Porcine Reproductive and Respiratory Syndrome (PRRS)

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Porcine Reproductive and Respiratory Syndrome (PRRS)

Weak piglet born after PRRS infection in the sow

Weak piglet born after PRRS infection in the sow

"PRRSV interacts with other pathogens to cause severe respiratory symptoms in finishing pigs."

The effects in breeding herds are reproductive failure and signs of respiratory disease. Weaned and finishing pigs suffer from respiratory disorders due to secondary infection, which are worsened by the immuno-modulatory properties of the PRRS virus (PRRSV).

About PRRS

For detailed information on PRRS in pigs also see the website www.porcilis-prrs.com.


PRRS virus is a single-stranded RNA virus. The etiology of PRRS virus was discovered in 1991 and isolated from swine in North America and Europe soon afterwards. It is present in most areas of the world. Currently, the countries of the world that are PRRS-free are Sweden, Norway, Finland, Switzerland, New Caledonia, New Zealand, Australia, Argentina, Brazil, and Cuba. The virus is highly infectious and is capable of infecting an animal with as few as 10 virions.


Order: Nidovirales

Family: Arteriviridae

Genus: Arterivirus.


Consequences of PRRS

The economic impact of PRRS in all production stages is substantial. The annual losses due to PRRS, as of 2011, are estimated at $668.58 million. This cost does not include the producers’ costs for vaccination against PRRS virus, treatments, diagnostics performed, or costs associated with the increased levels of biosecurity implemented to slow the spread of this virus. In a breeding herd, the losses are dramatic but, in general, only lasting for a few months until the breeding herd reaches stability. However, the reproductive problems may reoccur if the breeding herd becomes destabilized due to recycling of PRRSv from the finishing herd or excreting gilts.


Pathogenesis of PRRSV infection

The PRRS virus is transmitted by various means. The virus may spread through semen, which is of large concern in the swine industry due to widespread use of artificial insemination. Boars may have PRRS virus present in semen up to 92 days after the day of infection. Sows infected with PRRS during late gestation can shed the virus through the mammary glands, passing the virus to the piglets via the milk. Sows may also pass the virus to the feti across the placenta. This is most likely to occur during the last trimester of pregnancy.

The virus enters and replicates in macrophages and lymph nodes present in the lungs, components of the pig’s immune system that normally help protect the animal from pathogens. Once a farm is infected, virus spreads to the majority of the herd and is recirculated through birth and introducing new pigs in the herd. The virus may also rapidly spread between farms via the introduction of infected pigs, contaminated semen, and airborne transmission from neighboring farms. Disease may be subclinical or clinical. The syndrome presented, respiratory or reproductive, is dependent on the age of the pigs affected.


Clinical signs

During an epidemic of PRRS, two stages of disease are seen that affect pigs in different stages of production.

First stage: lasts 2 or more weeks

  • Affects 5 - 75% of pigs of all ages in the herd
  • Anorexia and lethargy for 1 - 5 days
  • May also include:
    1. Fever (102 - 106 degrees F)
    2. Rapid breathing or shortness of breath
    3. Blotchy red patches covering the body
    4. Blue-colored areas on body extremities

    Second stage: begins after or during first stage and lasts 1 - 4 months

    • Reproductive failure
    • Premature farrowings
    • High piglet mortality before weaning (up to 60%)
    • Stillborn or mummified piglets (7 - 35% of pigs in a farrowing unit are born dead)
    • Weak PRRSV-positive piglets (50% die soon after birth)
    • Delayed return to service
    • Lack of libido in infected boars
    • Decreased semen quality (decreased motility and defects)

prrs weak and stillborn
Stillborn and weak piglets at farrowing as a result of PRRS infection in the sow

Sows and Gilts

  • Reproductive failure
  • Anorexia
  • Fever
  • lethargy
  • pneumonia
  • Agalactia (lack of milk)
  • Red/blue discoloration of the ears and vulva
  • Subcutaneous and hind limb edema
  • Incoordination
  • Delayed return to estrus after weaning
  • In rare cases, death.

Neonatal piglets

Neonatal piglets can display a variety of clinical signs. The most characteristic are dyspnea (shortness of breath), tachypnea (rapid breathing), lethargy, starvation, and death.

Other clinical signs:

  • Splay-legged posture
  • Swelling of conjunctiva (tissues surrounding the eye)
  • Less common: tremors or paddling, bleeding from navel or other areas, and/or watery scours

Growers and finishing pigs

PRRSV infection alone is often subclinical. It is, however, indirectly responsible for huge economic losses in finishing herds due to its major role in the multi-factorial Porcine Respiratory Disease Complex (PRDC).

