Porcine Reproductive & Respiratory Syndrome (PRRS)

PRRS is caused by a virus which was first isolated and classified as an arterivirus as recently as 1991. The disease syndrome had been first recognised in the USA in the mid 1980′s and was called “mystery swine disease”. It has also been called blue ear disease. The name porcine arterivirus has been proposed recently.

The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.

Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.

A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.

It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.

The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.

PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.

Symptoms

Acute disease

When the virus first enters the breeding herd disease is seen in dry sows, lactating sows, sucking piglets and growers.

Sows

Clinical signs in dry sows during the first month of infection

  • Short periods of inappetence spreading over 7-14 days, 10-15% of sows at any one time.
  • The body temperature may be elevated to 39-40°C (103-105°F).
  • Abortions, often late term, may occur at a 1-6% level. These are often the first signs to be noted.
  • Transient discoloration (blueing) of the ears may be seen (2% level. Blue ear disease).
  • Some sows farrow slightly early. 10-15% over the first 4 weeks.
  • Increased returns occur 21-35 days post-service.
  • Prolonged anoestrus and delayed returns to heat post-weaning.
  • Coughing and respiratory signs.

Clinical signs in farrowing sows in the first month of infection

  • Inappetence over the farrowing period.
  • A reluctance to drink.
  • No milk (agalactia) and mastitis – significant symptoms.
  • Farrowings are often 2-3 days early.
  • Discoloration of the skin and pressure sores associated with small vesicles.
  • Lethargy.
  • Respiratory signs.
  • Mummified piglets. 10-15% may die in the last 3-4 weeks of pregnancy.
  • Stillbirth levels increase up to 30%.
  • Very weak piglets at birth.
  • The initial phase of inappetence and fever will often take 3-6 weeks to move through.
  • Cyanosis or blueing of the ears is a variable finding and less than 5% of sows show it. It is transient and may last for only a few hours.
  • Coughing occurs in some sows and a few individual cases of clinical pneumonia may occur.
  • This acute phase lasts in the herd for up to 6 weeks, and is characterised by early farrowings, increases in stillbirths, weak pigs and an increase in the numbers of large mummified pigs that have died in the last three weeks of pregnancy. In some herds, these may reach up to 30% of the total pigs born. Piglet mortality peaks at 70% in weeks 3 or 4 after the onset of symptoms and only returns to pre-infected levels after 8-12 weeks. The reproductive problems may persist for 4-8 months before returning to normal, however in some herds it may actually improve on the pre-PRRS performance.
  • Longer term effects of PRRS on reproductive efficiency are difficult to assess, particularly in herds of low health status. In some there are increases in repeat matings, vulval discharges and abortions, all of which may be blamed on PRRS.
  • The effects of PRRS on reproduction efficiency in herds in which the infection has become enzootic have been observed in the field for up to 12 months after disease has apparently settled.

These are as follows:

  • A 10-15% reduction in farrowing rate (90% of herds return to normality).
  • Reduced numbers born alive.
  • Increased stillbirths.
  • Poor reproduction in gilts.
  • Early farrowings.
  • Increased levels of abortion (2-3%).
  • Inappetence in sows at farrowing.

Piglets

  • More diarrhoea.
  • Less viable piglets.
  • Increase in respiratory infections such as glassers disease.

Signs in boars

  • Inappetence.
  • Increased body temperature.
  • Lethargy.
  • Loss of libido.
  • Lowered fertility.
  • Poor litter sizes.
  • Lowered sperm output.

Weaners & Growers

When first introduced into an EP and App free growing herd there may be few signs:

  • A period of slight inappetence.
  • Mild coughing.
  • Hairy wasting pigs.
  • In some herds there are no symptoms.

If EP and/or virulent App are present but not under control in the herd:

  • An acute extensive consolidating pneumonia.
  • Formation of multiple abscesses.
  • Disease becomes evident within 1-3 weeks of weaning.
  • Pigs lose condition.
  • Diarrhoea may be seen.
  • Pale skin.
  • Mild coughing.
  • Sneezing.
  • Discharges from the eyes.
  • Increased respiratory rates.
  • Mortality during this period may reach 12-15%.

Once the acute period of disease has passed through PRRS virus normally only becomes of significance in the early growing period:

  • Severe pneumonia.
  • Periods of inappetence.
  • Wasting.

Pigs become infected as maternal antibody disappears and then remain viraemic for 3 to 4 weeks continually excreting virus. Clinical disease is seen in pigs 4 to 12 weeks of age:

  • Inappetence.
  • Malabsorption.
  • Wasting.
  • Coughing.
  • Pneumonia.
  • In this post-weaning period mortality can rise up to 12% or more and persist inspite of antibiotic treatments.

Secondary bacterial infections become evident in pigs at a later stage from 12 to 16 weeks of age:

  • Abscesses develop in the lungs and may spread throughout the body.
  • Lameness with abscesses.
  • Poor stunted growth.

Causes / Contributing factors

The following are common methods of spread and contribute to overall disease levels.

  • Droplet contamination from older pigs to younger pigs.
  • Nasal secretions, saliva, faeces and urine
  • Permanently populated houses maintain the virus at high levels, particularly in the first and second stage nurseries.
  • Movement of carrier pigs.
  • Airborne transmission up to 3km (2 miles).
  • Adult animals excrete virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
  • Mechanical means via faeces, dust, droplets and contaminated equipment, lorries etc.
  • Contaminated boots and clothing.
  • Vehicles especially in cold weather.
  • Artificial insemination but only if the boar is viraemic. This period is probably only 3-4 days.
  • The mallard duck and probably other species of bird.

Diagnosis

This is based on the clinical signs, post mortem examinations and the known presence of the virus in the herd or by serological examinations and isolation of the virus in a laboratory.

If the herd has not been exposed to PRRS then blood sampling and testing a minimum of 12 adult animals (preferably those that have been off their food at least three weeks) provides a reliable means of diagnosis.

 

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