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1.
Gizzard lesions were formed in specific-pathogen-free (SPF) white leghorn chickens inoculated with fowl adenovirus (FAV). The virus, serotype 1 FAV 99ZH strain (FAV-99ZH), was originally isolated from the gizzard mucosa of commercial broiler chickens exhibiting gizzard erosion with intranuclear inclusion bodies. Five-day-old and 53-day-old SPF white leghorn chickens were inoculated with FAV-99ZH by both oral and ocular routes and then examined at necropsy on days 3, 5, 7, 10, 14, and 21 postinoculation (PI). There were no clinical signs in any of the chickens after the inoculation. Focal gizzard lesions occurred macroscopically, however, in inoculated chickens at several experimental periods. FAV was recovered from tissue samples of the proventriculus, gizzard, pancreas, and rectum by day 10 or 7 PI but was not recovered from liver samples of any of the chickens. These results indicate that FAV isolated from gizzard erosion is able to reproduce gizzard lesions as necrosis and erosion in SPF white leghorn chickens and that it may have a greater degree of tissue tropism in gizzards and other digestive organs than in the liver.  相似文献   

2.
The pathogenicity of a serotype-1 fowl adenovirus (FAV-99ZH), which causes adenoviral gizzard erosion by oral inoculation in chickens, was investigated in specific pathogen-free white leghorn chickens. In trial 1, 14 chickens were inoculated intravenously with the virus at 21 days of age and euthanatized for necropsy within 1-14 days of inoculation. Gizzard erosion was grossly observed from day 7 postinoculation (PI), and histologically, FAV-99ZH antigen-positive, basophilic intranuclear inclusion bodies were seen in the gizzard lesions from day 7 to 11 PI. Necrotizing pancreatitis, and cholecystitis and cholangitis associated with the inclusions were observed from day 3 to 14 PI (pancreatitis) and from day 5 to 9 PI (cholecystitis and cholangitis), respectively. The inclusions were also observed in the epithelial cells of the cecal tonsils from day 3 to 5 PI. The virus was recovered from samples of the lesions. It was revealed that FAV-99ZH causes not only gizzard erosion but also pancreatitis, cholecystitis, and cholangitis by intravenous inoculation in chickens. In trial 2, 10 chickens were inoculated orally with the virus twice, at 13 and 36 days of age, and euthanatized for necropsy within 4-17 days after reinfection. Macroscopically, focal gizzard lesions were observed; however, neither necrosis nor inclusions were observed by microscopy. Moreover, FAV was not recovered from the gizzard or rectum of any of the chickens at necropsy. This suggests that the gizzard lesions occurred as a result of the primary infection, and that the chickens were able to resist reinfection.  相似文献   

3.
Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.  相似文献   

4.
The horizontal transmission ability of fowl adenovirus (FAV) serotype 1 99ZH strain, isolated from chickens exhibiting gizzard erosion, was investigated. Twelve 13-day-old specific pathogen-free chickens were inoculated orally with 10(6) TCID(50)/0.05 ml of the strain. An in-pen contact group (chickens in the same pen with inoculated chickens), hedge contact group (chickens in a pen connected with pens housing inoculated chickens), non-contact group (chickens in a separate pen placed at a distance of 70 cm from the connected pens), human exposure group (chickens in the next room and attended last every day) and negative control group were examined. Each group consisted of 11 or 12 uninoculated chickens. Gizzard lesions were grossly or histologically observed from 10 days after exposure (DAE) in the in-pen contact group, and from 15 DAE in the hedge contact and non-contact groups. The FAV gene was detected by polymerase chain reaction performed on cloacal swabs taken on 5 and 13 DAE from chickens in both contact groups, and on 20 and 26 DAE from those in the non-contact group. Serum neutralizing antibodies against FAV serotype 1 were detected in chickens from 13 and 26 DAE in both contact groups and in the non-contact group, respectively. In the human exposure and negative control groups, no infection was observed. We conclude that FAV-99ZH strain spreads rapidly through direct contact with inoculated chickens, and slowly through non-contact transmission, and that adenoviral gizzard erosion is reproduced by this horizontal transmission.  相似文献   

