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1.
The naturally occurring disease caused by San Miguel sea lion virus in fur seals was characterized by small fluid-filled vesicles 1 to 25 mm in diameter on the nonhaired portions of the flippers. Early epithelial lesions contained multifocal sites of cell lysis. The resultant microvesicles enlarged and coalesced, forming grossly visible macrovesicles. Mature vesicles progressed to involve all layers of the epithelium but did not involve the underlying dermis. Intradermal inoculation of vesicular exanthema of swine virus type A48 or San Miguel sea lion virus type 2 into otarid (fur) seal pups caused plaque-like lesions around inoculated coronary bands. These swellings regressed without rupture by 96 hours postinoculation. One seal inoculated with San Miguel sea lion virus had a linear lingual erosion at ten days postinoculation. Virus was isolated from this site and from two uninoculated sites, the tonsil and testicle. Contact controls showed no evidence of infection. Virus was isolated in low titers from some sites of inoculation and draining lymph nodes from seals infected with vesicular exanthema of swine virus. Virus was recovered more easily, in higher titers, and from more tissues, from seals infected with San Miguel sea lion virus. Inoculated seals tested after four to ten days seroconverted. Feeding swine seal tissues from the inoculation experiments resulted in seroconversion in swine which were fed tissues from seals infected with vesicular exanthema of swine virus but not in those which were fed tissues from seals infected with San Miguel sea lion virus.  相似文献   

2.
A virus was isolated from California sea lions (Zalophus californianus californianus) and northern fur seals (Callorhinus ursinus) in 1972. It was later named San Miguel sea lion virus (SMSV). State and federal livestock disease control agencies became concerned, because SMSV was found to be indistinguishable from vesicular exanthema of swine virus and to cause (in laboratory trials) clinical signs in swine similar to those produced by vesicular exanthema of swine virus. Ground carcasses of northern fur seals, salvaged after harvesting pelts, are fed to mink on ranches in the United States. Domestic swine are kept on some of these same ranches. Samples withheld from lots of this seal carcass mink food were found to contain SMSV (serotype 5) in titers of 10(6.1) and 10(6.8) tissue culture infective doses.  相似文献   

3.
The indirect immunofluorescence test is a rapid method for detecting the presence of vesicular exanthema of swine virus or San Miguel sea lion virus in cell culture. A serological relationship exists between vesicular exanthema of swine virus and San Miguel sea lion virus, as shown by the fluorescence-positive reactions between swine antisera to vesicular exanthema of swine virus A48 and San Miguel sea lion virus type 5 and cell cultures infected with San Miguel sea lion virus types 1, 2, 3, 4 and 5 as well as vesicular exanthema of swine virus B51, C52, D53, E54, F55, G55, H55, I55, J56 and K55. The indirect immunofluorescence test detects group-specific antibody to caliciviruses in swine sera.  相似文献   

4.
Vesicular exanthema of swine virus type A48 or San Miguel sea lion virus type 2, when inoculated intradermally into swine, resulted in fluid-filled vesicles at the sites of inoculation in the snout, coronary band, and tongue. Pigs that developed vesicles also had fevers. Secondary vesicle formation varied, depending on virus serotype. Viremia was found in one pig infected with San Miguel sea lion virus five days after infection. Virus was recovered from nasal-oral passages for up to five days after infection in both groups of pigs and from the gastrointestinal and urinary tracts of pigs infected with San Miguel sea lion virus. Neutralizing antibodies began to increase three days after inoculation and reached peak titers in seven to ten days. In the absence of secondary bacterial infection, healing was well advanced by ten days after inoculation. Lesions usually were limited to nonhaired portions of the integument and tongue. Individual epithelial cells became infected when a break in the skin allowed virus access to susceptible epithelial cells from either exogenous or endogenous sources. Individual infected cells ruptured and adjacent cells were infected, resulting in the formation of multiple microvesicles. Centrifugal coalescence of microvesicles led to formation of grossly visible macrovesicles. Lesions rarely developed from viral contamination of intact hair follicles. A mild virus-induced encephalitis was seen in pigs infected with vesicular exanthema of swine virus, and virus was recovered from brain tissue of pigs infected with San Miguel sea lion virus.  相似文献   

