Aujeszky's disease

Both domestic pigs and wild swine are the only natural reservoir hosts of Aujeszky’s disease virus (ADV) and able to survive a productive infection. It remains unexplained whether other members of the artiodactyl suborder Suina are susceptible to ADV. The virus can infect a wide range of other mammals, in particular animals in close contact with pigs such as sheep, cattle, goats cats and dogs. In those species the disease caused is nearly always fatal, but the virus is rarely shed and transmitted from such animals. Reports of horses contracting ADV are very rare (Mettenleiter et al., 2012).

Aujeszky’s disease (AD) is spread in domestic or wild swine and has an almost worldwide distribution, particularly in regions with high population densities of domestic swine. There are only a few regions where the disease has never been endemic in the domestic pig population, such as Norway, Australia, and most of the Southeast Asian islands. In recent years, strict implementation of national eradication programmes has resulted in virtual disappearance of the infection from domestic pigs in several parts of the world, e.g. Europe, North America and New Zealand.

The current dimension of the regional occurrence of AD in eastern and southeastern Europe, Latin America, Africa, and Asia is difficult to assess as information from those countries is often fragmentary, incomplete or even lacking. Recently, severe clinical outbreaks with high morbidity and lethality have been reported from China.

The distribution in the summary table is mainly based on information available from OIE or the European Union (EU). For current information on disease incidence, see OIE's WAHID database.

The following is partly taken from:
Mettenleiter TC, Ehlers B, Müller T, Yoon K-J, Teifke JP, 2012. Herpesviruses. In: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, eds. Diseases of Swine, 10th edition. Chichester, UK: John Wiley & Sons, 412-446.

Clinical diagnosis

The presence and severity of clinical signs, as well as morbidity and mortality, depend on the age and immunological status of the pig. Furthermore, the route of infection and the virulence of the Aujeszky's disease virus (ADV) strain are important factors. In general, clinical signs manifest as neurological signs in young (sucking and weaned) and respiratory signs in older pigs. The disease is therefore more easily diagnosed in herds with both weaning or sucking and older pigs. Sow aborting is often one of the earlier signs of a herd being affected.

ADV infections in fully susceptible swine result in high morbidity and mortality, especially in juvenile animals in which meningoencephalitis and viremia-associated signs predominate. In neonatal pigs less than 7 days of age, the disease may be characterized by sudden death with few, if any, clinical signs. In 2- to 3-week-old piglets, severe signs of central nervous system (CNS) involvement, for example, trembling, incoordination, nystagmus, oposthotonos, epileptiform-like seizures, convulsion, tremor, ataxia, and paralysis, are seen with mortality up to 100%. Suckling pigs with neurological signs usually die within 24-36 h of onset of disease.

Older animals (3-6 weeks of age) may show neurological signs, but usually develop age-dependent resistance. Mortality may decrease to 50% by the fourth week of age and to less than 5% in 5-month-old pigs and even lower as the age of the infected pigs increases. Clinical signs can be present for 6-10 days. Animals may recover within a few days, but lose weight over the course of the disease. In finishing and fattening pigs, because of the population density, clinical signs can amplify and animals often die from secondary bacterial pneumonia. Signs in gilts and sows depend on the phase of gestation and include embryonic death, resorption of fetuses, mummified fetuses, abortion, or stillbirth, in addition to respiratory signs and fever. Pigs surviving a ADV infection become latently infected.

In the case of coinfections with other swine viruses, for example, porcine reproductive and respiratory syndrome virus (PRRSV), porcine circovirus type 2 (PCV2), and swine influenza virus (SIV), a severe and often fatal proliferative and necrotizing pneumonia (PNP) may develop in weaning and postweaning pigs.

Laboratory diagnosis

Rapid detection of viral infection is essential for the effective control of AD. Clinical observations are only sufficient to lead to a suspicion of AD because the infection produces no pathognomonic clinical signs or gross post-mortem lesions in swine. Therefore, laboratory confirmation is required.

Viral antigen can be detected using immunoperoxidase and/or immunofluorescence staining with polyclonal or mAbs on impression smears and cryosections of tissues, for example, brain, lungs, and tonsils. Diagnosis is confirmed by virus isolation in conventional cell cultures requiring about 2-5 days. In the absence of any obvious CPE, blind passages should be performed. ADV can be isolated from secretions and excretions and from tissues, for example, brain, tonsils, lungs, and spleen, of infected animals. In latently infected pigs, the trigeminal ganglion and tonsils are the most consistent sites for virus isolation. As there is no CPE characteristic of ADV, and CPE may vary with the prevailing ADV strain and the cell line used, virus identity is confirmed by immunofluorescence, immunoperoxidase, or neutralization assays using specific antisera or mAbs.

Viral DNA can be detected by direct filter hybridization, DNA hybridization dotblot assay, ADV-specific PCR, nested and real-time quantitative PCR (qPCR) assays with the latter ones being the method of choice for detection of ADV in secretions or organ samples under routine conditions. Several conventional PCRs targeting genes encoding gB, gC, gD, or gE have been established, but there is as yet no internationally agreed upon standard.

According to OIE for routine testing, the virus neutralization (VN) test and ELISAs are standard reference serological test to detect ADV specific antibodies. Robust and sensitive indirect or competitive ELISAs detect antibodies against the complete ADV or against distinct viral antigens. The latex agglutination test (LAT) and immunoblotting are alternatives. VN and LAT are highly reliable but cannot differentiate between antibodies resulting from natural infection or vaccination. The development of ELISAs able to detect serum antibodies against gE (or gC or gG) allowed for the differentiation of infection from vaccination and led to the “marker” or differentiating infected from vaccinated animal (DIVA) concept. These ELISAs became a key part of AD eradication programs.

For more information on diagnostic tests for international trade purposes see the relevant chapter in the World Organisation for Animals Health’s (OIE) ‘Manual of Diagnostic Tests and Vaccines for Terrestrial Animals’ (www.oie.int).

Measures to prevent infection of a herd in an area where the disease is endemic include isolation of domestic pigs from ADV infected feral pigs or wild boar, prevention of entry onto the premises of contaminated fomites, and potentially infected people and animals.

Modern eradication programmes involve measures such as use of vaccines, removal of latently infected animals, and quarantine. The use of blanket vaccination with inactivated (particularly in breeding animals) and modified live virus vaccines (in finishers) to control of disease, but not infection is no longer practised.

Today, a combination of modern genetically modified live deletion (gE, gC or gG) marker vaccines against AD and differential ELISAs to discriminate between vaccinated, ADV-uninfected animals from wild-type ADV-infected animals (DIVA strategy - test and removal) is the method of choice for eliminating ADV from domestic pigs

Depopulation of infected herds can be applied in the final phase of an eradication programme to facilitate achieving an AD-free status.

For measures to be taken to determine the AD status of a country or zone, and recommendations for importation of pigs for breeding, rearing and slaughter from countries and zones with different AD statuses see chapter Chapter 8.2., Infection with Aujeszky's disease virus of the OIE Terrestrial Animal Health Code (http://www.oie.int/fileadmin/Home/eng/Health_standards/tahc/2010/en_chapitre_aujeszky.htm).