Since the discovery and characterization of PMWS in western Canada in 1995, the significance and dissemination of post-weaning multisystemic wasting syndrome (PMWS) has grown. For the purpose of this presentation I will use Porcine Circovirus- Associated Disease (PCVAD) instead of PMWS because the name PMWS does not include the variety of clinical presentations associated with the disease. This syndrome is characterized by respiratory, digestive, hemolymphatic, vascular, and renal lesions associated with Porcine circovirus-2 (PCV-2) infection. Clinical signs and lesions are observed in late nursery (8-10 weeks of age), and finisher pigs, 2–3 wks after placement. Affected pigs present all or some of the following: cough, diarrhea, anemia, icterus, poor body condition, generalized lymphadenopathy and skin lesions. In 2004, 2005 and part of 2006 PCV-2-associated disease showed a dramatic increase in the Eastern provinces of Canada. It should be noted that the PCV-2 isolated from these new cases presented significant changes in its genome. Due to the sudden appearance of these genetic changes and the severity of clinical disease and mortality seen in the Eastern provinces swine production, it has been proposed that these outbreaks were caused by the dissemination of a new strain of higher virulence. As of today, this hypothesis has not been proven experimentally or by field studies. However, Dr. Carl Gagnon from the University of Montreal is performing studies in order to prove this hypothesis. Up until the summer of 2006 in the Western Provinces, PCVAD was a sporadic finding. However the picture has changed from the sporadic form to the epizootic form on several farms. Veterinarians in the West report 3 different manifestations of PCVAD: Type I: Sporadic occurrence, minimal effect on long term mortality, mainly wasting presentation fitting with the PMWS case definition. Type II: Persistent PCVAD signs. Mortality is elevated, maybe doubled in the affected age group and there is an increase in the number of cull pigs sold. Type III: Epizootic, severity varies with presence of concurrent disease, especially PRRS. Mortality ranges around 8 to 25% in 8- to 13-week-old pigs. Management, immune stimulation or vaccination also seem to play an important role in the presentation of this syndrome. Harding (2006) posed a very interesting hypothesis where “the key to controlling and preventing PMWS in any herd regardless of PMWS status, location, strain or co-factors involved is to reduce and maintain PCV2 viral load below this biologically critical “threshold”. As mentioned before PMWS was first described in 1995, however, retrospective studies have shown that both PCV2 infection and clinical cases of PMWS were present as early as 1985 indicating that PCV2 is not a new virus. These findings, together with the fact that PCV2 infection is present in almost 98 % of the swine farms around the world clearly suggest that PCVAD is a multifactorial disease. Remember that if herd evidence suggests an association between vaccination practices and PCV2- associated disease, re-evaluation of use and timing of certain vaccines is important. Good management practices should be exercised, i.e. strict and true all-in-all-out, early removal of runt pigs and of those that don’t respond to treatment, and reduction of mixing and moving of pigs; reduction of viral load by using disinfectants both in buildings and transport vehicles have been demonstrated to be efficacious against PCV2, and if it is an option, consider changing pig genetics if there is enough evidence that there is a predisposition at the farm. Finally, as commercial vaccines have become available in North America, reports generally seem to agree that vaccines are an effective tool in the control of PCVAD; therefore a combination of the above measures and vaccine might provide the control strategy for this interesting, complex but devastating syndrome.