5.
Colostrum-deprived neonatal Northern fur seal pups (Callorhinus ursinus) were exposed to San Miguel sea lion virus type 5 (SMSV-5) by feeding them fish (Girella nigricans) infected with virus or fish infected with both the sea lion lung worm larvae (Parafilaroides decorus) and virus. Virus infection was demonstrated in 8 of 9 pups, and 1 of these developed a vesicular lesion on the flipper. In this sequence, P decorus larvae exposed to SMSV-5 were fed to G nigricans held at 15 C in a salt water aquarium; 32 days later, these fish were killed, then fed to the fur seal pups. The vesicle developed 22 days subsequent to this and SMSV-5 was reisolated from the lesion. The SMSV-5 was shown to persist for at least 23 days in infected neonatal fur seals. Attempts to establish P decorus infection in Northern fur seal pups were apparently unsuccessful.  相似文献   

6.
Immunoelectron microscopic comparisons of caliciviruses   总被引:4,自引:0,他引:4  
Using immunoelectron microscopy, 9 serotypes of vesicular exanthema of swine virus (VESV) were compared with 5 serotypes of San Miguel sea lion virus and 7 additional calicivirus isolates from marine animals. In addition, swine caliciviruses and marine caliciviruses were compared with the vaccinal strain of feline calicivirus (FCV) F-9. Of 9 VESV types, 8 showed common antigenicity with San Miguel sea lion virus. Of 9 VESV types, 2 showed common antigenicity with FCV F-9. All 12 marine caliciviruses showed common antigenicity with VESV, but not with FCV F-9.  相似文献   

7.
Two new serotypes of San Miguel sea lion virus (SMSV), designated SMSV-4 and SMSV-5, were studied in vivo and in vitro. The host cell spectrums were compared with SMSV-1, SMSV-2, and vesicular exanthema of swine virus type A-48. Based on the result of these broad host spectrums, a numerical scoring system was devised for ranking each virus on the basis of its potential for infecting terrestrial mammals, including the important domestic species.  相似文献   

8.
A new serotype of calicivirus was isolated from California sea lions (Zalophus californianus) with severe vesicular disease. Neutralizing antibodies were found in 27 of 82 (32.9%) serum samples from California sea lions and in 15 of 146 (10.3%) serum samples from Steller sea lions (Eumetopias jubatus) tested. The seropositive animals were widely dispersed along the margins of the eastern Pacific basin, from the Bering Sea to the Santa Barbara Channel. Seropositive samples were found from as early as 1976 through the present time. This new calicivirus serotype, San Miguel sea lion virus type 13, was inoculated into weaned pigs, resulting in induction of severe vesicular disease, which spread to all pigs, including uninoculated pen contacts. Virus was continually shed by most of the pigs throughout the 2-week duration of the experiment.  相似文献   

9.
A prevalence survey for hookworms (Uncinaria spp.) was done in northern fur seal (Callorhinus ursinus) and California sea lion (Zalophus californianus) pups on San Miguel Island, CA, in 2000. Intestines of dead pups were examined for adult hookworms in July. These parasites were found in 95% of 20 fur seal pups and 100% of 31 sea lion pups. The number of hookworms varied from 4 to 2142 (mean = 760) in fur seal pups and from 20 to 2634 (mean = 612) in sea lion pups. A direct relationship was evident between body condition and number of hookworms in the pups; that is, pups in poor condition had fewer hookworms than those in good condition. There was a decline in the number of hookworms in sea lion pups in 2000 compared to collections in 1996. Eggs of Uncinaria spp. were found in rectal feces (collected in late September and early October) of none of 35 (0%) live fur seal pups and 41 of 48 (85%) live sea lion pups. Packed cell volume values, determined for most of the same live pups, were essentially normal for C. ursinus but were much lower than normal for most Z. californianus. Hookworm larvae were not found in blubber of fur seal and sea lion pups or in rookery sand in July. Rookery sand, positive for live hookworm larvae when put in a refrigerator, was negative at removal 2.5 years later. The average number of eggs in utero of female hookworms was 285 for three specimens from a fur seal pup and 281 from three specimens from a sea lion pup. One hookworm larva was recovered from milk stripped from the teats of a stranded Z. californianus female at The Marine Mammal Center, Sausalito, CA.  相似文献   

