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1.
Intracerebral inoculation of field-isolates as well as established strains of equine herpesvirus-1 (EHV-1) in suckling mice results in viral replication in neurons and glial cells and induces encephalitis. By intraperitoneal (i.p.) inoculation, no histological lesion was observed in the central nervous system (CNS) in suckling mice with the EHV-1 HH1 strain (HH1), whereas a neuroadapted variant (NHH1) produced by serial passage of HH1 in the mouse brain caused severe encephalomyelitis after i.p. inoculation. The purpose of this study was to determine the route of neuroinvasion after i.p. inoculation of NHH1 and to clarify the effects of the brain passage on viral neuroinvasion. NHH1, but not HH1, targeted splenic and pulmonary macrophages and omental fat cells on days 1 and 2 post-inoculation (p.i.). From days 1 to 3 p.i., cell-associated viremia was occurred in NHH1-infected mice, but not in HH1-infected mice. On day 4 p.i., viral antigen was detected in a few endothelial cells, perivascular glial cells and neurons in the CNS in NHH1-infected mice. The number of viral antigen-positive cells increased markedly after day 5 p.i. In contrast, no viral antigen-positive cell was detected in the CNS in HH1-infected mice, except for a few nerve cells in the thoracic cord on day 4 p.i. These results suggest that NHH1 neuroinvasion is hematogenous and is correlated with enhanced extraneural virus growth.  相似文献   

2.
Suckling mice are serviceable in many virological experiments because they are sensitive to various virus species. Simpson & Groupé (2) succeeded in adapting the Beaudette strain of infectious bronchitis virus (IBV) to suckling mice, using the intracerebral route of inoculation. A study of the properties of a Finnish strain of infectious bronchitis virus (IBVF) has been published recently (1). It successfully established the intracerebral adaptation of IBVF to suckling mice. The suckling mice were 100 % sensitive to this virus strain up to an age of 12 days. Symptoms of the central nervous system with a typical clearly discernible gibbosity in the vertebral column were elicited after an incubation period of 2—3 days, and the animals died 3—4 days after the inoculation. Parallelly with IBVF, transmission experiments with other IBV strains were carried out. The present paper is a report on the results of these experiments.  相似文献   

3.
The tumorigenic properties of 3 turkey adenoviruses (CUA, NC-K, and MST) isolated from turkeys with respiratory tract disease and injected into neonatal hamsters (Mesocricetus auratus) have been determined. One of 30 adenovirus isolates (CUA) induced tumors at the site of inoculation (subcutaneously or intracranially) in neonatal hamsters. The tumors were identified as fibrosarcomas and undifferentiated sarcomas. The tumors were found to be free of infective virus, but hamsters which had tumors produced antibody to the virus-specific tumor antigen detectable by the complement-fixation test. The antibody titers for the tumor antigen were from 1:8 to 1:16. Abnormalities were not observed in the major organs collected from hamsters inoculated with the virus. Inoculations of hamster embryo cells and of adult and baby hamster kidney cells with the 3 turkey adenoviruses at a high multiplicity of infection did not produce transformed cells in monolayers. Hamster cells were permissive for CUA virus, since cytopathic effect was observed in 3 to 5 days after inoculation.  相似文献   

4.
An attenuated respiratory disease vaccine against feline viral rhinotracheitis (FVR) and feline calicivirus (FCV) disease was evaluated for safety and efficacy in specific-pathogen-free cats. Twenty cats were vaccinated twice intramuscularly, with 28 days between vaccinations. Ten unvaccinated cats were used as contact controls. Adverse effects were not noticed after vaccination, and the vaccinal virus did not spread to contact controls. Arithmetical mean serum-neutralizing titers against vaccinal FCV strain F9 and challenge FCV strain 255 were 1:13 and 1:15 at 28 days after the 1st inoculation. These titers increased to 1:45 and 1:196 after the 2nd inoculation. After challenge exposure of vaccinated cats to virulent FCV 255 virus, mean titers increased to 1:129 and 1:865, respectively for F9 and 255 viruses. The F9 postchallenge mean titer for vaccinated cats was 21.5 times higher than that for the 8 contact controls that survived challenge exposure. The arithmetical mean serum neutralizing titer for FVR was low (1:2) after the 1st vaccination, but increased to 1:35 after the 2nd vaccination. Challenge exposure to virulent FVR virus resulted in a marked anamnestic immune response (mean titer of 1:207, compared with 1:12 for contact controls). In general, vaccinated cats remained alert and healthy after challenge exposure with FCV-255, whereas unvaccinated contact control cats developed definite signs of FCV disease, including central nervous system (CNS) depression (6 of 10) and dyspnea indicative of pneumonia (5 of 10). Two controls died of severe pneumonia. A mild fibrile response was detected in 28% of vaccinated cats, compared with a more severe febrile response in 78% of control cats. Some vaccinated cats developed minute lingual ulcers that did not appear to be detrimental to the health of the cat. After FVR challenge exposure, vaccinated cats were free of serious clinical signs. Five of 18 vaccinated cats had mild signs of FVR, including an occasional sneeze, low temperature, and mild serous lacrimation for 1 or 2 days. Contact controls developed definite clinical signs of FVR. The combined FVR-FCV vaccine appears to be safe and reasonably efficacious. Vaccination against FCV disease and FVR should be part of the routine feline immunization program.  相似文献   

