Outbreak Of Equine Viral Arteritis Research Articles

Outbreak of equine viral arteritis in the UK 2019

Outbreak of equine viral arteritis in the UK 2019

Investigating an outbreak of equine viral arteritis at two connected premises.

In early 2019, four stallions in the south of England tested positive for equine viral arteritis following routine prebreeding screening. Here, a team from Defra and the APHA describe the epidemiological investigation that was carried out to determine the origin of infection and the potential for its transmission across the country.

Equine viral arteritis: A respiratory and reproductive disease of significant economic importance to the equine industry

SummaryEquine arteritis virus is the causative agent of equine viral arteritis, a respiratory and reproductive disease that affects the members of the familyEquidae. The virus was first isolated from the lung of an aborted fetus after an extensive outbreak of respiratory disease and abortion on a Standardbred breeding farm near Bucyrus, Ohio, in 1953. Since then, periodic outbreaks of equine viral arteritis have been reported in a number of countries around the world. This disease may result in significant economic loss to the equine industry due to the occurrence of abortion in pregnant mares, neonatal mortality, and establishment of the carrier state in stallions. This article provides an extensive review on equine arteritis virus, epidemiology, disease, pathogenesis, and prevention and control measures.

The Recent European Isolate (08P178) of Equine Arteritis Virus causes Inflammation but not Arteritis in Experimentally Infected Ponies

In the last two decades, outbreaks of equine viral arteritis (EVA) have been reported in Europe, but little is known about these European isolates of equine arteritis virus (EAV). EAV European strain (08P178, EU-1 clade) isolated from one of these recent outbreaks is able to cause clinical signs on experimental infection. The aim of the present study was to investigate the microscopical lesions induced by this isolate after experimental infection of ponies. Animals were killed at 3, 7, 14 and 28 days post infection (dpi). At 3 dpi, lesions were essentially restricted to the respiratory tract and intestines and were characterized by mild multifocal epithelial degeneration and associated mononuclear cell infiltration. Lesions were more severe at 7 dpi and by 14 dpi, respiratory lesions were even more severe and lymphoplasmacytic infiltrates extended to other organs. At 28 dpi, lesions were still present in the viscera. In all specimens the most prominent histological change was intraepithelial, subepithelial and perivascular lymphoplasmacytic infiltration, ranging from mild and multifocal to extensive and diffuse. No signs of arterial damage such as infarcts, haemorrhages or necrosis were found. In conclusion, infection of naïve animals with the European 08P178 strain of EAV is associated with inflammation, but not arteritis.

Emergence of novel equine arteritis virus (EAV) variants during persistent infection in the stallion: Origin of the 2007 French EAV outbreak was linked to an EAV strain present in the semen of a persistently infected carrier stallion

During the summer of 2007, an outbreak of equine viral arteritis (EVA) occurred in Normandy (France). After investigation, a link was suggested between an EAV carrier stallion (A) and the index premise of the outbreak. The full-length nucleotide sequence analysis of a study reference strain (F27) isolated from the lung of a foal revealed a 12,710 nucleotides EAV genome with unique molecular hallmarks in the 5′UTR leader sequence and the ORF1a sequence encoding the non-structural protein 2. The evolution of the viral population in the persistently infected Stallion A was then studied by cloning ORFs 3 and 5 of the EAV genome from four sequential semen samples which were collected between 2000 and 2007. Molecular analysis of the clones confirmed the likely implication of Stallion A in the origin of this outbreak through the yearly emergence of new variants genetically similar to the F27 strain.

