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Porcine reproductive and respiratory syndrome (PRRS)

Background and history

Porcine Reproductive and Respiratory Syndrome (PRRS) is a viral disease that has two overlapping clinical presentations; complications with reproduction and respiratory disease in pigs of any age. PRRS is the most economically significant disease to affect US swine production since the eradication of classical swine fever and costs the United States pig industry around $650 million annually, and recent estimates in Europe determined that it costs almost 1.5b€ every year.

The PRRS virus (PRRSv) can affect all age groups. Reproductive impairment or failure is more obvious in sows or gilts, but can, and does, affect boars. The respiratory syndrome is more often observed in young growing pigs but also occurs in naïve finishing pigs and older breeding stock. PRRS infects all types of herds including high or ordinary health status and both indoor and outdoor units, irrespective of size.

The PRRSv destroys up to 40% of the pigs macrophages* removing a significant part of the pig’s defence mechanism which allows secondary infections by bacteria and other viruses, particularly those that affect the respiratory system such as Swine Influenza, to proliferate and cause damage.

A 2010 Royal Veterinary College MSc study confirmed a high prevalence of PRRS in the English pig population with a greater prevalence in high pig-dense areas, and the AHDB Pork states that more than 60% of herds were affected by 2011 - indicating that current control measures have much room for improvement.

Clinical signs

The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRSv 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 clear, however, what is known is that the higher the health status of the herd, the less severe are the disease effects – possibly due to less/ better controlled opportunist pathogens in the pigs environment. Another theory is that as the virus mutates (changes) as it spreads between herds, sometimes it results in a mild strain and at other times a highly virulent strain.

When the PRRSv enters a herd with an ordinary herd health status, but that is Enzootic Pneumonia (EP) and Actinobacillus pleuropneumoniae (App) free, then if clinical signs are observed then they can been in dry sows, lactating sows, some boars, sucking piglets, growers and finishers.

Respiratory presentation

Acute disease

  • A period of slight inappetence and mild coughing but in some herds there are no symptoms at all.

NB: If EP and/or virulent App are present in the herd, the clinical signs may become severe with an acute extensive pneumonia which gradually forms multiple abscesses in the lungs. Clinical signs are evident as early as one week after weaning with the piglets losing condition with pale skin, mild coughing, sneezing and increased respiratory rates. Mortality during this period may reach 12-15%.

Endemic (established) disease

  • Once the acute period of disease has passed through a breeding and finishing herd PRRSv typically only becomes of significance in the early growing period, where severe endemic pneumonia can persist with periods of inappetence and wasting of pigs.
  • Weaners and growers may become infected as their maternal antibody disappears and they can then continually shed the virus for 3 to 8 weeks.
  • Permanently populated houses maintain the virus at high levels, particularly in the first and second stage accommodation.
  • Clinical disease is seen in pigs from 4 to 12 weeks of age and it is characterised by a fairly predictable time of onset, inappetence, malabsorption and wasting, coughing and 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 from abscesses that develop in the lungs. These infections spread to other parts of the body, particularly joints with increased lameness.
  • A carrier state exists in the pig that can last for 2-3 months.

Reproductive presentation

Clinical signs in dry sows during the first month of infection (Acute)

  • Short periods of inappetence spreading over 7-14 days – up to 15% of sows at any one time.
  • The body temperature may be raised from 39-40ºC (103-105ºF).
  • Abortions, often late term, may occur at a 1-6% level. These are often the first signs to be noted.
  • Transient blue discoloration of the ears may be seen (but only about 5% of herd)
  • 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.

The inappetence may be quite short, often no longer than 12-24 hours, and the sow may eat only half her feed. Thus in the dry sow house there may be episodes when up to 10% of sows at any one time will be slightly off their food. In group housing, this inappetence may not be so noticeable. In herds where sows are subjected to wide fluctuations in environmental temperature, or if the management is poor and nutrition marginal, then the signs are likely to be more severe. Furthermore, in these types of herds, abortion levels are often elevated considerably.

Clinical signs in farrowing sows in the first month of infection (Acute)

  • Inappetence and a reluctance to drink
  • Agalactia (no milk) and mastitis.
  • Early farrowing- often 2-3 days early.
  • Discoloration of the skin and pressure sores associated with small vesicles (blisters).
  • Lethargy with abnormal 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 the breeding herd. 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 farrowing, increased 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.

Signs in boars

  • Inappetence.
  • Increased body temperature.
  • Lethargy.
  • Loss of libido.
  • Lowered fertility.
  • Poor litter sizes.
  • Lowered sperm output.
  • Defective acrosome (tip of sperm responsible for egg penetration).

Long-term effects

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 mating, vulval discharges and abortions, all of which may be attributed to PRRS.

The effects of PRRS on reproduction efficiency in herds in which the infection has become enzootic (regularly seen) 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 farrowing
  • Increased levels of abortion (2-3% but rises up to 50% have been reported).
  • Inappetence in sows at farrowing.

Some herds report that PRRS continues to be associated with reproductive failure and increases in repeats (5-10%) on a normal and abnormal cycle for as long as 6 months after the acute episode has subsided.

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 the PRRSv 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.

Causes

The PRRSv can be introduced to a herd via;

  • Nasal secretions, saliva (nose –to-nose contact, fighting)
  • Faeces and urine – indoor and outdoor kept
  • Vectors, such as flies, birds (especially the Mallard duck), access to slurry or contaminated carcasses.
  • Permanently populated houses / pens maintain the virus at high levels, particularly in the weaner and early grower pens.
  • Movement of carrier pigs – replacement stock, new stock, exhibiting pigs
  • From sow to piglet during pregnancy, with a higher probability of transmission the later the sow is infected during pregnancy
  • Semen from infected boars including AI – this period is probably less than a week
  • Contaminated needles
  • Airborne transmission up to 3km (2 miles) – problematic in high pig dense areas
  • 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, boots, clothes, vehicles, especially in cold weather

Prevention

Vaccination – can control clinical signs and reduce the shedding of the virus. Modified live vaccines have been clinically proven to be the most effective and there is a choice available.

Not buying in new stock for eight months to allow PRRS to reduce within the herd.

Consult your veterinarian for a control plan of treatment to minimise further transmission and assist in recovery where possible. This may include exposing naïve gilts to the infection alongside vaccination at least six weeks prior to exposure or vaccination to gain a PRRSv immune status.

Treatment

In the absence of medication to treat viruses, treatment is aimed at preventing secondary infections, both respiratory and enteric (gut) until an immunity builds up. With PRRS however, it is essential during the acute phase to prevent the multiplication of bacteria that normally would have been destroyed by macrophages. Antibiotic treatment should be given for 3-4 weeks to all sows and boars immediately the disease is diagnosed or suspected. If necessary commence with water soluble antibiotics followed by in-feed medication. Prompt treatment usually reduces abortions, stillbirths, mummified pigs and early farrowing caused by secondary bacteria.

  • Extra warmth should be a priority including extra bedding, a heat lamp for younger piglets.
  • Piglets should be injected with either long-acting oxytetracycline or amoxycillin on days 3, 7 and 14 after farrowing.
  • Electrolytes should be given to counteract dehydration.