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Pseudorabies in Pigs

(Aujeszky Disease, Mad Itch)

By

Scott A. Dee

, DVM, MS, PhD, Pipestone Veterinary Services

Last full review/revision Jan 2021 | Content last modified Jan 2021

Pseudorabies is an acute, often fatal, viral disease with a worldwide distribution. Swine are the primary host, but other species are also occasionally infected. Clinical signs include reproductive failure and CNS and respiratory signs in growing pigs. The diagnosis is suspected based on clinical signs and confirmed by serology, PCR, or viral isolation. There is no specific treatment, but highly effective vaccines are available. The disease is reportable and has been successfully eradicated from commercial swine in the USA.

Pseudorabies is an acute, frequently fatal disease with a worldwide distribution that affects swine primarily and other domestic and wild animals incidentally. The pseudorabies virus has re-emerged as a significant foreign animal disease pathogen in the USA 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 USA but is still present at low levels in wild pigs.

Etiology

Pseudorabies virus is a DNA herpesvirus. The pig is the only reservoir host, but the virus can infect cattle, sheep, cats, dogs, and goats as well as wildlife, including raccoons, opossums, skunks, and rodents. Reports of human and equine infection are rare. Only one serotype of pseudorabies virus is recognized, but strain differences have been identified, particularly in China, where a highly virulent type has been reported.

Epidemiology

Pseudorabies virus can be transmitted via nose-to-nose or fecal-oral contact. Indirect transmission commonly occurs via inhalation of aerosolized virus. Data from England indicate that virus may travel via aerosols for up to 2 km in certain weather conditions. Other studies have demonstrated that the virus can survive for up to 7 hours in nonchlorinated 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 pelleted hog feed; and for 4 days in straw bedding. The virus is enveloped and, therefore, inactivated by drying, sunlight, and high temperatures (≥37°C [98.6°F]). Dead-end hosts, such as dogs, cats, or wildlife, can transmit the virus between farms, but these animals survive only 2–3 days after becoming infected. Birds do not seem to play a role in transmission.

Clinical Findings and Pathogenesis

Clinical signs of pseudorabies virus in pigs depend on the age of the affected animal. Young swine are highly susceptible, and losses may reach 100% in piglets <7 days old. In general, signs of CNS disease (eg, tremors and paddling) are seen. If weaned pigs are infected, respiratory disease is the primary clinical problem, especially if complicated by secondary bacterial pathogens. Pseudorabies virus has been reported to inhibit the function of alveolar macrophages, thereby reducing 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 are seen in infected pigs of all ages. Mortality can be very low (1%–2%) in grower and finisher pigs but may reach 50% in nursery pigs. Sneezing and dyspnea are frequently seen, 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, the primary site of viral replication is nasal, pharyngeal, or tonsillar epithelium. The virus spreads via the lymphatics to regional lymph nodes, where replication continues. 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.

Viral excretion begins ~2–5 days after infection, and virus can be recovered from nasal secretions, tonsillar epithelium, vaginal and preputial secretions, milk, or urine for >2 weeks. A latent state, in which virus is harbored in the trigeminal ganglia, may exist. In swine with latent infections, shedding may 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 recrudescence.

Lesions

Gross lesions of pseudorabies virus infection are often undetectable. Serous rhinitis, necrotic tonsillitis, or hemorrhagic pulmonary lymph nodes may be seen. 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, as well as necrotic bronchitis, bronchiolitis, and alveolitis, are commonly seen. Focal areas of necrosis are often found in the liver, spleen, lymph nodes, and adrenal glands of macerated fetuses.

Diagnosis

  • Suspected based on reproductive failure in sows, along with high mortality and CNS signs in piglets

  • Can be confirmed by serology, PCR, and virus isolation

In addition to the gross and microscopic lesions, other diagnostic aids to identify pseudorabies virus include virus isolation, PCR fluorescent antibody testing, and serologic testing. Brain, spleen, and lung are the organs of choice for virus isolation. Nasal swabs can be used for isolation of virus from acutely infected animals. The nasal specimens must be stored and transported in cold, sterile saline with antibiotics to suppress bacterial growth. The fluorescent antibody test can be performed using tonsil or brain.

Many serologic tests are now available, including serum neutralization, ELISA, and latex agglutination. Serum neutralization, which is the standard test, requires 48 hours to complete. An ELISA has been developed as a screening assay for large volumes of sera; however, specificity may be poor. False-positive results are typically reassessed using the serum neutralization test. After infection, antibodies can be detected within 6–7 days using the latex agglutination test, within 7–8 days using the ELISA, and within 8–10 days using the serum neutralization test.

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 in swine are based on the deletion of certain genes (gI, gIII, or gX) from the vaccine virus. Swine vaccinated with a gene-deleted vaccine do not mount an antibody response to the protein coded for by the deleted gene. In contrast, infection with field virus results in antibodies against these proteins.

Colostral antibodies to pseudorabies virus may be present until pigs are 4 months old (similar to porcine parvovirus). Therefore, paired samples or serologic profiles may be necessary in grower and finisher pigs to assess decreasing levels of maternal antibody and to ensure that pigs are vaccinated at the appropriate time.

Treatment and Control

  • No specific treatment, but highly effective vaccines are available

Although there is no specific treatment for acute infection with pseudorabies virus, vaccination can alleviate clinical signs in pigs of certain ages. 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, helps reduce viral shedding and improve survival. 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 vaccines, the thymidine kinase gene has also been deleted; thus, the virus cannot infect and replicate in neurons. It is recommended that breeding herds be vaccinated quarterly and that finisher pigs be vaccinated after levels of maternal antibody decrease. Regular vaccination results in excellent control of the disease. Concurrent antibiotic therapy via feed and IM injection is recommended to control secondary bacterial pathogens.

Numerous programs have been developed for eradication of pseudorabies virus. As of 2014, all 50 states in the USA are considered free of the disease in commercial pigs; however, the virus appears to be endemic in feral pig populations and has been identified on game ranches. Effective strategies for eradication of pseudorabies include whole-herd depopulation, a test and removal strategy, and offspring segregation. Although effective, whole-herd depopulation is costly and time consuming. Usually, problems other than pseudorabies virus (eg, genetic improvement) need to be resolved before whole-herd depopulation can be cost effective.

Key Points

  • Pseudorabies virus is a reportable disease caused by a DNA virus.

  • The commercial pig industry in the USA is currently free of the virus.

  • Vaccination is very effective.

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