5.
The pathogenicity of serotype 8 fowl adenovirus (FAV), isolated from gizzard erosions of slaughtered broiler chickens, was investigated. In experiment 1, 29 5-day-old specific-pathogen-free (SPF) chickens were inoculated with the isolates of serotype 8 FAV, M013 (group 1) or G0054 (group 2) strain, via an oral route. There were no clinical signs in any of chickens after inoculation, and mild gizzard erosions were observed macroscopically and microscopically in three inoculated chickens of group 2. FAV was recovered from gizzards and rectums but was not recovered from pancreas and livers from chickens in both inoculated groups. In experiment 2, 27 1-day-old SPF chickens were inoculated with the G0054 strain by intramuscular route. Five, 6, and 3 inoculated chickens died on days 3, 4, and 5 postinoculation (PI), respectively. Four, 3, 1, and 1 inoculated chickens became moribund with severe clinical signs such as ruffled feathers, severe depression and closed eyes from days 3 to 6 PI, respectively. Macroscopically, the common characteristic of the gross lesions of dead chickens and euthanized moribund chickens was discoloration of liver. FAV was recovered from the gizzard, liver, pancreas and rectum. Virus titers in the liver and pancreas were high until day 6 PI. Histologically, necrotizing hepatitis and pancreatitis with intranuclear inclusion bodies were observed in the inoculated chickens. These results indicate that some strains of serotype 8 FAV are able to reproduce not only gizzard erosion by oral inoculation but inclusion body hepatitis (IBH) by intramuscular inoculation.  相似文献   

6.
The pathogenicity of serotype 1 group I avian adenovirus (GIAAV) strains isolated from gizzard erosions for 1-wk-old specific-pathogen-free (SPF) chickens was investigated. In Experiment 1, SPF chickens inoculated orally with a serotype 1 strain (Tokushima2000/GE) of GIAAV isolated from gizzard erosion in broilers were euthanatized and necropsied from 3 to 12 days after inoculation. Clinically, there were no significant signs in the chickens inoculated with Tokushima strain. The gizzards were found macroscopically to be dilated with liquefied contents. The koilin layer of the gizzard exhibited multifocal white lesions with occasional erosions. Gross lesions of the koilin layer (white foci and erosion) appeared at 3 days after inoculation and persisted until 12 days after inoculation. The gross lesions were most severe at 9 days after inoculation. Histologically, multifocal degeneration, necrosis, and loss of the glandular epithelial cells with intranuclear inclusions, liquefactive change of koilin substance, and erosive lesions of koilin layers and surface epithelium of the gizzards were observed. Macrophages increased in the focal areas of the lamina propriabelow the liquefactive koilin substances. Immunohistochemically, intranudear inclusions were positive against GIAAV antigen. Histologic lesions of gizzards were most severe at 7 and 9 days after inoculation, but the frequency of intranuclear inclusions was greatest at 5 days after inoculation. In Experiment 2, the pathogenicities of four strains of serotype 1 GIAAV for 1-wk-old SPF chickens were compared. Three strains isolated from gizzard erosion had similar pathogenicities but one strain from a normal chicken was not pathogenic for chickens. These results suggest that gizzard erosions by serotype 1 GIAAV infection may occur in broiler chickens in Japan.  相似文献   

