Diseases

Swine Vesicular Disease

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Control Tools

  • Diagnostics availability

  • Commercial diagnostic kits available worldwide

    Two companies commercialise an ELISA kit for detection of antibodies.

    Reagents for antigen detection ELISA and for antibody detection by competitive ELISA (as described in the OIE manual) are available from the two OIE reference laboratories

    GAP: No commercial kit is available for RT-PCR, that has become the gold test for virus detection in samples with low virus load, like faeces.

  • Commercial diagnostic kits available in Europe

    See Section “Commercial Diagnostic kits available worldwide”.

  • Diagnostic kits validated by International, European or National Standards

    The 5B7-competitive ELISA for antibody detection is reported in the OIE manual, but also commercial ELISAs underwent validation in several EU National Reference laboratories. They performed similarly well in proficiency tests run by the EU Reference Laboratory and could be considered as reference screening tests.

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

    All assays mentioned at 16.3 section are reported in the EC Decision 2000/428 and in the O.I.E. Manual of Diagnostic tests and vaccines for terrestrial Animals.

  • Commercial potential for diagnostic kits in Europe

    Low, as a national surveillance programme is implemented only in Italy.

  • DIVA tests required and/or available

    Not required, as vaccine is not authorised or used in Europe nor worldwide.

  • Opportunities for new developments

    Currently available diagnostic tests are valid tools. The newly described real time RT-PCR tests have been validated on only a small number of samples. More validation and comparison with conventional PCR and virus isolation would be desirable.

    GAPS:

    Observed variability in genome segments target of real-time PCR affects detection of a few strains. Improvement in order to detect all strains with a single real-time PCR would be desirable.

    Rather than new developments, a modification of recommendations for use of available tests should be considered.

    For example, extensive experience suggests that, for antibody detection, ELISA is more reliable and robust than VNT, so that there is no need to confirm by VNT multiple positive samples detected by ELISA. VNT can remain the reference test to confirm the singleton reactor cases.

    Similarly, RT-PCR proved to be more sensitive and reliable than virus isolation (still indicated as the gold standard test).

  • Vaccines availability

  • Commercial vaccines availability (globally)

    None.

  • Commercial vaccines authorised in Europe

    None and not permitted to use vaccines.

  • Marker vaccines available worldwide

    None.

  • Marker vaccines authorised in Europe

    None.

  • Effectiveness of vaccines / Main shortcomings of current vaccines

    Not applicable as no vaccines in use.

    Vaccination is not convenient as a control tool for SVD. Although humoral response with neutralizing antibodies is expected to be effective against SVD, cost/benefit evaluation of vaccine production does not support this practice because: the disease is mostly sub-clinical and studies indicate that a DIVA strategy is difficult to be developed for SVDV.

  • Commercial potential for vaccines in Europe

    None, see previous points.

  • Regulatory and/or policy challenges to approval

    Not applicable at present.

  • Commercial feasibility (e.g manufacturing)

    No clear market.

  • Opportunity for barrier protection

    Barrier protection not applicable by vaccination.

  • Opportunity for new developments

    Not required and applicable, based on above considerations.

  • Pharmaceutical availability

  • Current therapy (curative and preventive)

    None, not applicable.

  • Future therapy

    None, not applicable.

  • Commercial potential for pharmaceuticals in Europe

    None.

  • Regulatory and/or policy challenges to approval

    Not applicable.

  • Commercial feasibility (e.g manufacturing)

    Not required.

  • Opportunities for new developments

    Not required, not applicable.

  • New developments for diagnostic tests

  • Requirements for diagnostics development

    See “Opportunities for new developments”.

    GAPS:

    Development / validation of real-time RT-PCR able to detect all virus variants by a single test.

    Extended sequencing of isolates with new technologies like NGS for full genome sequence would help in selection of best matching primers and probes for application in new RT-PCR assays, in addition to provide indications of virus evolution.

  • Time to develop new or improved diagnostics

    2 years for the above gaps to be filled.

  • Cost of developing new or improved diagnostics and their validation

    Main cost is for human resources and vary in different labs/countries. Sequencing and development studies for diagnostic test development could be quantified in the range 300,000-400,000 euro, including personnel costs.

    Strategic samples are essential and are available in very few labs.

    Restrictions in place for handling infectious material in BSL3+, authorized labs.

