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The new field strains of rabbit haemorrhagic disease virus (RHDV), characterised by different reactivity in ELISA similar to antigenic variant of RHDVa and non-haemagglutinating isolate, are described. The specimens were isolated from small rabbitries from natural outbreaks suspected of rabbit haemorrhagic disease (RHD) and from experimentally-infected animals. RHD was confirmed on the basis of high mortality rate, clinical and necropsy features, and positive results in HA, ELISA, and RT-PCR. The isolates were able to infect unvaccinated rabbits but laboratory animals immunised with a commercial vaccine were fully protected. The immunisation of rabbits with three different inactivated field strains demonstrated the seroconversion and efficacy of the experimental vaccines against challenge with virulent strains of RHDV.
Vesicular stomatitis (VS) is a viral disease of horses, cattle and swine caused by vesiculoviruses (VSV) of the Rhabdoviridae family. The disease is a zoonosis. VS is endemic in the Western Hemisphere, where its incidence is confined to the warmer regions of North America, as well as Central and South America with tropical climate. The article presents the most important issues concerning the historical background and current status of the disease and its etiological agent. The impact of climatic and ecological conditions on the emergence of new outbreaks and virus strain evolution is discussed, as well as the role of insects in the epidemiology of infections and limited possibilities of specific prevention. The importance of VS virus as a vaccine and oncolytic vector and prospects for its use in the prevention of human infectious diseases and cancer therapy are also highlighted.
The field outbreak of RHD that occurred late summer 2012 on a small-scale rabbit-rearing operation in Poland and the usefulness of techniques for RHD virus diagnosis are described. During the epizootic, the overall mortality rate of rabbits older than two months was 77%. Eight liver specimens collected from dead unvaccinated rabbits (aged 3-5 months) underwent virological examinations. RHDV specific antigen was detected in two out of eight liver homogenates by haemagglutination (HA) test and ELISA, one of the two being negative in HA assay. However the presence of genetic material of RHD virus was confirmed by RT-PCR and real-time RT-PCR in all liver samples tested. Based on antigen reactivity in ELISA and sequencing of PCR amplicons of the VP60 gene, the RHDVa subtype strain was identified as the cause of infection. The partial genome sequence of a field isolate (STR 2012), comprising the C-terminus of the polymerase gene and the full capsid protein gene, revealed 91% nucleotide homology to reference FRG89 RHDV isolate and 97% to strain Triptis representing the RHDVa variant. Serological evidence of an RHD outbreak in the STR rabbit-rearing operation was confirmed in a serum sample collected from an unvaccinated surviving rabbit. A cross-reactivity examination of RHDV positive serum revealed a decrease in HI titre against the STR 2012 field antigen, and a decrease in the RHDVa control antigen as compared to classic RHDV.
Rabbit haemorrhagic disease (RHD) was first recognized in China in 1984. In Europe, the disease appeared in 1986 in Italy, and in the following years RHD was observed in many other European countries, including Poland in 1988. The disease is caused by RHD virus (RHDV), classified as a representative of the Lagovirus genus within the Caliciviridae family. Lagoviruses include the non-pathogenic rabbit calicivirus (RCV) and the European brown hare syndrome virus (EBHSV). There are three basic variants (subtypes) of pathogenic RHD viruses: classic (RHDV) and antigenic subtypes RHDVa and RHDV2 (RHDVb), distinguished on the basis of epidemiological characteristics, infectious properties and antigenic and genetic modifications. Phylogenetic analysis of RHDV revealed the presence of five genogroups (G1-G5) with similar time of isolation, regardless of the place of occurrence. RHDVa strains are genetically more variable than RHDV, and all RHDVa strains belong to genogroup G6. RHDV2 was diagnosed for the first time in 2010 in domestic and wild rabbits in France, and later in the Iberian Peninsula, and it was called RHDVb. Like the previously identified variants of the RHD virus, RHDV2 spreads to other regions of the world, and in 2011-2016 it was diagnosed in many European countries, North America, Africa and Australia. Strains of RHD2 form a separate, uniform phylogenetic group and are more similar to the non-pathogenic rabbit calicivirus than to pathogenic RHDV and RHDVa. Infections with different variants of RHD viruses are a serious epidemiological, diagnostic and immunological problem. Advanced antigenic changes in RHD viruses limit the usefulness of standard RHD vaccines in controlling the disease.
