Understanding pseudorabies in pigs leads to prevention

Pseudorabies (PRV, Aujeszky's disease) is a severe, infectious herpes virus disease affecting swine of all ages.

Prevention is always more profitable than treatment, especially for diseases that are difficult to treat. | Dusan Petkovic, istockphoto.com
Prevention is always more profitable than treatment, especially for diseases that are difficult to treat. | Dusan Petkovic, istockphoto.com

Pseudorabies (PRV, Aujeszky's disease) is a severe, infectious herpes virus disease affecting swine of all ages. Humans are resistant, but cats, dogs, sheep, cattle, horses, monkeys, rats and raccoons are susceptible. The acute epizootic form of the PRV primarily occurs in näive pig herds without previous exposure or immunity. 

Signs of the acute form are abortion, stillbirths, mummifications and infertility in sows; diarrhea, high fever and central nervous system CNS signs (tremors and convulsions) in piglets; and coughing and sneezing in older swine. The death rate in suckling pigs can approach 100 percent, but is typically less than 10 percent in weaned pigs and low (less than 2 percent) in older pigs (if no complications). Some high virulence strains can cause sow mortality, and in growing-finishing pigs, mortality with CNS signs and severe pneumonia, while some low virulence strains may not cause any noticeable disease whatsoever.

Chronic PRV in pigs

Chronic enzootic PRV is a pneumonia and cough in growing-finishing pigs. Pigs under continuous-flow management become infected at about 10 to 12 weeks of age as the long-lasting maternal antibody levels fall and the virus begins to move pig to pig. The grow-finish system becomes a pseudorabies virus factory, and the virus attacks the upper and lower respiratory tract. Secondary infections with Strep, Pasteurella, Actinobacillus and Mycoplasma are common. PRV is intensified by PCV-2, PRRS and CSF. 

Learn more about how to prevent PRV: Improving the pig's environment

How PRV is spread

PRV is spread by contaminated trucks and infected breeding animals. It exists in nasal and oral secretions and semen, but it is absent from feces and urine. PRV is spread by contact with infected pigs or contaminated surfaces but can spread within the air space of a pig barn. Cold weather tends to preserve PRV, and it can spread from farm to farm over a distance of 3 km in cool, moist air. PRV virus is destroyed in less than one week in warm weather, and it is killed on clean surfaces by most common swine farm disinfectants, except for iodines.   

Necropsy findings

Lesions at necropsy are not especially diagnostic for PRV other than the occasionally observed white necrotic foci in the liver and spleen of piglets that have died from PRV. Tonsillar necrosis may be observed. The nasal cavity may be severely inflamed and reddened or hemorrhagic to fibrinonecrotic.  There is interstitial pneumonia with interlobular edema that may be superimposed on an anteriorventral bacterial pneumonia. Small blotches of hemorrhage and necrosis may be seen on lungs. Histopathology reveals a non-suppurative to mixed-cell meningoencephalitis. Perivascular cuffing and gliosis are common. There may be focal necrosis in the liver, bronchi and bronchioles, the lung parenchyma, tonsil and sometimes the gut. Sometimes, intranuclear inclusions are observed.

Differential diagnosis and confirmation

PRV can resemble PRRS, PCV-2, classical swine fever (CSF), Actinobacillus pleuropneumonia (APP), Salmonellosis, enzootic pneumonia and “shaker pig disease.” Several of these diseases often occur together, particularly APP as a sequela to PRV. PRRS and PCV2 occur predominantly in nursery pigs, while PRV troubles emerge in growing-finishing pigs, but PRRS/PCV2 continues into grow-finish while PRV is occasionally seen in nursery age pigs. Herds with chronic PRV issues may have chronic CSF as well. Diagnosis can be confirmed by PCR, histopath, immunohistochemistry, virus isolation and by serology.

