Different Approaches to Handling Circovirus
By John Harding, DVM, University of Saskatchewan - This article, presented at the London Swine Conference, is summarized by Jaydee Smith/OMAFRA and was reviewed by the editor of the Pork News and Views newsletter for accuracy and appropriateness.
19 June 2006
4 minute read
Post-weaning multisystemic wasting syndrome (PMWS) has grown to become a serious disease affecting the global swine industry. Porcine Circovirus type 2 (PCV2) contributes to PMWS, porcine respiratory disease complex (PRDC), proliferative and necrotizing pneumonia (PNP), and possibly other conditions.
Several classic clinical signs of PMWS form the basis of a preliminary diagnosis, including enlarged lymph nodes, wasting, dyspnea, diarrhea, pallor, and jaundice. While all of these will not be noted in a single pig, affected farms will present with the majority, if not all, over a period of time. Confirmation of PMWS requires the presence of clinical signs, hallmark histological lesions, and the identification of PCV2 within lesions.
Although PCV2 infection is clearly a necessity and is the only virus consistently recovered from PMWS cases, other co-factors are required for the induction of PMWS. These may include other diseases such as PRRS, mycoplasma, swine influenza and parvovirus, immune stimulation or vaccination, or the absence of good production practices (i.e. other general stresses). Virtually all commercially raised pigs are subclinically infected with low levels of PCV2, yet most remain healthy. By contrast, very high levels of PCV2 are consistently recovered from pigs with PMWS. In fact, the amount of PCV2 in tissues and serum of PMWS pigs (viral load) is correlated with the severity of clinical signs and histological lesions in experimentally and naturally infected pigs. Thus, amplifying viral load is critical for the development of PMWS. In pigs, as in all species, antigen presenting cells (APCs) play a fundamental role in the early immune response by presenting foreign antigens such as viral particles to the effector cells of the immune system. In healthy subclinically infected pigs, PCV2 is contained within APCs in a quiescent state that does not impact APC function, but results in persistent low level PCV2 infection. Co-factors may induce PMWS by attracting PCV2-infected APCs to sites of immune stimulation or infection, where PCV2 is amplified beyond a critical biological “threshold” leading to PMWS lesions through a number of immune mechanisms, and ultimately the dissemination of PCV2 to distant systemic sites.
The author suggests that the key to controlling PMWS in any farm regardless of PMWS status, location, strain or co-factors involved is to reduce and maintain PCV2 viral load below this biologically critical “threshold”.
Public domain research documenting the efficacy of experimental vaccines is limited, but experimental and field research available is promising. The products under development are targeted at both the breeding herd, to enhance the passive immunity of piglets, and the feeding herd, to initiate active immunity post-weaning. Both killed and attenuated live vaccines are in the pipeline. The use of autogenous vaccines has been suggested, however, it is unlikely that autogenous PCV2 would be effective, and more importantly may not be safe, because PCV2 is difficult to grow in tissue culture, and is very resistant to inactivation.
While the emergence of a new PCV2 strain has received considerable attention in eastern Canada, the superior virulence of these strains is unproven. Until vaccines are widely available in Canada, the key to controlling severe PMWS is to implement good production practices and eliminate co-infections to prevent the amplification of viral load.
Newsletter editied by John Bancroft - Swine Grower Finisher Specialist/OMAFRA - May 2006
