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The presence of the pseudorabies virus (PRV) genome in infected hosts has previously been studied by standard hybridization techniques, which showed the viral genome to be present at very low levels in infected tissues. The recently introduced polymerase chain reaction (PCR) procedure provides an alternative and rapid means of amplifying small quantities of specific DNA sequences. We applied this technique to a study of pigs infected by PRV. The sequence selected for amplification consisted of 222 base pairs lying in the gene coding for the glycoprotein gp50. We used a pair of 20-mer oligonucleotides flanking this sequence as primer and a cloned Stu-Nde fragment containing the sequence as target DNA. To avoid the tedious DNA extraction procedure we performed PCR directly on disrupted cells and detected specific amplification after 25 cycles of PCR with the thermostable Taq DNA polymerase. Amplified products were detected by gel electrophoresis directly. Nasal samples from experimentally and naturally infected pigs were tested by this PCR technique. When compared with tissue culture and serological tests, detection by gel electrophoresis of PCR amplified fragments provided excellent specificity and sensitivity. We concluded that PCR amplification will be a valuable tool for rapid diagnosis of PRV infection in pigs, taking less than 1 h to complete.

Pseudorabies virus (PRV) was isolated from 9 of 44 PRV-vaccinated seropositive sows on 5 of 11 farms. Although serum-neutralization antibody titers were 1:16 to 1:256, 28 virus isolates were obtained from tonsil, nasal, or buccal swab samples from 9 sows given 2 ml of dexamethasone/kg of body weight IM for 5 days. Pseudorabies virus was isolated from 6 of 20 sows (3 of 5 farms) given a killed-virus vaccination. Virus was obtained from 3 of 24 sows (2 of 6 farms) given modified-live virus and killed-virus vaccination. Evaluation of the 9 PRV with 5 restriction endonucleases revealed 4 PRV existing genotypes. The 9 isolated types of PRV appeared to be indistinguishable by Kpn I and BamHI restriction endonuclease analysis; however, when analyzed with Sal I, HinfI, and Pst I, isolates 7 (farm D), 8 (farm C), and 9 (farm B) had numerous differences. Isolates 1, 2, 3, and 4 (farm F) and 5 and 6 (farm G) appeared to be the same genotype when further analyzed with Pst I, HinfI, and Sal I.

An enzyme-linked immunosorbent assay was developed for the detection of Aujeszky's disease virus antigen in tissue extracts and in nasal swabs. The enzyme-linked immunosorbent assay is based on two different monoclonal antibodies with specificity for the gII glycoprotein of Aujeszky's disease virus. Viral antigen was detected in 81 of 93 tissue extracts prepared from virus-infected organs. Fifteen outbreaks of Aujeszky's disease were analyzed in this study, and they were all identified by the gII antigen enzyme-linked immunosorbent assay.

A non-suppurative encephalitis accompanied by intraneuronal intranuclear inclusions were observed in the brain from a cow that died within 10 hours of developing nervous signs. Immunogold-silver staining located Aujeszky's disease virus antigen in neuronal cytoplasm and the virus was isolated from large volumes of suspensions of nervous tissues and tonsils. Fattening pigs in adjacent buildings had high antibody titres to Aujeszky's disease virus. The methods by which the cow could have acquired infection are considered, and the significance of transient low titres of antibodies to Aujeszky's disease virus in in-contact cows is discussed.

A deterministic mathematical model of the population biology of pseudorabies in swine was used to clarify some of the basic features of the host-virus relationship and to inquire into the circumstances that promote or impede virus persistence in a single herd. When the basic reproductive rate of the infection (ie, the number of secondary infections resulting from the introduction of a single infective animal into a wholly susceptible herd) is greater than unity, the model suggests that the number of infective individuals in the herd will undergo highly damped oscillations to a final equilibrium level. The most important determinants of virus persistence are herd size and the density at which sows are maintained. There is a threshold density of susceptible individuals below which the virus will eventually be eliminated from the herd, even when specific control measures are lacking. Test and removal strategies hasten virus elimination when herd density is already below threshold, but are otherwise likely to succeed only when the removal of latent infections reduces the basic reproductive rate of the infection below unity. Vaccination strategies may also result in virus elimination, but only in relatively small herds.