5.
Venezuelan equine encephalitis (VEE) viruses cause natural outbreaks in humans and horses and represent a significant biothreat agent. The effect of tunicamycin on the course of the disease in mice with VEE was investigated, and the combined effects of these agents was characterized. CD-1 mice given 2.5 microg of tunicamycin had >1,000-fold more virus in the brain 48 hours after infection with the virulent VEE strain V3000 and > or =100-fold of the attenuated strain V3034 at all tested times than did untreated mice, indicating enhanced neuroinvasion. Tunicamycin did not alter the viremia profiles of these viruses nor the replication of V3000 in the brain itself. Tunicamycin alone caused ultrastructural blood-brain barrier damage, yet neuroinvasion by V3000 in treated mice appeared to occur via the olfactory system rather than the blood-brain barrier. Tunicamycin-treated, V3000-infected mice also exhibited earlier and more severe weight loss, neurological signs, neuronal infection, neuronal necrosis and apoptosis, and inflammation than untreated, V3000-infected mice. The mean survival time of tunicamycin-treated, V3000-infected mice was 7.3 days versus 9.9 days for untreated, V3000-infected mice. These studies imply that animals that ingest toxins similar to tunicamycin, including the agent of annual ryegrass toxicity in livestock, are conceivably at greater risk from infections by encephalitis viruses and that humans and horses exposed to agents acting similar to tunicamycin may be more susceptible to encephalitis caused by VEE viruses. The exact mechanism of tunicamycin-enhanced neuroinvasion by VEE viruses requires further study.  相似文献   

6.
Two 7-year old Arabian racing horses were reported to show typical AHS symptoms in Qatar and died shortly after. The horses had been vaccinated with formol inactivated vaccine approximately 10 days before the onset of the disease. Blood samples from these horses were collected and AHS virus isolated from one sample after intracerebral (i.c.) inoculation into suckling mice. The virus identity was confirmed by complement fixation test (CFT) using the virus antigen and reference type 9 of AHS virus hyperimmune serum. The serotype of the isolated virus was identified by serum neutralization test (SNT) using reference types of AHS virus. Two possibilities of the original source of this infection were suggested. The infection might be due first to the natural endemic occurrence of the virus in the country and secondly, to the presence of residual infectious virus in the inactivated vaccine.  相似文献   

7.
The effect of Sendai virus infection on the splenic primary plaque-forming cell (PFC) response to sheep RBC in 2 strains of mice, with contrasting susceptibility to Sendai viral pneumonia, was examined. Mice were given single inoculations of sheep RBC, which varied relative to time of inoculation with Sendai virus, PFC were counted 6 days later, and were compared with PFC responses from noninfected mice. The IgM- and IgG-PFC responses were augmented in resistant C57BL/6J mice 7 and 9 days after inoculation with Sendai virus (sheep RBC given 1 and 3 days after inoculation with Sendai virus, respectively) and in susceptible DBA/2J mice 7, 9, 10, and 13 days after inoculation with Sendai virus. Augmentation was restricted mainly to IgM-, IgG3-, and IgG2b-PFC. The number of splenic background antitrinitrophenyl sheep RBC PFC in mice of both strains was examined during the course of Sendai virus infection. Only a marginal increase in background PFC was seen in C57BL/6J mice on or after viral inoculation day 11 and no change was seen in DBA/2J mice. Serum of infected mice also was examined sequentially for alpha/beta interferon (IFN). Despite vigorous lung IFN production, infected mice rarely had detectable circulating IFN. Seemingly, Sendai virus infection can induce transient hyperresponsiveness to a nonviral antigen.  相似文献   

