Reproductive performance of apparently healthy cattle persistently infected with bovine viral diarrhea virus.

A Holstein-Friesian bull and three Holstein-Friesian cows were seronegative for bovine viral diarrhea (BVD) virus but were persistently infected with the virus. Virus was isolated from buffy coat cells and nasal and lacrimal secretions during their lifetime, and they remained free of clinical signs of BVD. The three cows were pregnant when purchased, and they gave birth to full-term calves. One calf lived only a few hours, one calf became ill and died within a few days, and one calf became ill and was euthanatized within a few weeks. One cow was then bred and became pregnant but aborted a 7-month fetus. A second cow was bred approximately 5 months after parturition but did not conceive. The third cow was necropsied 6 weeks after calving, because of loss of weight. Although the bull's semen contained BVD virus when seropositive cows were bred, normal calves were born. When seronegative heifers were bred, they became seropositive to BVD virus within two weeks, with higher titers in six weeks. On heifer conceived after one service but aborted a 6-month fetus. Three others continued to have estrous cycles until their titers rose to 1:128, then they conceived and gave birth to normal calves. Another heifer conceived on the first service, had a titer of 1:128 two weeks after breeding, and gave birth to a normal calf.     

Indirect transmission of bovine viral diarrhoea virus at calving and during the postparturient period

Two trials were designed to investigate whether bovine viral diarrhoea virus (BVDV) could be transmitted after the birth of persistently infected calves, even if they were removed immediately after birth. In trial 1, 11 calves were actively exposed to fetal fluids and uterine lochia collected from cows that had delivered calves persistently infected with type 1 BVDV. One calf that was exposed to a sample taken on the day of calving seroconverted. In trial 2, six calves were housed in stables where persistently infected calves were being born and then removed immediately from their dams and from the stable unit within two to three hours. One of four calves in close contact with the cows after delivery seroconverted and one of two calves housed within the same stable unit became infected.     

Rift Valley fever virus-induced encephalomyelitis and hepatitis in calves.

Three calves (Nos. 1, 2 = 7 days old; No. 3 = 21 days old) were inoculated subcutaneously with virulent Rift Valley fever (RVF) virus. All calves became viremic and clinically ill, but the two 7-day-old calves were moribund and were euthanatized subsequently on post-inoculation day (PID) 3. Highest viral titers were measured in the serum, with lesser concentrations in the brain, heart, spleen, and liver of these animals. Viral antigens were detected by immunohistochemical analysis only in the livers, where positive staining was localized in coalescing foci of hepatocellular necrosis. The 21-day-old calf appeared to recover after viremia and pyrexia but became lethargic and ataxic and was euthanatized on PID 9. The calf was no longer viremic, and RVF virus was isolated only from the brain. Microscopic examination of the central nervous system revealed diffuse perivascular infiltrates of lymphocytes and macrophages, multifocal meningitis, and focal areas of neuronal necrosis and aggregates of macrophages, lymphocytes, and neutrophils throughout all regions of the brain and cervical spinal cord. There was positive immunohistochemical staining for viral antigens within the cytoplasm of neurons and glial cells throughout the central nervous system. Thus, RVF virus can cause encephalomyelitis in calves, and the specific virologic diagnosis can be made by immunohistochemical localization of viral antigens in formalin-fixed tissues.     

Bovine Viral Diarrhea Virus and Escherichia Coli in Neonatal Calf Enteritis

This study was initiated to determine the etiologic and pathogenic significance of an American strain of bovine viral diarrhea (BVD) virus (strain NADL-MD) in enteritis of neonatal calves (calf scours).

Three colostrum-fed calves from dams exposed intravenously to BVD virus at 6, 16 and 25 days prepartum, respectively, had moderate diarrhea persisting until the eighth day of life. The BVD virus was isolated from all 3 calves and persisted up to 93 days in 1 calf, indicating either that BVD was transmitted in utero or via the dam's milk.

Three specific pathogen free (SPF) calves permitted dams' colostrum for the first 4 feedings and then given milk replacer were exposed orally on the day of birth to BVD virus. One calf died of neonatal enteritis 28 hours post-exposure and at necropsy the BVD virus was isolated from several of its organs. The remaining 2 calves had a mild diarrhea persisting to the eighth day of age.

Two calves permitted dams' colostrum ad lib. for 72 hours, and then weaned, were exposed orally to BVD virus. Both calves had a mild persistent diarrhea and BVD virus was isolated from their blood for 56 days post-exposure.