Over the last three decades, a variety of approaches have been investigated to develop new types of bluetongue virus (BTB) vaccines, ranging from baculovirus-expressed subunit vaccines to live vector vaccines. DNA vaccines against BTV consist of DNA plasmid expressing different BTV proteins after inoculation of the animals. The recombinant viral vector vaccines against BTV are based on recombinant viruses that express desired BTV antigens in the host upon inoculation. Viruses such as vaccinia, modified vaccinia Ancara (MVA), capripox, canarypox, herpes, myxoma and fowlpox viruses have been used as vectors of BTV genes. The reverse genetics (RG) systems for BTV are useful tools for BTV vaccine development. Disabled infectious single-cycle (DISC) vaccines make it possible to restore virus replication and can be used for differentiating infected from vaccinated animals (DIVA). These vaccines are based on the production of a modified virus with a deletion in one or more genes that are essential for virus replication. Another approach for BTV vaccine development using RG is the disabled infectious single-animal (DISA) vaccine, generated by deletion of NS3/NS3a expression. DISC and DISA vaccines can mimic the natural tropism of the virus and can express BTV proteins at the site of infection. Important advantages of these new generation vaccines over the conventional BTV vaccines are their high efficacy as well as the possibility of applying them for DIVA. At present, there are a number of novel laboratoryscale BTV vaccines that could meet vaccine profiles required for different field situations. However, further development and licensing of these vaccine candidates for many BTV serotypes is needed in order to prepare for future BT outbreaks. To date, all novel BTV vaccines described in this paper are still under laboratory testing. They are not available commercially, and the time of their application in the field is still indefinite.
Foot-and-mouth disease virus (FMDV), in contrast to the antigen used for the production of FMD vaccine, can replicate in animals. As a result of infection the specific antibody to the viral structural proteins (SPs) and non-structural proteins (NSPs) of FMDV are synthesized. The laboratory diagnostic methods based on individual NSPs, e.g. 3D, 2C and 2B, as well as polypeptides, such as 3AB and 3ABC can be used for differentiation of infected and vaccinated animals (DIVA). This article presents the aim, principle, methods and results of applying DIVA strategy in the eradication of foot-and-mouth disease. The marker vaccines which enable differentiation between infected and vaccinated animals and appropriate ELISA serological tests for detection of antibodies to the NSPs of FMDV have been described. DIVA strategy makes it possible to reduce the economic losses and restore possibilities of international trade in animals and animal products. This strategy may be an alternative of the administrative “stamping-out” eradication method. The essential aim of DIVA strategy is realization of the so-called “vaccinate-to-live” policy, which is based on the principle that vaccinated animals exposed to FMDV will not transmit the virus. These animals are not epidemiologically risky, and therefore do not have to be eliminated. It is necessary to develop new vaccines and improve those already used as well as the application of reliable diagnostic tests to detect FMDV in vaccinated livestock populations.
Medycyna Weterynaryjna
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2010
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tom 66
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nr 08
s.538-543,rys.,tab.,bibliogr.
A number of diseases have similar or identical clinical symptoms as does foot-and-mouth disease, including swine vesicular disease (SVD), vesicular stomatitis (VS), rinderpest (RP) and peste des petits ruminants (PPR). SVD is an acute, highly contagious viral disease of pigs caused by a virus belonging to the genus Enterovirus in the family Picornaviridae. VS is a vesicular disease of horses, cattle and pigs caused by vesiculoviruses of the family Rhabdoviridae. RP and PPR are acute viral diseases caused by the Morbillivirus genus within the family Paramyxoviridae. Classic descriptions of RP refer to it as a highly fatal disease of domestic cattle, buffaloes and yaks. PPR affects sheep and goats and occasionally small wild ruminants. Laboratory investigations are a key to their precise diagnosis. The most important data regarding these diseases are presented in this article.
