Control Tools

• Diagnostics availability

• Commercial diagnostic kits available worldwide

  Largely available now

  Variety of qPCR tests for viral material in samples.

  Virus neutralisation tests for detection of antibodies (no commercial and only used in research) – unlikely commercial use).

  IPMA and ELISAS are the standard tests in most laboratories.

  PCV2 IHC or PCV2 ISH available in most laboratories worldwide.

  GAPS:

  Diagnosis is still complex, best made at the herd level with the necessary help of local laboratories, and high cost is an issue in a lot of cases and countries.

  Most growing / finishing pigs will display antibodies to PCV2 and/or PCV2 in serum but not all are “spreading PCVD”. An additional “risk marker” for spread of disease is needed, we do not have predictive tools.

  Taking into account that vaccination worldwide is very significant, tests aimed to differentiate vaccinated from naturally infected pigs may be of interest for studying infection dynamics in the vaccination context.

• Commercial diagnostic kits available in Europe

  See above, section “Commercial diagnostic kits available worldwide”.

• Diagnostic kits validated by International, European or National Standards

  Most kits are validated by state diagnostic labs.

• Diagnostic method(s) described by International, European or National standards

  Probably not easy to establish as yet.

• Commercial potential for diagnostic kits in Europe

  The existing tests are probably adequate.

  GAP: Consider pen-side test that assess need and/or impact of vaccination.

• DIVA tests required and/or available

  Not required and of little value as yet if agent is ubiquitous.

  GAP: May be useful in certain areas like in boars or SPF herds. However, as long as infectious pressure is lower and some batches may reach slaughterhouse seronegative against PCV2, to discriminate between natural infection or vaccination would be desirable.

• Opportunities for new developments

  Penside (e.g. micro-array) tests for diagnosis and estimate of viral load would be helpful if clear cut-offs are established. Need for predictive tools.

• Vaccines availability

• Commercial vaccines availability (globally)

  The major companies providing vaccines appear to be able to provide the supplies necessary worldwide.

• Commercial vaccines authorised in Europe

  Vaccines now freely available in Europe.

• Marker vaccines available worldwide

  No vaccines sold as marker vaccines are available, however, the subunit vaccines could be regarded as marker vaccines if diagnostic tests were developed targeting virus subunits not present in the vaccines.

  GAP: DIVA capability of sub-unit vaccines needs to be assessed.

• Marker vaccines authorised in Europe

  None.

• Effectiveness of vaccines / Main shortcomings of current vaccines

  All the vaccines appear to be successful in reducing losses due to PMWS and are capable of producing raised levels of colostral protection and to protect young piglets prior to acquisition of infection in the growing phase.

  GAPS:

  Mass vaccination by the intra-muscular route of the pig population is needed; possible improvements would be to reduce the number of injections or replace them with other easier routes and consider combinations.

  Improvement of combined vaccines is needed.

• Commercial potential for vaccines in Europe

  Probably limited in the short-term as adequate solutions are in place, but it is likely that as more knowledge of the pathogenesis of PCV2 infections is generated it may be possible to develop new vaccines based on molecular advances.

  GAPS:

  See also section “Effectiveness of vaccines/main shortcomings of current vaccines”.

  Consider options that could reduce production costs and allow better export outside of EU (Asia and Africa).

• Regulatory and/or policy challenges to approval

  GAP: The lack of very demonstrative challenge model is an obstacle to RA approval.

• Commercial feasibility (e.g manufacturing)

  Depends on demand for other vaccines eg new swine flu etc and priorities but PCV2 is the second major viral threat to pigs behind PRRSV.

  GAPS:

  See also section “Effectiveness of vaccines/main shortcomings of current vaccines”.

  Reduction of production costs would always benefit access.

  The ability to market a new vaccine against a sudden very significant genetic variant and an emergency situation is not present.

• Opportunity for barrier protection

  Very limited due to ubiquitous and resistant nature of virus.

• Opportunity for new developments

  The vaccines work, however improved vaccines and vaccination schedules would be great.

