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Nature of the disease
Aujeszky’s disease (AJD) is a viral disease due to porcine herpesvirus-1 which belongs to the Alphaherpesvirinae subfamily, Herpesviridae family. 

The disease causes neurological troubles very similar to rabies (hence the name pseudorabies) but also reproductive and respiratory disorders. It is of greatest economic significance in pigs but can also affect a large number of mammals. 

OIE List B disease
Susceptible species
Pigs (Sus scrofa domesticus and Sus scrofa scrofa are the main host. Sporadic cases occur in cattle, sheep, goats, horses, dogs, cats, foxes and rodents. There is no transmission to humans.
AJD occurs in most European countries. The USA, Mexico, Cuba, Brazil, Venezuela, Japan, Taiwan, south east Asia. In recent years the disease has increased in incidence and severity in many intensive pig farming regions.
In the Pacific, AJD occured in New Caledonia up to 1984 and in New Zealand (North Island) and in French Polynesia (serological evidence) up to 1999, it is known to occur in Samoa, Tonga, Vanuatu, Wallis and Futuna and among wild pigs in Papua New Guinea. It has never been reported from Australia. 
Clinical signs (see pictures)
In pigs, AJD usually spreads rapidly through newly infected herds. Clinical signs are most likely to be seen in newborn piglets and breeding sows. Most severe disease occurs in young pigs.


Piglets < 2 weeks old, prostration, death within hours. 

Older piglets show:

  • Fever,
  • Loss of appetite, and depression,
  • Vomiting,
  • Respiratory difficulty,
  • Central nervous system signs — incoordination, ‘goose-stepping’ gait, drowsiness, muscular twitching, convulsions, involuntary eye movements, paralysis
  • Mortality rate 20–100%

Weaner pigs show signs as above, with respiratory signs (coughing, sneezing, laboured breathing, conjunctivitis) more prominent. Mortality rate is 5–10%

Grower and finisher pigs show respiratory disease which may be mild but spreads rapidly. Mortality low (1–2%)

Adult pigs:

  • Disease often mild or inapparent
  • In pregnant sows may see abortion, mummified foetuses, still births, and weak trembling piglets

Cattle and sheep 

  • Disease is almost invariably fatal.
  • Intense itchiness of localised area of skin
  • Licking, rubbing, self -mutilation
  • Incoordination
  • Prostration and weakness
  • Clonic convulsions, teeth grinding,
  • Rapid shallow breathing and cardiac irregularities
  • Death in about 2 days after onset of clinical signs

Dogs and cats 

  • Clinical signs similar to ruminants
  • Intense pruritus and self-mutilation
  • Whimpering and howling
  • Paralysis of the pharynx and intense salivation
  • Clonic convulsions
  • Death in 1-2 days
Post-mortem findings (see pictures)
At post-mortem, gross lesions often minimal or absent in pigs. There may be:
  • Purulent inflammation of the nasal lining, pharynx and tonsils
  • Congestion or consolidation of the lungs
  • Congested meninges
  • Congested lymph nodes with small haemorrhages
  • Small white to yellow necrotic foci in liver and spleen of affected animals and aborted foetuses
  • Necrotic placentitis

In other species often the only lesions are oedema, congestion and haemorrhage of the spinal cord.

Differential diagnosis 
  • Porcine polioencephalomyelitis (Teschen)
  • Rabies
  • Classical swine fever and African Swine Fever
  • Haemagglutinating encephalomyelitis virus infection
  • Erysipela
  • Nipah virus
  • Streptococcal meningoencephalitis
  • Hypoglycaemia
  • Organic arsenic and mercury poisoning
  • Salt poisoning
  • Other causes of abortion — the presence of signs in young pigs should assist in differentiation
  • Swine influenza
  • Congenital tremor
Specimens required for diagnosis 
Nasal swabs from live pigs can be collected and submitted for virus isolation. Specimens must be kept in cold temperature with saline solution and antibiotics.

