状、抗体检测和攻毒保护测定。结果显示,该疫苗对低抗体鸽有保护作用,对30日龄幼龄鸽和120日龄青年鸽的最小免疫剂量分别为0.05,0.2mL/只。因此,为了确保疫苗的免疫效果,在PPMV-Ⅰ(S-1株)灭活疫苗制造及检验规程中疫苗用法用量规定:幼龄鸽肌肉注射,0.2mL/只;青年鸽和种鸽肌肉注射,0.5mL/只。     

Avian paramyxovirus type 1 infection of racing pigeons: 3 epizootiological considerations

During July to December 1983 birds in 192 racing pigeon lofts were confirmed as infected with paramyxovirus type 1 virus on the basis of disease signs alone when contact with infected cases was known (10) or with supporting serology (130), virus isolation (eight) or both (44). These outbreaks were mainly concentrated in south Wales (89) and Dorset (40). In all, 29 counties of Great Britain were involved. In the majority of outbreaks (69 per cent) activities associated with racing were strongly implicated in the spread of the disease but trade in birds, stray bird contact, loft visits and contact at shows were also possible methods of spread. Although considerable variation was seen in the pathogenicity of the viruses isolated from affected birds there were no apparent epizootiological links between isolates of similar virulence.     

Avian paramyxovirus type 1 infections in racing pigeons in California. I. Clinical signs, pathology, and serology.

An outbreak of diarrhea and neurological disease in California racing pigeons caused by avian paramyxovirus type 1 (PMV-1) is documented. Predominant clinical signs were polydipsia, ataxia, poor balance, torticollis, head tremors, inability to fly, and diarrhea that was unresponsive to therapy. Gross pathologic findings were often unremarkable or non-specific. The predominant histologic lesions were interstitial nephritis, chronic tubular necrosis, lymphoplasmacytic infiltration within the kidney, liver, and pancreas, and focal non-suppurative encephalitis. Pigeons from 20 submissions demonstrated characteristic clinical signs of PMV-1 infection. Pigeons from 17 submissions exhibited typical histopathology. Serologic evidence of PMV-1 infection was present in pigeons from 13 submissions, and PMV-1 was isolated from pigeons received in six submissions. None of these pigeons had been vaccinated against PMV-1.     

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.     

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.     

Unusual biphasic disease in domestic pigeons (Columba livia f. domestica) following experimental infection with Sarcocystis calchasi

A novel Sarcocystis species has recently been reported in the domestic pigeon (Columba livia f. domestica) as intermediate host, causing severe central nervous signs similar to Paramyxovirus-1 or Salmonella Typhimurium var. cop. infection. Transmission of the parasite via the northern goshawk (Accipiter gentilis) as definitive host has been established. Experimental infection of domestic pigeons with sporocysts excreted by experimentally infected northern goshawks reproduced the natural infection in the pigeon, proving the causative role of the parasite in the disease. Here, we describe in greater detail the course of the fulminant biphasic disease depending on the infectious dose. Pigeons infected with 10(3) or 10(4) sporocysts showed clinical signs of polyuria and apathy around 10-11 days postinfection (dpi) and sudden neurological signs 51-57 dpi as a second phase of disease. Pigeons infected with higher doses died within 7-12 dpi, also showing polyuria and apathy but without nervous signs. At necropsy, livers and spleens had multifocal necroses and infestations with parasitic stages, namely, schizonts. Moreover, lesions and schizonts were also found in the lung, bone marrow, and next to blood vessels in the connective tissue of various organs. Pigeons infected with 102 sporocysts remained symptomless until 58-65 dpi, when sudden central nervous signs occurred. Major histopathologic findings of pigeons with neurological signs were encephalitis and myositis of virtually every skeletal muscle with high infestations of sarcocysts. Only mild myocarditis and very few cysts were found in the heart muscles. Importantly, a sentinel pigeon developed identical lesions when compared to those of low-dose infected pigeons, suggesting a risk of mechanical transmission of sporocysts from freshly infected to uninfected pigeons in a flock. By contrast, chickens failed to develop any clinical signs or pathologic lesions in the same experiment. The findings further characterize the new highly pathogenic disease in domestic pigeons, which clinically mimics paramyxovirosis and salmonellosis in both phases of the disease and exclude chickens as further intermediate host species.     

Inhibition of lymphocyte proliferation by bovine trophoblast protein-1 (type I trophoblast interferon) and bovine interferon-alpha I1.

Bovine trophoblast protein-1 (bTP-1) is a Type I interferon secreted by the bovine trophoblast from about Day 15 of pregnancy. It is not known whether bTP-1 has functional properties in common with other interferons. The aim of the present study was to determine whether bTP-1 inhibits proliferation of lymphocytes induced by mitogens, mixed lymphocyte cultures (MLC) and interleukin-2 (IL-2) and, if so, whether this activity is similar to that of a related interferon, bovine interferon-alpha I1 (bIFN-alpha I1). Stimulation of lymphocyte proliferation caused by phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM) was inhibited by bTP-1 and bIFN-alpha I1 without any reduction in cell viability. Maximum or near-maximum inhibition (less than 50%) was achieved at concentrations of 0.5-5.0 nM of bTP-1 and bIFN-alpha I1. Cells stimulated with PWM were less inhibited than cells stimulated with PHA and Con A. Both bTP-1 and bIFN-alpha I1 inhibited MLC to a greater degree than lectin-stimulated cells (maximum inhibition was 78% or greater). Also, bTP-1 and bIFN-alpha I1 slightly inhibited incorporation of [3H]thymidine ([3H]TdR) induced by the combination of phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), and calcium ionophore A23187. Finally, bTP-1 and bIFN-alpha I1 had bimodal effects on incorporation of [3H]TdR by IL-2-induced lymphocytes. Incorporation of [3H]TdR was increased at 0.005 nM and 0.05 nM concentrations while higher concentrations caused a slight decrease in [3H]TdR incorporation. Results confirm that bTP-1 inhibits lymphocyte proliferation in a manner similar to that caused by the leukocyte-derived interferon, bIFN-alpha I1. Incomplete inhibition of mitogen-induced proliferation and differences in degree of inhibition between various stimulators suggest that bTP-1 and bIFN-alpha I1 preferentially inhibit certain lymphocyte subpopulations. Local inhibition of lymphocyte proliferation caused by bTP-1 may help protect the allogeneic conceptus from immune responses to fetal antigens or regulate the release of cytokines from endometrial lymphocytes.