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Historic Krakow in Poland: The setting of a mid-2007 international veterinary conference that delivered an important update on routes of circovirus infection in pigs.
on June 30, 2009

Circovirus sheds through the nose

Ideas over PMWS control may have to be revised in the light of new research findings

Poland's delightful and historic city of Krakow was the scene recently for reports of new evidence that could affect our ideas on controlling PMWS and the other diseases associated with porcine circovirus PCV2. The reports related to European research indicating that nasal shedding of the virus may be an important route of infection.

This came during the 5th International Symposium on Emerging and Re-emerging Pig Diseases, organised by Professor Zygmunt Pejsak and his team from the National Veterinary Research Institute in Pulawy, Poland, and supported by the Jagiellonian University in Krakow. A focus on emerging diseases in pigs in 2007 inevitably means looking mainly at the latest information on PMWS, PRRS and swine influenza. In Krakow, the conference attended by about 1100 delegates from around the world, was dominated by porcine circovirus diseases and especially the post-weaning multisystemic wasting syndrome.

A keynote lecture on PMWS by John Ellis from the University of Saskatchewan, Canada, recounted the progress made over the last 10 years towards understanding the disease. He said porcine circovirus type 2 (PCV2) had moved "from the arcane to near centre stage in veterinary virology" after its epidemic spread across the continents. Despite this increased profile in research, however, it continues to present more questions than answers. Much of the confusion has related to the debate over the significance of PCV2 in the post-weaning complex.

Bear in mind that the multifactorial nature of disease is a fact of life in modern pig production systems. For PMWS and other circovirus-related diseases, said Dr Ellis, the virus PCV2 is now considered as "the necessary, but usually not sufficient cause". In other words, it needs to be present, but it does not usually cause the disease signs by acting on its own.

Preventive measures

How the virus causes the disease in some pigs and not in others is still an open question. Controversial, too, is whether it has mutated to become more pathogenic, given that PCV2 has been around for many years. Most control programmes to date have revolved around the 20 'Madec principles' (Table 1) which have been largely successful in many countries with the chronic form of the disease. In North America the focus is now on the use of vaccines, for piglets and for sows. The Krakow conference was told that the effects of vaccination against PCV2 alone have been beyond practitioners' expectations.

But the real news of the meeting was in a research paper given by Danish workers (Hjulsager and others). They showed the dynamics of PCV2 infections in piglets from naturally immune but PMWS-affected herds, in comparison with pigs which did not show PMWS. In particular, PCV2 was found in the nose by quantitative PCR from as early as one week of age (see Figure 1). No proof was offered that this came directly from the sows because they had not been swabbed. But the early transmission is suggestive of the direct sow-to-piglets route. It seems from these results that nasal shedding may play a more important role in the route of circovirus infection than was previously thought.

Disease delayed

A significant viraemia meaning virus particles in the blood, the major determinant of potential disease expression did not occur until 9 weeks of age and continued to increase to 12 weeks, when the trial was terminated. The late viraemia and subsequent faecal shedding were presumably due to circulating passive antibodies in the blood, passed on from the sow's colostrum. It had no effect on nasal colonisation and excretion in the piglets.

By contrast, although the pigs classified as non-PMWS-affected showed a similar early nasal infection and viraemia at 9 weeks of age, this had started to fall by 12 weeks of age (presumably as the pig's own immune system started to cope with the virus challenge). Faecal swabs followed a similar pattern to blood results, with shedding of virus increasing in the PMWS-affected pigs and falling in the negative pigs (see Figure 2).

These findings strongly support Dr François Madec's earlier concerns about the potential spread of infection by nose-to-nose contact, across open pens, especially at a litter level or in mixed-source groups. They also highlight that deficiencies in the immune response to the virus will allow it to continue to develop into PMWS. The causes of those deficiencies are only now becoming apparent. Among them are stress, concurrent infections and breed type. On the positive side, several authors in Krakow reported that vaccination had given an enhanced immunity under European conditions confirming previous results for vaccines in North American field trials.PIGI

Only one really new disease was reported in Krakow a viral condition described by Australian veterinarians as porcine mycocarditis syndrome. It took the form of an increase in stillborn piglets, mummifications and pre-weaning losses (up to 50%). Pathological changes comprised a multi-focal, non-suppurative myocarditis (inflamed heart muscle) consistent with a viral infection. A virus could not be cultured initially, although materials from affected piglets were able to affect foetuses when injected into the uterus. Specialised techniques using RNA fragments from the viral material showed the virus to be related to the pestivirus group, although unlike any existing pestivirus such as classical swine fever virus or bovine viral diarrhoea in cattle.

Figure 1 and 2, disease expressed by virus levels did not start until about 9 weeks old, whether or not the source herd was affected by PMWS, but then showed contrasting patterns of increase and decrease by 12 weeks.
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