  GAPS:

  Efficient vaccination schedules and criteria for start of vaccination taking into account maternal interference/ protection and cost-benefit.

  See also section “Effectiveness of vaccines/main shortcomings of current vaccines”.

• Pharmaceutical availability

• Current therapy (curative and preventive)

  None.

• Future therapy

  None predicted.

  GAP: May be new generations of T-cell stimulants will be developed or intermediary metabolism modulators.

• Commercial potential for pharmaceuticals in Europe

  At the moment probably slight.

• Regulatory and/or policy challenges to approval

  Probably none necessary at the moment.

• Commercial feasibility (e.g manufacturing)

  As such a huge disease with no obvious world wide differences in virus it will be possible to produce vaccines for world wide use and not have to consider drug therapy.

• Opportunities for new developments

  As molecular understanding of viral pathogenicity so new developments may take place.

  GAP: The effect of existing antiviral drugs against PCV2 is not known; this might have bearings on similar small “circular” human viruses which roles are not yet clearly understood.

• New developments for diagnostic tests

• Requirements for diagnostics development

  GAPS: See section “Commercial diagnostic kits available worldwide”. Penside tests to facilitate estimate of viral load.

• Time to develop new or improved diagnostics

  Impossible to say as will be based on elucidating pathogenicity and immunological characteristics yet unknowns.

  GAP: This sort of test would enable vaccination to precede active infection so the sooner the better, as well as managements of vaccination at the herd level and cost control.

• Cost of developing new or improved diagnostics and their validation

  Classical for similar tests.

• Research requirements for new or improved diagnostics

  Continuing EU wide support for multidisciplinary approaches to PCV2 research.

  GAP: Especially, surveillance of PCV2 populations and elucidating pathogenicity and immunological markers.

• Technology to determine virus freedom in animals

  Unlikely to be made possible unless there is a great reduction in the level of this naturally occurring virus.

• New developments for vaccines

• Requirements for vaccines development / main characteristics for improved vaccines

  Mass vaccination by the intra-muscular route of the pig population is needed for effective control now

  Continual search for easier administration eg in the water or in the aerosol form is necessary for farmer co-operation in reducing the incidence of pig disease.

  GAPS: Possible improvements would be to reduce the number of injections or replace them with other easier routes and consider combinations.

• Time to develop new or improved vaccines

  This process is already continuing in those companies associated with pig vaccine production.

• Cost of developing new or improved vaccines and their validation

  Classical for similar products.

  GAP:

  An accepted challenge model for animal of various ages in non infected and infected situations is not available.

  Any challenge model to assess PCV2 effect on reproductive parameters is not available.

• Research requirements for new or improved vaccines

  Continuing research on the fundamental immunology of the pig and its relation to PCV2 infection (Pathogenicity, immunology).

• New developments for pharmaceuticals

• Requirements for pharmaceuticals development

  Probably not applicable until new antivirals become effective in farm animals.

• Time to develop new or improved pharmaceuticals

  Unknown, as yet no pharmaceuticals exist yet.

• Cost of developing new or improved pharmaceuticals and their validation

  Unknown, as yet no pharmaceuticals.

• Research requirements for new or improved pharmaceuticals

  Unknown, as yet no pharmaceuticals.

Disease details

• Description and characteristics

• Pathogen

  Porcine circovirus type 1 is a non-pathogenic virus found as a contaminant of porcine cell lines and in pigs. Porcine circovirus type 2 (PCV2) is associated with several disease manifestations in pigs. No pathotypes of type 2 have been found although the isolated strains of type 2 are now called 2a (older or 422 like pattern), 2b (newer or 321 like pattern), and 2c (identified in archived tissues in Denmark). Recently a new strain has been identified and has been named 2d; a potential genotype 2e has been proposed as well. Most of the strains or isolates of the virus appear to have high level of homogeneity at the nucleotide level. PCV2 is the necessary but not usually self-sufficient cause of a variety of manifestations of what has become known as porcine circovirus diseases (PCVD); the most important PCVD is PCV2-systemic disease.