8.
Highly pathogenic H5N1 avian influenza viruses were isolated in 9 large-billed crows that died in Kyoto and Osaka prefectures in Japan from March to April in 2004. We studied 3 of the 9 crows using standard histologic methods, immunohistochemistry, and virus isolation. The most prominent lesions were gross patchy areas of reddish discoloration in the pancreas. The consistent histologic lesions included severe multifocal necrotizing pancreatitis, focal degeneration and necrosis of neuron and glial cells in the central nervous system, and focal degeneration of cardiac myocytes. All of these tissues contained immunohistochemically positive influenza viral antigens. The virus was isolated from the brain, lung, heart, liver, spleen, and kidney of the crows examined. Thus we concluded that highly pathogenic avian influenza virus was associated with clinical disease, severe pathologic changes, and death in the 3 crows.  相似文献   

9.
The present study describes the pathogenesis of infection of chicks with a new avian reovirus strain, belonging to the so-called enteric reovirus strains (ERS) that is capable of causing central nervous system signs in SPF white leghorns. After intramuscular (IM) or oral inoculation birds were either observed for clinical signs or sacrificed for macroscopic, histological and virological examination for 21 days. Virus isolation was performed on the brain, leg muscle, hock joint, liver and spleen. For the detection of viral antigen the immunohistochemistry (IHC) technique was performed on the caudal part of the cerebrum, spinal cord including spinal ganglia and right N. Ischiadicus. High mortality (79% in 7 days) was seen in birds that were inoculated IM. Survivors were depressed and stayed small until the end of the experiment. One bird had tremor and showed torticollis at 9 days after IM inoculation. Birds that were inoculated orally were depressed from day 4 and stayed small until the end of the experiment. One bird showed a torticollis at 10 days after inoculation. After both IM and oral inoculation ERS was isolated from the brain between 3 and 10 days after inoculation. Other examined organs were positive for virus isolation from day 1 or 5 until day 21. IHC revealed viral antigen positive cells in the Plexus chorioideus (plexus epithelial cells or cells within the underlying connective tissue) and in a spinal ganglion. The results indicate that the pathogenesis of ERS infection in chickens bears some resemblance with that of the mammalian reoviruses serotype 1 in mice.  相似文献   

10.
BACKGROUND: Eastern equine encephalitis (EEE) virus is a mosquito-borne togavirus (alphavirus) that causes severe (often fatal) encephalitis in many mammalian species, but it has not been reported previously in South American camelids. Hypothesis: South American camelids can become naturally infected with EEE virus and show encephalitic signs similar to those observed in other affected species. ANIMALS: Nine cases (8 alpacas and 1 llama, aged 3.5 weeks to 12 years) were identified; 4 of 9 were 510 weeks old. All cases were from the East Coast of the United States and presented in late summer and fall. METHODS: A retrospective study was performed to include confirmed cases of EEE in camelids in North America before 2006. RESULTS: Eight of nine (89%) camelids died or were euthanized in extremis, with the mean time to death of 2 days. Clinical signs were consistent with encephalitis and included fever, lethargy, ataxia, seizures, recumbency, torticollis, opisthotonus, and vestibular signs. No consistent hematologic abnormalities were identified, and cerebrospinal fluid contained an increased protein concentration in the single camelid analyzed. No successful therapy was identified. EEE was confirmed by alphavirus detection by using immunohistochemistry (IHC) and polymerase chain reaction (PCR) in the central nervous system (CNS) and by serology. Findings included polioencephalitis with lymphocytic perivascular cuffing; neutrophil infiltration; gliosis; neuron satellitosis; necrosis; and edema, with intracytoplasmic alphavirus within neurons and glial cells. No virus was detected in extraneural tissues. CONCLUSIONS AND CLINICAL IMPORTANCE: In endemic areas, EEE should be considered a differential diagnosis for young and adult camelids with CNS disease. Brain histopathology with indirect IHC or PCR is diagnostic.  相似文献   

11.
Intramuscular or intravenous inoculation of 5 Columbia black-tailed deer (Odocoileus hemionus columbianus) with virus of epizootic hemorrhagic deer disease (EHD) did not produce overt clinical disease. Two white-tailed deer (Odocoileus virginianus) exposed identically died in 5 to 6 days. There were no significant lesions in 1 black-tailed deer euthanatized on postinoculation day 5. The EHd virus was not isolated from the spleen of that deer. Seroconversion occurred in black-tailed deer, from zero EHD virus antibody titer before inoculation to titers of 1:128 to 1:256 after inoculation.  相似文献   