    GAPS:

    Despite reasonable costs, no funds have been dedicated internationally to research and development on SVD for several years.

  • Research requirements for new or improved diagnostics

    See Section “Requirements for diagnostics development” and “Diagnostics availability – Opportunities for new development”.

  • Technology to determine virus freedom in animals

    The disease is mainly subclinical, evidence of SVD-freedom must be based on laboratory investigations, in particular:

    • RT-PCR methods for evidence of no virus shedding in faeces)
    • Serological screening for evidence of absence of antibodies.
    GAP: Evidence of disease freedom based only on absence of clinical signs is inadequate, given the sub-clinical occurrence of the infection. Nevertheless, active laboratory-based surveillance to demonstrate virus freedom is applied only in Italy.

  • New developments for vaccines

  • Requirements for vaccines development / main characteristics for improved vaccines

    Not required.

  • Time to develop new or improved vaccines

    Not applicable.

  • Cost of developing new or improved vaccines and their validation

    High.

  • Research requirements for new or improved vaccines

    None , vaccination not applicable.

  • New developments for pharmaceuticals

  • Requirements for pharmaceuticals development

    None.

  • Time to develop new or improved pharmaceuticals

    Not applicable.

  • Cost of developing new or improved pharmaceuticals and their validation

    Not applicable.

  • Research requirements for new or improved pharmaceuticals

    None.

Disease details

  • Description and characteristics

  • Pathogen

    Swine Vesicular Disease virus (SVDV) is a member of the genus Enterovirus within the family Picornaviridae, and is a porcine variant of the human pathogen coxsackie B5 virus. The virus has a positive sense single-stranded RNA genome encoding four capsid proteins (VP1, VP2, VP3 and VP4) assembled in a capsid of icosahedral symmetry, and several non-structural proteins.

  • Variability of the disease

    Phylogenetic and molecular clock studies suggest that SVDV evolved from approximately 1940 onwards as a genetic recombination of the human pathogen coxsackievirus B5 to which it is antigenically related and coxsackievirus A9 for which sequence similarity has been detected in the genome coding for non-structural proteins.

    SVDV occurs as a single serotype, in which four congruent groupings were found in both the genetic and antigenic properties of the virus. The most recent group consists of viruses isolated from the European Union since 1992. Isolates of this variant, collected in a 25-year period mostly in Italy, showed a gradual nucleotide substitution rate. Two genomic sublineages have been described within the most recent group, one evolved in Italy and another one detected firstly in Portugal in 2003 (and again in 2006) and later on also in Italy. A recombinant event between these two sub-lineages has been demonstrated in isolates from Italy.

    SVDV is unrelated to other porcine enteroviruses.

  • Stability of the agent/pathogen in the environment

    Temperature:

    Generally very stable.

    Preserved by refrigeration and freezing, inactivated at 56°C (> 4 log10 reduction per hour).

    pH:

    Resistant at pH 2 - 12.

    Disinfectants:

    In the environment and in the presence of organic matter, SVDV is inactivated by sodium hydroxide 1%, and formaldehyde ≥ 2%.

    Survival:

    SVDV is extremely resistant and can survive for several months in the environment. Resistant to fermentation and smoking processes. The estimated time needed for 1 log10 reduction at 4°C is approximately 60 days. It has been shown that SVD virus can be detected in hams cured for 180 days, in dried sausages for >1 year, and in processed intestinal casings for >2 years.

  • Species involved

  • Animal infected/carrier/disease

    Swine (domestic and wild pigs) are the only susceptible species.

    The carrier state was experimentally shown to be a very rare sequel to infection with SVD virus and is therefore not significant in the epidemiology of the disease.

  • Human infected/disease

    SVD virus has evolved from the human enterovirus coxsackievirus B5 to which it is antigenically related, but transmission of CV-B5 between pigs does not occur. Seroconversion or disease was never reported in farmers or veterinarians working with infected pigs; however, seroconversion in humans has rarely occurred in laboratory workers associated with mild flu-like clinical disease, with exception of one case of association with meningitis.

  • Vector cyclical/non-cyclical

    None.

  • Reservoir (animal, environment)

    Pigs are the only species that are naturally infected. No reservoir hosts are known.