Purified DNA from 45 isolates of suis herpes virus 1 (SHV1) collected between 1980 and 1987 from clinical outbreaks of Aujeszky's disease on French farms was compared by restriction fragment pattern (RFP) analysis. The BamHI generated RFPs were found to be distinguishable, confirming RFP analysis as a potential epidemiological tool. The RFP could be assigned to two established major electrophoretic types and different subtypes. The RFP analysis indicated that the majority of outbreaks were caused by ADV with a central European genome type. The heterogeneity of RFPs among PRV isolates recovered from the central nervous system, lung, and foetus was not restricted specifically to one clinical entity. Variations in the virulence of the 45 isolates studied in mice, chicks, or piglets were unrelated to the RFP subtypes. One unusual RFP has been described for one strain of low virulence.

Cloned pseudorabies virus (PRV) sequences representing over 80% of the viral genome were radiolabeled and individually hybridized to nucleic acid in the trigeminal ganglia of acutely and latently infected swine. In acutely infected animals, all cloned probes hybridized to PRV RNA and DNA. In contrast, during latency transcription was found to be limited to a selected region, corresponding to the IE gene, analogous to that of two other alpha-herpesviruses. Viral DNA was not detected in latently infected neurons by in situ hybridization.

A fully age-structured deterministic model of the population biology of a pseudorabies epizootic in a farrow-to-finish operation was used to examine the disease-related change in productivity following the initial disease episode. A strategy involving continual sow vaccination was compared with various strategies involving the vaccination of growing pigs, as well as sows. The model suggests that vaccinating growing pigs, in addition to the breeding herd, results in only a relatively small improvement in long-term productivity following a pseudorabies epizootic.

Direct immunoperoxidase labelling on impression smears of brain and pharynx was compared with virus isolation and direct immunofluorescence for the detection of Aujeszky's disease virus in experimentally-infected pigs. Immunoperoxidase labelling was as sensitive as immunofluorescence and more sensitive than virus isolation for tissue that had been stored at room temperature (approximately 20 degrees C) for up to 144 h.

The interaction between pseudorabies virus (PRV) and Pasteurella multocida was investigated to determine whether single or combined infections result in pneumonia in 6- to 7-week-old pigs. The effect of the PRV-P multocida challenge exposure on feed consumption, rate of gain, and extent of pneumonic lesions appeared dependent on the PRV dose; however, pneumonic lesions were of bacterial pneumonia. Pigs inoculated with a virulent strain of PRV plus P multocida developed severe pneumonia, whereas pigs given PRV only did not develop pneumonia. Modified-live PRV vaccine had no effect on the occurrence of pneumonia. Average daily gain was most depressed in pigs given the highest dose of virulent PRV plus P multocida.

Forty European starlings (Sturnus vulgaris) were inoculated orally with pseudorabies virus. Subsequent attempts to isolate the virus from feces, liver, lung and kidney of the birds were negative; antibody against the virus could not be detected in their serums.

On seven fattening farms and seven breeding farms, investigations were carried out to examine whether Aujeszky virus was capable of persisting in particular animal groups or units of the farm as a productive infection following a virologically verified outbreak. After an outbreak on fattening farms, virus persisted temporarily as newly arrived piglets became systematically infected. On the farms on which this could be accurately followed, virus persistence continued for at least 1 1/2 to 2 months. However, this cycle of infection was found to be interrupted on each farm within approximately three months after the outbreak, which resulted in a gradual return to a totally sensitive animal population, so that new outbreaks could occur. On the seven swine breeding farms, virus persistence in the farrowing house was examined by placing seronegative sentinel piglets with sows during the immediate post-partum period. Twelve sentinel piglets were placed in the various farrowing houses for a total period of sixty-seven weeks, during which time 172 sows farrowed. None of these piglets became seropositive during their stay on the breeding farms. The results of this study show that Aujeszky's disease virus did not persist on breeding farms and that the productive infection on fattening farms in only transient following an outbreak. Therefore, it is very likely that new outbreaks of the disease are due to reintroduction of Aujeszky's disease virus on the farm. Though the role of latent carrier animals cannot be totally disregarded, natural reactivation of latent virus is believed an exception rather than the general rule.

