In a susceptible (unvaccinated) herd large numbers of pigs may be clinically affected and some sows may abort. Mortality in suckled piglets is high but much lower in growing pigs. Unfortunately, it can spread on the wind so standard precautions of farm biosecurity cannot be entirely relied on to keep it out. On the credit side, there is only one serotype of the virus and attenuated vaccines are highly effective.

Clinical signs

The susceptible breeding herd
The earliest sign is usually a few pregnant sows aborting. If there is a farm dog in close contact with the pigs, it may develop a severe acute nervous disease which is distressing to see and which always progresses to death. The farms cats disappear presumed dead. In newborn piglets an acute severe fatal nervous disease develops. This is first evident by rough haired listless appearances. They stop sucking and within 24 hours, tremble, become incoordinated, salivate excessively and go into convulsions, rolling their eyes forward and backward. They often emit a high pitched squeal.

Affected suckled piglets may show a variety of clinical signs such as walking in circles, sitting like a dog, or lying on their sides paddling their legs. Some may vomit and others may develop diarrhoea. They die within 24-36 hours of the onset of nervous signs. Mortality in piglets may be very high, approaching 100%. Subsequent litters may be born weak and/or start showing clinical signs as soon as they are born.

If there are weaned pigs on the farm, the younger most recently weaned ones develop early signs similar to, but milder than, the suckled piglets and fewer of them develop nervous signs and die. Vomiting and diarrhoea are sometimes a feature. If the virus is a pneumotropic strain, causing pneumonia as well as nervous signs, older weaned pigs start sneezing, develop a nasal discharge, breath heavily and start coughing. The virus infection tends to cause flare-ups of enzootic pneumonia caused by Mycoplasma hyopneumoniae and may trigger off secondary bacterial infections such as Pasteurella multocida and Actinobacillus pleuropneumoniae.

Affected weaned pigs run a high fever 41-42ºC (106-107ºF). Many of those that develop nervous signs and/or severe pneumonia die but the death rate is usually less then 10%. Most of the rest recover fully in 5-10 days but some may be left stunted and grow poorly.

The susceptible grower-finisher herd
The earliest signs here are usually depression, lack of appetite, staring coat and fever 41-42ºC (106-107ºF) and respiratory diseases similar to those described above for older weaners are common. Relatively few pigs develop nervous signs or they may be mild (e.g. muscle tremors). Although all, or nearly all of the growers and finishers may be affected, most recover in 5-6 days and start to grow well again when they have recovered their appetites. The mortality is usually less than 2%.

Variations on the above clinical picture
These are common partly because of variations in the virulence of different strains of the virus and partly because of the differing immune status of pigs. If the virus is a mild one a herd may seroconvert to become positive in routine serological tests without the pig attendants being aware of anything seriously wrong. All strains of the virus have an affinity for nerves. Some also tend to have a strong affinity for the respiratory tract causing severe pneumonia while others do not.

In modern pig production cattle are not usually reared in close proximity to pigs but on those farms where they are some of the cattle may become sick, develop a relentless itching and die. Farm cats may also develop nervous signs and die.

Diagnosis

Lesions on nose of piglet

In acute severe outbreaks a strong presumptive diagnosis can be made on the typical clinical signs, particularly those in newborn piglets. The diagnosis is strengthened further if dogs, cats, cattle or horses are affected. On the other hand, in milder outbreaks and in grower-finisher herds where there are no sucking piglets, diagnosis may be difficult or impossible. Furthermore, even when sucking piglets are involved this disease can easily be confused with porcine reproductive and respiratory syndrome (PRRS) which is caused by an entirely different type of virus. Both diseases cause abortions, the birth of weak and premature litters and a high piglet mortality but in PRRS there are no nervous signs in piglets and weaners. The disease in grower/finisher pigs can also be confused with influenza which results in similar clinical signs and takes a somewhat similar course.

To confirm the diagnosis you will have to resort to laboratory tests. Whole dead young piglets should be submitted if possible. If not, tonsils and smears made from the pharyngeal region on microscope slides can be submitted. See chapter 15 (Swabbing). The laboratory should be able to do a rapid fluorescent antibody test (FAT) and have the results in a matter of hours. This test is fairly reliable in sucking piglets but much less so in grower/finisher pigs and so a negative result may be false and unreliable.

In grower/finisher pigs virus isolation has to be attempted and this delays the result considerably. The best tissues to submit for this are brain, spleen and lung which should be kept chilled on ice during transport. If no dead pigs are available nasal swabs can be submitted and should be sent in transport medium containing antibiotics. Blood samples from pigs in the early stage of the disease and from recovered pigs can be tested for rising antibodies but this delays the result about two weeks.

Rhinitis in snout of pig with Pseudorabies

Virus isolation is carried out in cell cultures. The virus produces changes in the cells (cytopathic effects) and can be demonstrated by fluorescent antibody tests.

A variety of serological tests have been developed for aujeszky's virus including serum neutralisation tests, ELISAs, and latex agglutination tests. The ELISA is usually the test of choice and yields results fairly quickly. ELISA kits are commercially available and some of them are able to differentiate antibodies produced by gene deleted vaccine virus from those produced by natural infection from a wild virus.

Post-mortem lesions

Lesions on post-mortemed lung

AD damages the pig's nervous system but this damage (i.e. lesions) can only be seen through a microscope, not with the naked eye.