  • Description of infection & disease in natural hosts

  • Transmissibility

    Direct contact with infected pigs or indirect contact via contaminated people, the environment and non-animate objects. Transmission route: oral (main), skin and mucosal lesions. Infectious sources: faeces (major), vesicular fluid, contaminated meat scraps and swill. Airborne transmission of SVDV is insignificant. In many areas transmission of SVD between farms seems to occur with extremely low incidence, but the control of SVDV transmission in a densely populated livestock area can be difficult, as experienced in an area with 2500 pigs/km2 in Lombardy, Italy, where apparently unconnected outbreaks occurred within a 3 km protection zone during 3 months, despite the use of stamping out and stringent control measures adopted for eradication.

  • Pathogenic life cycle stages

    Not applicable.

  • Signs/Morbidity

    SVD is characterised by development of vesicles on the coronary band (sometimes resulting in loss of the hoof), interdigital spaces, and occasionally on snout, lips, tongue and teats; shallow erosions may be seen on the knees. Pigs may become temporarily lame. Transient fever up to 41°C can occur. Recovery is usually complete within two to three weeks.

    The disease may be subclinical, mild or severe, depending on the strain of virus involved, the route and dose of infection, and the husbandry conditions. Morbidity rate in herds may be low but high in pen/contact groups. The main importance of SVD is that it is clinically indistinguishable from foot-and-mouth disease and other vesicular diseases. However, outbreaks of SVD that have occurred during the last decade have been characterised by less severe, or no clinical signs.

  • Incubation period

    The incubation period is between 2 and 7 days.

  • Mortality

    Mortality due to SVD is extremely rare.

  • Shedding kinetic patterns

    Affected pigs may excrete virus from the nose and mouth and in the faeces up to 48 hours before the onset of clinical signs. Most virus is produced in the first 7 days after infection, and virus excretion from the nose and mouth normally stops within 1 - 2 weeks. Virus has once been detected up to 3 months in the faeces, but mostly virus is gone from faeces earlier. All tissues contain virus during the viraemic period.

  • Mechanism of pathogenicity

    SVD virus has tropism for epithelial tissue (skin and mucosa of digestive tract). Vesicle formation is the only known lesion directly attributable to the infection.

  • Zoonotic potential

  • Reported incidence in humans

    Very few human cases have been reported many years ago in laboratory workers with contact with SVDV, but never in farmers or veterinarians working with infected pigs.

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

    Almost none.

  • Symptoms described in humans

    Clinical signs included mild influenza-like symptoms (fever, malaise) with generalized abdominal and muscle pain and weakness. One case was associated with an aseptic meningitis. All human cases recovered without sequelae.

  • Estimated level of under-reporting in humans

    None.

  • Likelihood of spread in humans

    None.

  • Impact on animal welfare and biodiversity

  • Both disease and prevention/control measures related

    At present, SVD has often a sub-clinical course and usually the direct impact of the disease in pigs is quite low. The restriction of animal movement (protection and surveillance zones) may cause sanitary and welfare problems.

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

    No.

  • Slaughter necessity according to EU rules or other regions

    According to EU legislation a stamping out policy must be applied in infected premises. In seropositive herds where virus is not detected, seropositive pigs must be slaughtered.

  • Geographical distribution and spread

  • Current occurence/distribution

    SVD was first recorded in Italy in 1966. Later, outbreaks occurred in several European countries and Eastern Asia during the 1970s, early 1980s; then the disease has continued to persist in Italy until the present day and has reappeared in the European Union, outside Italy, on sporadic occasions since 1992. In Italy, the frequency of detecting SVD virus is decreasing, with only 1-4 cases per year detected in clinically normal pigs during surveillance activities in the last five years, and restricted in the two non-accredited southern regions. The other European countries are considered free of SVD. Uncertainty remains on the presence of SVD in some countries in Asia.

    GAP: Due to the current prevalent sub-clinical course of the disease, clinical inspection is often ineffective; so that it is necessary to resort to laboratory diagnosis for SVD surveillance. The extent of occurrence of SVD virus outside of Italy is not absolutely clear, since most countries do not undertake the extensive laboratory-backed surveillance needed to be sure of freedom.

  • Epizootic/endemic- if epidemic frequency of outbreaks

    Apart from very sporadic clinical cases in Europe, SVD is now sporadically detected only in southern Italy; occasional outbreaks or rarely epidemic waves have occurred in central or northern regions, from where infection has been rapidly eradicated.