The aim of this paper is to present the recent changes in the global distribution of bluetongue (BT) and epizootic hemorrhagic disease (EHD) in the world. Both of these arboviral infections are widespread in the territory of many continents. BT is currently endemic in many tropical, sub-tropical and temperate regions of the world (Africa, southern Asia, Australia, the Middle East, and the Americas), between latitudes 50°N and 35°S, during times of the year that are optimal for vector activity. In Europe, BTV serotypes 1, 2, 4, 8 and 16 are currently circulating in many regions of continent. The range of EHDV lies approximately between latitudes 35°S and 49°N. EHDV infection of wild and domestic ruminants has been reported in the America, Africa, Asia, Australia, the Middle East as well as some islands of the Indian Ocean. Recently it has also been recorded in cattle in countries surrounding the Mediterranean Basin including: Israel, Turkey, and northern African countries such as Morocco, Algeria and Tunisia. So far there has been no report of EHDV being present in Europe, but there has been only limited surveillance for subclinical infections in wild cervids. The global range of BT and EHD and their aetiological agents have changed remarkably in recent years, most notably with the incursion to Europe of multiple virus serotypes. The enormous genetic diversity of these orbiviruses can lead to the emergence of viruses with unique biological properties, such as a capacity for horizontal and vertical transmission. Reassortment of the genes of invasive orbiviruses with those viruses already present in environment has facilitated the successful introduction and spread of novel reassortant progeny between episystems.
Medycyna Weterynaryjna
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2010
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tom 66
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nr 12
s.799-804,bibliogr.
Over the years since ancient through contemporary times, rinderpest has been a lethal threat to cloven-hoofed animals, especially cattle. In this review, the most particular facts connected with the occurrence and eradication of this mortal plague of animals were presented. The history of the struggle against rinderpest is closely bound with the foundation of the first veterinary school, as well as the World Organization for Animal Health (OIE). The FAO/OIE declaration of rinderpest global eradication is expected to be announced in the near future.
Foot and mouth disease (FMD) is the most contagious disease of domesticated and wild cloven-hoofed animals, caused by a virus of the Aphthovirus genus in the Picornaviridae family. Foot and mouth disease virus (FMDV) exists as seven different serotypes (O, A, C, Asia 1, SAT 1, SAT 2, SAT 3), which are not uniformly distributed across the globe. Six of the seven serotypes of FMD (O, A, C, SAT 1, SAT 2, SAT 3) occur in Africa, four (O, A, C, Asia 1) in Asia, and only three (O, A, C) in South America. FMD-endemic areas of the world are high-risk zones for introducing FMD to countries free of the disease. In 2010-2011 and at the beginning of 2012, FMD caused by different serotypes occurred in Asia, Africa and South America. It also occurs in Europe, in Bulgaria. Asia is still the main source of outbreaks for the Middle East and Europe. In the period considered, the dominant serotype was O, and no serotype C was observed. It is noteworthy that serotype C has not been recorded since 2004. Its disappearance has not yet been explained. This article presents key information on the outbreaks of FMD around the world based on the data from Office International des Epizooties (OIE) and the World Reference Laboratory for Foot-and-Mouth Disease (WRL FMD).
Peste des petits ruminants (PPR) is a contagious and fatal disease of sheep and goats which significantly affects the production of meat and milk, farm incomes and people’s overall standard of living, contributing to famine and poverty, especially in developing countries of Africa and Asia. This publication presents issues concerning the emergence of this disease of domestic and wild small ruminants, the characteristics of the disease agent and epidemiological situation for over 70 years. The article concentrates on the growing risk of the spread of the disease to new areas. The authors present information concerning the prevention and effective control of the disease, as well as the possibilities of limiting its spread. The latest views on the prospects for developing a global program of eradicating this transboundary animal disease are also discussed.
