首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 281 毫秒
1.
Chickens were infected with an avian adenovirus group II isolate previously obtained from chickens exhibiting splenomegaly in commercial broiler flocks. The isolate was inoculated orally in 6-week-old experimental chickens, which were euthanatized and necropsied 6 days postinoculation. The primary gross lesions found were splenomegaly and splenic mottling. Numerous tissues from 12 chickens were taken for histologic evaluation. Histologic lesions included splenic reticuloendothelial cell hyperplasia with intranuclear inclusions. Lymphocytic degeneration was seen in the lungs of most chickens examined. Lung hemorrhage and edema with endothelial disruption and congestion of pulmonary arterioles were found less frequently. The splenic lesions in the chickens were similar to those seen in turkeys naturally infected with hemorrhagic enteritis, and the lung lesions resembled those seen in pheasants naturally infected with marble spleen disease.  相似文献   

2.
Acute pulmonary edema, splenomegaly, and ascites were observed in a disease outbreak in adult white and pearl guinea fowl. The clinical history and gross and microscopic lesions resembled those described for marble spleen disease of pheasants and avian adenovirus group II splenomegaly of chickens. A small number of intranuclear inclusion bodies were found in liver, spleen, and lung sections of affected guinea fowl. Attempts to isolate virus and serological tests to detect the presence of viral antigens were unsuccessful. Adult female pearl guinea fowl experimentally exposed to pheasant and turkey isolates of type II avian adenoviruses developed gross and microscopic lesions similar to those seen in the field outbreak. The pheasant isolate was the more virulent. Intranuclear inclusion bodies were observed in liver, spleen, and lung sections of pearl guinea fowl inoculated with either of the virus isolates, and direct immunofluorescent examination revealed viral antigen in the spleen and lung.  相似文献   

3.
Three serologically indistinguishable viruses from the avian adenovirus type-II splenomegaly virus of chickens, marble spleen disease virus of pheasants, and hemorrhagic enteritis virus of turkeys, were analyzed by restriction endonuclease fingerprinting. The DNA from these viruses were examined with 6 restriction endonucleases (Bgl II, EcoRI, HindIII, Hha I, Xho I, and BamHI). Markedly different DNA cleavage patterns were found in these virus isolates with all the 5 enzymes, except with BamHI, suggesting genetic differences between isolates of adenovirus type II. Restriction endonuclease analyses were found to provide a method for distinguishing genetically different, and yet serologically similar, strains of avian adenovirus type II.  相似文献   

4.
Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.  相似文献   

5.
The polypeptides of serologically related viruses of hemorrhagic enteritis (HE) in turkeys, marble spleen disease (MSD) in pheasants, and splenomegaly in chickens (SMC) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed by protein immunoblotting with polyclonal antibodies to HE virus (HEV). The viral polypeptides II, III, IV, V, VI, and VII were detected on SDS-PAGE with the size range from 18 to 97 kDa in HEV. Viral polypeptides II, III, V, VI, and VII were detected in MSD virus and virus of SMC. Protein immunoblotting of viral proteins with anti-HEV serum revealed antigenic differences between the 3 viruses of avian adenovirus type-II examined. The differences were that the polypeptides II, III, IV, V, VI, and VII were identified in HEV and the polypeptides II, V, VI, and VII were identified in MSD virus and virus of SMC. The bands of penton base (polypeptide III) and fiber (polypeptide IV) were seen in HEV only by protein immunoblotting.  相似文献   

6.
Outbreaks of influenza were diagnosed in two turkey breeder flocks on the same premises in eastern North Carolina during the "dark-out" period of recycling for a second lay. Clinical history included increased mortality from acute death with no apparent predisposing illness. Mortality attributed to the disease was 4.5% in one flock and 3.3% in the other. Necropsy findings included severe diffuse congestion and edema of both lungs, with little or no pleural exudate. Spleens were moderately to markedly enlarged and mottled, and kidneys were swollen and congested. Microscopic lesions included moderate to severe serofibrinous pneumonia with severe pulmonary congestion. Splenic changes included fibrin deposition and severe congestion, and severe congestion was noted in kidneys. Influenza virus (H1N1) was isolated from pools of tissues including lung, spleen, liver, and kidney, and both flocks seroconverted to influenza (H1N1) virus.  相似文献   