If clinical signs are present, they are usually respiratory, including:

  • Fever
  • Sneezing
  • Hyperpnea (rapid breathing)
  • Dyspnea (shortness of breath)
  • Pneumonia
  • Lethargy
  • Periocular edema (swelling of conjunctiva)
  • Oculonasal discharge (Discharge from nasal passages and eyes)
  • Rough hair coats
  • Red, blotchy skin
  • Anorexia

Experimental challenge of SPF pigs with PRRSV alone usually produces no clinical signs.


Interactions between PRRSV and other pathogens
PRRSV interacts with other pathogens to cause severe respiratory symptoms in finishing pigs.

Mechanism of interactions

The mechanism by which PRRSV interacts with other pathogens is still under investigation. However, it has been demonstrated experimentally that interactions with the following pathogens increases the pathological effects of PRRS:

  • Swine Enzootic Pneumonia
  • Streptococcus suis
  • Streptococcus suis Actinobacillus suis
  • Salmonella choleraesuis
  • Bordetella bronchiseptica
  • Glasser Disease
  • Pasteurella multocida
  • Swine Influenza virus
  • Porcine respiratory corona virus
  • Aujeszky’s disease virus
  • Porcine Circovirus (Associated) Disease (PCVD) type 2 (PCV2)

The role of PRRSV

It is still not possible to conclude which are the most important combinations of pathogens or to define the importance of PRRSV in the severity of respiratory disease in finishing pigs. This is difficult to prove experimentally due to difference in pathogenicity of virus strains, timing of infections, serological status of pigs, and stress factors due to housing and/or management. Clinical experience in the field has shown that the occurrence of new respiratory pathogens result in increasingly complex respiratory problems and improved performance has been observed in PRRSV-vaccinated herds.


Diagnosis of PRRSV infection

The symptoms presented by pigs infected by PRRS can be indicative of several other diseases, and concurrent infections with other viral or bacterial pathogens can further complicate the diagnosis of PRRSV. To definitively diagnose PRRSV, laboratory methods must be used to confirm the presence of the PRRS virus, its protein products, or host antibodies against the virus. Diagnostic methods used to confirm presence of PRRSV infection are:

  • Serology - ELISA or IFA tests for the presence of antibody. However, the presence of antibody cannot itself establish an ongoing infection, as antibodies remain present in the serum after exposure and initial infection from the virus are completed.
  • Virus isolation (VI) via oral fluid or samples from the tonsils or lymph nodes
  • Reverse Transcriptase Polymerase Chain Reaction (RT-PCR)
  • Nucleotide or amino acid sequencing
  • Microscopic analysis of tissues from necropsied animal
    1. The best tissues or samples will likely come from the lung, lymph nodes, tonsils, spleen, and possibly bronchoalveolar lavage.
    2. PRRS virus usually leads to lesions, which may be mild or severe, in infected pigs and are most likely found in the lungs and surrounding lymph nodes. These lesions can be indicative of PRRS but can be caused by other concurrent infections as well, so identification of the virus will provide the most definitive diagnosis.


PRRS control in different pig herds
For both growing and finishing pigs as well as for breeding stock the following has proven effective:

  • Vaccination
    • A live vaccine for vaccinating the whole herd is available. SeeVaccines for more information.
  • Management strategies
    • As always, management practices have an important part to play. Gilts entering the breeding unit need to be acclimated, and strict adherence needs to be paid both to the all-in/all-out principle and the unidirectional flow of animals during the nursery and growing phases.
    • The PRRS virus is inactivated by most of the common disinfectants, such as phenol and formaldehyde. Disinfection of the facilities of all production stages is important in removing the virus from the environment.



    The most effective method of removing the chance of subsequent PRRS infections on a farm is through the process of elimination through complete herd immunity. This is accomplished by inoculation of the entire herd with live PRRS virus through the use of modified-live vaccine. Due to the slow nature of immunity development of swine to this virus, the herd should be isolated from any new incoming gilts or seed stock for at least 200 days. This will allow the entire herd to develop sufficient immunity to the virus and can stop the spread of the virus to susceptible new breeding stock brought onto the farm after this time period. In addition, any new boars brought onto the property should be isolated and kept out of the breeding herd for at least 60 - 90 days and after a negative serological test for PRRS. Implementing the elimination process can allow producers to remove this virus from the property and animals and help prevent further infections of PRRS in the future.