Airborne Aujeszky's disease virus was recovered from looseboxes containing groups of pigs infected with virus strains from England, Northern Ireland and Denmark from days 1 to 7 after infection. Pigs sampled individually excreted most airborne virus on days 2 and 3 after infection. On a 24 hour basis the maximum amount of airborne virus excreted per pig was log10 5.3 TCID50. Subclinical infection was transmitted from a clinically affected group of pigs to a seronegative group held in separate looseboxes when air was drawn through ducting connecting one box with the other. Tissues taken from pigs killed at varying times after infection showed that the main sites of virus replication were in the head and neck region. Aujeszky's disease virus was detected for up to 40 days in a range of tissues taken from pigs at the acute stage of disease and stored at -20 degrees C.

Two groups of adult boars were inoculated with a field strain of pseudorabies virus (PRV) by intranasal droplet; one group was given 5 x 10(5) median tissue culture infective doses (TCID50), and the other, 5 x 10(6) TCID50. (A third group was maintained as controls.) Ejaculates were examined twice a week for volume, sperm numbers, sperm morphology, and presence of PRV. Severe clinical disease with fever followed administration of the larger virus dose. Death (one boar), testicular degeneration, and transient elevation in spermatozoa with proximal cytoplasmic droplets were seen in different members of this group. The smaller dose resulted in seroconversion, but did not produce signs of disease. In this group, volume, sperm numbers, and sperm morphology did not decline when compared with base-line values or data of control animals. The virus was not isolated from semen. Effects of PRV infection on semen quality in boars seem to be related to the associated clinical signs of systemic disease.

Clinical and epizootiologic studies have been carried out in the course of one year on a farm with a permanent Aujeszkys disease infection as well as virologic and serologic investigations, performed seven times, with a total of 70 fattened pigs. No clinical symptoms of Aujeszky's disease have been established during the period of investigation, while the epizootiologic status have invariably spoken of the fact that the infection had a stationary course on this farm. The virus was isolated from meat and bone marrow, which posed the question of veterinary and sanitary inspection of meat obtained from such animals. The virologic results were varying by months, the peak percent values of positive animals and organs being established over the winter-spring period. Serologically, the results have agreed with the findings in the virologic studies: most significant were the variations in the months during which there was a highest percent of positively reacting animals and organs. It has been assumed that the disease was maintained in a latent form on the farm investigated, showing certain variations as to its manifestation, with no trend in terms of spontaneous recovery.

Six isolates of Suid herpesvirus 1 (SHV-1) collected from clinical outbreaks of Aujeszky's disease (AD) in Jutland in January-February, 1985, were compared by restriction fragment pattern (RFP) analyses with older SHV-1 isolates from Jutland as well as with SHV-1 isolates from different parts of West Germany and Ireland. The RFP analysis indicated that the outbreaks were caused by SHV-1 isolates introduced from abroad.

The K strain of Aujeszky's disease virus (ADV) grown in Vero cells was used to vaccinate pigs. Following intramuscular inoculation, the pigs remained healthy, no vaccine virus was excreted and virus could be detected only at the inoculation site. One inoculation gave good protection against challenge with a virulent strain of ADV, and the amount of virulent ADV excreted was geatly curtailed. Following vaccination only low leads of serum neutralizing antibody were detected (geometric mean titre 1/2), but three weeks after challenge very high levels were found (GMT 1/1773). Intranasal vaccination gave similar results. There was minimal excretion of vaccine virus. The clinical reaction on challenge was less severe than in the intramuscularly challenged group, although lower antibody levels were detected three wekks following challenge (GMT 1/483). A field trial, using this strain given subcutaneously, indicated that one inoculation of this vaccine is effective.

Serum samples were collected from 42 raccoons trapped in a pseudorabies enzootic area of Missouri. All samples were negative for neutralizing antibodies to pseudorabies virus (PRV). Raccoons were orally exposed with one of four dose levels of PRV. The raccoons were found to be susceptible to moderately large doses of PRV tissue culture infective dose (10(4) - 10(5) TCID50). All raccoons given 10(3) TCID50 of PRV survived and did not develop clinical signs. The PRV was consistently isolated from tonsillar swabs collected from raccoons that died after exposure. The PRV was also isolated from the brain, tonsils, lungs, and salivary glands of raccoons that died. It was isolated from samples of the brain and tonsils collected from a raccoon 5 days after death. Neutralizing antibodies to PRV could not be detected in the serum of raccoons that survived PRV exposure. Tonsillar swabs and tissue samples collected from these raccoons were free of PRV. The results indicated that the raccoon may serve as a short-term reservoir for PRV, but it is unlikely to have an ipizootiologic role as a long-term, subclinical carrier of the virus.