7.
The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.  相似文献   

8.
Two pheasants maintained in outdoor closed pen died within several days after having a history of depression. On necropsy, the spleens from both pheasants were enlarged about 3 times of their normal size and appeared mottled in color varying white to red. Histopathologically, there were diffuse severe follicular necrosis in the spleen and congestion and edema in the lung. Intranuclear basophilic inclusion bodies, which are strongly positive to group II avian adenovirus with immunohistochemistry, were noted in the spleen.  相似文献   

9.
Five black-footed penguins (Spheniscus demersus) admitted to the Southern African Foundation for the Conservation of Coastal Birds, in Cape Town, South Africa, died from malaria infection. Evidence for malaria as the cause of death included antemortem clinical signs, parasitemia, splenomegaly, pulmonary edema, and the presence of histologically visible schizonts in the reticuloendothelial system. A portion of the malarial small subunit ribosomal ribonucleic acid gene was detected by polymerase chain reaction from postmortem blood samples from all the birds. A species-specific variable region of this gene was compared with the same region on genes from other known avian malarial organisms, establishing that Plasmodium juxtanucleare was involved.  相似文献   

10.
Highly pathogenic avian influenza (HPAI) was diagnosed in broiler breeders, submitted to the National Veterinary Research and Quarantine Service in South Korea. Grossly, the dead breeders had lesions consistent with HPAI, including pancreatic mottling, splenomegaly, pulmonary edema and congestion, and hemorrhages in the mucosa of the proventriculus, gizzard and small intestine, and on the serosal surface. Microscopically, there were necrotized hepatitis and pancreatitis, lymphocytic meningoencephalitis, myocarditis, and interstitial pneumonia. Influenza viral antigen was demonstrated in areas closely associated with histopathologic lesions. The AI virus was isolated from cecal tonsils, feces, trachea, and kidney of the chickens. The isolated virus was identified as the highly pathogenic H5N1, with a hemagglutinin proteolytic cleavage site deduced amino acid sequences of QREKRKKR/GLFGAGLFGAIAG. In order to determine the pathogenicity of the isolate, eight 6-week-old specific pathogen free chickens were inoculated intravenously with the virus, and all the birds died within 24 hr after inoculation. This is the first report of an outbreak of HPAI in the chickens in South Korea.  相似文献   

11.
Seventy-two 13-week-old ring-necked pheasants were inoculated orally with 5.0 x 10(2) tissue-culture infective dose (TCID) of cell-culture-propagated marble spleen disease virus. Inoculated birds exhibited neither mortality nor clinical disease. Gross and histologic lesions were typical of marble spleen disease. The mean splenic weight was significantly (P less than 0.02) higher in inoculated birds than in controls between 6 and 10 days postinoculation (PI). The histologic splenic lesions, which consisted of reticuloendothelial cell hyperplasia, intranuclear inclusions within reticuloendothelial cells, and lymphoid depletion, were most prominent between 6 and 10 days PI. In a second experiment, 1-day-old pheasants were chemically bursectomized by dosing birds with 1.2 mg cyclophosphamide on 3 consecutive days. At 7 weeks of age, 54 bursectomized birds were inoculated orally with 5.0 x 10(2) TCID of marble spleen disease virus. Gross and histologic lesions were detected in one of the inoculated pheasants, but the mean splenic weight was not significantly different from control birds at any time PI. These results are evidence of the role of the bursa of Fabricius in the pathogenesis of marble spleen disease.  相似文献   

