ABSTRACT

Developing methods to control PRRS is both a critical and long-standing challenge for the swine industry. To quote Dr. Mark Fitzsimmons, Swine Graphics, Webster City, Iowa: Abasic PRRS virus information, particularly in the area of immunity and transmission, is conspicuous by its absence. In short, there is a lot we do not know yet about PRRSV and hence its predictable and effective control which I wish I could share with you today. However, we have come a long way from the days of Mystery Swine Disease, Abortus Blau, Porcine Epidemic Abortion and Respiratory Syndrome, and EMC virus.

PRRS control strategies that work have been developed, each however usually limited to specific types of situations and production types. This presentation will attempt to clearly define essential concepts of PRRSV-pig “biology” and then review control strategies for PRRS, both conventional and unconventional. It is by necessity only an overview, hopefully providing a clear basis and framework for weighing different approaches to PRRS control. For more details on PRRS control I strongly urge you to read the applicable sections of the Producer Edition of 2003 PRRS Compendium produced by the National Pork Board (United States) and edited by Drs. Zimmerman, Yoon, (Iowa State University) and Neumann (National Pork Board). This is an excellent document which provides a practical review of scientific knowledge as well as current, albeit untested methods used for controlling PRRS (scientific proof often follows practical and effective innovations).

For a more detailed review of current scientific knowledge read the 2003 PRRS Compendium, second edition. Both are available (for $30US) in a single CD from the US National Pork Board at: http://porkstore.pork.org/

PRRSV-PIG “BIOLOGY” AND IMMUNOLOGY

PRRS is particularly a disease of LARGE three-site or single-site swine herds which use management short-cuts that don’t meet the needs of the pigs or designs which compromise both internal and external biosecurity.

Continuous flow rooms, buildings, and possibly sites, as well as breeding barns which receive susceptible gilts regularly enable continuous virus replication (constant source of susceptible pigs), holding-back of poor-doers (Typhoid Marys), short time for cleaning, disinfecting, and DRYING of rooms and transports, inadequate isolation and testing of breeding stock, semen, inadequate pre-immunization of breeding replacements prior to entry, etc, etc, etc. Continuous virus replication enables maximum PRRSV mutation and ultimately “escape” from the herds’ initial immune responses. Typhoid Mary hold-backs infect younger groups of pigs, ensuring they repeat the same PRRSV-associated disease-losses of their predecessors.

Definitions:

Modified-Live Virus (MLV): PRRSV which has been altered in the laboratory to reduce its virulence or pathogenicity in an effort to make it safe(r) for use as a live-virus vaccine.

Virulent Live Virus (VLV): Unaltered or Wild-Type PRRSV isolated from a diseased pig. VLV can be grown and multiplied unchanged in Porcine Alveolar Macrophage (PAM) cultures, from blood or lung tissue from purposefully infected PRRSV-free pigs, or from diseased pigs within herds during PRRS outbreaks. In the last case, it is imperative to collect the blood or tissues from febrile aborting sows or weak-born febrile piglets if it is to be used later to immunize / acclimatize gilts in isolation or perform whole-herd exposure and closure (see below).

Horizontal infection (transmission): PRRSV infection comes from another pig of the same age or production group (all-in all-out flow) or within the same room where pigs of different ages are housed together (CF production and breeding herds). Virus transfer occurs by exchange of saliva, blood, or semen. Therefore, mixing pigs from different litters or pens (causes fighting and exchange of saliva and blood) or not changing needles or blades between litters, pens, or at times pigs, helps horizontal transmission. We all know the impact PRRSV-infected semen can have!

Vertical infection (transmission): PRRSV infection comes from the sow either in utero (across the placenta ~ 70 days at the earliest) or from milk, oral / nasal contact. In utero infection has the most severe impact on piglet immune system and duration of (persistent) PRRSV infection.

Persistent infection or “persistence”: Ability of PRRSV to stay in an infected pig for weeks and months after infection. PRRSV may persist in these pigs, be shed, and infect other pigs over 80 to 100 days (maybe longer??). Persistence seems to be a result of a slowed development of FULLY protective immunity (ability to eliminate the virus) by some unknown effects of PRRSV on the pig. PRRSV persistence after infection is the reason recommendations are made for both long periods of time for herd closures when attempting herd virus elimination or for duration of isolation during acclimatization after exposing new gilts to VLV.

Further Information

To continue reading this article, including tables, click here (PDF)

To view the summary page and the other articles in this series, click here

June 2006