Description of the first recorded major occurrence of equine viral arteritis in France

The vast majority of equine arteritis virus (EAV) infections are inapparent or relatively mild, but may occasionally cause outbreaks of equine viral arteritis. The event observed in France during the summer of 2007 was the most important seen in the country, with mortality and disruption of economic activity. To describe the different stages seen during the outbreak and to show how molecular tools were used for both the detection and management of the crisis. EAV detection was performed by real-time reverse transcription-polymerase chain reaction (RT-PCR) in blood, nasal swabs, semen or organ samples. Characterisation of EAV strains was performed by sequencing the ORF5 fragment. The outbreak affected 18 premises in 5 counties in western France, which represented the index, 8 primary and 9 secondary premises. Artificial insemination in draught horses was responsible for the virus spread. Eight mortality cases were observed, including one fetus, 5 young foals and 2 mature horses. Forty-three individuals had positive results by real-time RT-PCR. The range of measured cycle threshold (Ct) values varied from 19.8 to 40.4 depending on the biological samples. Phylogenetic analysis revealed that the 33 isolated strains all clustered within the EU-2 subgroup. The mortality rate attests to the virulence of the strain involved in this outbreak. Real-time RT-PCR was used for the first time in order to follow-up an epidemic disease in horses. The early detection of 3 signals with high Ct values attest the importance of taking low signals into account in field conditions.

Preventing venereal disease in horses

Colleagues will be aware of the recent outbreaks of equine viral arteritis (EVA) in France and of contagious equine metritis (CEM) in the USA. The British Equine Veterinary Association (BEVA) would like to remind all veterinary surgeons involved in the practice of artificial insemination (AI) in

Phylogenetic characterisation of the G L sequences of equine arteritis virus isolated from semen of asymptomatic stallions and fatal cases of equine viral arteritis in Denmark

The study describes for the first time the phylogenetic relationship between equine arteritis virus (EAV) isolated from asymptomatic virus-shedding stallions and fatal cases of equine viral arteritis (EVA) in an European country. EAV was isolated from three dead foals and an aborted foetus during three different outbreaks of EVA. From these fatalities, the complete open reading frame 5, encoding the EAV G L protein, was amplified by reverse transcription-polymerase chain reaction and subjected to nucleotide sequence analysis. Furthermore, DNA sequences were obtained from virus isolated from semen samples of seven virus-shedding, but clinically healthy, Danish stallions. DNA sequence alignment revealed an overall divergence of 0–14 and 0–10% at the nucleotide and amino acid levels, respectively. Phylogenetic analysis including 24 previously published sequences revealed that European as well as North American “types” of EAV were present in the semen of asymptomatic carrier stallions and in fatal cases of EVA. Our results reveal that the presence of EAV-shedding stallions in Denmark represents a potential source of severe EVA.

Serological surveillance of equine viral arteritis in the United Kingdom since the outbreak in 1993.

Serological analysis of blood samples submitted to the Animal Health Trust showed that during 1995, 185 of 9203 unvaccinated horses (2.0 per cent) tested positive for antibodies to equine arteritis virus (EAV), and that during 1996, 46 of 8851 unvaccinated horses (0.52 per cent) tested positive. During both years thoroughbreds were the predominant breed tested and only a small proportion of these (<0.3 per cent), consisting predominantly of imported mares, were seropositive. In contrast, among standardbred horses, from which samples were actively solicited in 1995, 84 of 454 (18.5 per cent) were seropositive. Among standardbreds there was a difference in prevalence between types of horses, with 3.7 per cent of racing horses, 25 per cent of non-racing horses and 41 per cent of stallions testing seropositive. Investigations of seropositive stallions identified during 1994 and 1995 demonstrated that clinically inapparent equine viral arteritis (EVA) had occurred previously in the UK. Of 50 seropositive stallions, nearly half were standardbreds and nearly all had been imported from either North America or the European Union. Whether 34 seropositive stallions were shedding virus in their semen was established either by test mating, by the serology of the covered mares, or by investigation by MAFF following the introduction of the Equine Viral Arteritis Order 1995. Nine of the stallions (26.5 per cent) were identified as presumptive shedders of EAV in semen and among specific breeds, viral shedding was identified in six of 15 (40 per cent) standardbreds and three of nine (33 per cent) warmbloods. In contrast with the outbreak of EVA in the UK in 1993, no signs of disease typical of EAV infection were reported during these investigations, even in mares test mated to stallions shedding the virus.

Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis.

An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of equine viral arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of equine arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific viral variants that occur in the semen of particular carrier stallions.

Genetic divergence with emergence of novel phenotypic variants of equine arteritis virus during persistent infection of stallions.