12.
A pathological study was conducted on 32 turkeys that died of sudden death with perirenal hemorrhage syndrome. Turkeys were selected from routine necropsy cases in a diagnostic laboratory. A higher incidence was observed in heavy tom turkeys. In addition to the characteristic gross lesions of perirenal hemorrhage, splenomegaly, and pulmonary congestion, turkeys in most cases had a hypertrophic cardiopathy. Microscopic lesions included moderate-to-marked acute passive congestion of all tissues examined (32/32), severe perirenal hemorrhage (32/32), and splenic lymphoid depletion (25/32). Changes in the thyroid follicular epithelium of most birds suggested an increased glandular activity. No lesions suggestive of arterial hypertension were observed. Adenoviral infection was detected in only four of 32 birds. Bacteriological cultures revealed no significant pathogen. Results suggest that sudden death in turkeys with perirenal hemorrhage is caused by an acute congestive heart failure consecutive to a hypertrophic cardiopathy. The perirenal hemorrhage would be a consequence of a severe passive congestion in kidneys.  相似文献   

13.
The response of ring-necked pheasants to inoculation with three strains of cell-culture-propagated type II avian adenovirus was examined. Marble spleen disease (MSD) virus of pheasants and both avirulent and virulent strains of hemorrhagic enteritis virus (HEV) of turkeys all induced typical gross and microscopic splenic lesions of MSD; neither MSD-associated lung lesions nor mortality were noted in inoculated pheasants, regardless of strain of virus used. Pheasants inoculated with a cell-culture-propagated avirulent strain of HEV were properly immunized against challenge with virulent HEV, as indicated by seroconversion and by protection against virus-induced splenic lesions. We conclude that these strains of type II avian adenovirus are comparable in pathogenicity for pheasants and cannot be distinguished. Further, absence of MSD-associated lung lesions and mortality in pheasants maintained under controlled laboratory conditions suggest that other environmental factors are probably involved in induction of such lesions and mortality in field cases of MSD.  相似文献   

14.
Causes of sickness and death in approximately 30,000 chickens in 5 meat breeder flocks were investigated between May 1979 and April 1980. Approximately 23% of disease was due to neoplasms; 81% of these were Marek's disease despite vaccination against this infection. Other frequent diagnoses included cellulitis (15%), respiratory disease (14%), lesions of the reproductive tract (11%) and tenosynovitis/arthritis (9%). Antibodies to Mycoplasma gallisepticium, avian adenovirus, infectious bursal disease virus and reticuloendotheliosis virus were present in all flocks. Antibody to Newcastle disease virus (NDV) was found in 2 flocks but titres were not considered protective against a virulent NDV challenge. Antibody to egg drop syndrome 1976 virus was found in 2 flocks comprised of the same breed of bird.  相似文献   

15.
Between January 1997 and March 1998, 11 cases of H7N2 avian influenza (nonpathogenic) were diagnosed at the Laboratory of Avian Medicine and Pathology, Kenneth Square, PA. These cases involved either commercial leghorn laying hens or leghorn pullets raised in Pennsylvania. Grossly and histologically, the most striking lesion associated with disease was salpingitis, usually with edema and occasionally with oviduct necrosis. Fluid, fibrinous, and egg yolk material in the peritoneum (egg yolk peritonitis) as well as pulmonary congestion and pulmonary edema were also frequently seen. Oviduct lesions have rarely been described in association with avian influenza infections in previous outbreaks. Mortality in affected houses was mild to moderate (less than 4% total mortality during the outbreak), with concurrent mild to moderate egg production declines (2%-4% at the time of disease onset).  相似文献   

16.
A poultry research facility that housed 2400 Peterson x Hubbard cross broilers (48 pens of 50 chicks each) experienced 4% mortality within 24 hr of chick placement. Mortality started within 4 hr of placement, and within 72 hr, cumulative mortality had reached 52%. Mild dyspnea was the only clinical sign noted in some chicks prior to death. The primary gross lesion noted in the chicks submitted was moderate to severe pulmonary congestion. The lungs of four of these chicks sank in formalin, and blood-tinged fluid was noted in the mouth and nares of two chicks. The microscopic lesions noted in the affected chicks were moderate to severe pulmonary edema and congestion. The diagnosis indicated to the submitter was that pulmonary edema caused by exposure to an unidentified noxious gas caused the death of the chicks. The poultry house environment was tested for sulfur dioxide, oxides of nitrogen, carbon monoxide, carbon dioxide, and volatile organic compounds (as produced by combustion engines); all tests were negative for significant levels of these compounds. A second broiler flock was placed in the same facility and the mortality at 6 wk was 11%, which was greater than the 2.5%-4.7% mortality seen in the previous four flocks on the farm. Further investigation revealed that the only change in management practice in this facility prior to the onset of the severe mortality problem was the replacement of 48 heat lamp bulbs (one for each pen). The new heat lamp bulbs were polytetrafluoroethylene (PTFE) coated. PTFE gas intoxication has been reported in several exotic avian species, but this intoxication has not been previously reported in a poultry flock.  相似文献   