Latency of pseudorabies virus (PRV) was established in 8 of 9 pigs born to 2 vaccinated sows. Pigs had high, low, or no maternal antibody titers at the time of the initial inoculation. At postinoculation months 3 to 4, latent PRV could be reactivated in vivo by the administration of large doses of corticosteroids. In most pigs, the stress-simulating treatment resulted in recrudescence of virus shedding after lag periods of 4 to 11 days. In 3 pigs, virus shedding was without clinical signs of disease, whereas clinical signs that developed in 4 pigs appeared to be due to the corticosteroid treatment, rather than to the reactivation of PRV. Pigs with a log10 neutralizing antibody titer of less than or equal to 2.55 at the onset of corticosteroid treatment had a booster response. Reactivated PRV spread to sentinel pigs housed with the inoculated pigs. Reactivation of PRV was also demonstrated in vitro. Explant cultures of trigeminal ganglia from pigs killed between postinoculation months 4 to 5 produced infectious virus. Restriction endonuclease analysis indicated that the reactivated PRV was indistinguishable from virus isolated shortly after the primary infection. Seemingly, pigs with maternal antibodies can become latently infected and therefore may be regarded as potential sources of dissemination of PRV.

A latent pseudorabies virus infection was established in pigs despite vaccination with a modified-live pseudorabies virus vaccine. Although the vaccinated pigs developed high concentrations of antibody, virus was recovered from the tonsils and lungs of pigs treated with dexamethasone three months after inoculation with virulent virus. These results may explain why vaccination programs have failed to eliminate the persistence and spread of virulent pseudorabies virus in infected herds.

Genomic sequences of pseudorabies virus, a porcine herpesvirus, were amplified by the polymerase chain reaction from cells of infected cultures, nasal cells and organs from acutely diseased as well as from organs of latently infected pigs.

All of the eight 5-day-old pigs orally given pseudorabies (Aujeszky's disease) virus developed tonsillitis. The initial changes occurred in the subepithelial area between the lymphoid nodule and the crypt epithelium, showing a characteristic pattern of necrosis. The necrosis became more severe and gained access into the lymphoid nodule and crypt epithelium. Coincident with the histopathologic changes, numerous specific immunofluorescences were detected, first in the nucleus and in some parts of the cytoplasm of cells distributed in the subepithelial area. The fluorescence subsequently spread into adjacent lymphoid nodules and crypt epithelial cells. Ultrastructurally, many enveloped virus particles were detected in the center of the necrosis. Thereafter, the crypt epithelial cells also underwent degeneration, and a small number of virus particles were detected in the nucleus of the degenerating epithelial cells. In the more advanced stage, the enveloped virus particles were discharged into the crypt lumen.

An attempt was made on a swine-breeding complex, where the virus of Aujeski's disease was demonstrated to interrupt the inapparent epizootic process of the disease. The persistence of the virus on the complex was demonstrated via virologic investigations of organs of pigs with respiratory symptoms and studies of sera of various groups of animals. A batch of pigs was divided into three groups of which one was left untreated, one was vaccinated at the time of weaning, and one was vaccinated at the age of 14 days, using as many as 10 vaccinal doses with one dose of a live vaccine being used at the moment of weaning. During fattening the pigs were kept in isolation and under clinical observation with the study of organs and sera. Wild virus was demonstrated only in the group of twice vaccinated pigs. It was established that the manifold vaccinations of sucking pigs on farms that were enzootic in terms of Aujeszky's disease, using a live vaccines, with the isolation of the animals right after weaning could contribute to the interruption of the inapparent epizootic process.

Pharyngeal swab samples were collected at a central Iowa abattoir from 6,010 market-weight slaughter hogs from September 1, 1979 to August 31, 1980. The swab samples were examined for cytopathic viruses by inoculation of monolayer cultures of continuous line of swine testicular cells. Of the 6,010 swab samples tested, transmissible gastroenteritis virus was isolated from 91 (1,51%), pseudorabies virus was isolated from 431 (7.17%), and porcine enterovirus was isolated from 21 (0.35%). Although all 3 viruses were identified throughout the year, transmissible gastroenteritis and pseudorabies viruses were found more frequently during the winter and early spring. In contrast, porcine enterovirus was detected more frequently during the spring and summer.

