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Porcine reproductive and respiratory failure (PRRS)

By Dr Annie Labuschage and Dr Peter Evans, Charles Street Vets
Until recently, South Africa has been one of the few countries that have never experienced an outbreak of PRRS.  This disease has been present in the US and Europe since the middle to late ‘80s and pork producers have battled with the consequences of this disease ever since. PRRS is recognised as one of the most economically significant diseases facing the modern pig industry.  In acute outbreaks one can loose as much as US$255 per sow and US$15 per pig.  Losses are ongoing and after the initial acute stage losses, one can expect to loose around US$76 per sow per year.
What causes PRRS?
PRRS is caused by a virus, which belongs to the family Arteriviridae. It is a single stranded RNA virus.  We differentiate between the American and European strain.  Before this virus was isolated, the disease was known as Mystery Swine Disease or Blue Ear disease.  The disease is highly infectious with only 10 virus particles needed to cause disease via the intranasal route.  Other routes (oral, eye, vaginal) require more particles to establish infection.
The PRRS virus has an affinity for macrophages, especially those found in the lung.  Macrophages are part of the body’s defence mechanism and are responsible for removing bacteria and viruses before they cause disease.  This does not happen in the case of PRRS. Instead of being removed, this virus multiplies in macrophages and ultimately destroys them.  Up to 40% of the macrophages can be destroyed, removing a huge portion of the body’s defence mechanism.  The animal is therefore more susceptible to other diseases.
The virus is very stable at cooler temperatures, at a neutral pH and in cases of a high humidity.  Drying quickly inactivates the virus.  It should be kept in mind that although outside temperatures might be soaring, that there will be many places on a farm where the conditions are just right for the virus to survive.

How does this disease spread?

The disease is introduced into clean herds most often via infected breeding animals.  The second most common way is via infected semen.

  • Droplet contamination from older pigs to younger pigs.
  • Nasal secretions, saliva, faeces and urine
  • Movement of carrier pigs.
  • Airborne transmission up to 3km (2 miles).
  • Mechanical means via faeces, dust and droplets.
  • Contaminated boots and clothing.
  • Contaminated equipment, lorries etc, especially in cold weather.
  • Artificial insemination but only if the boar is viraemic. This period is probably only 3-4 days.
  • Probably several species of bird, especially the mallard duck

What are the clinical symptoms of this disease?
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 39-40ºC
  • Abortions, often late term, may occur at a 1-6% level. These are often the first signs to be noted.
  • Transient discolouration (bluing) 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.
  • Clinical signs in farrowing sows in the first month of infection
  • Inappetence over the farrowing period.
  • Lethargy and a reluctance to drink.
  • No milk (agalactia) and mastitis – significant symptoms.
  • Farrowings are often 2-3 days early.
  • Discolouration of the skin and pressure sores associated with small vesicles.
  • 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.

Cyanosis or bluing 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.
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.
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.
Piglets

  • More diarrhoea.
  • Less viable piglets.
  • Increase in respiratory infections such as glässers disease.
  • Signs in boars
  • Inappetence, lethargy and fever .
  • Loss of libido and lowered sperm output
  • Lowered fertility and poor litter sizes
  • 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 with the formation of multiple abscesses
  • Disease becomes evident within 1-3 weeks of weaning.
  • Pigs lose condition.
  • Diarrhoea may be seen.
  • Pale skin.
  • Mild coughing and sneezing with increased respiratory rates
  • Discharges from the eyes.
  • 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 in spite of antibiotic treatments.
How do we treat/control this disease?
Because a virus causes this disease, it cannot be treated with antibiotics.  The only way to get rid of it is to manage it properly, although this is easier said than done.  The virus can be transmitted from the sow to her piglets while they are still in the uterus and this will lead to the presence of persistently infected carrier animals.
These animals shed the virus continuously and therefore they constantly infect animals that have not been exposed to the virus before.  The virus can circulate for indefinite periods of time within a herd in this way.
There are a few vaccines available on the market.  Some of them are dead while others are live.  Unfortunately there are some problems complicating the whole issue.
The PRRS virus is genetically unstable and has a high rate of mutation.  A very real outcome due to this characteristic is that although animals have been vaccinated with a dead vaccine, they can still get the disease. The function of dead vaccines is to expose the body to disease causing bacteria/viruses without the risk of the animals becoming sick.  The body will form antibodies against the specific virus/bacteria and when the animal comes in contact with the real virus it will have the necessary defence mechanisms in place.
However, in the case of the PRRS virus, vaccine failure is possible because the antibodies do not recognise the virus particles.
Generally, modified-live vaccines are more efficacious than killed vaccines. However, modified-live vaccines are able to replicate, spread through populations, and mutate to a more fit status.
The possibility therefore exist of these vaccine strains to revert to full-blown disease causing strains.  They have also complicated the issue of whether a herd is infected by a “wild” strain or by a vaccine strain as diagnostic methods fail to distinguish between the two.
Conclusion
From the above it is evident that controlling the disease is difficult and that the best way by far is to keep it out of your herd!  This is why the South African pig industry demanded a slaughter-out policy when this disease was diagnosed in certain herds in our country.  The disease is extremely erosive and therefore certainly one we can do without!

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