The only gross lesions that can be seen by the naked eye are those in the lungs and respiratory tubes and areas of necrosis on the tonsils and abdominal organs. . An untrained pig person would not be able to distinguish AD lesions from those caused by influenza, PRRS, Mycoplasma hyopneumoniae, Actinobacillus pleuropneumoniae, or Pasteurella multocida so, unless you are veterinary trained it is probably a waste of time to open up pigs suspected of having died of AD.

Treatment

• There is no treatment available specifically against the virus.
• No treatment is effective in sucking pigs.
• Antibiotics will prevent secondary infections particularly of the respiratory system and also reduce bacterial damage.

Management control and prevention

Vaccination of the herd

• In countries which are free of the AD virus, vaccination is not practised and generally is not allowed.
• In enzootic and high risk areas routine vaccination is practised and may be compulsory as part of an eradication scheme. The great break-through in vaccination was the development of gene-deleted attenuated-virus marker vaccines. In these a small part of the genetic code of the viral DNA has been removed so that not only is the virus non-pathogenic when it multiplies in the pigs (thus producing immunity but no disease) but also it fails to stimulate a full complement of antibodies. This is because the missing piece of genetic code is not coding for one antigen. This is therefore absent from the vaccine virus.
• Special commercially-available serological test kits can distinguish antibodies which have been stimulated by the marker vaccine from those that have been stimulated by natural infection with a gene-complete wild virus. Pig herds in a control and eradication area can thus be vaccinated to protect them from the worst ravages of virulent AD virus and at the same time serologically screened for natural infection. The widespread use of gene-deleted marker vaccines in a controlled region has the added advantage of suppressing the spread of wild virus and thus reducing its level in the region.
• There is only one main serotype of AD virus which produces a strong long-lasting immunity. Vaccinated pigs can become infected but multiplication of the virus in the pigs' tissues is limited and so less is shed into the environment.
• Vaccination also prevents the virus from crossing the placenta of pregnant sows to infect the unborn piglets.
• Piglets which are suckled by vaccinated sows receive colostral protection which lasts about 6-10 weeks. This is the age when the virulent AD virus would do most damage. During this time the pigs cannot be vaccinated successfully because the maternal antibodies neutralise the vaccine virus before it has had time to stimulate an immunity.

National or regional control and eradication programmes

• Individual countries and regions within countries are variously trying to suppress or eliminate the AD virus (e.g. Ireland, Norway, the Netherlands, France, the USA, and Mexico). The approach used in most of these is blanket vaccination of all 8-12 week old commercial slaughter pigs with a relatively cheap inactivated vaccine. Breeding stock is vaccinated with a longer lasting gene-deleted vaccine over a limited period to reduce the level of virus in the pig population This is combined with routine testing of sow sera using the differential ELISA to monitor for natural infection. Tests have also been developed for use on colostrum which is easier to collect than blood. The disease may also be made notifiable (i.e. when a veterinarian diagnoses it he has to report it to the authorities who take the appropriate action).
• The USA government increased its funding in the year 2000 and an Accelerated Pseudorabies Eradication Programme was introduced. This aims to rapidly remove infected animals in herds when they are first diagnosed.

On-farm eradication
First try and identify how it arrived before deciding which is the best option. If your herd is infected and the disease is in a stable state there are various methods of eradicating it.

• Slaughter the herd, clean and disinfect the premises and repopulate with negative breeding stock. This is expensive and is unlikely to be cost effective in most commercial herds.
• In a weaner production unit, vaccinate all the breeding stock with gene-deleted vaccine. Later test all the sows with the differential ELISA and remove those that are positive for wild virus.

Follow this by one of two options:

1. Depopulate the weaner accommodation and rear the pigs elsewhere. Then, after all the grower/finishers have been slaughtered and/or the youngest of them reared elsewhere, gradually restock the weaner, grower and finisher accommodation as subsequent sows are weaned or
2. Change to a three-site or multi-site system with all-in all out rooms or buildings.

On-farm precautions

• If your herd is free of AD virus you should of course endeavour to keep it free but it is not always easy to do so particularly in a pig-dense area.
• Unfortunately, the AD virus can spread on the wind several km over land and much further over water, so standard precautions of farm biosecurity such as those described earlier in chapter 2 cannot be entirely relied on to keep it out of your herd.
• Also, semen from infected boars is thought to spread it so the use of artificial insemination with bought in semen could in theory contaminate the herd.
• Rats, which are normally thought of as dead end hosts, also become infected and are said to spread it from farm to farm. This possibility is disputed by some authorities.
• Infected pigs can become long-term sub-clinical carriers. Any replacement pigs coming on to the premises should come from known safe sources and be quarantined. These should as a minimum be physically separated from your pigs, for at least a month, preferably six weeks and blood tested prior to integration.
• AD virus can be carried on the tonsils of the wild boar and be excreted intermittently. Make sure the farm is pig-proof.

The causal agent is a herpes virus and like the herpes viruses of humans (e.g. the causes of cold sores and chicken pox) the AD virus can lie latent in the pig's nerve cells. Stress (e.g. the stress of transport) can reactivate it and the pig starts to shed virus again. The main spread between pigs is aerosol and nose to nose contact. It is not spread in faeces or urine.