Of 13 SPF, colostrum-deprived calves exposed orally or intranasally at birth to the BVD virus, 4 had severe diarrhea and died of neonatal enteritis from 38 hours to 13 days postexposure. Isolations of BVD virus were made from several of the organs of the calves at necropsy. All of the 9 surviving calves had a moderate to severe diarrhea frequently persisting for 7 to 10 days, and BVD virus was isolated from the survivors up to 103 days postexposure.

Several strains of Escherichia coli were isolated from calves after the second day of life, but were neither pathogenic for mice, nor serologically related to strains of E. coli usually associated with outbreaks of calf scours. Four colostrum-deprived SPF calves were exposed orally at birth to a strain of E. coli isolated from the intestine of the calf with the most acute symptoms and fatal neonatal enteritis. None of the four calves receiving the E. coli had diarrhea. One calf, however, had respiratory distress and died on day 5.

Two SPF colostrum-deprived control calves had neither diarrhea nor respiratory distress.

The above findings support the conclusion that BVD virus should not be overlooked as a primary cause of the neonatal calf enteritis complex.

     

Isolation of bovine adenovirus type 7 from calves with pneumonia and enteritis.

Bovine adenovirus type 7 was isolated from a 10-month-old calf with fibrinopurulent pneumonia and from 2 newborn calves with pneumoenteritis. The viruses were isolated on calf lung and adrenal gland cell cultures and were identified as serotype 7 by immunoelectron microscopy and serum-neutralization tests.     

Evaluation of the pathogenic potential of cervid adenovirus in calves.

Four 3-month-old Jersey calves and three 3-month-old Holstein calves were inoculated with cervid adenovirus and monitored for clinical signs until necropsied between 10 and 42 days postinoculation. The neonatal Jersey calves had received colostrum, and the Holstein calves were colostrum deprived. Preinoculation and postinoculation serum samples were tested for antibodies to the cervid adenovirus, bovine adenovirus type 6, bovine adenovirus type 7, and goat adenovirus type 1. Virus isolation was performed on kidney, nasal secretion, and/or lung homogenates in fetal white-tailed deer lung cells. Negatively stained preparations of feces from Jersey calves were examined weekly using an electron microscope, and weekly blood samples were collected for complete blood counts. Full necropsies were performed on all calves. A complete selection of tissues was evaluated for microscopic changes, and immunohistochemistry was performed on all tissues using a polyclonal antibody to deer adenovirus. No clinical signs were observed in the calves during the study period. Following inoculation, colostrum-deprived calves developed low antibody titers to deer adenovirus, while the Jersey calves that received colostrum did not. Calves that received colostrum had high antibody titers to bovine adenovirus type 7 and goat adenovirus type 1. No consistent gross or microscopic lesions were seen. Adenovirus was not observed in negatively stained preparations of feces. Immunohistochemistry results did not demonstrate virus in all tissues examined microscopically, and virus was not isolated from lungs, nasal secretions, and kidneys.     

EXPERIMENTAL ENCEPHALOMYOCARDITIS VIRUS INFECTION IN CALVES

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.     

Infectivity of bovine adenovirus type 5 recovered from a polyarthritic calf with weak calf syndrome.

Bovine adenovirus type 5, isolated from newborn calves with a polyarthritic disease known as "weak calf syndrome" caused a mild, self-limiting illness in susceptible calves. The induced illness was characterized by marked pyrexia and occasionally by mild diarrhea. It was concluded that the virus may contribute to morbidity and mortality associated with the weak calf syndrome by adding to the stress and debilitation caused by cold wet weather and by bovine viral diarrhea (BVD) virus, which has also been isolated from tissues of calves affected with weak calf syndrome.     

OBSERVATIONS OF SW AINSONA GALEGIFOLIA POISONING IN CATTLE IN NORTHERN NEW SOUTH WALES

A mild interstitial pneumonia with mononuclear cell infiltration was produced in calves following intra-tracheal inoculation of the BIL adenovirus. Viral antigen appeared early in the regional lymph node. An interstitial reaction developed early in the lungs, and pneumonic lesions and infective virus were present by the third day after inoculation. Virus spread rapidly to trachea, tonsils and nasal mucosa, and was excreted from the third to eighth day. Upper and lower respiratory tissues continually harboured virus until the 12th day, when the experiment was terminated. The virus was isolated from the livers of two calves. All tissues yielded low concentrations of virus, and only the lung showed pathological reactions. The reactions were qualitatively similar to known adenovirus pneumonias, but considerably milder, and lacked the characteristic necrotic and proliferative bronchiolar changes.     