  GAPS:

  The molecular characterization of PVC2 has largely been used in phylogenetic analysis but the impact of the diversity and impact of specific mutations on vaccine cross-protection and virulence has not been assessed.

  There is a need to continue surveillance and the evolution of the PCV populations, as vaccination pressure increases.

  There is a need to access the biological impact of diversity.

• Variability of the disease

  There are some indications that the severity of the disease is linked to the emergence of specific genotypes (genotype 2b). The variability of disease may, however, also be related to many other factors such as immune status to PCV2, time of infection, pig genetics, standards of management in the widest sense, and in particular to the health of the herd and the other concurrent diseases.

  GAPS:

  The history and circumstances for PCV2 emergence are largely unknown; and it is not possible to predict the appearance of new, more pathogenic versions of the virus.

  The role of co-infections with other small DNA-virus could be of importance in future vaccine development and deserves further studies. Nowadays, an apparent genotype shift from PCV2b to PCV2d is occurring, but the cause of it is unknown. Ten-to-fifteen years ago, the shift from PCV2a to PCV2b was linked with occurrence of severe outbreaks of disease.

• Stability of the agent/pathogen in the environment

  The virus is the smallest of the porcine viruses (together with porcine parvovirus, with which PCV2 occasionally occurs) and it is one of the most ubiquitous and resistant viruses. It is stable, resistant to pH 3.0, chloroform and to temperatures of 70 degrees C for 15 minutes. On the farm, only heat or steam in combination with Virkon S at the maximum strength is effective. If there is any organic matter PCV2 will survive. In farrowing accommodation this is usually the case and PCV2 is readily available to infect newborn piglets.

  GAP: There is little information obtained specifically with PCV2 on survival in biological products (meat and meat products, pig sera and/or semen, etc…).

• Species involved

• Animal infected/carrier/disease

  All species of pigs appear to be affected including wild boar and feral animals. Many pigs are infected without displaying clinical symptoms of disease and some of these animals act for certain as carriers.

  GAPS: Identification of infected animals that is likely to spread PCV2 and thereby contribute to the spread and development of PCVD.

• Human infected/disease

  No evidence of human infection.

  GAPS:

  Some vaccines used for humans have been found to contain PCV2 and other small DNA viruses, but studies have not shown any impact on human health to date.

  Some human cell lines can be infected with PCV1 or PCV2.

• Vector cyclical/non-cyclical

  No evidence of vectors. Probably most pigs are infected.

  GAP: This aspect has not been explored, but should be addressed if herds are to be declared free of the virus.

• Reservoir (animal, environment)

  There has not been found to be any reservoirs. It is closely related to other circoviruses, in particular, Psittacine beak and feather disease virus, Canary circovirus, Goose circovirus, and Pigeon circovirus. This group of viruses are distant related to plant viruses but there has not been any evidence to suggest that these may be a reservoir.

  GAP: This aspect has not been explored, but should be addressed if herds are to be declared free of the virus.

• Description of infection & disease in natural hosts

• Transmissibility

  Transmits easily because of ubiquitous nature in the environment but in experiments PCV2 in-contacts are not always infected and certainly does not always produce disease. It depends also on the levels of immunity against the virus and the dosis.

  GAPS: Sensitive bio-assays to assess transmissibility from semen in parallel to PCR counts and transmissibility to pregnant gilts and sows are lacking.

• Pathogenic life cycle stages

  Pig to pig transmission either direct or indirect has been identified as the only cycle.

  GAP: The role of piglets persistently infected at births need to be clarified.

• Signs/Morbidity

  There is a wide variety of clinical syndromes produced or associated with this virus. Known collectively as PCVD, the first to be identified was the Postweaning Multi-Systemic Wasting Syndrome (PMWS; nowadays referred as PCV2-systemic diseases) in which disease in young pigs was characterised by wasting, fever, lethargy, weight loss, dyspnoea, jaundice, lymphadenopathy (lymphoid depletion, necrosis, histiocytosis, viral inclusions and syncytia) and the presence of detectable PCV2 in the tissues (ISH or IHC detection). In many pigs, thymic atrophy and granulomatous enteritis were also identified. Not all the pigs with PCV2 infection develop PMWS. When there is co-infection with parvovirus and/or PRRSV, the disease is much worse.