The persistently infected carrier stallion is the critical natural reservoir of equine arteritis virus (EAV), as venereal infection of mares frequently occurs after breeding to such stallions. Two Thoroughbred stallions that were infected during the 1984 outbreak of equine viral arteritis in central Kentucky subsequently became long-term EAV carriers. EAV genomes amplified from the semen of these two stallions were compared by sequence analysis of the six 3' open reading frames (ORFs 2 through 7), which encode the four known structural proteins and two uncharacterized glycoproteins. The major variants of the EAV population that sequentially arose within the reproductive tract of each carrier stallion varied by approximately 1% per year, and the heterogeneity of the viral quasispecies increased during the course of long-term persistent infection. The various ORFs of the dominant EAV variants evolved independently, and there was apparently strong selective pressure on the uncharacterized GP3 protein during persistent infection. Amino acid changes also occurred in the V1 variable region of the GL protein. This region has been previously identified as a crucial neutralization domain, and selective pressures exerted on the V1 region during persistent EAV infection led to the emergence of virus variants with distinct neutralization properties. Thus, evolution of the EAV quasispecies that occurs during persistent infection of the stallion clearly can influence viral phenotypic properties such as neutralization and perhaps virulence.

Phylogenetic characterization of a highly attenuated strain of equine arteritis virus from the semen of a persistently infected standardbred stallion.

An avirulent, novel variant of equine arteritis virus (EAV; CA95G) was isolated from the semen of a persistently infected Standardbred stallion. The CA95G virus caused subclinical infection and seroconversion in susceptible horses, and virus was isolated only once from blood and nasal secretions collected from 6 experimentally infected horses. Sequence analysis of genes encoding the known EAV structural proteins shows that this highly attenuated strain of EAV is genetically similar to virulent field strains of EAV and, in particular, to a strain of EAV that was isolated during an outbreak of equine viral arteritis in western Canada in 1986. Not only is the carrier stallion the critical natural reservoir of EAV, but genetic diversity of the virus is generated in the course of persistent infection of carrier stallions. The subtle genetic changes that facilitate and maintain persistent EAV infection of the stallion's reproductive tract likely influence phenotypic properties of the virus such as virulence.

Clinical features of the 1992 outbreak of equine viral arteritis in Spain

During 1992, a widespread outbreak of Equine viral arteritis (EVA) occurred at a riding establishment near Barcelona, Spain. A total of 31 out of 186 horses on the premises displayed clinical signs, most frequently, fever, depression, mild ventral and limb oedema and a vesicular-erosive stomatitis, with hypersalivation, petechiations and small ulcerations. Affected horses developed illness of varying severity with only a few exhibiting a severe form of the disease and no mortality was recorded. Haematological and blood biochemical examination the most severely affected horses revealed a thrombocytopenia, slight leucocytosis with neutrophilia, lymphopenia and eosinopenia, an increase in plasma fibrinogen and a small rise in serum proteins and indirect bilirubin values. Diagnosis was confirmed by demonstration of seroconversion to equine arteritis virus in acute and convalescent phase sera. Attempted isolation of the virus from citrated blood samples proved unsuccessful.

First recorded outbreak of equine viral arteritis in the United Kingdom.

Equine viral arteritis was diagnosed for the first time in the United Kingdom in 1993. The outbreak began on a non-thoroughbred stud in south Nottinghamshire and spread to five other premises through chilled semen used for artificial insemination and from acutely and subclinically infected mares returning home. The outbreak was contained on these six premises by means of voluntary movement restrictions. The most commonly observed clinical signs were typical: pyrexia with depression, and conjunctivitis with periorbital oedema; nasal discharge, and oedema of the distal limbs, prepuce and mammary glands were less common. The first mare to be covered by a recently imported stallion was the first animal to be affected. The mare was resident and no new mares had arrived on the stud during the previous five months. About 100 animals became infected during the outbreak, including three indigenous stallions. Equine arteritis virus was isolated from semen and heparinised blood samples and seroconversions were demonstrated by using the equine arteritis virus neutralisation test. Although the outbreak was contained, the free movement of animals within the European Union increases the possibility of infected stallions being introduced into the UK.