EXPERIMENTAL ADENOVIRUS PNEUMONIA IN CALVES

A mild interstitial pneumonia with mononuclear cell infiltration was produced in calves following intra-tracheal inoculation of the BIL adenovirus. Viral antigen appeared early in regional lymph node. An interstitial reaction developed early in the lungs, and pneumonic lesions and infective virus were present by the third day after inoculation. Virus spread rapidly trachea, tonsils and nasal mucosa, and was creted from the third to eighth day. Upper and lower respiratory tissues continually harboured virus until the 12th day, when the experiment was terminated. The virus was isolated from the livers of two calves. All tissues yielded low concentrations of virus, and only the lung showed pathological reactions. The reactions were qualitatively similar to known adenovirus pneumonias, but considerably milder, and lacked the characteristic necrotic and proliferative bronchiolar changes.     

Alimentary Tract Manifestations of Bovine Adenovirus Infections

Two calves and a feedlot steer with systemic bovine adenovirus infection had hemorrhagic and necrotizing lesions confined to the digestive tract. In one calf there was severe, multifocal, necrotizing, hemorrhagic rumenitis, omasitis, abomasitis, enteritis and colitis. Small intestinal lesions were predominantly in Peyer's patches. Multifocal necrotizing abomasitis was the principal change in the other calf. Large amphophilic intranuclear inclusions typical of bovine adenovirus were common in swollen vascular endothelial cells. Bovine adenovirus was isolated from the former calf.The steer had diffuse hemorrhagic enterocolitis and large numbers of BAV inclusions in vascular endothelial cells of the intestinal lamina propria. Serum-neutralization tests to bovine adenovirus type 3 on acute and convalescent samples from six clinically affected in-contact animals revealed fourfold elevations in two.     

Disease in a dairy herd associated with the introduction and spread of bovine virus diarrhoea virus

In January 1982 an outbreak of diarrhoea among adult dairy cows in a closed herd of approximately 200 milking animals was shown to be caused by the introduction of bovine virus diarrhoea virus (BVDV). Affected animals showed a significant reduction in milk yield. One animal died and four were culled. Eight cows aborted and one weak calf was born. Of 121 calves born that year, 26 died, mostly from pneumonia, but five aged from three weeks to five months had enteric lesions of mucosal disease. Subsequent investigations of the whole herd in 1983 and 1984 showed that virus spread among the adults was slow and that BVDV continued to make a major contribution to calf losses. Again the greatest cause of loss was suppurative or fibrinous pneumonia. Overall, BVDV was isolated from 36 animals. Isolation of virus from a wide range of tissues of individual animals confirmed that they were viraemic at death. Viruses from calves dying of pneumonia and from aborted fetuses were non-cytopathic in tissue culture. Isolates showing varying degrees of cytopathogenicity were obtained only from tissues of one calf with a congenital neurological defect and the seven animals with enteric lesions consistent with a diagnosis of mucosal disease. Blood from all 89 BVDV antibody-free animals older than three months was tested for the presence of BVDV. Altogether, 12 calves were identified as persistently viraemic and all were apparently healthy when bled. Only two matured normally, four grew poorly and six died.(ABSTRACT TRUNCATED AT 250 WORDS)     

A paravaccinia virus isolated from cattle.

Isolation of viruses from calves with acute respiratory tract disease were attempted on bovine embryonic lung cell cultures. An isolate obtained from one calf with oral lesions and respiratory disease, designated 44-M-E482, was characterized as a paravaccinia virus on the basis of biological and physical properties. The calf from which the paravaccinia virus 44-M-E482 was isolated did not possess serum neutralizing antibody in its convalescent sera; neither did experimentally inoculated calves possess serum neutralizing antibody to the isolate. However, a low titer of serum neutralizing antibody was produced in one calf after several intravenous injections of the virus. Inoculation of calves with 44-M-E482 into the oral mucosa, skin, nasal cavity and pharynx did not cause any noticeable illness or lesions. The relation of 44-M-E482 to the viruses which cause bovine papular stomatitis and pseudocowpox is discussed.     

