PMWS & PDNS Technical Zone Back to the Technical Zone Sign up for the Mailing list Go to the Discussion Forum thePigSite.com would like to thank Merial who's kind support made the publication of this article possible.

The first two days of the conference discussed comparative virology of DNA viruses of plants, birds, pigs and primates followed by two full days devoted entirely to the above diseases.

The meeting was sponsored by the French food safety agency (fafssa), The Institute for Animal and Agriculture Production (ISPAIA.), OIE, SFM, Fort Dodge, Merial, Intervet, Sogeval Laboratory and The Bretagne Region. It was an extremely well organised conference with excellent presentations and detailed proceedings published by the ESVV. Further details can be obtained from the Internet at www.zoopole.com.

The meeting was attended by over 300 delegates from most countries across the world particularly North America and Europe, where the diseases are now endemic with post weaning mortalities often reaching 30% or more and continuing.

Dr John Harding from Canada opened the conference and discussed the emerging and clinical studies of the diseases highlighting other conditions associated with PMWS including congenital tremors (CT) prenatal myocarditis, and necrotising pneumonia (PNP). Porcine circovirus type 2 (PCV2) now established as the initiating agent.

PCV2 is present is both diseased and healthy pig populations often at 100% level. PMWS is presented by wasting, usually commencing 2-3 weeks post weaning with dyspnoea, enlarged lymph nodes, diarrhoea, pallor and jaundice. Symptoms however vary from one farm to another and also may include coughing pyrexia, meningitis and sudden death. The disease does not affect sows or sucking pigs, only weaners with the peak incidence usually between 7 and 15 weeks of age.

This paper highlighted the lack of understanding on epidemiology or indeed the emergence of the disease. Work in Canada demonstrates that PCV2 actively circulates in the early post weaning stages and that horizontal transmission is a significant factor in the epidemiology. Current controls consist of all-in/all-out production with high levels of disinfection and hygiene between batches and the controlling of current disease on the farm.

Stocking densities are crucial overstocking being a major contributing factor. He reported that preliminary studies suggested certain genotypes are more susceptible than others and that both vertical and horizontal spread occurred. PCV2 is also shed in semen and may play a role in its dissemination. The other strain of circovirus PCVI in now considered non pathogenic.

The second paper by Joaquim Segalés from Spain discussed the pathological findings. These include non-collapsed lungs, broncho-pneumonia, enlargement of lymph nodes, a reduction in the size of the liver, jaundice, pale multiple foci in the kidneys and often gastric ulceration. In the lymphoid tissues, lymphocyte depletion, histiocytic inflammation and intracytoplasmic inclusion bodies with the presence of syncytial cells are characteristics of the disease. Interstitial pneumonia, interstitial nephritis and moderate to intense hepatitis are also often evident. The detection of PCV2 in tissues is carried out using in-situ hybridisation, immuno-histochemistry and indirect immunofluorescence.

Dr Sogalés also proposed a possible pathogenesis that in farrowing, nursing and growing pigs infection was by inhalation, followed by replication and systemic distribution of the virus. This could result in sub-clinical infection in an early phase. This could progress into a late phase with PMWS developing. The systemic distribution of the virus could result in antibody/antigen complexes leading to PDNS.

Dr Andre Jestin (France) discussed Porcine circovirus highlighting there are two groups within the family circoviridae. The first which includes PCV types 1 and 2 also contains some of the circoviruses in birds. The second group contain chicken anaemia virus (CAV) which is now classified within the circoviridae as gyrovirus.

He reported that the current prevalence of PCV2 in Brittany farms revealed a high serological response in fully grown sows and pigs on all farms and at 93% of pigs from 11-17 weeks of age were found positive in the herds with typical PMWS compared to only 54% in herds without symptoms. This is an important feature in that PCV2 is also present in many herds that do not show evidence of disease.

Dr Marinao Domingo (Spain) looked at the role of immunosuppression in PMWS. He reported that PCV2 is now considered the prime etiological factor in PMWS and its role as an immunosuppressive agent is now under active debate and supported by many areas of research. The end result of PCV2 invasion into lymphoid tissue is severe lymphoid depletion. There was active discussion at the conference as to whether this immunnosuppression is followed by immunostimulation and that it is probably a combination of these two factors that decide whether there is progression from an initial viraemia into disease.

Dr John Ellis from the UK presented an active debate on the role of satisfying Koch postulates in relation to PCV2. He reviewed PMWS and other concurrent infections in the field and discussed the significance that some herds have reported reproductive problems, associated with PCV2, with abortions or weak pigs and in particular myocarditis in new-born piglets.

He highlighted the fact that co-factors are required for full expression of PCV2 related diseases. These include porcine parvovirus (PPV), procine reproductive respiratory disease virus (PRRSV), encephalo-myocarditis virus and probably other as yet unidentified agents.

Dr Gordon Allan from Northern Ireland stimulated the audience with the results of his and co-workers experimental models and co-infections. It was at this stage that some "meat" started to appear from a practitioner level in the field.

His paper summarised work from various scientists in the field both from Canada USA, Denmark, Switzerland, Belgium and France (work supported by the EU). These results looked at infections in gnotobiotic (GN) and colostrum fed (CF pigs) and the conclusions drawn from this.

It is now been shown that piglets infected with PCV2 alone do not develop clinical disease but only show very mild histopathological changes. However piglets co-infected with PCV2 and porcine parvovirus (PPV) developed severe clinical disease and gross lesions of PMWS. Piglets infected with PPV or PCV1 did not develop disease or have gross or histological lesions.

