The efficacy of 4 commercial porcine reproductive and respiratory syndrome virus (PRRSV) modified-live vaccines (MLV), against PRRSV-1 and PRRSV-2 was evaluated and compared in growing pigs. Two of the vaccines were based on PRRSV-1 and two on PRRSV-2. There were no significant differences between each of the two PRRSV-1 MLV vaccines and the two PRRSV-2 MLV vaccines respectively based on virology, immunological, and pathological evaluations. Vaccination with either of the PRRSV-1 MLV vaccines resulted in reduced PRRSV-1 but not PRRSV-2 viremia. Additionally, vaccination with either of the PRRSV-1 MLV vaccines resulted in reduction of lung lesions and PRRSV-1 positive cells in PRRSV-1 challenged pigs but had no significant effect in PRRSV-2 challenged pigs. In contrast, vaccination with either of the two PRRSV-2 MLV vaccines resulted in the reduction of both PRRSV-1 and PRRSV-2 viremia. The PRRSV-2 MLV vaccines were also able to effectively reduce lung lesions and PRRSV positive cells after challenge with either PRRSV-1 or PRRSV-2. Our data suggest that while vaccination with PRRSV-1 MLV vaccines can be effective against PRRSV-1, only PRRSV-2 MLV vaccines can protect against both Korean PRRSV-1 and PRRSV-2 challenges in this study.

A total of 23,322 specimens collected between 2014 and 2017, froma total of 2,592 cases, were received in Veterinary Research Institute, Ipoh (VRI) from various states in Malaysia and testedfor common bacterial, viral, and parasitic diseases in pigs. The highest occurrence of isolated bacteria from 771 samples whichtested positive were Salmonella (47.38%) and Escherichia coli (15.68%), followed by Staphylococcus (6.62%), Streptococcus (5.57%), Klebsiella pneumonia (4.88%), Pseudomona (3.38%), Acinetobacter (3.14%), Aeromonas (2.79%), Enterobacter (2.44%), one each of Bacillus and Pasteurella multocida (1.74%), Enterococcus (1.39%) and Corynebacterium (1.05%). 1.74% of each bacteria detected were Moxarella, Aspergillus, Burkholderia andChromobacterium. Positive samples tested by ELISA was Japanese encephalitis virus (JEV) (9.15%), Aujezsky disease virus (ADV)(5.37%), porcine cirvo-virus-2 (PCV2) (5.09%) and porcine reproductive and respiratory syndrome virus (PRRSV) (4.52%). Positive amples tested by the molecular test wasPCV2 (1.62%), PRRSV (1.32%) and classical swine fever virus (CSFV) (0.4%). Serology tests were conducted on 11,305 samplesand reported positive for Brucella suis (15.32%), Brucella abortus (0.62%), Brucella melitensis (0.85%), and melioidosis (0.05%). Parasitology analyses on 99 samples. revealed presence of 10.1% coccidia and 1% each of helminths and Sarcocystis. Within the 4-year period, there were no positive samples for porcine parvovirus (PPV), Nipah virus, swine influenza virus (SIV), and bacteria of Johne’s disease and leptospirosis. Continuous assessment is required to establish a comprehensive baseline data of swine diseases in Malaysia.

Pathogens causing significant respiratory disease in growing pigs include Porcine reproductive and respiratory syndrome virus, Porcine circovirus 2, swine influenza virus, porcine respiratory coronavirus, Mycoplasma hyopneumoniae, and Bordetella bronchiseptica. The objective of this research was to characterize the respiratory excretion of these pathogens by acutely infected pigs. Pigs were inoculated under experimental conditions with 1 pathogen. Samples were collected from the upper respiratory tract and exhaled air. All pathogens were detected in swabs of the upper respiratory tract, but only M. hyopneumoniae and B. bronchiseptica were detected in expired air from individually sampled, acutely infected pigs. These findings suggest either that the acutely infected pigs did not aerosolize the viruses or that the quantity of virus excreted was below the detection threshold of current sampling or assay systems, or both, at the individual-pig level.

