The Pig Site Backroom
PMWS/PDNS Meeting in Stoneleigh, UK - This document summaries a number of the issues that were discussed and came out of the PMWS conference in Stoneleigh, UK in November 2001. The main issues dicussed at the conference relating to Controlling PMWS and PDNS are covered in our main "Controlling PMWS" Document.
There seemed to be a general consensus from the meeting that this disease is spreading and that eventually every-one will get it. i.e. it will become endemic.
The concept was also accepted that the the causative virus (PCV2 or other unknown) is present for some time before the clinical signs of disease appear.
How the disease is spread is still a mystery, the consensus of the meeting was that birds, pigs and AI were all implicated. This makes it difficult to keep the disease out and probably explains the general feeling that the disease will become endemic.
It was accepted that "fresh" genetics had to be brought onto the farm, this means either bringing in gilts or AI, both of which it was felt appear to have a risk.
Several producers stated they considered they got the disease in their closed herds when they were forced to change AI suppliers due to the foot-and-mouth crisis.
Others also highlighted the effect of the foot-and-mouth crisis and suggested the additional stress caused by movement restrictions and subsequent overcrowding was the precipitating factor that caused the disease on their farm
Some interesting facts emerged highlighting that a smaller percentage of sows generated the bulk of the diseased pigs, however there seemed to be no evidence at this time that certain sows were persistent offenders. More data is needed.
It was generally agreed that immunity to the virus does exist, but where the immunity comes from and why some pigs and not other have it remains a mystery.
Of all the things mentioned there seemed to be a consensus that REDUCING STOCKING DENSITY seemed to have the most effect.
Gordon Allan reported on a rather interesting finding. It appears that many piglets are viraemic (i.e. infected with PCV2) but only those with low colostral antibody develop disease. This raises the possibility that more effort is needed to raise antibody production in the sow and hence higher colostral antibodies for the piglet. He suggested that hyperactivity of the immune system was allowing the virus to enter and deplete lymphoid tissues in those piglets with low colostral antibodies to PCV2, resulting in disease.
On the positive side, several producers reported they had managed to lower their mortality to single figures and in some cases to below 5% using the above procedures. So perhaps there is some light at the end of the tunnel.
Finally the conference highlighted two critical points.