  • Seasonality

    No.

  • Speed of spatial spread during an outbreak

    SVD diffusion is mainly related to movement of pigs, means of transport and contaminated material and personnel. High herd density may also play a role in spread between herds. However, SVD may have a limited tendency to spread even between pens of the same farm.

    GAP: Bio-security measures based on principles of direct prophylaxis are not always correctly implemented to prevent incursion of SVD in a farm or in a “new territory”.

  • Transboundary potential of the disease

    SVD is a transmissible disease that has the potential for very serious and rapid spread, irrespective of national borders.

    GAP: Increased risk due to subclinical course of disease.

  • Route of Transmission

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

    Direct contact with infected pigs or indirect contact via contaminated materials, environment, personnel, fomites. Faecal contamination is a major source of virus spread, often within contaminated vehicles.

  • Occasional mode of transmission

    Via contaminated meat scraps and swill.

  • Conditions that favour spread

    Overcrowding, mixing and transporting animals, transport of pigs in contaminated lorries. Late diagnosis, non clinical infection.

    GAP: The subclinical course of SVD may facilitate its diffusion.

  • Detection and Immune response to infection

  • Mechanism of host response

    Humoral response with development of virus neutralizing antibodies is the most important, known mechanism of host reaction to infection.

    GAP: In the absence of pressure to develop a vaccine, immunological research has not been a priority.

  • Immunological basis of diagnosis

    Detection of specific antibodies in serum, by ELISA and Virus Neutralisation test, is indicative of present or past infection. On the basis of the typical kinetics of occurrence for the different immunoglobulins, antibody isotyping is useful to ascertain the time of exposure to infection; detection of IgM is indicative of recent infection within a pig herd.

  • Main means of prevention, detection and control

  • Sanitary measures

    EU legislation provides for: stamping out, restriction of pig movements (protection and surveillance zones), cleansing and disinfection, restrictions on swill feeding and on importation of pig products from SVD-affected regions.

    GAP: In many countries SVD detection is based on clinical evidence. SVD has often a sub-clinical course and when the disease is identified it may have already spread.

  • Mechanical and biological control

    Stamping out and destruction of affected and in contact pigs, standstill, cleansing and disinfection. Correct implementation of bio-security measures for prevention.

  • Diagnostic tools

    The diagnosis of SVD requires the facilities of a specialised laboratory. In case of clinical occurrence, differential diagnosis with FMD is essential, and due to the common subclinical course, laboratory investigations are the only mean to scientifically exclude virus circulation.

    Diagnostic tests for virus detection:

    • RT-PCR
    • Virus isolation in susceptible cell cultures accompanied by an identification assay
    • ELISA for antigen detection (only suited for vesicular tissue and virus identification in infected cultures)

    Diagnostic tests for antibodies detection:

    • Competitive ELISA (based on monoclonal antibody) as screening test
    • Virus Neutralization test as confirmatory test
    • Isotype specific ELISA, for IgG and IgM identification

    GAPS: See Section “Diagnostics availability – opportunities for new developments”.

  • Vaccines

    There is currently no commercial vaccine available against SVD. Vaccination is not applicable in EU.

    Experimental inactivated vaccines against SVDV have been developed but vaccination of pigs has never been undertaken in the field. Vaccination is not a suited/convenient mean of prevention and control (see also answer at Section “Vaccines availability -Effectiveness of vaccines/main shortcomings of current vaccines”).

  • Therapeutics

    None.

  • Biosecurity measures effective as a preventive measure

    Health status certification (holding/animal/product), application of rigorous cleansing and disinfection procedures, restrictions on movement of animals, and limiting introduction of possible contaminated materials to farms.

    GAP: The health status certification (farm/animal) can only be proved by appropriate lab investigations.

  • Border/trade/movement control sufficient for control

    Certification on the origin of the animals/product plus health status certification.

    GAP: Certifications are based on the surveillance activities performed, at present there are not harmonized surveillance rules.

  • Prevention tools

    Health status certification (holding/animal). Application of rigorous cleansing and disinfection procedures. Control on animal movements. Ban on swill feeding. Application of biosecurity measures.

    GAP: On the basis of clinical symptoms, it may be difficult to recognize affected animals, also during the acute phase.