Objective-To inoculate white-tailed deer (Odocoileus virginianus) during the sixth or seventh week of gestation with bovine viral diarrhea virus (BVDV) and observe for signs of reproductive tract disease during a 182-day period. Animals-10 pregnant white-tailed deer (8 seronegative and 2 seropositive [control deer] for BVDV). Procedures-Deer were inoculated with 1 of 2 deer-derived BVDV strains (RO3-20663 or RO3-24272). Serum anti-BVDV antibody titers were determined prior to and 21 or 35 days after inoculation. Virus isolation (VI) procedures were performed on tissues from fetuses and does that died and on blood samples collected from live fawns. Ear notch specimens obtained from live fawns were assessed by use of BVDV antigen-capture ELISA (ACE). Results-Both RO3-20663-inoculated seropositive deer gave birth to apparently normal fawns. Among the RO3-24272-inoculated seronegative deer, 1 died, and 1 aborted and 1 resorbed their fetuses; among the RO3-20663-inoculated seronegative deer, 3 died, 1 aborted its fetus, and 1 gave birth to 2 fawns that were likely persistently infected. On the basis of VI and ACE results, those 2 fawns were positive for BVDV; both had no detectable neutralizing anti-BVDV antibodies in serum. Conclusions and Clinical Relevance-Reproductive tract disease that developed in pregnant white-tailed deer following BVDV inoculation was similar to that which develops in BVDV-exposed cattle. Methods developed for BVDV detection in cattle (VI, immunohistochemical evaluations, and ACE) can be applied in assessments of white-tailed deer. Fawns from does that had serum anti-BVDV antibodies prior to inoculation were protected against BVDV infection in utero.

We studied the uptake and sequential transneuronal passage of pseudorabies virus (PRV) in rat CNS by use of a combination of immunohistochemistry and in situ hybridization. Protocols for rapid detection of PRV by immunohistochemistry and in situ hybridization in rats with PRV infection of the CNS after intranasal instillation of a wild-type strain of PRV were optimized in vitro, using porcine kidney-15 cells. Pseudorabies virus-specific hybridization signals appeared in the cytoplasm and nucleus of PRV-infected porcine kidney-15 cells by postinoculation (PI) hour 6. In tissue sections of PRV-infected rats, PRV nucleic acids were detected in areas of the rat brain in close proximity to the areas in which PRV antigens were evident. The PRV was initially found in the nucleus of trigeminal ganglion neurons at PI hour 24. At PI hour 72, PRV antigens were observed in the mid-brain, and 24 hours later, in the telencephalon. We also found evidence of specific progressive transsynaptic transmission of the virus, and, on the basis of that, we have constructed a map of the synaptic contacts and pathways in the brain. Therefore, combined use of immunohistochemistry and in situ hybridization was useful for characterizing the pathogenesis of PRV in the CNS of rats after intranasal inoculation, following a pattern that mimics PRV infection of the natural host.

Pseudorabies virus (PRV) nucleic acids in the trigeminal ganglia and tonsils of swine latently infected with the virus were analyzed. By use of DNA-polymerase chain reaction (PCR), 14 of 14 trigeminal ganglia and 12 of 14 tonsils were positive for PRV genomes. By use of RNA-PCR, RNA containing the large latency transcript splice junction were detected in 4 of 4 trigeminal ganglia and 4 of 5 tonsils. In general, results of both PCR procedures indicated that the amounts of PRV DNA and RNA per microgram of cellular nucleic acids were higher in trigeminal ganglia than in tonsils. Identification of peripheral tissues that harbor latent PRV is an important asset for PRV research. The presence of large latency transcript in tonsil tissues, in the absence of virus replication, is a critical characteristic, which indicates that the tonsil is a site of PRV latency. For diagnostic purposes, animals need not be euthanatized to obtain their nervous tissue to determine latency; instead, tonsil biopsy specimens could be obtained from live animals for analysis. For pathogenesis studies, multiple specimens obtained sequentially from the same animal would be available for examination for the duration of the experiment.