  In the early cases in the UK there was also a severe skin /kidney syndrome called Porcine Dermatitis and Nephropathy Syndrome (PDNS) which was extremely difficult to differentiate from ASF/CSF but which was later shown to be associated with PCV2, but has been also associated with secondary bacterial disease with a hypersensitivity reaction usually to gram negative bacteria eg Pasteruella and Mannheimia. It is characterised by red-purple discolouration in the skin marking vasculitis and the deposition of immune complexes which also cause a severe necrotising glomerulonephritis. Another reported syndrome is the Reproductive failure which is manifested as mid-late term abortions or farrowings with increased numbers of stillborns and mummies. In many cases the piglets have enlarged flaccid hearts with myocarditis with demonstration of moderate to high amount of virus in the lesions. One publication has suggested that PCV2 may be associated with congenital tremor but there has not yet been universally accepted and experimental proof is lacking to date.

  Sporadically, Encephalitis has been reported with PCV2, but also linked to PMWS status.

  Some reports link PCV2 infection with ear-necrosis outbreaks, but its relationship is rather unclear.

  GAPS:

  The role of PCV2 in PDNS has not been clarified; this syndrome is still mostly a mystery and we do not know its causes.

  The role of PCV2 on reproductive disorders has been relatively poorly investigated under field conditions. Moreover, its potential association with embryo death and return-to-estrus deserve much more investigation, mainly field investigation.

• Incubation period

  Varies considerably, probably 14-28 days.

  GAP: Pure effect of possible pathotypes has not been elucidated.

• Mortality

  Very variable, may be from 1-40%.

  GAP: Pure effect of possible pathotypes has not been elucidated.

• Shedding kinetic patterns

  As far as one can tell the virus can be shed from all available surfaces, orifices and secretions including blood, colostrum faecal material and semen.

  GAP: Kinetics and circumstances of shedding are mostly unknown and should be studied in details.

• Mechanism of pathogenicity

  The exact cell types involved in the replication/spread and pathogenicity of PCV2 infections has still not been definitively determined, even it is known that epithelial and endothelial cells play a major role (together with a low proportion of macrophages and even some subsets of lymphocytes). There is a high involvement of other pathogens. PRRSV may concurrently occur in 40% of the cases, M. hyo in 27%, and other bacterial species in >10%. In a few cases swine influenza virus is involved. There is a strong association between PCV2 and PRRSV in PDNS cases. PCV2 as a single causative occurrence is a rare event.

  Certainly PCV2 reduces PRRSV vaccination efficiency. Some of the worst cases are seen in conjunction with porcine parvovirus type 1 (classical parvovirus). This combination of the two smallest viruses requiring cell structures to replicate them occurs in approximately 15% of the cases.

  The occurrence of enzootic pneumonia is also an exacerbating factor and some authorities have thought that the immune stimulation associated with M. hyo vaccination may potentiate PMWS.

  The mechanism of pathogenicity is still largely unknown. The virus is so small it does not possess a virally encoded DNA polymerase and therefore relies on the host cell enzymes. It replicates best in the cells in the S phase of the cell cycle, eg myocardiocytes in late gestation, kidney around birth and the 2 weeks after and then in epithelial and endothelial cells and cells of the macrophage/monocyte system. It probably attaches to receptors through heparin sulphate and glycos-aminoglycans and is then replicated in the cell and released in huge amounts from the cells. It is probably stored in the dendritic cells. The virus or parts of the virus (nuclic acid) is found in a non-replicative form in dendritic cells and are belived to modify the cytokine profile of these antigenpresenting cells. The degree of severity of clinical signs and the severity of the lymphoid depletion may have a direct correlation with the amount of circulating virus detected in the blood.

  GAPS:

  The mechanisms of pathogenicity are largely unknown.

  The potential immune modulatory role of PCV2, especially its effect on professional antigen presenting cells needs to be clarified.