7.
The fiber gene sequence and pathogenicity of the serotype-1 fowl adenovirus (FAdV-1) isolated from gizzard erosions and from clinically normal chickens were compared among isolates. The FAdV-99ZH strain, which induced gizzard erosions, had a nucleotide sequence of the long fiber gene that was different from that of the Ote strain, which did not induce gizzard erosions. The differences could be distinguished by use of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. The long fiber gene of 16 FAdV-1 isolates from gizzard erosions and 10 FAdV-1 isolates from the feces of clinically normal chickens was examined by use of PCR-RFLP analysis. All 16 FAdV-1 isolates from gizzard erosions had the same restriction patterns as those of strain 99ZH; however, 10 FAdV-1 isolates from normal chickens were classified into 3 groups. Specific-pathogen-free (SPF) chickens were inoculated orally with 2 FAdV-1 isolates from gizzard erosions or 3 FAdV-1 isolates from clinically normal chickens to determine the pathogenicity of each strain. Two of 2 FAdV-1 isolates from gizzard erosions induced gizzard erosions. Two of 3 FAdV-1 isolates from normal chickens had the same PCR-RFLP patterns as those of the Ote strain, but did not induce any gizzard erosions. However, 1 FAdV-1 isolate from clinically normal chickens had the same PCR-RFLP pattern as that of strain 99ZH and induced gizzard erosions. These results indicate that there are FAdV-1 strains that have different pathogenicity; one strain induces gizzard erosions, and the other does not. Use of PCR-RFLP analysis of long fiber genes may be able to distinguish between these two strains.  相似文献   

8.
Groups of approximately 20 one-day-old chickens were inoculated with G-4260, the reference strain of avian nephritis virus (ANV), or saline. Based on mortality rates from severe nephritis in comparable experiments, light Sussex chickens generally were more susceptible than Rhode Island red (RIR) chickens. Mortality was greater in those given broiler starter than those given other feeds, and was greater when light Sussex chickens were given broiler starter feed and cold-stressed at 15 +/- 1 C for 2 hr daily during the first week rather than brooded normally. Inoculation with G-4260 either orally or by intraperitoneal injection produced similar results in RIR chickens. Thirty-three inoculated chickens died of severe nephritis between 4 and 12 days postinoculation, and 24 (73%) of them had visceral urate deposits. Inoculated inbred white leghorn Line 15 chickens with maternal antibody to ANV were brooded normally and given broiler feed: they were susceptible to infection as evidenced by subsequent histological lesions in the kidneys and serology, but mortality was not a feature. There were no deaths from nephritis in inoculated non-inbred white leghorn chickens free of maternal antibody to ANV that were given broiler feed and brooded normally. These results have implications in standardizing experimental conditions for the study of mortality induced by G-4260 and similar viruses.  相似文献   

9.
The enteropathogenicity of avian reoviruses (ARVs), isolated from chickens affected with malabsorption syndrome (MAS) from The Netherlands and Germany was studied. In the first trial seven different ARVs isolated from MAS cases were inoculated in 1-day-old specific pathogenic free (SPF) white leghorns. The pathogenicity was compared with 2 ARVs isolated from cases of tenosynovitis, namely reference strain S1133 and a Dutch strain. Although a difference in the severity of the clinical disease was observed, all reoviruses could induce vacuolar degeneration and sloughing of the epithelium of the small intestine at day 2 post inoculation (PI) till day 7 PI. Two Dutch and one German ARV derived from MAS causing the most severe intestinal lesions at day 2 PI, were further studied in the second trial using SPF broilers. These reoviruses did not cause weight gain depression in the broilers although lesions in the small intestine were present from day 1 up to day 4 PI and were more severe than in the white leghorn chickens. In one of the inoculated groups apical denuded villi were already present at day 1 PI. At day 7 PI the small intestine of the infected broilers appeared to be normal. Reovirus antigen was detected in the cytoplasm of the enterocytes at the tip and middle section of the affected villi both in layers and in broilers. To study the role of intestinal CD4+ and CD8+ T-cells and macrophages/monocytes in the pathogenesis of ARV, the numbers of these cells of the jejunal villi of one infected and the control broiler groups were compared. CD4+ T-cells were detected in low numbers and only in the infected broiler group at day 14 PI. The numbers of CD8+ T-cells and macrophages/monocytes were significantly higher in the infected broiler group than in the control broiler group at day 7 and 14 PI and at day 7 PI respectively. Our study indicates that the reovirus alone cannot induce intestinal lesions as found in MAS chickens. Moreover, CD8+ T-cells may play a major role in the pathogenesis and or reovirus clearance in the small intestine.  相似文献   

