Pseudorabies is an acute, often fatal viral disease with a worldwide distribution. Swine are the primary host; however, other species (cattle, sheep, goats, cats, and dogs) are incidental hosts. Clinical signs in pigs include reproductive failure in sows, CNS signs in newborn pigs, and respiratory signs in growing pigs. The diagnosis is suspected on the basis of clinical signs and confirmed by virus identification (PCR assay, virus isolation) and/or serological testing (ELISA). No specific treatment exists for the disease in pigs or the incidental hosts. Highly effective vaccines are available and prevent disease in swine. Pseudorabies is reportable and has been successfully eradicated from commercial swine in the US.
Pseudorabies is an acute, frequently fatal disease with a worldwide distribution that affects swine primarily and other domestic and wild animals incidentally. The virus that causes pseudorabies, Varicellovirus suidalpha1, has reemerged as an important foreign animal disease pathogen in the US because of the emergence of highly virulent strains in China.
Clinical signs in pigs include reproductive failure in pregnant sows and CNS and respiratory signs in growing pigs. Pseudorabies is a reportable disease and has been successfully eradicated from commercial swine in the US but is still present in wild pigs.
Etiology of Pseudorabies in Pigs
Varicellovirus suidalpha1 (formerly pseudorabies virus) is a member of the herpesvirus family, subfamily alphaherpesvirus, also referred to as Suid alphaherpesvirus 1. As such, the virus has a propensity to infect cells of the CNS. Swine (including wild boars and domestic pigs) are the primary natural hosts; however, the virus can infect cattle, sheep, goats, cats, and dogs, as well as wildlife, including raccoons, opossums, skunks, and rodents (1). Reports of human and equine infection have been described but are extremely rare.
Only one serotype of V suidalpha1 is recognized, but two distinct genotypes have been described. The genotype I strain is mainly prevalent in Europe, the US, and parts of China, whereas the majority of genotype II strains are isolated from Asia, particularly China. Genotype II has undergone mutations, presumably because of immune pressure, and evolved into novel variant strains that continue to cause problems and warrant updated vaccines.
Epidemiology of Pseudorabies in Pigs
V suidalpha1 can be transmitted via the respiratory route (saliva, nasal secretions) nose-to-nose. Other routes of transmission include fecal-oral contact, via semen, and via fomites. Indirect transmission can occur via inhalation of aerosolized virus.
Studies have demonstrated that the virus can survive for up to 7 hours in unchlorinated well water; for 2 days in anaerobic lagoon effluent and in green grass, soil, feces, and shelled corn; for 3 days in nasal washings on plastic and in pelleted hog feed; and for 4 days in straw bedding (2, 3, 4, 5). V suidalpha1 is enveloped and therefore inactivated by drying, sunlight, and high temperatures (≥ 37°C [98.6°F]) (6).
Incidental hosts typically become infected through close contact with pigs or by consuming contaminated raw porcine tissues. For susceptible animals other than pigs, infection causes acute disease characterized by severe pruritus (known as "mad itch"), and animals survive only 2–3 days after becoming infected. Horses, chickens, and nonhuman primates are largely resistant to infection. Incidental hosts, such as dogs, cats, and wildlife, can transmit the virus between farms. The levels of virus in these animals are generally relatively low; however, experimentally infected lambs have been found to shed virus in nasal secretions at levels similar to naturally infected piglets (7). Birds do not seem to play a role in transmission (8).
In addition, the virus causes endophthalmitis and encephalitis in humans (9, 10).
Clinical Findings and Pathogenesis of Pseudorabies in Pigs
Clinical signs of pseudorabies in pigs depend on the age of the affected animal. Young swine are highly susceptible, and losses can reach 100% in piglets < 7 days old. In general, CNS signs (eg, tremors and paddling) occur in affected newborn pigs. In weaned and growing pigs, respiratory disease is the primary clinical problem, especially if complicated by secondary bacterial pathogens. V suidalpha1 has been reported to inhibit the function of alveolar macrophages, thereby decreasing the ability of these cells to process and destroy bacteria.
A generalized febrile response (41–42°C [105.8–107.6°F]), anorexia, and weight loss occur in infected pigs of all ages. Mortality rates can be very low (1–2%) in growing-finishing pigs but can reach 50% in nursery pigs. Sneezing and dyspnea are frequently observed, and CNS involvement is reported occasionally. Clinical signs in nonporcine species, such as cats, dogs, cattle, and small ruminants, include sudden death, intense local pruritus, CNS signs (circling, maniacal behavior, paralysis), fever, and respiratory distress.
After natural infection in pigs, the primary site of viral replication is nasal, pharyngeal, or tonsillar epithelium. The virus spreads via the lymphatics to regional lymph nodes. Virus also spreads via nervous tissue to the brain, where it replicates, preferentially in neurons of the pons and medulla. In addition, virus has been isolated from alveolar macrophages, bronchial epithelium, spleen, lymph nodes, trophoblasts, embryos, and luteal cells.