10.
Caliciviruses have, for the 1st time, been shown experimentally to infect a primate. Twenty-four hours after being inoculated with San Miguel sea lion virus (SMSV), an African green monkey developed a febrile response and vesicular lesions at injection sites. Virus was recovered from lesion material 96 hours later and from the stool at 48 hours. Possible human infection with SMSV was indicated by serologic evidence. Three persons working with 4 distinct serotypes of SMSV developed neutralizing antibody titers to 2 SMSV types. The positive serum-neutralization test results were confirmed, using immunoelectron microscopy to demonstrate complexes of viruses and antibodies.  相似文献   

11.
Studies on the aetiological agents of rabbit haemorrhagic disease (RHD) and European brown hare syndrome show that the viruses responsible for these infections can be placed in the family Caliciviridae. Established members of this group are vesicular exanthema virus (prototype), San Miguel sea lion virus and feline calcivirus. The human hepatitis E virus and the Norwalk agent may soon be included. The RHD virus genome consists of a positive stranded RNA molecule composed of 7437 nucleotides. A major subgenomic RNA of 2.2 kb, colinear with the 3' end of the genomic RNA, can also be recovered from infected liver tissue, and both RNAs are enclosed within viral capsids formed by a single major protein of approximately 60 kDa. Electron microscopic examination of organ suspensions from diseased animals shows two types of particle; 35-40 nm complete virions have the regularly arranged cup-shaped depressions typical of calcivirus morphology, and 23-25 nm smooth particles resulting from degradation of the outer surface structures of the complete virions.  相似文献   

12.
In apparent or nonprogressive Aleutian disease virus infection was considered a subclinical but persistent viral infection in which infected mink did not develop tissue lesions, hypergammaglobulinemia, or high antibody titers. Transmission of Aleutian disease virus from mink with this type of infection was measured. Mink with inapparent Aleutian disease appeared healthy and had normal gamma-globulin values, but were capable of transmitting the disease by direct and indirect horizontal contact. The risk of direct or indirect horizontal transmission from mink with inapparent infection was less than from mink with progressive Aleutian disease. Infection also was directly transmitted from the dam to the kits, but again the risk of infection from dams with inapparent infection was less than from dams with progressive Aleutian disease. Mink infected from their dams before weaning developed the disease more slowly than mink which became infected after weaning.  相似文献   

13.
This paper describes the relationship of a canine calicivirus, named No.48, to other human and animal caliciviruses, based on phylogeny of the 3' half of its genome. It was found that No.48 constitutes a unique lineage, most closely related but distinct from feline and San Miguel sea lion caliciviruses.  相似文献   

14.
Virus-neutralizing antibody and immunity after infection with foot-and-mouth disease virus was studied for 128 days in a group of swine. Antibody first appeared at 3 days, rose to peak levels between 7-10 days, and regressed to a plateau by 28 days. After 28 days, there was little change in mean antibody titres.

An attempt to reinfect 10 swine at 28 days was not successful. At 128 days, the immune status of 4 convalescent swine neutralized more than 4 logarithms of virus in an in vivo titration. However, in another group of 5 convalescent swine, one developed vesicular lesions when exposed to infected swine.

Efforts to demonstrate latent virus in one pig 128 days after infection were not successful.

  相似文献   

15.
Virus isolation was attempted from 262 field samples of vesicular material collected during the outbreaks of vesicular exanthema of swine in the U.S.A. from 1952-54. Using primary swine kidney culture, viral cytopathogenic agents were isolated from 76.3% of the samples. However, an overall recovery rate of 82.1% was obtained after samples negative in tissue culture were inoculated intradermally in susceptible swine. All vesicular exanthema of swine virus isolates were identified as serotype B51 using complement fixation and serum neutralization tests. Two isolates did not react with antisera to known vesicular agents of swine and failed to produce vesicles or clinical signs of disease upon inoculation in swine. One vesicular exanthema of swine virus isolate from tissue of equine origin was pathogenic for swine but produced limited vesiculation at the site of intradermalingual inoculation in the tongue of a pony infected experimentally. Type B51 virus was reisolated from lesions produced in the pony and the pony became seropositive for virus type B51.  相似文献   