10.
Transmissible viral proventriculitis (TVP) was experimentally reproduced in 2-wk-old specific-pathogen-free chickens and commercial broiler chickens by eyedrop inoculation of adenovirus-like virus (AdLV), isolate R1 1/3. No clinical signs and no weight gain depression were observed in chickens inoculated with AdLV (R11/3); however, gross and microscopic lesions characteristic of TVP were present in proventriculi of inoculated chickens. Proventriculi of AdLV (R11/3)-inoculated chickens were markedly enlarged, compared with sham-inoculated controls, by day 7 postinoculation (PI). Microscopic lesions in proventriculi of inoculated chickens were detected beginning on day 3 PI and consisted of degeneration and necrosis of glandular epithelium, ductal epithelial hyperplasia, replacement of glandular epithelium with ductal epithelium, and diffuse interstitial lymphoid infiltration; no microscopic lesions were observed in other tissues. AdLV (R11/3) antigens were detected in proventriculi by immunohistochemistry on days 3-10 PI in inoculated SPF chickens and days 3-21 PI in inoculated commercial broiler chickens; no viral antigens were detected in other tissues. AdLV (R11/3) was reisolated from proventriculi of inoculated SPF and commercial broiler chickens on days 5 and 7 PI. No virus, viral antigens, or lesions were detected in proventriculi collected from sham-inoculated chickens. These findings indicate an etiologic role for AdLV (R11/3) in TVP.  相似文献   

11.
Pathogenicity of a fowl adenovirus (FAV), JM1/1 strain of serotype 1 derived from gizzard erosions of a broiler chicken, was examined to specific pathogen-free (SPF) chickens pre-treated with infectious bursal disease viruses (IBDVs) or cyclophosphamide (CY). Virulent IBDVs, classical type, were inoculated orally at 3 days of age of SPF chickens. CY was treated subcutaneously for 3 days after hatch. FAV was given orally at 30 days of age. At 40 days of age, all chickens were bled and autopsied for serology and gross observation. Gizzard lesions were ranked by the scores depending on their severities. IBDV- or CY-treated chickens showed significantly higher gizzard lesion scores than non treated birds. There were no gross lesions in any other organs except for bursal atrophy. Serologically, antibody production against FAV was highly suppressed by IBDV infection or CY treatment.  相似文献   

12.
The virulence of six pigeon-origin isolates of Newcastle disease virus (NDV) was evaluated before and after passage in white leghorn chickens. Four isolates were defined as pigeon paramyxovirus-1 (PPMV-1) and two isolates were classified as avian paramyxovirus-1 (APMV-1) with NDV monoclonal antibodies. The four PPMV-1 isolates were passaged four times in chickens, and the APMV-1 isolates were passaged only once. Infected birds were monitored clinically and euthanatized. Tissues were collected for histopathology, in situ hybridization with a NDV matrix gene digoxigenin-labeled riboprobe, and immunohistochemistry with an anti-peptide antibody to the nucleoprotein. Mean death time, intracerebral pathogenicity index, and intravenous pathogenicity index tests performed before and after passage in chickens demonstrated increased virulence of the passaged PPMV-1 isolates and high virulence of the original isolates of APMV-1. Sequence analysis of the fusion protein cleavage site of all six isolates demonstrated a sequence typical of the virulent pathotype. Although the pathotyping results indicated a virulence increase of all passaged PPMV-1 isolates, clinical disease was limited to depression and some nervous signs in only some of the 4-wk-old specific-pathogen-free white leghorns inoculated intraconjunctivally. However, an increased frequency of clinical signs and some mortality occurred in 2 wk olds inoculated intraconjunctivally with passaged virus. Histologically, prominent lesions in heart and brain were observed in birds among all four groups inoculated with the PPMV-1 isolates. The behavior of the two pigeon-origin APMV-1 isolates when inoculated into chickens was characteristic of velogenic viscerotropic NDVs and included necro-hemorrhagic lesions in the gastrointestinal tract.  相似文献   