Virus can be recovered from nasal secretions, tonsillar epithelium, vaginal and preputial secretions, milk, or urine (11). A latent state, in which virus is harbored in the trigeminal ganglia, typically exists in infected pigs. In pigs with latent infections, shedding can resume after periods of stress, such as farrowing, crowding, or transport. Experimentally, corticosteroid injections (dexamethasone, 2 mg/kg, IM) for 5 consecutive days have induced reactivation of latent virus (12).
Lesions
Gross lesions of V suidalpha1 infection are often undetectable. Serous rhinitis, necrotic tonsillitis, or hemorrhagic pulmonary lymph nodes may be visible. Pulmonary edema, as well as pneumonic lesions of secondary bacterial pathogens, may be present. Necrotic foci (2–3 mm in diameter) may be scattered throughout the liver. Such lesions are typically found in young (< 7 days old) piglets.
Microscopically, nonsuppurative meningoencephalitis is a characteristic lesion that can be present in gray and white matter. Mononuclear perivascular cuffing and neuronal necrosis may also be present. The meninges are thickened as a result of mononuclear cell infiltration. Necrotic tonsillitis with the presence of intranuclear inclusion bodies commonly occurs, as do necrotic bronchitis, bronchiolitis, and alveolitis. Focal areas of necrosis are often found in the liver, spleen, lymph nodes, and adrenal glands of macerated fetuses.
Diagnosis of Pseudorabies in Pigs
Suspected based on reproductive failure in sows and CNS signs in young piglets
Definitive diagnosis: PCR assay, ELISA
Clinical signs and a history of reproductive signs in sows, neurological signs in newborn pigs, and respiratory signs in growing-finishing pigs are important in suspected pseudorabies. Pseudorabies diagnosis requires identifying the presence of the virus in an infected animal. Detection of virus can be achieved through virus isolation in cell culture systems and most commonly through molecular tests, such as PCR assay to detect viral DNA. Brain, spleen, and lung are the organs of choice for virus detection. Nasal swabs can be used for sampling virus from acutely infected animals.
Serological tests, including serum neutralization, ELISA, and latex agglutination, are used for antibody detection. Serum neutralization requires 48 hours to complete. ELISA, the most commonly used test and the fastest, is valuable as a screening assay for large volumes of sera and in differentiating infected from vaccinated animals.After infection, antibodies can first be detected within 6–8 days (13).
Pearls & Pitfalls
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A differential ELISA has been used to differentiate antibodies produced as a result of vaccination from those produced as a result of natural infection. The vaccines used for pseudorabies are based on the deletion of certain genes (gE, TK, and others) from the vaccine virus. Pigs vaccinated with a gene-deleted vaccine do not mount an antibody response to the viral protein deleted from the marker vaccine. Both infected and vaccinated pigs develop antibody responses to the essential structural viral protein gB. Using the ELISA for the two corresponding viral proteins provides a differentiation of infected from vaccinated animals (DIVA). Using the marker vaccine and corresponding ELISA-based testing, the eradication strategy was successful in commercial swine in the US and other countries.
Colostral antibodies against V suidalpha1 may be present until pigs are approximately 4 months old. Therefore, paired samples or serological profiles may be necessary in growing-finishing pigs to assess decreasing levels of maternal antibody and to ensure that pigs are vaccinated at the appropriate time.
Treatment and Control of Pseudorabies in Pigs
No specific treatment
Highly effective vaccines for control
No specific treatment exists for acute Varicellovirus suidalpha1 infection.
Vaccination can prevent the development of clinical signs in pigs. Typically, mass vaccination of all pigs on the farm with a modified live virus vaccine is recommended. Intranasal vaccination of sows and neonatal piglets 1–7 days old, followed by IM vaccination of all other swine on the premises, has been recommended (14, 15, 16). The modified live virus replicates at the site of injection and in regional lymph nodes. Vaccine virus is shed in such low levels that mucous transmission to other animals is minimal.
In gene-deleted marker vaccines, the thymidine kinase gene has also been deleted; thus, the virus cannot infect and replicate in neurons. Quarterly vaccination is recommended in breeding herds, and finishing pigs should be vaccinated after levels of maternal antibody decrease. Regular vaccination results in excellent control of the disease. Concurrent antimicrobial therapy via feed and IM injection is recommended to control secondary bacterial pathogens.
Numerous programs have been developed for eradication of V suidalpha1. Since 2004, all 50 states in the US have been considered free of the disease in commercial pigs. The virus appears to be endemic in feral pig populations, however, and has been identified on game ranches. Isolated transmission of V suidalpha1 from feral swine to commercial pigs and to hunting dogs has occurred.