  • Surveillance

    At present, in many countries surveillance for SVD is based on clinical evidence. Since SVD has often a sub-clinical course, clinical surveillance must be supported by appropriate sampling and laboratory investigations such as serological surveillance and/or detection of SVDV in random sampling of pen-floor faeces.

    GAP: Surveillance in the EU is based on the assumption that in case SVD enters a susceptible population, clinical symptoms are observed. According to the knowledge acquired on the disease, clinical surveillance has a low sensitivity for detecting virus circulation.

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

    A number of European and Far Eastern countries have eradicated SVD in the 70’s, 80’s and 90’s. Since then, the only reported cases were in Taiwan (2000, 2004), in Portugal (2002, 2003-4, 2006) and Italy (still present). In case of outbreak, EU legislation provides for a rigorous stamping out policy.

    GAP: Due to the frequent subclinical nature of SVD virus infection and the lack of information on surveillance, the global distribution of the virus cannot be ascertained with certainty.

  • Costs of above measures

    Nowadays the cost of SVD is mainly linked to the control measures applied (active serological and virological surveillance and eradication plan in Italy, serosurveillance in The Netherlands and until recently in Spain, stamping out and stringent control on trade when infection occurs), rather than to the real outcome of the disease in susceptible species (morbidity is very low, mortality is nil).

    GAP: Control measures applied seem disproportionate to the real impact of the disease.

  • Disease information from the WOAH

  • Disease notifiable to the WOAH

    No.

  • WOAH Terrestrial Animal Health Code

    Not applicable.

  • Socio-economic impact

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

    Not applicable.

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

    Not applicable.

  • Direct impact (a) on production

    The direct impact of SVD is low, mobility is low and mortality nil.

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

    SVD is of economic importance because surveillance, control and eradication measures are costly.

  • Indirect impact

    Countries which are known to have the disease face embargoes on the export of pigs and by products. Several months of interruption of activity in herds affected by SVD outbreaks.

  • Trade implications

  • Impact on international trade/exports from the EU

    Outbreaks result in embargo on the export of pigs and pork products.

    GAP: Due to the pathogenesis of SVD, the risk of virus being present in muscle meat is considered to be low (short viraemic period, no replication of virus in the muscles).

  • Impact on EU intra-community trade

    In case of an SVD outbreak quarantine measures and movements standstill are applied in the affected area.

    GAPS:

    The control measures foreseen in case of SVD seem disproportionate.

    See also Section “Impact on international trade/exports from the due to existing regulations“.

  • Impact on national trade

    See Section “Impact on EU intra-community trade due to existing EU regulations” .

  • Main perceived obstacles for effective prevention and control

    Difficulties in clinical diagnosis due to the often undisclosed course of the disease, import from countries where the SVD status is not regularly assessed.

    GAP: The disease was included among the List A for the clinical similarity to FMD. Since January 2015 SVD is no longer listed. In recent cases no clinical disease was reported.

  • Main perceived facilitators for effective prevention and control

    Fast and robust diagnostic tools.

    Surveillance methodologies and appropriate tests to detect unapparent infection.

    In case SVD occurs clinically, diagnostic tests are available to differentiate SVD and FMD.

  • Links to climate

    Seasonal cycle linked to climate

    No.

  • Distribution of disease or vector linked to climate

    No.

  • Outbreaks linked to extreme weather

    No.

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

    No.

Risk

  • The risks are associated with the movement of pigs or contaminated materials and transport means from countries where the disease is not diagnosed due either to inadequate surveillance systems or to sub clinical occurrence.

    The interruption of active surveillance in countries where the infection is not eradicated would most likely cause the spread of undisclosed infection in free areas.

    Reversion of clinical reappearance cannot be excluded.

Main critical gaps

Conclusion

  • The main importance of SVD is that it is clinically indistinguishable from FMD, and any outbreaks of vesicular disease in pigs must be assumed to be FMD until investigated by laboratory tests and proven otherwise. However, subclinical infection has been the most frequent condition observed during recent years.

Sources of information

  • Expert group composition

    Expert group members are included where permission has been given

    Emiliana Brocchi - Istituto Zooprofilattico Sperimentale della Lombardia e dell Emilia Romagna (IZSLER) - [Leader]

    Aldo Dekker, ID-Lelystad, Laboratory of Vesicular Diseases, The Netherlands

  • Reviewed by

    Project Management Board.

  • Date of submission by expert group

    May 11th, 2016