13.
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   

14.
Two outbreaks of gizzard erosion in slaughtered broiler chickens in Japan were examined pathologically and microbiologically. The prevalences of such lesions were 9%-11% and 4%-50% in the affected flocks. Affected chickens had no clinical signs. Group I fowl adenovirus (FAV) serotype 1 was isolated from gizzard lesions. Histologically, gizzard mucosa were necrotic. Intranuclear inclusion bodies were seen in the enlarged nuclei of degenerating epithelial cells of the gizzard. The keratinoid layer in the erosion was edematous and desquamated and contained degenerative cells. Moderate to marked inflammatory cell infiltration was observed in the lamina propria and perivascular connective tissue in the submucosa and muscle layer. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies within degenerating epithelial cells. Ultrastructurally, numerous viral particles were demonstrated in the inclusions.  相似文献   

15.
Impact of BSE on Livestock Production System   总被引：1，自引：0，他引：1  
A total of 240 unvaccinated day-old broiler chicks, which had been found to be negative for antibodies against FAV-4, were divided into four groups of 60 chicks each. Group A was fed aflatoxin at 1 ppm from 7 days to 7 weeks of age. Group V was infected intra-abdominally at 14 days of age with 0.2 ml of FAV-4, having a titre of 105.5 TCID50 per 0.2 ml. The combined group AV was given the aflatoxin and infected with FAV-4. The fourth group C served as the control. More pronounced clinical signs, a higher mortality rate (56.7%), and reductions in body weight gain and in the organ to body weight ratios of the bursa and spleen were recorded in group AV. A significant (p<0.01) reduction in the HI antibody titre following vaccination against Newcastle disease, and of skin thickness in the delayed hypersensitivity test following sensitization with DNCB, indicated an additive immunosuppressive effect from aflatoxin and FAV-4 on the humoral and cell-mediated immune responses in group AV compared to groups A and V. Microscopically, marked depletion and degeneration of lymphocytes in the thymus, bursa, spleen and caecal tonsils were observed in group AV up to 5 weeks PI.  相似文献   

16.
Gharaibeh S 《Avian diseases》2008,52(1):106-110
A low pathogenic avian influenza virus (AIV) serotype H9N2 affected many commercial flocks in the Middle East in late 1990s and early 2000s. Due to the varying pathogenicity ofAIV H9N2 reported in previous studies, this study was carried out to determine the pathogenicity of a Jordanian isolate of H9N2 in broiler and specific-pathogen-free (SPF) chickens. Mild tracheal rales were observed in the broilers but not in the SPF birds starting 3 days postinfection (DPI) and until the end of the experiment at 16 DPI. Infected chickens had gross and histologic changes limited to the respiratory system (sinuses, trachea, lungs, and air sacs) characterized by congestion and lymphoplasmacytic inflammation. However, the lesions in the broiler chickens were more severe than those in the SPF chicks. Furthermore, the virus caused significant (P = 0.004) reduction (230 g) in average body weight of the infected broiler group compared with the uninfected broiler group. Both broiler and SPF-infected groups seroconverted, and they had a geometric mean titer of 2(8.2) and 2(9.3), respectively, on the hemagglutination inhibition test at 16 DPI. Cloacal virus shedding was not detected by 9 DPI and 15 DPI in broiler and SPF-infected groups, respectively. This study demonstrated the pathogenic nature of the local Jordanian H9N2 isolate and the variation from what it has been reported in other countries of the region. Regional effort should be directed to start an eradication program of this disease because of its pathogenicity for chickens, wide distribution, and possible interference with surveillance for H5N1 serotype.  相似文献   

17.
M Brugh 《Avian diseases》1992,36(4):968-974
Avian influenza (AI) virus A/chicken/Alabama/7395/75 (H4N8), a putatively non-pathogenic virus associated with a self-limiting outbreak of severe disease in commercial layers, was selectively passed in chickens or in cell cultures and then in chickens to determine whether virus with increased pathogenicity would emerge. When 20 derivatives of the parental virus were each inoculated intranasally and intratracheally in leghorn hens, mortality rates ranged from zero (0/24) to 25% (6/24); mortality was 4% (1/24) for hens inoculated with the parental virus. Many virus reisolates (51/144) from hens that died exhibited high pathogenicity, killing at least six of eight intravenously inoculated 4-week-old chickens. Most derivatives examined produced plaques in trypsin-free cell cultures more efficiently than the parental virus, but the highest plaquing efficiencies observed (10%) were lower than would be expected (100%) for highly pathogenic subtype H5 or H7 AI viruses. These results confirm that the Alabama H4N8 virus can acquire increased pathogenicity upon passage in chickens and suggest that it may have acted alone in producing the severe disease observed in laying chickens in Alabama.  相似文献   