Two pseudorabies virus (PRV) poly(A)+ RNAs, 2.0 and 0.95 kilobases, were detected in the trigeminal ganglia of latently infected pigs. These RNAs were partially colinear at the 3' end. They were located in the BamHI J fragment (0.706 to 0.737 map units), 3' of the PRV immediate-early gene. A potential polyadenylation signal was also identified in BamHI-J. The direction of transcription of the latency-associated RNAs was antiparallel (i.e., opposite in polarity) to that of the PRV immediate-early mRNA.

A 2-year-old sow with a relatively low virus-neutralization (VN) titer (1:8) against pseudorabies virus (PRV) was brought to the National Animal Disease Center for observation and study. The sow was kept in isolation for approximately 6 weeks, and repeated nasal and tonsillar swabs for virus isolation and blood samples for VN tests were obtained during this interval. At the end of 5 weeks' observation, the sow was injected IM with 200 mg of dexamethasone and was euthanatized 1 week later. Parts of the two trigeminal ganglia, tonsillar tissue, and nasal secretions were cultured in porcine kidney cells. The rest of the trigeminal ganglia was extracted with phenol and tested for presence of the PRV-DNA genome by hybridization with tritiated complementary RNA. The PRV was isolated from the trigeminal ganglia only, and the PRV genome was demonstrated in the same tissue. This latently infected sow was a potential shedder of PRV.

The spread of antibody to Aujeszky's disease virus through a susceptible pig herd was monitored after the probable introduction of infection by a recently purchased boar. The infection spread slowly through the herd but no clinical signs of Aujeszky's disease were seen. The strain of virus isolated was designated NIA-6. It has been characterised by a series of experimental infections and extends the known range of virulence of isolates of Aujeszky's disease virus made in Northern Ireland. The strain caused no disease in four-week-old piglets and is therefore less virulent than other isolates from Northern Ireland pigs. However, it killed rabbits and a proportion of experimentally infected two-week-old piglets, which differentiates it from the avirulent bovine isolate (NIA-4).

Three strains of pseudorabies virus were intranasally inoculated into 10-week-old pigs and the pathogenesis of the infection was compared. Virulent NIA-3 virus caused widespread necrotic lesions in nasal mucosa, rapidly invading the stroma and infecting axons of olfactory nerves within 24 h of inoculation. Intermediate virulent virus 2.4N3A, a mutant strain derived from NIA-3, caused less necrosis of the mucosa and did not reach axons of olfactory nerves until 72 h after inoculation. Bartha virus strain K, a non-virulent virus strain, caused a mild infection in the superficial layers of nasal epithelium. Viral antigens were not detected in stromal fibroblasts or nerve cells. The inflammatory response of the pigs varied with the virus strains used: after infection with NIA-3 virus mainly neutrophils infiltrated the nasal mucosa, whereas after infection with 2.4N3A virus and Bartha virus, mainly macrophages and lymphocytes infiltrated the nasal mucosa.

This study was designed to determine the effects of experimental inoculation with pseudorabies virus on the reproductive tracts of young adult boars. Pseudorabies virus was inoculated intranasally into 12 boars and intrapreputially into four boars. All animals seroconverted after nasal or preputial inoculation. Semen abnormalities were observed 21 days postinoculation with partial recovery by 50 days postinoculation. Virus was isolated from the preputial sheath of two intrapreputially inoculated boars 12 days postinoculation. It was concluded that pseudorabies virus infection can be established via preputial inoculation and that decreased spermatogenesis and infertility can result.

Pseudorabies virus-induced cell fusion in rabbit kidney cells can be prevented by Concanavalin A added early after infection. The infected cells are not agglutinated and the infectivity of cell-free virus is not reduced. Sera from productively infected animals also inhibit polykaryocytosis, whereas a hyperimmune serum directed against virus structural components has no effect. 2-Deoxy-d-glucose reversibly disturbs virus-induced fusion and reduces significantly the virus infectivity.

The occurrence of the pseudorabies virus (PRV, herpes suis 1) genome in various neural tissues of latently infected pigs was investigated. During the latent phase of infection, between 7 and 52 weeks p.i., the average amount of PRV DNA ranged between 0.3 and 0.05 genome copies per cell. The results obtained by in situ cytohybridization and reassociation kinetic experiments indicated that each latently infected cell harbored at least 30 viral genome copies. PRV DNA could be demonstrated in similar frequencies (about 30% of cases) in the trigeminal ganglia, the olfactory bulb, and the medulla oblongata, and less frequently in the brain stem and the spinal cord. Southern blot analysis showed that in general the physical state of the latent genome was linear and nonintegrated. Only in 2 of 15 animals could the presence of circular or concatemeric viral DNA be observed. Thus, we could show that over a period of 13 months after infection the PRV genome persisted both qualitatively and quantitatively in a stable state in different areas of both the peripheral and the central nervous system.

