porcine reproductive and respiratory syndrome

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4 th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29 th – July 2 nd , 2003 References 1. Andreyev, V.G., Scherbakov, A.G., Pylnov, V.A., and Gusev, A.A.: Genetic heterogeneity of PRRSV in Rusia. In Procedings of the Third International Symposium on Porcine Reproductive and Respiratory Syndrome (PRRS). pp 211-212. 2. Forsberg, R., Oleksiewicz, M.B., Petersen, A.M.K., Hein, J., Bøtner, A., and Storgaard, T.: A molecular clock dates the common ancestor of European-type porcine reproductive and respiratory syndrome virus at more than 10 years before the onset of the current epidemic. Virology, 289: 174-179, 2001. 3. Forsberg, R. Storgaard, T., Nielsen, H. N., Oleksiewicz, M. B., Cordioli, P., Sala, G., Hein, J., and Bøtner, A.: The genetic diversity of European type PRRSV is similar to that of the North American type but is geographically skewed within Europe. Virology, 299: 38-47, 2002. 28 4. Indik, S., Valicek, L., Klein, D., and Klanova, J.: Variations in the major envelope glycoprotein GP5 of Czech strains of porcine reproductive and respiratory syndrome virus. Journal of General Virology 81, 2497-2502, 2000. 5. Oleksiewicz, M.B., Bøtner, A., Toft, P., Grubbe, T., Nielsen, J., Kamstrup, S., and Storgaard, T.: Emergence of porcine reproductive and respiratory syndrome virus (PRRSV) deletion mutants: correlation with the porcine antibody response to an antigenic site in the ORF3 structural glycoprotein. Virology 267:135-140, 2000. 6. Stadejek, T., Stankevicius, A., Storgaard, T., Oleksiewicz, M. B., Belák, S., Drew, T., and Pejsak, Z.: Identification of radically different variants of porcine reproductive and respiratory syndrome virus (PRRSV) in Eastern Europe: Towards a common ancestor for European and American viruses. Journal of General Virology, 83: 1861-1873, 2002.
4 th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29 th – July 2 nd , 2003 PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME: CONTROL AND VACCINOLOGY Kelly M. Lager Virus and Prion Diseases of Livestock Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa 50010, USA Porcine Reproductive and Respiratory Syndrome (PRRS) was first recognized about 16 years ago in the eastern United States as epidemics of maternal reproductive failure and severe respiratory disease in young pigs. At that time PRRS was known as Mystery Swine Disease (MSD) since its cause was unknown. Following the initial reports, MSD epidemics were quickly recognized throughout swine dense regions across the United States and Canada sparking some debate about whether the disease had spread rapidly from the original cases, or were veterinarians just becoming more aware of the clinical signs associated with MSD. This debate broadened with the first reports of MSD in Western Europe during the fall and winter of 1990. During this time there was much speculation about the cause of MSD although it was generally accepted that the etiology was infectious and the etiologic agent was most probably a virus. This assumption was confirmed in spring of 1991 when Dutch scientists discovered the virus that caused MSD or PRRS (64). This virus is now known as the PRRS virus (PRRSV) and it has been classified as a member of the Arteriviridae virus family for which equine arteritis virus is the prototype (40). By the early 1990s PRRS had become a pandemic, and to this day it is still causing significant losses for the swine industry. At the beginning of the PRRS story veterinarians and pork producers tried to fight this new disease with the tools that were available, common sense. Field observations suggested PRRS was an infectious disease and the assumption was the infectious agent causing PRRS would behave like any theoretical infectious agent; i.e., it would replicate in swine, it would be shed from infected swine for some period of time, it would spread among swine, and it would induce an immune response in swine that would protect them from clinical disease upon re-exposure. Using this logic, veterinarians implemented control plans in herds undergoing epidemics and prevention plans in herds deemed at risk of becoming affected by the disease. Basically, these control and prevention programs centered around the concept of exposing or immunizing naïve animals to the infectious agent through the use of cull animals (usually sows that had aborted) and the feedback of substances assumed to contain the infectious agent, e.g., feces, stillborn pigs, aborted fetuses, and placenta. In addition to these strategies, the practice of replacement-animal quarantine was encouraged. From the early days of MSD or PRRS it became apparent that the epidemiology of this disease was not simple. As the data from field studies began to accumulate, it appeared the MSD agent (PRRSV) could be transmitted through the use of contaminated semen collected from boar studs even though the boar studs in question may have been clinically normal (51). At times, direct spread of PRRSV indicated some sort of a chronic carrier state must exist for the virus. This hypothesis was based on the observation that swine could be moved from one herd that was clinically normal, although it had experienced a PRRS epidemic in the past, to another herd and the recipient herd would then develop PRRS. Indirect spread of PRRSV, i.e., spread of the virus not involving the direct contact of swine or the use of contaminated semen, was believed to occur. Another part of the epidemiology puzzle was an apparent cyclical form of the Key words: PRRSV, Control, Vaccinology 29 disease where herds underwent epidemics in a periodic pattern of every 9 to 18 months or so. All of these observations indicated the etiology of PRRS was complex and with the discovery of PRRSV, and the subsequent avalanche of PRRSV-related research, it became apparent that this virus was not a typical, theoretical infectious agent. In fact, this virus and the virus/host relationship have unique qualities that produce novel problems for the control and prevention of PRRS. The purpose of this paper about PRRS control and vaccinology is to review the past, comment on the present, and speculate about the future. Of course this paper will have a bias that is based on the experience of its author, a veterinary virologist working in a government laboratory located in the central United States. Before beginning a PRRS commentary, it is important to state a few general comments. First, despite all of the currently available technology and all that is known about PRRS, this disease still has plenty of mystery. Second, PRRS is a constant challenge for everyone in the swine industry trying to control, prevent, and eliminate this disease. Lastly, it is quite apparent that there is no simple answer to the PRRS problem and there seems to be few complex answers that work consistently in a herd over time. I will begin this paper with comments on epidemiology, immunology, and vaccines, followed by how this knowledge might be applied to control and prevent PRRS, and then conclude with speculation about the future. EPIDEMIOLOGY Etiologic agent - PRRSV is classified as a member of the Arteriviridae virus family in the order Nidovirales (13). Since a discussion of PRRSV properties is beyond the scope of this paper, only relevant information about the virus and how it relates to the control and prevention of PRRS will be discussed. Routes or Modes of Transmission Direct Transmission - Direct transmission defined as PRRSV transmitted between swine due to close contact or through the use of infected semen. When thinking about direct PRRSV transmission it is important to think of animals as young and old since the likelihood of virus transmission seems to be dependent on the age of the animal at the time of infection. For the sake of this paper, old swine will be defined as 6 to 7 months of age or greater. Young swine will be defined as about 4 weeks of age since most research involving pigs utilizes 3- to 5-weekold pigs. Keep in mind, my definitions are arbitrary and reflect research that has been published and my understanding of that research. Of course others may have a different opinion and one must always remember that when dealing with PRRS there are very few black and white issues. I believe the response of old swine to a PRRSV infection is the easiest to understand and the best place to start the discussion. Old Swine Susceptibility - Swine can be infected by oronasal, intravenous, intramuscular, intravaginal, and intratracheal
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