Swine vesicular disease (SVD) was first observed in Italy in 1966, where it was clinically recognised as foot-and-mouth disease (FMD). SVD virus (SVDV) was subsequently isolated in an FMD vaccine trial in Hong Kong. At the beginning of the 1970s, it spread to several other European and Asian countries: Bulgaria, Austria, Italy, Great Britain, Poland, former Soviet Union (Ukraine), Romania, France, Germany, Belgium, Switzerland, the Netherlands and Japan, and lasted until the beginning of the 1980s. After that period, SVD outbreaks were sporadic. The disease was almost forgotten until it flamed up again in 1992 in the Netherlands. Once again it spread to several other European countries, such as Belgium, Spain, Portugal and Italy. Since 1995, SVD has been reported in Europe almost exclusively in Italy, except two isolated outbreaks in Portugal. Since the last two SVD outbreaks in 2014 in the Potenza province (Basilicata region), no new SVD outbreaks have been reported either in Italy or in any other European country. The clinical resemblance of SVD to FMD highlights the need for its reliable identification and discrimination. Differentiation from FMD, though not possible clinically, is feasible if appropriate diagnostic tests are applied. Improvements in diagnostic techniques are making differential diagnosis of vesicular disease increasingly affordable, feasible and easy, and nowadays, portable devices are capable of a rapid and accurate differentiation of SVDV from FMDV infections on site. As these tests become economical and as competent laboratory services become more and more accessible, the restrictions originally imposed on SVD because of its similarity to FMD will no longer be justified. This, together with the fact that in recent years SVD has been predominantly asymptomatic, makes it necessary to rethink the measures currently in place for the control and diagnosis of SVD. Therefore, by the decision of OIE, the SVD chapter was removed from the Terrestrial Code in January 2015. Consequently, the European Commission (EC) informed the Pirbright Institute that the EU Reference Laboratory for SVD would no longer receive financial support. Moreover, the EC position is that notification requirements have ceased in January 2015.
Climate changes may have significant impact on animal health, including changes in the distribution and seasonality of vector-borne diseases. Arboviruses, such as bluetongue virus (BTV), are particularly susceptible to climate change because of their small size and their ability to adapt to variations in the temperature of the environment. Climate also has long-term indirect effects on the transmission of BT via its effects on the distribution and availability of suitable habitats. Changes in BT incidence in Europe have been matched by spatio-temporal changes in regional climates, including the specific climatic drivers of BTV infection. The climate changes are responsible for the occurrence and distribution of BT through their impact on the viral vectors. Changes in climate, i.e. temperature, precipitation, humidity, wind, etc., can influence various aspects of the Culicoides vectors’ life cycle, including survival, population numbers, vector-pathogen interactions, pathogen replication, vector behaviour and, of course, its distribution. Different species of Culicoides have different environmental tolerances, and the optimal temperature and humidity levels for populations of Afro-Asiatic species, such as C. imicola, are different from those for Palearctic species, such as the C. obsoletus and C. pulicaris groups. However, the biotic processes of changing vector roles and distribution have been as important as the climatic process in driving the invasion of Europe by multiple BTV strains. The enhanced transmission of BTV by indigenous European vectors has been instrumental in the spread and persistence of infection in cooler and wetter areas of different regions of Europe after the invasion. The vectorial capacity of Culicoides is dynamic and climate-mediated, making it difficult to state unequivocally that particular species cannot or will not be involved in transmission – even of strains that enter Europe unexpectedly from geographically remote regions.
Senecavirus A (SVA) is a single representative species of the Senecavirus genus within the family Picornaviridae. This review presents the current knowledge regarding SVA epidemiology, transmission, pathogenesis, clinical signs, differential diagnosis and control measures. SVA is not debilitating, but significant because of its resemblance to acute, highly contagious and economically devastating viral diseases, such as FMD. The incubation period of SVA is 4-5 days, the viremia period is short, lasting 3 to 10 days post infection (dpi). SVA shedding lasts up to 28 days. SVA can be shed by oral and nasal secretions and by faeces. The virus excretion peak occurs between 1 and 5 dpi, especially in oral secretions, which contain higher virus loads relative to nasal secretions and faeces. SVA lesions are found most frequently on the snout, lips and tongue, as well as on hooves, specifically, on coronary bands, dewclaws, hoof pads and in interdigital space. The vesicles quickly rupture to form ulcers that may be covered by serofibrinous exudates. The ulcers begin to repair in 7 days, and the regeneration of epithelium is usually complete within 2 weeks. Since clinical lesions induced by SVA are indistinguishable from those observed in other vesicular diseases of swine, accurate and reliable laboratory differential diagnosis is critical to the precise identification of the infectious agent. SVA has potential cytolytic activity and high selectivity for tumour cell lines with neuroendocrine properties versus adult normal cells. Because of its potential oncolytic activity, the virus can be useful in human cancer therapy. The example of SVA shows that the risk of emerging infectious diseases in swine populations is high and that emerging diseases of swine have significant potential impact on the productivity and economics of the pork industry. The SVA infection is currently limited to the United States, Canada, Brazil, China and Thailand. However, descriptions of the SVA infection in Asia suggest that the virus is not restricted to a specific geographic region and may be distributed on a global scale in the future.
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