  Factors that activate the replication of PCV2 need to be identified, especially in PMWS phases when all tissues seem to be suddenly involved.

• Zoonotic potential

• Reported incidence in humans

  Never reported.

• Risk of occurence in humans, populations at risk, specific risk factors

  None.

• Symptoms described in humans

  None.

• Estimated level of under-reporting in humans

  Not likely to have occurred.

• Likelihood of spread in humans

  Not likely to have occurred.

• Impact on animal welfare and biodiversity

• Both disease and prevention/control measures related

  The ubiquitous nature of the virus, its resistance in the environment and as yet not understood effects on the host make it very difficult to control. It is a great blessing that the vaccines available appear to exert such a good degree of control.

  GAP: Clarifying the circumstances of PCV2 emergence as a pathogen could help understand the evolution of viral populations in changing environments and may be of interest for the study of microbial biodiversity in general.

• Endangered wild species affected or not (estimation for Europe / worldwide)

  Probably not as vaccination will protect although wild boar can be affected.

  GAP: Situation unknown in Africa.

• Slaughter necessity according to EU rules or other regions

  Only as a welfare case.

• Geographical distribution and spread

• Current occurence/distribution

  Worldwide.

• Epizootic/endemic- if epidemic frequency of outbreaks

  Endemic.

  GAP: The possible trend of cyclical smaller epidemics in a globally endemic situation should be explored.

• Seasonality

  Not yet identified.

• Speed of spatial spread during an outbreak

  Progressive spread through a unit over 3-6 months. Virus has been around years before been associated to any pathogenicity despite that typical PMWS lesions has been described years before the big outbreaks. This is one of the big puzzles of the PMWS “epidemic”.

  GAP: Identification of factor(s) that contribute to the pathogenicity of PCV2 infection.

• Transboundary potential of the disease

  Will cross if pigs or pig related products cross.

• Route of Transmission

• Usual mode of transmission (introduction, means of spread)

  PCV2 is usually introduced from infected pigs directly or indirectly. PMWS always behaves like an infectious disease.

  GAPS: Most pigs are seropositive to PCV2, how to identify those that contributes to the spread of PCVD. The dynamics over time within herds are also unknown at present and so is the reason for the apparent shift in age preference over time.

• Occasional mode of transmission

  Probably through semen from boars or AI. Possibly blood or needles or aerosol spread.

  GAPS: See above section “Transmissibility”.

• Conditions that favour spread

  Only one- lack of cleaning with complete removal of organic material and disinfection using approved disinfectant such as Virkon S at full strength.

  GAPS:

  See above section “Transmissibility”.

  The massive use of vaccination has diminished significantly the infectious pressure with PCV2. This implies a change in the epidemiology of the virus, creating subpopulations of animals (including those to be used as gilts) which are seronegative and susceptible to the viral infection.

• Detection and Immune response to infection

• Mechanism of host response

  Neutralising antibodies and cellular immune response (measured as IFN-gamma producing cells) are considered the major immunological components in order to control infection. In PDNS there is a hypersensitivity type 3 reaction triggered and then pro-inflammatory stimulation predisposes to secondary bacterial infection. PCV2 is immunosuppressive however; on the contrary immunostimulation has been shown to promote PMWS development.

  GAPS:

  Clarification of the immune modulatory role of PCV2.

  The role of cell-mediated immunity to PCV2 is not yet known and should be investigated.

  Lack of understanding of PDNS, which might be related to hypersensitivity.

