PMWS/PCVD - Is There a Way to Its Control?

David G S Burch  BVetMed MRCVS
Veterinarian, Octagon Services Ltd

(Published in "Pig International" June 2006)

PMWS (post-weaning multisystemic wasting syndrome) or as it is increasingly being referred to as PCVD (porcine circovirus disease), is sweeping across Northern America and they are experiencing the same devastating, high mortality (30-40%) in young growing pigs, as we saw in Europe and Asia in the late nineties. In Europe, the acute effects of the disease have largely died down and we are living with the chronic effects where mortality figures range from 0-10%, depending on the success in controlling the disease and the implementation and effect of the 'Madec 20 points', to reduce stress, pig-to-pig contact, improve hygiene and reduce challenge. The disease/mortality is now occurring later in the chronic form of the disease in the early finishing stages (see Graph), not in the nursery/grower stage seen in the acute form.

Graph:  Mortality of pigs by Age due to PMWS

(Source: based on Madec and others, 2000)

There is still the disparity of sizes between affected and unaffected pigs (see Photo), the so-called 'enter the finishing shed at 30 kgs and come out at the end at 30 kg syndrome', when all the others are 100 kg. This effect is equally as damaging as mortality on production efficiency.

The disease has been 'associated' with porcine circovirus type 2 (PCV2) but there are supporters of other factors, which lead to the expression of the disease. Factor X (possibly another virus still undetected), PCV2 mutation, immunostimulation by vaccines, immunosupression by other viruses (PRRS and PPV), bacterial infections, genetics, feeding, mycotoxins, almost anything and everything have been associated.

Photograph of a Thin Undersized Pig affected by PMWS - "The 30kg syndrome"

Photograph of a Thin Pig affected by post-weaning multisystemic wasting syndrome - PMWS disease of swine


The disease has spread like an infectious agent, across countries and now, even continents. Pig movement and contact, semen and proximity to infected premises all seem to play a major role. The acute form (high mortality) followed by a build up in the herd immunity and the subsequent chronic form (lower grumbling mortality) all suggest that it is caused by an infectious agent. Macrophages (the bodies immune cells that eat up foreign proteins and even bacteria), usually full of ingested PCV2, appear to have invaded and destroyed the lymph cells in the lymph nodes. The lymph cells produce the body's immune response to an infection, both through antibody production and stimulation of the cell-mediated response, where cells not antibodies help to overcome the infection. Whether it is just the PCV2 infection alone, which causes the initial damage to the lymphoid cells and this then attracts the macrophages to destroy its own immune system is still not clear and further work on the mechanisms involved needs to be done.

We have waited a long time for a vaccine to be produced, but a vaccine against what, if there are a number of other viruses and factors potentially involved? At last, a PCV2 vaccine for use in sows has been produced and has recently been provisionally licensed in Canada. It has been available in France and Germany under a provisional licensing system also and the results have shown that there can be improvements in growth rate and reductions in mortality by stimulating the sow's immunity and passing higher levels of maternal antibody to the piglet. In the case of na´ve herds, in primary breakdown, high-risk areas, such as Canada, this vaccine could potentially reduce the acute effects (high mortality) of the disease.

Recent work however, by McKeown and others (2005), researchers from Blacksburg, Virginia and Ames, Iowa have demonstrated that the presence of high levels of maternally derived antibodies prevents the onset of viraemia (PCV2 circulating in the blood) but does not at low levels or when levels fall after several weeks. This work tends to support the acute and chronic forms of the disease observations. The acute form is when there is no or low antibodies i.e. in the face of primary breakdown from virus challenge and the chronic form is dependent on maternal antibody levels in the piglets preventing the disease in the early stages but as they subside and challenge occurs, disease is expressed later.

Further, recent developments with new PCV2 vaccines given to young growing pigs have shown outstanding results in field trials, offering protection throughout the growing and finishing period and reduced mortality to almost pre-PMWS times. This is highly significant in three ways. Firstly, it demonstrates the efficacy of the PCV2 vaccine; secondly, it confirms that the disease expression is primarily as a result of PCV2 infection and thirdly it shows that vaccination of piglets, i.e. immunostimulation in young pigs, is not important, if the primary virus (PCV2) is controlled.



Madec, F. and others (2000) Post-weaning multisystemic wasting syndrome in the pig: a new challenge for veterinary research and practice. Pig Journal, 45, 69-75.

Mckeown, N. E and others (2005) Effects of porcine circovirus type 2 (PCV2) maternal antibodies on experimental infection of piglets with PCV2. Clinical and Diagnostic Laboratory Immunology, 12, 11, 1347-1351.


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