18.
Gizzard erosion in broiler chickens was investigated at 18 slaughterhouses in Japan. The condition was observed in 13 of them, and adenoviral gizzard erosion (AGE) was diagnosed histologically, immunohistochemically and virologically in the eroded gizzards from nine of these 13. The antigen-positive intranuclear inclusion body of group 1 fowl adenovirus was observed in the epithelial cells of the affected gizzards, and fowl adenoviruses were isolated from the lesions. In two of the slaughterhouses the total weights of the gizzards disposed of in three years were 3590 kg (0.40 per cent of the gizzards inspected) and 2880 kg (0.19 per cent). Sixteen of the 19 outbreaks of gizzard erosion on 15 farms that were confirmed in three of the slaughterhouses, including the previous two slaughterhouses, were diagnosed as AGE, and the condition was suspected in the other three outbreaks. Most of the adenoviruses isolated were identified as serotype-1 by PCR-restriction fragment length polymorphism. No apparent clinical signs were observed in any of the affected flocks.  相似文献   

19.
Seven 19-day-old broiler chickens affected with hydropericardium syndrome (HPS) with pancreatic necrosis and gizzard erosions were investigated pathologically and virologically. Mortality increased after 13 days of age in a flock on a broiler farm. The mortality rate of the flock reached 10% by 19 days of age. Macroscopically, the chickens had hydropericardium (the characteristic gross change of HPS), pinpoint white foci in the pancreas, and ventricular erosions. Histologically, the chickens had multifocal hepatic necrosis with intranuclear inclusions in hepatocytes, a marked increase of macrophages in the spleen and lung, mild epicardial edema, multifocal necrosis of pancreatic acinar cells with intranuclear inclusions, focal necrosis of the ventricular koilin layer, and degeneration of the ventricular glandular epithelium with intranuclear inclusions. Immunohistochemically, intranuclear inclusions in the liver, pancreas, and ventriculi were stained positively against group I avian adenovirus (GIAAV) antigens. Ultrastructurally, 67-nm diameter viral particles were present in intranuclear inclusions. Virologically, serotype 4 of GIAAV was isolated from the liver, heart, and kidney of affected chickens. The pathologic changes of the present cases differ from previous cases of HPS; therefore, the present strain of GIAAV may have different pathogenicity for chickens than the previous virus strain of HPS.  相似文献   

20.
An avian adenovirus (AAV) was isolated from liver samples of two 2-wk-old broiler-breeder flocks obtained from grandparents vaccinated at 10 and 17 wks of age with an autogenous inactivated vaccine containing the European AAV 8 (8565 strain) and 11 (1047 strain) serotypes (AAV8/11 vaccine). Affected broiler-breeders exhibited clinical signs and macroscopic and microscopic lesions associated with inclusion body hepatitis (IBH). The isolated adenovirus, identified as Stanford, was molecularly characterized as European serotype 9. The pathogenicity of the Stanford strain was confirmed after inoculation of specific-pathogen-free (SPF) chickens at 1-7 days of age, causing 100% and 20% mortality, respectively. The level of protection against IBH was evaluated in two broiler-breeder progenies from AAV 8/11-vaccinated grandparent flocks and a commercial broiler flock by challenge at 1 or 7 days of age with the AAV 8 and 11 serotypes and/or the Stanford strain. The broiler-breeder progenies and the commercial broiler flock exhibited protection against IBH after challenge. No significant differences in mean body weights were observed at 3 wk of age in any of the evaluated groups. We conclude that broiler-breeder progenies from 30- to 50-wk-old grandparents vaccinated with the AAV 8/11 vaccine were adequately protected against challenge with the AAV 8 and 11 serotypes and the Stanford strain.  相似文献   

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