• Immunological basis of diagnosis

  Pigs with PCV2 infections appear to mount a strong PCV2 specific antibody response, mostly directed against the ORF2 capsid. The maternal antibodies appear to decrease during the period 3-11 weeks depending on the sows’ antibody levels and then increase to around 15 weeks in PMWS affected herds or later in subclinically infected herds. Experimentally, antibodies appear about 14 days after infection whereas neutralising antibodies appear about 21 days post-infection. In pigs with PMWS compared with pigs with PCV2 infection but no PMWS there are lower levels of neutralising antibody and IgM isotype antibodies. IgM antibodies indicate active infection. In sub-clinical pigs increased IL-10 leads to a higher ratio of IgG to IgM. High neutralising antibody titres do not necessarily mean there is protection. It may be that PCV2 employs a decoy mechanism to avoid the defences. Interleukin IL-10 is responsible for the suppression of TH1 cells. Generally, IL-10 and pro-inflammatory cytokines are increased in PCV2 infections and there is a decrease in general antiviral responses. The role of interferons is not understood, but a significant IFN-alfa and IFN-gamma responses are related to protection. Complex and multifactorial mechanisms occur in PCV2 induced PMWS. In an infected, but asymptomatic animal, PCV2 may co-exist with the host by undergoing minimal replication and inducing a limited host, balanced TH1/TH2 response. There are many triggering factors of the disease process eg stress, exposure to other pathogens, host genetics and at the molecular level these probably induce increased viral replication.

  GAPS:

  The mode of action has only begun to be delineated; kinetics of responses are as important as the responses themselves and should be documented; we could benefit from acquiring more information about responses directed against ORF1 protein.

  Serological tests are not helpful for diagnosis as most pigs are seropositive; we lack any predictive test that would identify pigs that will indeed progress to severe disease

• Main means of prevention, detection and control

• Sanitary measures

  Effectiveness is only complete with all in/ all out, cleaning and disinfection with recognised disinfectant, use of hospital units for sick animals and reduction of stock density.

• Mechanical and biological control

  None, except implementation of tender loving care for piglets, i.e. proper management with minimum disruption (Francois Madec’s 20 point plan).

• Diagnostic tools

  Clinical signs, gross post-mortem, particularly enlarged inguinal lymph nodes, histopathology with demonstration of PCV2 material by IHC or ISH. Quantification of virus load has been used for diagnosis in some countries but the results are doubtful as a diagnostic tool to predict clinical impact.

  GAP: Reliable diagnostic parameters for diagnosis of PCVD on live animals should be established, especially if they have some predictive value.

• Vaccines

  Vaccines for control of PCV2 infections in sows and piglets are available both Baculovirus expressed and inactivated full-virus vaccines.

  GAP:

  Conditions in which maternal immunity interference occurs should be defined.

  Impact of viral diversity on vaccine coverage should be accessed in more details.

• Therapeutics

  Not available.

• Biosecurity measures effective as a preventive measure

  No real control except general biosecurity. Herd closure and eradication may be possible, but is not widely used.

  GAP: It is not clear if herds can be declared and remain free of PCV2 – some projects have shown that reintroduction into negative herds occurs frequently but more studies are needed.

• Border/trade/movement control sufficient for control

  No real effective possibilities as PCV2 are ubiquitous.

  GAP: Methods for identification of carrier/shedding animals are needed.

• Prevention tools

  None except thorough cleaning and disinfection to reduce the level of virus uptake.

  GAP: Vaccination as a tool to avoid introduction of PCV2 in free herds should be examined.

• Surveillance

  Sequencing is necessary to plot changes in the virus over time and identification of genetic changes that may indicate sites of virulence in the genome and any new viruses.

  GAP: Mapping of genetic changes over time and geographic location could be useful.

• Past experiences on success (and failures) of prevention, control, eradication in regions outside Europe

  Vaccine provision and serious improvements in care of young piglets is highly successful.

  GAP: An eradication protocol was applied in a farm in Spain by means of mass vaccination. While vaccinating, the virus was not able to be found. More insights on mass vaccination programs at a regional level may help on assessing the real feasibility of eradication.

• Costs of above measures

  Impossible to estimate globally, although several tools or systems exist to monitor vaccination impact at farm or production sites levels.

  GAP: Refinements of economical tools to assess the impact of such endemic diseases are needed; they would be useful for most other similar diseases as PRRSV, M. hyo etc.

• Disease information from the OIE

• Disease notifiable to the OIE

  No.

• OIE disease card available

  No.

• OIE Terrestrial Animal Health Code

  N/A.

• OIE Terrestrial Manual

  N/A.

