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.
The full gap analyses matrices for Swine Vesicular can be found on the website and downloaded here.
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.
All assays mentioned under section (Main means of prevention, detection and control-Diagnostic tools) are reported in the EC Decision 2000/428 and in the O.I.E. Manual of Diagnostic tests and vaccines for terrestrial Animals.
Low, as a national surveillance programme is implemented only in Italy.
Not required, as vaccine is not authorised or used in Europe nor worldwide.
None.
None.
None.
Not applicable as no vaccines have been used. Vaccination has been shown not to be 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, in the last period of circulation in Europe, was mostly sub-clinical and studies indicate that a DIVA strategy was difficult to be developed for SVDV.
None, see previous points.
Not applicable at present.
No clear market.
Barrier protection not applicable by vaccination.
Not required and applicable, based on above considerations.
None, not applicable.
None, not applicable.
None.
Not applicable.
Not required.
Not required, not applicable.
See “Opportunities for new developments”.
Not applicable following what has been stated above.
Not applicable following what has been stated above
See Section “Requirements for diagnostics development” and “Diagnostics availability – Opportunities for new development”.
The disease is mainly subclinical, evidence of SVD-freedom must be based on laboratory investigations, in particular:
Not required.
Not applicable.
High.
None , vaccination not applicable.
None.
Not applicable.
Not applicable.
None.
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 of about 7.4 Kb encoding four capsid proteins (VP1, VP2, VP3 and VP4) assembled in a capsid of icosahedral symmetry, and several non-structural proteins.
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 encoding 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, which circulated in Italy until 2015, 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 and the sequences analysis pointed out the presence of two sub-lineages 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.
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 40 days (upper 95% one-sided prediction interval 33 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.
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.
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 the exception of one case of association with meningitis.
None.
Pigs are the only species that are naturally infected. No reservoir hosts are known.
Direct contact with infected pigs or indirect contact via contaminated people, the environment and non-animated 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.
Not applicable.
The incubation period is between 2 and 7 days.
Mortality due to SVD is extremely rare.
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. The 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.
SVD virus has a tropism for epithelial tissue (skin and mucosa of the digestive tract). Vesicle formation is the only known lesion directly attributable to the infection.
There are reports of seroconversion to SVDV in laboratory workers handling the agent and there have been no reported cases of seroconversion or disease in farmers or veterinarians working with infected pigs.
Almost none.
Clinical disease in humans is reported to be mild, it includes 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.
None.
None.
In the last years of circulation in Italy, SVD had mainly a sub-clinical course and the direct impact of the disease in pigs was low. The restriction of animal movement (protection and surveillance zones) to be applied in case of occurrence may cause sanitary and welfare problems.
No.
No European rules are currently present for SVD, since the disease is not present in the list set out in Annex II of EU Regulation 2016/429. In the past, a stamping-out policy was applied on infected premises. In seropositive herds where virus was not detected, seropositive pigs were slaughtered.
SVD was first recorded in Italy in 1966. Later, outbreaks occurred in several European countries and Eastern Asia during the 1970s, and early 1980s; then the disease has continued to persist in Italy until 2015 when the last viral detection was recorded. The last serological positivity was detected in 2017. All European countries are considered free of SVD now.
See section on- (current occurence/distribution)
SVD transmission is mainly related to the movement of pigs, transport vehicles and contaminated material and personnel. Introduction through contaminated feed has occurred several times. High herd density may also play a role in the spread between herds. However, SVD may have a limited tendency to spread even between pens of the same farm.
All European countries are SVDV-free and there is no evidence of SVDV circulation outside Europe, especially in the neighbouring countries. However, when it is present, SVD is a transmissible disease that has the potential for very serious and rapid spread, irrespective of national borders.
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.
Via contaminated meat scraps and swill.
Overcrowding, mixing and transporting animals, transport of pigs in contaminated lorries. Late diagnosis, non clinical infection. The subclinical course of SVD may facilitate its diffusion.
Humoral response with development of virus neutralizing antibodies is the most important, known mechanism of host reaction to infection.
Detection of specific antibodies in serum, by ELISA and Virus Neutralisation test, is indicative of present or past infection. Based on 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.
When SVD was still circulating in Europe, the EU legislation provided for: stamping out, restriction of pig movements (protection and surveillance zones), cleansing and disinfection, restrictions on swill feeding and importation of pig products from SVD-affected regions.
Stamping out and destruction of affected and in contact pigs, standstill, cleansing and disinfection. Correct implementation of bio-security measures for prevention.
There is no commercial vaccine available against SVD. 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 means of prevention and control (see also answer at Section “Vaccines Availability-Effectiveness of vaccines/main shortcomings of current vaccines”).
None.
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.
Certification on the origin of the animals/product plus health status certification.
Health status certification (holding/animal). Application of rigorous cleansing and disinfection procedures. Control on animal movements. Ban on swill feeding. Application of biosecurity measures.
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. Currently not surveillance plans are in place for SVD.
A number of European and Far Eastern countries 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 (until 2015). In case of an outbreak, EU legislation provided for a rigorous stamping out policy. Nowadays Europe is considered SVDV free.
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.The cost of SVD during its circulation was mainly linked to the control measures applied (serological and virological surveillance 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.No
GAP
Not applicable
GAP
Not applicable
Not applicable.
https://www.woah.org/fileadmin/Home/eng/Health_standards/tahm/3.09.08_SVD.pdf
GAP
Not applicable.
Not applicable.
Not applicable.
The direct impact of SVD is low, mobility is low and mortality nil.
SVD is of economic importance because surveillance, control and eradication measures are costly.
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.
Outbreaks result in an embargo on the export of pigs and pork products. Currently, SVD virus-free guarantees are often required for the export of pigs and pork products. In particular, the antibody detection ELISA is performed on serum samples.
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).GAP
The control measures foreseen in case of SVD seem disproportionate. See also Section “Impact on international trade/exports from the due to existing regulations“.See Section “Impact on EU intra-community trade due to existing EU regulations” .
No.
No.
No.
No.
Difficulties in clinical diagnosis due to the often undisclosed course of the disease.
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.
The most recent detection of SVDV in Italy was in 2015, and no serologically positive pigs have been identified since 2017. No further SVD outbreaks have been reported elsewhere in Europe or in any other countries globally.
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.
The main importance of SVD is that it can be 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.
Expert group members are included where permission has been given.
Giulia Pezzoni, WOAH/FAO reference laboratory for SVD, Istituto Zooprofilattico Sperimentale della Lombardia e dell’Emilia Romagna (IZSLER), Italy - [Leader]
Aldo Dekker, WBVR-Lelystad, Laboratory of Vesicular Diseases, The Netherlands
Donald King, WOAH Reference Laboratory for SVD, The Pirbright Institute, UK
Aurore Romey, ANSES, Animal Health Laboratory, Virology Unit, (WOAH/FAO/EU reference laboratory for FMD), NRL for SVD, Maisons-Alfort, France
Tiziana Trogu, IZSLER
Project Management Board.
November 12th 2024
Defra:
WOAH Website
Centre for Food Safety and Public Health Iowa State University:
https://www.cfsph.iastate.edu/diseaseinfo/disease/?disease=swine-vesicular-disease&lang=en