16.
Bovine viral diarrhea virus (BVDV) is a pestivirus that is enzootic in most cattle populations throughout the world. This virus is present throughout the body of persistently infected (PI) cattle. Previous research has not assessed the cooking temperature at which BVDV in meat from PI cattle can be inactivated. Therefore, muscle tissue from 6 PI cattle was harvested, refrigerated, frozen, and heated to various internal temperatures. The concentration of virus present was determined by virus isolation. Average cell culture infective doses (50% endpoint; CCID(50)) of BVDV per gram of frozen, uncooked meat from PI cattle were 10(5.85) CCID(50)/g of whole cuts and 10(6.02) CCID(50)/g of ground meat. The virus in whole and ground meat was consistently inactivated when cooked to temperatures greater than or equal to 75°C. A second objective of this research was to thoroughly reassess if Vero cells were permissive to BVDV infection in our laboratory to provide further indication of whether primates, including humans, might be susceptible to BVDV. Vero cells were not permissive to infection with any of 43 different strains of BVDV that readily replicated in Madin Darby bovine kidney cells. In conclusion, this bovine pathogen, which is not considered to be a human pathogen, can be inactivated by cooking ground or whole cuts of meat to 75°C or higher. Care should be taken to ensure that susceptible hosts such as pigs are not fed improperly cooked meat, meat by-products, or waste food originating from PI cattle.  相似文献   

17.
Inapparent of nonprogressive Aleutian disease virus (ADV) infection is a subclinical but persistent virus infection of mink. Mink with the inapparent type of ADV infection when subjected to stress did not develop the progessive form of the disease. However, when challenged with a large dose of the virus, these mink did develop progressive Aleutian disease indicating that they were not highly resistant to the virus. Sera of mink with either the progressive of the inapparent type of ADV infection did not neutralise the virus. The anti-ADV antibody activity in mink with inapparent type of ADV infection was in the IgG fraction of the serum the same as in mink with progressive Aleutian disease. These data indicate that the resistance of the mink with inapparent infection as compared to mink with progressive Aleutian disease was not due to a difference in the class of immunoglobulin response to the virus. However, mink with progressive Aleutian disease showed a greatly increased immunoglobulin response.  相似文献   

18.
Nephrolithiasis has rarely been reported in marine mammals. During 2004 and 2005, two cases of nephrolithiasis were diagnosed during routine necropsy examination, one in a northern elephant seal (Mirounga angustirostris) and one in a California sea lion (Zalophus californianus). Nephroliths were found throughout both kidneys during necropsy examination, varying in size from 1-10 mm in diameter in the northern elephant seal and from 1-15 mm in diameter in the California sea lion. Necropsy and histopathology revealed nephroliths in association with renal pelvic dilation and pyelonephritis in both animals. In addition, hydronephrosis was noted in the sea lion. Nephroliths were composed of uric acid and ammonium urate in the northern elephant seal and of ammonium urate in the California sea lion. The underlying disease leading to nephrolith formation was not determined; however, it is hypothesized that unknown metabolic derangements due to morphologic or physiologic differences may have played a role. This is the first report of urate nephrolithiasis in the California sea lion and northern elephant seal.  相似文献   

19.
The characteristics of four United Kingdom isolates of swine vesicular disease (SVD) virus from 1981 to 1982 have been compared with those of an isolate obtained from the first outbreak of swine vesicular disease diagnosed in the United Kingdom in 1972. When the virus structural proteins were examined by polyacrylamide gel electrophoresis the four isolates from 1981-82 all had the same polypeptide pattern, which was different from that of the 1972 isolate. Immunodiffusion tests with the 1972 isolate and one 1982 isolate did not reveal any antigenic difference between the viruses but minor antigenic differences were shown by cross-neutralisation tests between the 1972 isolate and the four isolates from 1981-82. In experimentally infected pigs the 1972 isolate produced typical SVD lesions whereas the four more recent SVD viruses produced only very mild clinical disease. Clinical lesions scored numerically were four- to 10- and five- to 11-fold higher at seven and 14 days after infection for pigs infected with the 1972 isolate than with the four isolates from 1981-82. The serum of pigs infected with the 1972 isolate contained significantly higher levels of neutralising antibody than those of pigs infected with more recent isolates. The antibody titres of pigs with only primary lesions ranged from log10 1.9 to 2.8 and one clinically normal pig had a titre of log10 2.4 at 14 days after infection. Attention is drawn to the implication of these findings for SVD control policies based only on the recognition and reporting of clinical disease.  相似文献   

20.
Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.  相似文献   

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