12.
Immunologic phenomena in the effusive form of feline infectious peritonitis   总被引：15，自引：0，他引：15  
The effusive form of feline infectious peritonitis (FIP) was reproduced by injecting 12- to 16-week-old kittens intraperitoneally with a cell-free inoculum derived from the tissues of infected cats. The kittens used for the study were either positive for FIP virus-reacting antibodies before inoculation or they were seronegative. Seropositive kittens were obtained from a cattery where the natural infection was enzootic, and seronegative kittens were obtained from a specific-pathogen-free cattery. Only about half the kittens that were seronegative before inoculation developed disease or serum antibodies to the tissue-derived virus. Seronegative kittens that developed disease showed no signs of illness until 8 to 10 days after inoculation, and they lived for 7 to 14 days after clinical signs appeared. The onset of clinical disease coincided with the appearance of serum antibodies. In contrast, all of the seropositive kittens became ill within 36 to 48 hours after inoculation, and died within 5 to 7 days. If seronegative kittens were treated with immune serum or immunoglobulin (Ig)G, they developed disease with the same frequency, acuteness, and severity as seropositive kittens. Foci of hepatitis and serositis in seropositive kittens contained viral antigen, IgG bound to antigen, and complement. Serum complement activity also decreased several days before death in seropositive kittens inoculated with tissue-derived FIP virus. The temporal relationship of clinical disease and the appearance of serum antibodies, the more acute and severe nature of the disease produced in seropositive kittens, and the presence of antibody and complement in the lesions indicated that effusive FIP is immunologically mediated.  相似文献   

13.
One-to-70-day-old specific-pathogen-free chickens were infected with rotaviruses isolated from chickens, turkeys, and pheasants. Chicks infected at 1 or 7 days of age remained largely free of infection: virus could be isolated from a few chicks of these ages, but virus antigen could not be detected in the epithelial cells of the intestinal villi. Treating the virus with trypsin before inoculation did not markedly enhance virus infectivity. The same batches of virus successfully infected chickens at 56 and 70 days of age: virus could be isolated between 1 and 5 days postinfection, and virus antigen was detected in the epithelial cells of the intestinal villi. Rotaviruses isolated from pheasants were infectious for 49-day-old chickens. All infections in the older chickens remained subclinical.  相似文献   

14.
An immunohistochemical and histopathological study using the ABC technique was carried out to examine time-sequential virus spread in the central nervous system (CNS) of mice after inoculation with the CVS strain of fixed rabies virus by different routes; intracerebral (ic), intraocular (io), intranasal (in), intramuscular (im) and subcutaneous (sc). Only the ic and io inoculations caused fatal infections, so that detailed analysis was conducted on mice inoculated by these two routes. In ic-inoculated mice, viral antigens were detected mainly in neurons in the cerebral cortex and in the pyramidal cells and granular cells of the hippocampus. After io inoculation, viral antigen was first detected in the trigeminal nerve ganglia, following which it spreads to the cerebral cortex and cerebellum. In the hippocampus only a few cells were viral antigen-positive at the early stage after io inoculation. There were no inflammatory lesions or Negri bodies in the CNS of mice infected by either route. This suggests that clinical signs such as ataxia or depression leading to death may be due to the direct effect of the virus on the functions of neural cells, but not to inflammatory reactions. The ABC method will be useful for the early diagnosis of suspected patients or animals to have the disease when conventional histopathological and immunofluorescent antibody techniques can not detect lesions or viral antigens.  相似文献   

15.
Butylated hydroxytoluene (BHT) was evaluated for antiviral effectiveness on pseudorabies virus (PRV) in cell culture, mice, and swine. When relatively small amounts of BHT were mixed with PRV and incubated at 37 C for 30 or 60 minutes before inoculation into cell cultures, the cell cultures did not become infected with virus. The PRV was not infectious when the virus was treated with BHT and then inoculated intraperitoneally into mice, but was infectious when BHT and PRV were inoculated simultaneously or when BHT was inoculated either 30 or 60 minutes before PRV. Swine fed BHT-medicated feed for 10 days before they were intranasally exposed with virulent PRV did not have overt signs of pseudorabies, had a lower concentration of PRV in nasal mucus than did control swine, and had acceptable blood enzyme and cholesterol concentrations during the experiment. The BHT was detected in tissues of 2 swine after they were fed BHT-medicated feed for 10 days, and higher concentrations of BHT were detected in tissues of 3 swine given BHT feed for 29 days.  相似文献   