• Socio-economic impact

• Zoonosis: impact on affected individuals and/or aggregated DALY figures

  In some instance, it brought pig farmers to (the brink of) bankruptcy and despair; in early days was the direct cause of pig farms being closed. Probably little effect now with access to vaccination.

  Complete loss of profitability due to variation in growth rate increased morbidity and mortality and reproductive failure together with increased veterinary charges.

  GAP: See section “Main means of prevention, detection and control - Costs of above measurers”.

• Zoonosis: cost of treatment and control of the disease in humans

  See section “Impact on affected individuals and/or aggregated DALY figures”

• Direct impact (a) on production

  Huge potential impact (huge decrease in number of finishing pigs per sow per year), but impact has been mitigated now that vaccines are widely used.

  GAP: See section “Main means of prevention, detection and control - Costs of above measurers”.

• Direct impact (b) cost of private and public control measures

  Impossible to say but huge prior to vaccination.

  GAP: See section “Main means of prevention, detection and control - Costs of above measurers”.

• Indirect impact

  Indirect impact was on provision of supply of finishing pigs at the correct grade at the time required.

  GAP: See section “Main means of prevention, detection and control - Costs of above measurers”.

• Trade implications

• Impact on international trade/exports from the EU

  None probably except for exports to Australia.

• Impact on EU intra-community trade

  Probably few apart from some regulation from some countries on import of semen from other member states.

  GAP: See section “Transmissibility”.

• Impact on national trade

  Unknown.

  GAP: See section “Main means of prevention, detection and control - Costs of above measurers”.

• Main perceived obstacles for effective prevention and control

  None now there is effective vaccination.

  GAP: Need to control PRRS, Mycoplama and swine influenza infections as well.

• Main perceived facilitators for effective prevention and control

  Private veterinary surgeons instituting health control programmes based on vaccination schemes and biosecurity controls.

  GAP: Need to maintain surveillance of the viral populations under vaccination pressure.

• Links to climate

  Seasonal cycle linked to climate

  Not noticed so far.

  GAPS: Resistance and/or sensitivity to climate variations are not clearly known, although the virus is very resistant.

• Distribution of disease or vector linked to climate

  Not linked to climate at all.

• Outbreaks linked to extreme weather

  No linkage yet identified.

• Sensitivity of disease or vectors to the effects of global climate change (climate/environment/land use)

  None noted.

Risk

• Virus changes suddenly that present vaccines do not work and we are back to the original scenario.

  GAP: Continue to monitor PCV populations under vaccination pressure.

Main critical gaps

Conclusion

• We need to know why this virus existed in the pig population for a long time and then in the mid to late 1980s suddenly started to cause disease. This can only have happened due to a change in the virus (not yet shown); a change in the environment of the pig (increased production, loss of labour and therefore disappearance of care, Madec’s 20 point plan); or changes in the genetic makeup of the pig (loss of genes or selection of wrong criteria) and/or a combination of those.

  GAPS:

  The availability of effective vaccines might prevent funding more research as the threat is no so acute any more; however we do need to continue viral population monitoring, and to study pathogenicity and immunology especially for diagnostic improvements. A repeatable, reproducible model of experimental disease is still missing.

  Reliable economical tools for fine costs/benefits assessments are also needed.

Sources of information

• Expert group composition

  Expert group members are included where permission has been given

  Lars Erik Larsen, National Veterinary Institute, Technical University of Denmark (DTU) - [Leader]

  Catherine Charreyre, Merial/Boehringer Ingelheim

  Tanja Opriessnig, The Roslin Institute, University of Edinburgh, UK

  Joaquim Segalés, CReSA-IRTA and Universitat Autònoma de Barçelona, Spain

  Caroline Fossum, Swedish University of Agricultural Sciences (SLU), Sweden

  Gordon Allan, Queen’s University Belfast, Northern Ireland, UK

  Poul Baekbo, SEGES, Denmark

• Reviewed by

  Project Management Board.

• Date of submission by expert group

  10 October 2016

• References

  26th April 2011.