Bovine immunodeficiency virus (BIV) is prevalent in beef and dairy cattle, yet the mode(s) of BIV transmission are undefined. Using polymerase chain reaction, which specifically targeted a 235-bp, highly conserved region of the BIV pol gene, BIV-infected leukocytes were detected in the blood and milk of BIV-seropositive cows. These data confirm the presence of BIV in milk and identify the potential for lactogenic transmission of this virus.

A nested polymerase chain reaction (PCR) test was developed to examine infection with the bovine lentivirus, bovine immunodeficiency-like virus (BIV), in cattle. Primers were designed to amplify 2 separate regions of the pol and env segments of the BIV genome. Two calves were experimentally infected with an isolate derived from the original strain of BIV, R29, or with a recent field isolate, FL491. Serial blood samples were collected and examined by virus isolation, protein immunoblot, and nested PCR. The nested PCR test detected BIV infection by 3 days after inoculation, earlier than the other 2 methods, and continued to identify infected cattle 9 to 15.5 months after inoculation, even when results from virus isolation and serology became negative. Nested PCR also detected multiple-size env products in samples obtained later in the infection from the calf that received FL491, giving evidence that viral quasispecies were selected during in vivo replication of the virus. Results indicated that the nested PCR test is more sensitive than virus isolation or serology for the detection of BIV infection in cattle.

The consequences of inoculation of bluetongue virus (BTV) serotype 11 into 16 susceptible cows either at the time of breeding or at specified stages of pregnancy were studied. The cows were free of BTV or epizootic hemorrhagic disease virus, and none had antibodies to BTV before virus inoculation. A group of 4 cows was mated naturally to a bull reported to shed BTV (CO75B300 strain) in the semen. The bull was suspected of infecting cows at mating with BTV-11, which subsequently transplacentally infected the developing fetuses and induced persistently infected and congenitally malformed progeny. Two groups of 4 pregnant cows were inoculated with an insect-derived strain of BTV-11 (CO75B300), one group by direct deposit into the uterus at estrus, the other, by intradermal and sc administrations. A 90-day fetus was inoculated in utero with virus from the same pool. Four pregnant cows were inoculated with sheep blood-passaged virus of the same BTV-11 strain (CO75B300) by intradermal and sc routes. Three cows were inoculated with BTV-free suspending fluids and ovine erythrocytes by the intrauterine and intradermal-sc routes and were used as in-contact controls.Infection with insect-derived BTV-11 was confirmed in 3 cows of 1 group by virus isolation and by detection of serum antibodies. The 4 cows inoculated with sheep blood suspension of BTV-11 developed viremia and produced antibodies to the virus. None of the cattle had clinical signs of bluetongue, other than 2 cows that had a slight rectal temperature increase on postinoculation day 4.All cows and fetuses that ranged in gestational age from 69 to 217 days appeared grossly normal at necropsy. Antibodies were not detected in fetal blood. Viral antigen was not detected in fetal tissues by inoculation into sheep or by immunofluoerscence, and viral RNA was not detected by use of the polymerase chain reaction. Developmental deformities were not seen in any fetus. The BTV-11 was not transmitted via the bull semen after natural mating. The BTV-11 strain CO75B300, isolated from this bull and passaged either as insect-derived or ovine erythrocyte suspensions, infected 8 cows. However, the virus was not transplacentally transmitted to their fetuses. It was concluded that there was no evidence for congenital BTV-11 infection in this study.

Recombinant equine interferon-beta 1 (reqIFN-beta 1) induces an antiviral state in blood mononuclear cells (BMC) of horses. Maximal protection against replication of vesicular stomatitis virus is achieved 6 hours after treatment with IFN in vitro and in vivo. Duration of the protective effect depends on the dose of IFN in vitro and in vivo. Availability of reqIFN-beta 1 in cultures of BMC for up to 48 hours does not prolong the antiviral state. The protective effect on BMC after treatment with IFN has similar duration in vivo and in vitro. Monitoring of the effect of IFN in vivo is, thus, simplified because the antiviral state may be recorded by testing cells twice (ie, before and 6 hours after application of interferon). All further tests may be performed in vitro. Multiple administrations of reqIFN-beta 1 do not prolong duration of the protective phases after each administration. Duration of the antiviral state depends only on the dose of reqIFN-beta 1.