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排序方式: 共有102条查询结果,搜索用时 15 毫秒
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The duration of immunity to an inactivated adjuvanted canine parvovirus vaccine. A 52 and 64 week postvaccination challenge study 总被引:1,自引:1,他引:0
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Povey RC Carman PS Ewert E 《The Canadian veterinary journal. La revue veterinaire canadienne》1983,24(8):245-248
Dogs were successfully isolated for a period of either 52 or 64 weeks following vaccination with an inactivated, adjuvanted canine parvovirus-2 vaccine. Antibody persisted in all ten vaccinated dogs, although in one case by 52 weeks postvaccination only virus neutralizing antibody, and not hemagglutination-inhibiting antibody, could be detected. Sentinel unvaccinated dogs housed alongside the vaccinated dogs throughout the study remained free of canine parvovirus-2 antibody until challenged. Upon oral challenge with canine parvovirus-2 infected material all unvaccinated dogs developed one or more signs of canine parvovirus-2 disease, shed virus and developed antibody. None of the vaccinated dogs became overtly sick. Of the five vaccinated dogs challenged 52 weeks after vaccination, three shed virus and one showed a significant rise in antibody. At 64 weeks after vaccination only one of the five challenged dogs shed virus and showed a boost in antibody titer. 相似文献
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The efficacy of a modified live-virus intranasal vaccine and a killed-virus adjuvanted parenteral vaccine in inducing protective immunity against feline viral rhinotracheitis (FVR) was evaluated in kittens with and without maternally derived FVR antibodies. The intranasal vaccine was given as a single dose to kittens 5 weeks old, and the parenteral vaccine was administered in 2 doses at 5 and 7 weeks of age. Seroconversion was delayed for 5 to 10 days in kittens with maternally derived antibodies, but occurred in all vaccinated kittens by 8 weeks of age. When virulent FVR virus was given, both vaccines provided satisfactory protection against disease but did not prevent infection. The results indicated that the modified live-virus intranasal vaccine or the killed-virus adjuvanted parenteral vaccine can be used successfully in kittens with residual maternally derived FVR antibodies. 相似文献
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Monensin controlled-release intraruminal capsule for control of bloat in pastured dairy cows 总被引:1,自引:0,他引:1
LB LOWE GJ BALL VR CARRUTHERS† RC DOBOS‡ GA LYNCH PJ MOATE PR POOLE† SC VALENTINE 《Australian veterinary journal》1991,68(1):17-20
Monensin, a polyether ionophore antibiotic, is potentially an important agent for bloat relief in dairy cows grazing temperate legume-based pasture. A series of studies was undertaken to determine the effect of monensin, when delivered continuously in the rumen of lactating dairy cows by means of controlled-release capsules (monensin CRC). Such devices release approximately 300 mg/head/day for 100 d. A short-term pilot study made at Ruakura, New Zealand, tested monensin CRC in cows selected for high susceptibility to bloat and grazing lucerne (Medicago sativa) or red clover (Trifolium pratense). Treatment significantly reduced the incidence of bloat, while milk yield and protein yield were increased. There was no effect on fat yield. Following the pilot study, 6 large-scale field experiments involving a total of 368 lactating dairy cows, were made in Australia and New Zealand to confirm the effectiveness of monensin CRC for bloat control and to measure the effect of such treatment on milk production and composition. A severe bloat problem occurred in 2 experiments, mild bloat occurred in 2 others, while no visual signs of bloat were observed in the remaining 2 experiments. Bloat was significantly (P less than 0.05) reduced by monensin CRC treatment when data was pooled over the 4 experiments in which bloat occurred. Daily milk yield was increased in all experiments from a mean of 17.7 in untreated groups to 18.8 kg/head/day (P less than 0.05) in monensin CRC-treated cows. Protein percentage was not affected by treatment, while there was a decrease from 4.29 to 4.10% fat, although total fat yield was not affected.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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Cohort studies were conducted on 29 pigs from 3 villages in the Highlands of Papua New Guinea. Animals ranged in age from 9 d to 5 m old. Three hundred and twenty nine faecal samples were collected from individual pigs followed over 3 to 6 w periods, and were examined for group A rotavirus antigen by ELISA, and rotaviral genomic RNA by polyacrylamide gel electrophoresis (PAGE). Electron microscopy was also conducted on selected samples. Group A rotavirus was detected in the faeces of 16 pigs with infected individuals coming from all villages. Non-group A rotavirus resembling group C was found in faeces from pigs from 2 villages. All of the group A rotaviruses examined had the same electrophoretype and this was distinct from that of the common type infecting humans in the area at the time of the study. None of the group A positive samples reacted with monoclonal antisera specific for human group A rotaviruses of serotypes 1, 2, 3, 4, or 8. The non-group A rotaviruses also all had identical electrophoretypes. In contrast to previous findings in intensive piggeries, rotavirus infection did not occur in all young pigs and was not limited to young animals under 2 m of age. Infected pigs varied in age from 12 days to 20 weeks of age. This pattern of infection was attributed to the non-intensive husbandry situations in the villages, with less opportunity for transmission to occur than in intensive piggeries. 相似文献
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Pathogenesis of canine parvovirus-2 in dogs: histopathology and antigen identification in tissues 总被引:2,自引:0,他引:2
The pathogenesis of canine parvovirus-2 was studied in orally inoculated conventional dogs using histopathological and peroxidase anti-peroxidase staining techniques. Lymphoid necrosis and depletion of lymphocytes from lymphoid tissues were most notable on days 5 and 6 after exposure. Lymphocyte hyperplasia occurred following day 7. Epithelial cell changes in segments of the small intestine were more severe on days 6 to 9 after exposure in areas associated with Peyer's patches and in the upper segments of the small intestine. The lymphocyte was the primary infected cell. Virus infected cryptal epithelial cells were not detected until 24 hours after the identification of infected cells in lymphoid tissues on day 4 after exposure. The majority of virus infected epithelial cells were found in crypts intimately associated with or adjacent to Peyer's patches in the upper segments of the small intestine. 相似文献