17.
  相似文献   

18.
Ten strains of adenovirus representing 10 serotypes were administered intratracheally to 3-week-old specific-pathogen-free chickens, which also received 2.5 X 10(5) colony-forming units of a pathogenic Escherichia coli intranasally. Those birds had been inoculated by eye drop at 1 day of age with a virulent infectious bursal disease virus (IBDV). Controls consisted of groups of chickens inoculated with: (a) IBDV and E. coli, (b) IBDV only, (c) E. coli only, and (d) no virus or E. coli. Gross pulmonary alterations at 5 days postinoculation (PI) included congestion and consolidation of one or both lungs of a chick inoculated with adenovirus serotype Ind-C and another inoculated with A-2. Histopathologic alterations in the lungs were those of multifocal interstitial and occasionally diffuse pneumonia. All 10 adenovirus serotypes elicited multifocal or diffuse pneumonia and bronchiolitis in one or more of the five birds per group necropsied at 5 days PI. T-8 and A-2 serotypes induced marked to serve diffuse pneumonia within 5 days; Ind-C, Stein, Tipton, 75-1A, B-3, and X-11 incited a mild diffuse pneumonia. In all groups, the pneumonic lesions were more severe 5 days PI than 12 days PI. Tracheitis was incited by Ind-C, Stein, T-8, and A-2 at 5 days PI; the lesions were minimal to marked in severity. None of the four control groups exhibited gross or histopathologic alterations except the two IBDV-infected groups, which exhibited bursal change.  相似文献   

19.
The pathogenicity of serotype 8 group I avian adenovirus (GIAAV) strains (TR630 and Saga97 strains) from inclusion body hepatitis (IBH) against cyclophosphamide (CY)-treated 3-wk-old specific-pathogen-free (SPF) chickens was examined. SPF chickens were inoculated intramuscularly with 10(7) plaque-forming units of viruses. Both strains from IBH could produce hydropericardium and mortality in CY-treated chickens as hydropericardium syndrome (HPS) that serotype 4 GIAAV strains cause, although they could not induce either hydropericardium or mortality in nontreated chickens. Histologically, hepatocytic necrosis with intranuclear inclusions, pancreatic acinar necrosis with intranuclear inclusions, and epicardial edema were seen in CY-treated chickens inoculated with GIAAV from IBH. Immunohistochemically, these inclusions were positive against GIAAV antigen. There were neither histologic lesions nor positive reactions against GIAAV antigen in nontreated chickens inoculated with GIAAV from IBH. From the present findings, pathogenic characteristics of IBH strains and HPS strains in the chickens were essentially the same.  相似文献   

20.
某宠物主人送检1只4月龄泰迪犬,初步确诊为冠状病毒感染,于输液过程中突然死亡。剖检可见整个肺脏呈深红色,肺叶边缘呈粉红色,切面深红色,支气管断端有大量红色液体渗出;剖开气管可见其浆膜面呈暗红色,腔内充满红色清亮液体;心脏左右心室扩张,质地柔软,心尖钝圆,呈心力衰竭心。对各个脏器取材进行病理组织学观察,主要病变表现为肺脏弥漫性淤血、水肿,心肌纤维局部溶解坏死。诊断该犬因感染冠状病毒后初次洗澡应激加重病情,并且随着大量静脉输液导致或加剧急性肺水肿发生,最终造成该犬急性死亡。对该病例进行了系统地病理剖检和组织病理学观察,为犬科动物和其他动物发生类似病症提供一定的参考。  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号