It is now concluded that other factors are required to initiate an invasion of PCV2 virus into the immune system and activate disease. Recent work has also shown that disease occurs when the pig is immunostimulated by PRRSV and it is this immunostimulation that allows PCV2 to become pathogenic. Immunostimulation has also been demonstrated with adjutants such as Freund incomplete and others used in vaccines. Other unidentified agents present in commercial pig environments are also believed to be involved in this complex pathogenesis.

Dr Daniel Todd from Northern Ireland discussed the current knowledge of avian circovirus in disease and suggested that further investigations of circovirus in avian species could well be fruitful in respect of PCV2 infection.

Dr Maurice Pensaert from Belgium discussed the transmission of PCV2 from the sow to the litter. He was able to show that inoculating virus into foetuses less than 75 days of age produced severe disease but after 75 days no gross lesions were observed. Further he was able to show that the foetuses inoculated at between 75 and 95 days of gestation had both virus and antibodies present but farrowed down normally. How this affects the development of PMWS is as yet to be determined but in the one experiment there was no evidence of immuno-tolerance.

He reported that PCV2 can naturally cross the placenta and replicate to a high degree in the foetus. It is thought however that the high immune status of the sow population makes it rather an exceptional rather than a normal event. This is an important observation because it highlights the risks and possible benefits of PCV2 exposure during pregnancy.

Dr Madec and co workers from Ploufragan in France highlighted on-farm observations and the results of preliminary analytical epidemiology. These workers have published a set of twenty housing and management recommendations for severely affected farms. These essentially highlight the normal parameters for disease control, all-in/all-out, hygiene, air quality, stocking density, reducing stress and mixing. Field results showing the positive effects of these changes are clearly demonstrated.

Their studies have shown that most if not all farms are infected with PCV2 and they conclude that farm practices are the main trigger factor to the development of the disease. UK veterinarians however debated this conclusion pointing out that the disease was developing in the UK as a new pathogenic organism entering a naïve population. Whereas in Canada the disease is reported to die out, in herds in Europe and particularly in the UK high levels of mortality are still persisting in some herds two years after the initial event.

With the disease appearing across many countries in the world and the fact that PCV2 has been known to be present for many years makes it difficult to accept that management practices are the sole stimulation to the development of PMWS/PDNS.

Dr Madec however reported on an extensive field study, which clearly shows the importance of fundamental basic management in controlling but not eliminating PMWS.

Oral communications session

The main lectures were followed by a series of 10 minute oral communications covering the world situation, antibodies and virus detection, epidemiology, experimental infection, experimental vaccination and therapeutics, 47 papers in total. Salient points from these presentations can be summarised as follows

• High levels of viral load might be important in the development of the disease.
• High levels of serum antibody are present in 11-17 week old pigs on diseased farms but only low levels in disease free farms.
• PCV2 has been demonstrated in nasal cavities in higher levels than in serum. This suggests that transmission is by direct contact. The virus may be present in the nose in pigs with no clinical symptoms.
• Viral circulation may be present after recovering from disease. The time of infection may be important in the clinical outcome.
• Boars may remain viraemic for at least 3 months viraemic boars may excrete virus for long periods.
• PCV2 infection has been detected in Belgium since at least 1969.
• PCV2 may be involved in reproductive disorders.
• Boar sero prevelence was very high > 95% in AI centres in France. Infection occurs on farm prior to entry into the stud.
• PCV2 in pregnant non immune sows does not appear to cross the placental barrier.
• PCV2 infection may occur at birth but the significance of this is unclear.
• PMWS can be produced by the inoculation of conventional seronegative piglets. Immuno-stimulation did not appear to be important in the development of disease.
• Maternal antibodies via colostrum appear to protect piglets against disease challenge. Pigs with low levels developed disease.
• An experimental vaccine appears to protect piglets to challenge.
• Trials indicate that immuno stimulating drugs can potentiate the effects of PCV2 infections making pigs more susceptible to disease.
• Acetominophen given in-feed for 10 days, 13 days after weaning significantly reduced mortality in controlled trials.
• 20ml serum taken from blood from 100kg pigs on an infected farm were injected into pigs at 35 days of age. Mortality rates compared to controls were dramatically and significantly reduced in 3 trials from 15-18% to 3 to 5%.

Further details of these short communications can be studied in the proceedings.

Merial have produced an excellent booklet of a review of selected literature which was available to all registrants. If you would like a copy please send an email to Merial Customers Services who will be pleased to send you a copy.

The pig site would be pleased to receive any comments suggestions, information etc to continue the debate.

Finally an urgent plea was made by many researchers for desperately needed funds for further work into this devastating disease.

Practical Conclusions

As a result of these presentations, we have summarised some possible practical extrapolations onto the farm. However these should be discussed with your veterinarian. Read also the first (Yorkshire farm) Case Study on PMWS in our PMWS Technical Zone.

1. Vaccinate sows before farrowing against parvovirus.
2. Vaccinate sows pre farrowing with a killed vaccine against PRRS (Progressis, Merial).
3. Improve PCV2 antibody in the colostrum through stimulation of the sow in late pregnancy.
4. Consider the use of serum from finishing pigs within the infected herd given before 5 weeks of age.
5. Follow the Madec principles of good management.
6. Reduce transmission by needles, teething instruments etc. Use cautery for detailing.
7. Consider changing the timings of vaccinations of pigs if appropriate.

© thePigSite.com 2001 - Keeping you informed for FREE

thePigSite.com would like to thank Merial who's kind support made the publication of this article possible.

---

NOTE: Reference to commercial products or trade names within information provided by thePigSite.com does not constitute an endorsement by the thePigSite.com and does not imply discrimination against any other similar products.