Vaccination for PRV

PRV vaccination is a useful tool in PRV control, but it does not protect completely. Vaccinated pigs are indeed less likely to become infected, have reduced illness and mortality rates, and shed much less virus than unvaccinated pigs. Emerging new “hot” Chinese strains of PRV are often blamed for vaccine failures, but variation in virulence has always been a feature of PRV. New type-specific vaccines are being produced, but the old Bartha K-61 vaccine still performs well when there are no complicating disease issues. All vaccines fail in heavy virus exposure and influential complicating and immunosuppressive factors. 

Vaccination of pigs is often not satisfyingly effective in controlling pig to pig transfers, but the vaccination of sows strongly inhibits sow to sow and sow to pig transmission. Modified live PRV vaccines generally produce better primary immunity and can be used intranasally, while killed PRV vaccines produce better booster effects.  

Gene deletion and DIVA vaccines

Vaccines with deletion in the gE (gI) locus attentuate the virus and permit differentiation of infected and vaccinated animals by a gE ELISA test. Common deletions include gC, gE, gG and TK. DIVA tests for gC (gIII) and gG (gX) deletions exist but are seldom used.

PRV control and elimination

Early PRV eradication focused on “stamping out” (forced depopulation) of infected herds, but it was slow and costly and failed because there were no changes in management practices; many depop/repop herds became reinfected. In elimination programs over the past 30 years, PRV is “walked off the farm” by invoking good biomanagement practices. PRV can be eliminated by exposure control via all-in/all-out management and timely vaccinations.  Exposure control by all-in/all-out management is the key, regardless of the virus strain. The advent of gene-deleted vaccines greatly aids the process.

Determine herd status. Find out what is the PRV status of the herd and where and when in production the infection is occurring. If gene-deleted DIVA vaccine is used in the piglets, one can discover the age at which pigs become infected and adjust vaccination and management accordingly. If sows are infected, piglets will carry the maternal antibody to gE (wild virus) for up to 15-16 weeks of age, but the maternal antibody is protective for only 7 to 9 weeks. Clean pigs can be produced from infected but vaccinated sows.

Adjust vaccination schedule. Typically, an intramuscular MLV vaccine is given at 7 to 9 weeks of age. Earlier intramuscular vaccination fails due to maternal antibody interference.   Intranasal MLV vaccination bypasses maternal Ab, and it is common practice in China to give intranasal vaccination to pigs at birth, but the immunity obtained is limited and short-lived. Intranasal vaccination is better done at weaning, but generally is not necessary unless a difficult PRV problem exists in the nursery. Sows should be mass-vaccinated every 3 to 4 months. Killed vaccine does effectively booster sow immunity, but MLV vaccination of sows can succeed. Mass vaccinate sows every 3 to 4 months, and the pseudorabies virus will cease to circulate in the sow herd — and a PRV-negative pig is weaned.

Control concurrent diseases. Diagnosis of herd problems should be done and efforts made to control major concurrent problems. Pigs with chronic PRRS and PCV2 fed suboptimal diets in poorly ventilated barns are not able to resist PRV, no matter how frequently they are revaccinated.

All-in/all-out management. PRV-negative pigs vaccinated and managed in an all-in/all-out system will remain negative. Exposure control is essential. The grow-finish virus factory must be shut down. Pigs should be in groups with not more than 2 week age intervals within each room or air space. Before a new batch of pigs is introduced, rooms are completely emptied, cleaned with an alkaline detergent and disinfected with a strong disinfectant. This system can produce PRV-negative gilts if all-in/all-out principles are not violated. All-in/all-out by grow-finish site is a good plan, but all-in/all-out by air space can succeed.

Accomplishing PRV elimination

Only gE-negative gilts and boars are fit for replacements. Incoming breeding animals must be tested negative for PRV gE before transport and tested again at the destination farm while still in their mandatory 60 day isolation. The virus does not spread among vaccinated sows even if positive, and with simple biosecurity measures, a farm will become negative for PRV by natural attrition and culling of positive sows in 2 to 3 years. PRV has been eliminated as an economic threat in many pork production systems by this method, and regions and whole countries can become free of pseudorabies.

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