奶牛四分胚分割研究

用玻璃针四等分7天的奶牛胚胎为四分(1/4)胚。同一胚胎2个四分胚装回空透明带内,另2个四分胚不装带,成对非手术移给受体奶牛。两次试验共分割胚胎(晚桑椹到囊胚期)11枚,得到42个四分胚。移植受体32头,有3头妊娠。最后,一头受体生出一对同卵双胎四分胚母犊,另一头产一四分胚母犊,均由装带四分胚发育而来。还有一头受体产一四分胚公犊,是由未装带的四分胚发育得到的。试验还分割一个8天囊胚,把一个无带四分胚先放在体外培养24小时再移入受体。结果获得一头四分胚母犊。     

Isolation and partial characterization of a calicivirus from calves

A calicivirus was isolated from 3 dairy calves in a herd with persistent calf respiratory tract problems. This virus, named Tillamook calicivirus, was not neutralized by 18 different calicivirus-typing serums available. The agent caused only minimal lesions in 2 experimentally exposed calves, but did establish a persistent infection with virus shedding for 45 days, after which time the experiment was terminated. Experimentally exposed swine developed clinical vesicular lesions. The possible origins, disease potential, and relationships to the exotic animal disease agent, vesicular exanthema of swine are discussed for this first calicivirus isolate of bovine origin.     

Some characteristics of a natural infection by parainfluenza-3 virus in a group of calves.

Parainfluenza-3 (Pi3) virus infection in a group of 25 calves is described. The virus was isolated from the lungs of four calve at days 6, 7, 13 and 55 after they were housed together at birth. Intracytoplasmic inclusion bodies were seen by light microscopy in bronchial and bronchiolar epithelial cells of two of these calves. Virus infected cells were detected by electron microscopy in three of the four calves. Haemagglutination inhibition antibodies to Pi3 virus were found in the sera of the calves. Despite the virus being present in the group from one week, a significant increase in antibody titre was found in only two animals although all the calves were in contact with each other during the study period. The pulmonary lesions in the four infected calves consisted of a bronchitis and bronchiolitis with infiltration of the walls and lumena of these structures by neutrophils and an adjacent neutrophil infiltration of alveoli some of which were collapsed.     

Transmission of Bovine viral diarrhea virus 1b to susceptible and vaccinated calves by exposure to persistently infected calves

Bovine viral diarrhea virus (BVDV) persistently infected (PI) calves represent significant sources of infection to susceptible cattle. The objectives of this study were to determine if PI calves transmitted infection to vaccinated and unvaccinated calves, to determine if BVDV vaccine strains could be differentiated from the PI field strains by subtyping molecular techniques, and if there were different rates of recovery from peripheral blood leukocytes (PBL) versus serums for acutely infected calves. Calves PI with BVDV1b were placed in pens with nonvaccinated and vaccinated calves for 35 d. Peripheral blood leukocytes, serums, and nasal swabs were collected for viral isolation and serology. In addition, transmission of Bovine herpes virus 1 (BHV-1), Parainfluenza-3 virus (PI-3V), and Bovine respiratory syncytial virus (BRSV) was monitored during the 35 d observation period. Bovine viral diarrhea virus subtype 1b was transmitted to both vaccinated and nonvaccinated calves, including BVDV1b seronegative and seropositive calves, after exposure to PI calves. There was evidence of transmission by viral isolation from PBL, nasal swabs, or both, and seroconversions to BVDV1b. For the unvaccinated calves, 83.2% seroconverted to BVDV1b. The high level of transmission by PI calves is illustrated by seroconversion rates of nonvaccinated calves in individual pens: 70% to 100% seroconversion to the BVDV1b. Bovine viral diarrhea virus was isolated from 45 out of 202 calves in this study. These included BVDV1b in ranch and order buyer (OB) calves, plus BVDV strains identified as vaccinal strains that were in modified live virus (MLV) vaccines given to half the OB calves 3 d prior to the study. The BVDV1b isolates in exposed calves were detected between collection days 7 and 21 after exposure to PI calves. Bovine viral diarrhea virus was recovered more frequently from PBL than serum in acutely infected calves. Bovine viral diarrhea virus was also isolated from the lungs of 2 of 7 calves that were dying with pulmonary lesions. Two of the calves dying with pneumonic lesions in the study had been BVDV1b viremic prior to death. Bovine viral diarrhea virus 1b was isolated from both calves that received the killed or MLV vaccines. There were cytopathic (CP) strains isolated from MLV vaccinated calves during the same time frame as the BVDV1b isolations. These viruses were typed by polymerase chain reaction (PCR) and genetic sequencing, and most CP were confirmed as vaccinal origin. A BVDV2 NCP strain was found in only 1 OB calf, on multiple collections, and the calf seroconverted to BVDV2. This virus was not identical to the BVDV2 CP 296 vaccine strain. The use of subtyping is required to differentiate vaccinal strains from the field strains. This study detected 2 different vaccine strains, the BVDV1b in PI calves and infected contact calves, and a heterologous BVDV2 subtype brought in as an acutely infected calf. The MLV vaccination, with BVDV1a and BVDV2 components, administered 3 d prior to exposure to PI calves did not protect 100% against BVDV1b viremias or nasal shedding. There were other agents associated with the bovine respiratory disease signs and lesions in this study including Mannheimia haemolytica, Mycoplasma spp., PI-3V, BRSV, and BHV-1.     