The presence of Aujeszky's disease virus was investigated in various organs and materials from experimentally infected dogs, employing the fluorescent antibody test (FAT), tissue culture and biological tests in rabbits. The FAT appeared less sensitive for virus detection than virus isolation in cell culture and rabbit tests. The virus distribution in the central nervous system was related to the site of inoculation.

A trial was conducted to study the sensitivity of the Aujeszky disease virus, present in the blood of pigs, to the effect of two preservatives: potassium thiosulphate ( K2S2O5 ) and hydrogen chloride (HCl). The sensitivity of the virus was determined on rabbits infected with pig blood containing Aujeszky disease virus with different additions of the two preservatives. As found, 0.5% of K2S2O5 and 3% of HCl are concentrations fully sufficient for the inactivation of all the viruses present in the blood. Blood preserved in this way can be used for feeding purposes in pig stocks without the hazard of introducing Aujeszky disease in healthy stocks via the blood included in feed rations.

A DNA-hybridization dot-blot technique was developed to detect the presence of pseudorabies virus (PRV) DNA in porcine tissue. Seven 32P-nick translated probes of high specific activity were prepared from transformed Escherichia coli plasmids into which Bacillus amyloliquefaciens H (Bam HI) restriction fragments of PRV-DNA had been inserted. Samples of DNA that had been extracted from porcine tissue or from PRV grown in tissue culture were transferred to nitrocellulose paper, using a microsample filtration manifold and were hybridized to the probes under high-stringency conditions. Under optimal hybridization conditions, the minimum detection amount of PRV-DNA was 10(-11) g, which is equivalent to 1 copy of the PRV genome/80 host cells. Four probes did not show cross hybridization with DNA extracted from tissues of known PRV-negative swine, and these were subsequently used to detect PRV-DNA in infected porcine tissues. Generally, correlation between virus isolation and hybridization data was good for tissues from swine that had died of acute PRV infection. Furthermore, PRV-DNA was present in specific tissues of all 4 seropositive swine that had recovered from pseudorabies and in which no infective virus or viral products were detected at necropsy. Pseudorabies virus DNA was present in the rostralis cerebral cortex (n = 2) or in the medulla oblongata (n = 1) and trigeminal ganglion (n = 1). This probably indicated the portal of entry of the virus into the CNS. In another seropositive pig, there was evidence of a productive infection in the tonsils, although virus was not isolated in a tissue culture system.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the sites of replication and the evolution of pseudorabies virus infection in boar genital organs, 5 Belgian Landrace boars were inoculated with pseudorabies virus unilaterally in the cavum vaginale of the testis. Virus replication took place only in cells of the tunica vaginalis of both cava vaginalia. Infection of the serosa led to exudative periorchitis and increased scrotal fluid, resulting in a severely swollen scrotal region. These experimental findings were similar to findings in boars with naturally acquired pseudorabies virus infection. Scrotal fluid contained large amounts of virus, making it a useful specimen for diagnosis of the disease in affected boars.

Clinical, virological, morphological, and immunofluorescence investigations were carried out on 22 pigs experimentally infected with two strains--a virulent one (V) of a 10(-3) titer, and a slightly virulent one (K) of a 10(-7) titer--of the virus of Aujeszky's disease as well as on contact pigs. Results revealed variations in the clinical and morphological manifestation of the disease in the individual groups. They were shown to be due to the strains of the virus that varied in virulence and tissue tropism. In the strain B-infected animals there were clinical symptoms characteristic of the disease, and the morphological changes in the central nervous system were of the nonsuppurative encephalitis type. The pigs infected with the K strain of the virus showed no clinical symptoms, while the contact animals manifested only respiratory troubles as well as interstitial pneumonia. It was demonstrated that the strains of slight virulence had weak nervotropic and pronounced pneumotropic characters. Complex virologic, morphologic and immunofluorescence investigations can be used for the diagnosis of the atypical forms of Aujeszky's disease and for the differentiation of the virulent from the slightly virulent strains of the virus.