Tissue specimens collected at post mortem can be submitted for virus detection, using the fluorescent antibody test, isolation on kidney cells or PCR techniques (mostly used to detect latent infection). Those specimens include spinal cord, lung, spleen, liver, kidney, lymph nodes, pharyngeal mucosa and tonsil. Conservation of the samples depends on the technique used. For the fluorescent antibody test they can be fixed on formalin. For PCR and isolation fresh chilled samples and preserved samples in neutral buffered saline can be submitted.

Serological tests are more commonly used. The two tests prescibed by OIE for international trade are ELISA and Virus Neutralisation. Sera should be collected from convalescent and recovered pigs.

AJD is highly contagious and is principally spread via the respiratory route. Infection within herds is rapid but may be slow between herds.

Oral and nasal secretions are a potent source of virus and direct contact between infected and susceptible pigs are the most important methods of spread. Most outbreaks result from introduction of infected pigs into susceptible herds. Latently-infected pigs are especially important in this context. Other methods include:

  • Via semen, vaginal secretions and transplacental infection
  • Via colostrum or milk
  • Via contaminated veterinary equipment e.g. needles and syringes
  • Virus can survive up to 5 weeks in pig meat — dogs fed meat from viraemic pigs become infected and die. Pigs have been reported to become infected through ingestion as well, although a higher dose of virus is required than by the respiratory route.
  • Wind-borne spread from farm to farm can occur under favourable conditions (described in England as up to 2 km)
  • The virus can resist weeks in anaerobic lagoon effluent, green grass, faeces and straw bedding. Thus environmental transmission from one herd to the other should be considered, specially in places where waste is not correctly drained nor treated.
  • The role of insect vectors is under investigation, rats could play a role of reservoir. The role of wild pigs in the Pacific region as reservoir should be explored.
Risk of introduction   
Movement of live pigs is considered the most likely method of introducing the disease. Risk analyisis should be conducted prior to importation of live pigs and semen and quarantine should carrefully monitor pigs and pig products trade.

NB several Pacific island countries (e.g. Tonga, Samoa) are already infected so inter-island movements are important to survey to limit the spread of the disease.

Control / vaccines  
Attenuated, inactivated (PRV) and gene-deleted vaccines have been developed. Vaccines protect pigs from clinical disease, reduce the amount and duration of virus excretion, but do not prevent latent infections. Virus can still be transmitted from vaccinated animals to susceptible contacts. 

For the control and elimination of the disease, several strategies have been described. The choice of the strategy should take into account the level of prevalence of the disease, its source and identified ways of transmission, the value of the genetic material and the possibilities to replace the breeding stock and the technical level of management:
  • Depopulation and repopulation: an effective and drastic method but very expensive and will result in the loss of all selected animals. Repopulation should be carried out 30 days after depopulation and screening should be organised 30 days after reintroduction.
  • Test and Removal: it is recommended when the prevalence is below 20%. The breeding herd is tested every month and positives are removed. Once two tests are consecutively negative, future tests can be at intervals of 4 months. When the prevalence is higher than 20% but lower than 50%, this method can be combined with vaccination of breeding herd using a killed vaccine on three occasions at six-month intervals.
  • Offspring segregation: the method requires two premises, one to accommodate the infected pigs and one to hold those free of disease. Breeding herds are vaccinated and selected offspring are removed at weaning (e.g. 4 weeks) and reared in the clean herd. They are then tested at 4 months old and all positives are removed. Tests are done every months and segregation is maintained until all positive gilts have been removed. The old herd is then progressively depopulated, the premises are disinfected, and repopulated after being empty for one month.
  • Other strategies consisting of combination of the above can be implemented to address specific situations.
  • GEERING WA, FORMAN AJ, NUNN MJ, Exotic Diseases of Animals, Aust Gov Publishing Service, Canberra, 1995, 440p
  • Office International des Epizooties, 2002
  • Pseudorabies, In Merck Veterinary Manual, National Publishing Inc. Eight ed, 1998, Philadelphia, p 964-966
  • Pseudorabies, In Veterinary Medicine, Saunders, Eight ed, 1997, London p. 1094-1103