Ultrastructural features of alveolar lesions in induced respiratory syncytial virus pneumonia of calves

Ultrastructural changes occurred in alveolar epithelium in the acute and repair stages of induced respiratory syncytial virus pneumonia induced in eight calves (calf Nos. 1-7, 3 to 6 days old and calf No. 8, 2 weeks old), using a bovine strain of respiratory syncytial virus. Five of the calves were Friesians, three were Hereford x Friesians, and all were male. Tissues from three mock-infected control calves (two Friesian, one Hereford x Friesian) were also examined. Evidence of respiratory syncytial virus infection was observed in both type I and type II pneumocytes from day 4 to day 8 after infection. Infection of type I pneumocytes frequently resulted in necrosis. The response of type II pneumocytes to respiratory syncytial virus infection varied and included hypertrophy, hyperplasia, and syncytial formation. In some infected type II pneumocytes, there were numerous irregular projections of the cell surface, associated with viral budding. Hypertrophy and hyperplasia of type II pneumocytes, epithelial syncytium formation, and irregular cytoplasmic projections from epithelial cells caused considerable thickening of respiratory membrane and occlusion of alveolar lumina. Neutrophils were frequently observed in close association with virus-infected epithelial cells, but evidence of respiratory syncytial virus infection and replication was not observed in alveolar macrophages or neutrophils. Proliferation of type II pneumocytes appeared to play a major role in maintaining the integrity of the alveolar epithelium during the acute stage of the experimental pneumonia. Increased numbers of type II pneumocytes were present on alveolar walls, particularly from 4 to 8 days after infection, and some alveoli were lined entirely by this cell type. In some areas, however, squamous epithelial cells were also involved in covering exposed alveolar basement membrane.     

Encephalitis induced by bovine herpesvirus 5 and protection by prior vaccination or infection with bovine herpesvirus 1.

Calves were intranasally challenged with bovine herpesvirus 5 (BHV5) and followed for the development of viral infection, clinical encephalitis, histologic lesions in the brain, and viral sequences in the trigeminal ganglia. Calves that were previously vaccinated with bovine herepesvirus 1 (BHV1, n = 4) or previously infected with BHV1 (n = 5) or that had not been exposed to either virus (n = 4) were compared. No calf developed signs of encephalitis, although all calves developed an infection as indicated by nasal secretion of BHV5 and seroconversion to the virus. Histologic lesions of encephalitis consisting of multifocal gliosis and perivascular cuffs of lymphocytes were observed in calves not previously exposed to BHV1. BHV5 sequences were amplified from the trigeminal ganglia of calves previously vaccinated and from calves not previously exposed to BHV1; calves sequentially challenged with BHV1 and later BHV5 had exclusively BHV1 sequences in their trigeminal ganglia. Administration of dexamethasone 28 days after BHV5 challenge did not influence clinical disease or histologic lesions in either previously unexposed calves (n = 2) or previously immunized calves (n = 2), although it did cause recrudescence of BHV5, as detected by nasal virus secretion.     

An outbreak of mucosal disease in a dairy herd

An outbreak of mucosal disease (MD) was studied in a dairy herd, comprising 12 cows, 9 heifers and 18 calves. During a period of 1 month, six 5 to 8 month-old calves showed typical signs of MD. They all died or were killed in extremis after 2-8 days with progressively worsening clinical signs. Post mortem lesions were examined in one calf. Non-cytopathogenic MD virus was isolated from serum or tissues from 3 clinically affected calves and from 1 healthy heifer. All cows and heifers except for the viremic one possessed neutralizing antibodies against bovine pestivirus. According to the current MD-pathogenesis concept, the affected calves were probably infected transplacentally during the first half of foetal life with pestivirus from the persistently infected heifer in the herd.