16.
Nine calves, were inoculated intravenously with the Innisfail strain of encephalomyocarditis (EMC) virus. Apart from a mild fever, no obvious clinical signs were noted. A low titre viraemia was demonstrated in all 5 calves from which blood was collected, and EMC virus was recovered from the myocardium of 3 of 6 calves at 2, 3 and 6 days after inoculation. Virus was not recovered from the central nervous system. No excretion of EMC virus in urine or faeces was detected in 3 calves. Histopathological lesions were present in brain tissue from only 1 calf, destroyed 14 days after inoculation, and in the heart muscle from another calf, destroyed 7 days after inoculation. Macroscopic lesions were not seen in these organs. Both neutralising and haemagglutination-inhibiting antibodies were produced within one week of infection, reached a peak in 3–4 weeks and persisted undiminished until 9 weeks after inoculation. By nitration on Sephadex G 200, it was shown that the early response was due to IgM type antibodies, and these were replaced by IgG antibody. One calf was inoculated intracerebrally with EMC virus. It developed a flaccid posterior paralysis and was destroyed 6 days later. Virus was recovered from the brain and spinal cord, but no significant histopathological lesions were detected in brain or spinal cord from this calf.  相似文献   

17.
Hyperimmune serum against feline viral rhinotracheitis was produced in a goat and conjugated with a fluorescent dye. Cell cultures infected with rhinotracheitis virus had positive immunofluorescence. Cell cultures infected with other feline viruses and herpesviruses of other species did not fluoresce. In cats experimentally infected with rhinotracheitis virus, the virus was isolated from nasal and conjunctival swabs 1 to 9 days after inoculation. Nasal smears stained with the conjugated antiserum fluoresced 1 to 9 days after inoculation when clinical disease was most apparent. Conjunctival smears had positive immunofluorescence 1 to 6 days, but not 9 days, after inoculation. On postinoculation day 23, rhinotracheitis virus was not isolated from nasal or conjunctival swabs and nasal and conjunctival smears did not fluoresce. Rhinotracheitis virus or feline calicivirus was isolated from naturally infected cats with upper respiratory tract disease. Nasal and conjunctival smears from rhinotracheitis virus-infected cats had positive immunofluorescence in all cast showing clinical illness. Smears from 1 clinically normal cat from which rhinotracheitis virus was isolated did not fluoresce. Nasal and conjunctival smears from calicivirus-infected cats did not fluoresce.  相似文献   

18.
Three bovine fetuses were inoculated in utero with approximately 10(3) plaque forming units of type 11 bluetongue virus. The gestational ages of the fetuses at the time of inoculation were 106, 113 and 122 days. They were spontaneously aborted 104, 65 and 109 days later, respectively, and the first and third of these fetuses were recovered. There was no grossly normal cerebral tissue, the meninges formed fluid filled sacs, and the cerebellums were reduced in size. Bluetongue virus was not isolated from the fetuses but the older one had neutralizing antibody. The three dams developed neutralizing antibody to bluetongue virus. The present work supports the observation by others that early fetal infections with bluetongue virus normally result in severe central nervous system damage and not in clinically normal, persistently infected calves.  相似文献   

19.
One-month-old Syrian hamsters of the APA and Std: golden strains were inoculated intraperitoneally with 10(5) PFU/head of the D variant of encephalomyocarditis (EMC) virus and examined virologically and pathologically up to 7 days after inoculation. APA hamsters developed apparent hyperglycemia due to pancreatic islet cell damage while Std:golden hamsters did not. Hamsters of both strains showed clear histopathologic changes in the testis with prominent viral replication as well as in the brain, heart and exocrine pancreas. The susceptibility to EMC virus-infection was higher in males than in females and in APA than in Std: golden hamsters.  相似文献   

20.
Effects of immunosuppression were compared in newly hatched chickens given cyclophosphamide (CY) after inoculation with avian nephritis virus (ANV). All CY-treated infected chickens died within 13 days after inoculation of the virus and had heavy urate deposits throughout the body. However, non-CY-treated infected, CY-treated noninfected, and non-CY-treated noninfected control chickens survived through the observation period. In a chronologic study, the value of serum uric acid in CY-treated infected chickens was more than 3 times higher than that in non-CY-treated infected chickens, and more than 9 times higher than in noninfected chickens. Serum uric acid values were coincident with the positive degree of ANV antigen in the tubular epithelial cells in the kidneys and with the severity of renal degeneration. Serologic and immunohistologic examinations did not reveal detectable antibody and IgG- and IgM-containing cells in the spleen and kidneys of CY-treated infected chickens. However, non-CY-treated infected chickens had an increased number of IgM- and IgG-containing cells and antibody against ANV on postinoculation day 6. These findings demonstrated that CY treatment enhanced the susceptibility of chickens to ANV infection.  相似文献   

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