Equine Viral Arteritis: Diagnostic and Control Measures.

A relatively large scale epizootic of equine viral arteritis (EVA) which occurred in Thoroughbreds at Arlington Park Race Course in the USA in 1993 [50], just after the first outbreak of EVA in non-Thoroughbreds in the United Kingdom [40, 95] remains vivid in our memory. It had been considered that the United Kingdom, Ireland, Australia, New Zealand and Japan were the few countries left free from EVA over the past few dozen years. However, serological evidence of EVA was found in Standerdbreds in Australia and New Zealand in 1990 and EVA has been in Australia since 1975, while confirmed clinical EVA was not recognized [42, 68]. The majority of horses infected with equine arteritis virus (EAV) seem to have a mild or subclinical form all over the world [5, 6, 12, 33, 39, 42, 45, 49-51, 53, 60, 64, 70, 73, 98]. In contrast, fatal cases in foals and a neonatal foal have been reported in Poland [34, 35] and the USA [93]. Furthermore, because EVA adversely affects racing [47, 50, 64] and results in a high rate of abortion in pregnant mares [9, 20, 34, 46], an outbreak of EVA in such horse populations may lead to significant economic loss. In recent years, there have been considerable number of international movements of horses for the purpose of trading, breeding and competition. Such movements could provide extensive spread of contagious diseases in horse populations which may be highly susceptible to exotic infectious diseases. Although only a few countries in the world including Japan have remained free from EVA, this article describes the clinical features and diagnosis of EVA, as well as the prevention and control of EVA, thus providing information which will be useful in minimizing suffering from a serious outbreak of EVA should it occur in horse populations that have been free of EVA.

Equine viral arteritis

break of equine viral arteritis (EVA) occurred on a considerable number of Thoroughbred breeding farms in Kentucky in 1984. Subsequent events have shown that this was a watershed event. That occurrence resulted in a dramatic increase in the significance with which this disease would henceforth be perceived by many horse industries worldwide. Greater awareness, surveillance, and improved diagnostic capability collectively have led to an increase in the number of reported outbreaks of EVA over the intervening years. Spread of this infection internationally can almost invariably be attributed to the movement of carrier stallions or shipment of virus-infective semen. The increase in number of confirmed outbreaks of the disease bears little relationship, however, to the known global distribution of the causal agent, equine arteritis virus (EAV). Based on the results of serosurveillance surveys and diagnostic testing, it would appear that the majority of cases of EAV infection continue to be asymptomatic. Where investigated, the virus has not been shown to be a significant cause of abortion or illness and death in young foals. Outbreaks at racetracks, sales yards, etc are very infrequent in occurrence.

Equine viral arteritis at a veterinary teaching hospital

An outbreak of equine viral arteritis (EVA) occurred at a veterinary teaching hospital in the summer and autumn of 1984. Clinical signs were observed in 16 out of 61 hospitalized horses and included ventral, limb and preputial edema, mild conjunctivitis with lacrimation, pyrexia and increased respiratory and heart rates. Of 16 clinically affected horses, 13 were undergoing experimental abdominal surgery and/or were involved in digestion experiments; 9 of the 13 were > 20 years of age. The three other clinically affected horses were client animals. Thirteen client horses developed serologic titers to equine arteritis virus in the absence of clinical signs. The risk of infection was associated with close contact, involvement in the experimental studies being conducted and length of hospitalization. The disease was mild, limited in spread and successfully controlled by quarantine.

Infectious disease incidence among horses in France, Ireland and the United Kingdom during 1984.

An outbreak of equine viral arteritis in the American state of Kentucky led to a temporary ban being imposed by France, Ireland and the UK on the importation of horses from the USA during 1984. Sporadic cases of influenza caused by the type 2 strain of the virus were confirmed in France throughout the year and cases of strangles in thoroughbred mares and foals were reported from all three countries. No cases of contagious equine metritis were confirmed among the thoroughbred breeding population, although a number of outbreaks of the abortion form of rhinopneumonitis occurred. A small number of clinical cases of equine infectious anaemia were confirmed in France.