Effective strategies for eradication of pseudorabies include whole-herd depopulation, test and removal strategies, and offspring segregation, all using diagnostic testing in tandem. Although effective, whole-herd depopulation is costly and time-consuming. Usually, problems other than V suidalpha1 (eg, genetic improvement) need to be resolved before whole-herd depopulation can be cost-effective.
Key Points
Pseudorabies is a reportable, potentially zoonotic disease caused by an alphaherpesvirus.
The commercial pig industry in the US is free of the virus; however, pseudorabies remains a problem for the global swine industry.
Vaccination using marker vaccines is effective in decreasing disease and in cleanup/eradication programs.
As V suidalpha1 evolves, vaccines must follow suit in order to remain protective.
Differential ELISA testing can be used as a screening test to differentiate antibodies produced as a result of vaccination from those produced as a result of natural infection.
For More Information
Pseudorabies. USDA Animal and Plant Health Inspection Service. Updated July 30, 2025. Accessed August 21, 2025.
Zheng HH, Fu PF, Chen HY, Wang ZY. Pseudorabies virus: from pathogenesis to prevention strategies. Viruses. 2022;14(8):1638.
References
Liu A, Xue T, Zhao X, et al. Pseudorabies virus associations in wild animals: review of potential reservoirs for cross-host transmission. Viruses. 2022;14(10):2254. doi:10.3390/v14102254
Trainer DO, Karstad L. Experimental pseudorabies in some wild North American mammals. Zoonoses Res. 1963;2:135-151.
Wittman G, Rziha HJ. Aujeszky’s disease (pseudorabies) in pigs. In: Wittman G, ed. Herpesvirus Diseases of Cattle, Horses, and Pigs. Kluwer Academic Publishers. 1989; 163-175.
Lomniczi B. Aujeszky’s disease (pseudorabies) in laboratory and captive animals. In: Darai G, ed. Virus Diseases in Laboratory and Captive Animals. Developments in Veterinary Virology; vol 6. Springer; 1988:205-218. doi:10.1007/978-1-4613-2091-3_12.
Medveczky I, Kovacs L, Kovacs Sz F, Papp L. The role of the housefly, Musca domestica, in the spread of Aujeszky’s disease (pseudorabies). Med Vet Entomol. 1988;2(1)81-86. doi:10.1111/j.1365-2915.1988.tb00052.x
Gong L, Deng Q, Xu R, Ji C, Wang H, Zhang G. Effects of physical and chemical factors on pseudorabies virus activity in vitro. BMC Vet Res. 2020;16(1):358. doi:10.1186/s12917-020-02573-3
He W, Auclert LZ, Zhai X, et al. Interspecies transmission, genetic diversity, and evolutionary dynamics of pseudorabies virus. J Infect Dis. 2019;219(11):1705-1715. doi:10.1093/infdis/jiy731
Mocsári E, Tóth C, Meder M, Sághy E, Glávits R. Aujeszky's disease of sheep: experimental studies on the excretion and horizontal transmission of the virus. Vet Microbiol. 1987;13(4):353-359. doi:10.1016/0378-1135(87)90066-6
Yang H, Han H, Wang H, Cui Y, Liu H, Ding S. A case of human viral encephalitis caused by pseudorabies virus infection in China. Front Neurol. 2019;10:534. doi:10.3389/fneur.2019.00534
Chen Y, Gao J, Hua R, Zhang G. Pseudorabies virus as a zoonosis: scientific and public health implications. Virus Genes. 2025;61(1):9-25. doi:10.1007/s11262-024-02122-2
Spickler AR. Aujeszky’s disease factsheet. Center for Food Security & Public Health. Updated January 2024. Accessed February 22, 2026. https://www.cfsph.iastate.edu/Factsheets/pdfs/aujeszkys_disease.pdf
Thawley DG, Solorzano RF, Johnson ME. Confirmation of pseudorabies virus infection, using virus recrudescence by dexamethasone treatment and in vitro lymphocyte stimulation. Am J Vet Res. 1984;45(5):981-983. https://pubmed.ncbi.nlm.nih.gov/6329047/
Aujeszky's Disease. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) of the World Organisation for Animal Health. 2018. https://www.woah.org/fileadmin/Home/eng/Health_standards/tahm/2.01.02_AUJESZKYS.pdf
Li S, Liu Y, Zhang Q, et al. Intranasal vaccination with gB adjuvanted by poly(I:C) induces complete protection against pseudorabies virus in swine. Vet Microbiol. 2026;314:110935. doi:10.1016/j.vetmic.2026.110935
Tizard IR. Porcine vaccines. Vaccines for Veterinarians. 2021;225-242.e1. doi:10.1016/B978-0-323-68299-2.00027-7
McCaw MB, Xu J. Protection against pseudorabies virus infection by intranasal vaccination of newborn pigs. Am J Vet Res. 1993;54(4):527-533. doi:10.2460/ajvr.1993.54.04.527
