Two outbreaks of neuropathogenic equine herpesvirus type 1 with breed-dependent clinical signs

Equine herpesvirus type 1 (EHV-1) is a worldwide spread pathogen of horses. It can cause abortion, respiratory and neurological disease and consequentially significant economic losses in equine industries. During 2009, two outbreaks of EHV-1 were confirmed in two stud farms in Eastern Croatia. The first outbreak occurred in February following the import of 12 horses from USA, serologically negative to EHV-1 before transport. Four mares aborted in the late stage of pregnancy and one perinatal death was recorded. Other six mares showed clinical signs of myeloencephalopathy with fatal end in four. One month later, the second EHV-1 outbreak was confirmed in stud farm about 100 km further with 17 abortions, three perinatal deaths and one mild neurological case. Epidemiological data showed that the disease was probably introduced in the first stud farm during international transport. The second outbreak started with the introduction of clinically healthy stallion from the first stud farm. Molecular characterisation and phylogenetic analysis confirmed that, despite different clinical signs, the identical virus caused both outbreaks. Both horse populations were free from EHV-1 infection before the outbreak and had not been vaccinated. Significant difference in clinical signs could be explained by different breed-related risk factors.     

Ataxia and paresis with equine herpesvirus type 1 infection in a herd of riding school horses

An outbreak of neurologic disease associated with serologic evidence of equine herpesvirus type 1 (EHV-1) infection occurred in a herd of 46 riding school horses. Ataxia and paresis were observed in 14 geldings and 5 barren mares. Eight affected horses had distal limb edema, 1 horse had a head tilt, and 3 others had urinary incontinence. Other clinical signs included fever, depression, and inappetance in 30 horses. Seven horses with neurologic signs were treated with acyclovir. Serum neutralizing antibody titers against EHV-1 increased 4-fold between acute and convalescent samples or exceeded 1: 256 in 19 of 44 horses, confirming recent infection. A significantly greater proportion of horses that seroconverted were mares ( P = .014). Of the 19 horses exhibiting ataxia and paresis, 17 made a complete recovery, 1 made a partial recovery, and 1 was euthanized.     

Polyneuropathy of Finnish horses characterised by inflammatory demyelination and intracisternal Schwann cell inclusions

REASON FOR PERFORMING STUDY: A neurological disorder characterised by pelvic limb metatarsophalangeal joint extensor paresis has been observed in numerous horses in Scandinavia for the last decade. Very little has been formally reported and there have been no detailed assessments of the neurological signs or neuropathological lesions. OBJECTIVES: To describe the epidemiological and pathological features of an outbreak of 'Scandinavian knuckling syndrome' in a riding stable in southern Finland. METHODS: Clinical neurological examination of 4 cases and neuropathological assessment of tissues of one case were performed. RESULTS: Eleven out of 17 horses fed on ryegrass from a common source showed progressive clinical signs of metatarsophalangeal extensor paresis necessitating euthanasia of 7 horses. Nervous system lesions in one horse consisted of a novel demyelinating, mildly inflammatory peripheral neuropathy, with BiP/GRP positive rough endoplasmatic reticulum Schwann cell inclusions. CONCLUSIONS: The clinical signs and lesions documented differ from any previously described equine polyneuropathy and suggest a primary Schwann cell lesion. POTENTIAL RELEVANCE: The classification of this disease as a novel demyelinating polyneuropathy may assist focused epidemiological investigations.     

Clinical signs and humoral immune response in horses following equine herpesvirus type-1 infection and their susceptibility to equine herpesvirus type-4 challenge.

A group of three horses was experimentally infected with equine herpesvirus type 1 (EHV-1) and showed clinical signs characterised by a biphasic febrile response, leucopenia and cell associated viraemia accompanied by virus shedding from the nasopharynx. A second exposure to the virus 18 days later resulted in the isolation of virus from the nasopharynx of one horse. This and a further group of three EHV-1 seropositive horses were subsequently infected with equine herpesvirus type 4 (EHV-4) 147 days after the initial EHV-1 infection and virus was shed from the nasopharynx in the absence of clinical disease. Following the first EHV-1 infection, virus specific immunoglobulin M (IgM) was present by day 5 and remained high until the second exposure at day 18 at which point levels decreased. In contrast, EHV-1 specific IgG, detected at day 6 peaked at day 18, after which time levels remained high. Virus neutralising antibodies and antibodies able to mediate antibody-dependent cellular cytotoxicity were present by day 10. The immune response to EHV-1 is discussed with reference to the disease.     

Equine Viral Respiratory Pathogen Surveillance at Horse Shows and Sales

Equine respiratory viral infections cause significant worldwide disease and economic loss. Common causes include equine influenza virus (EIV) and equine herpesviruses-1 and -4 (EHV-1 and -4), and risk of exposure to these agents may be highest in young horses commingling at sales and competitive events. A surveillance study was conducted at two horse shows and two Thoroughbred sales to determine whether horses shed EHV-1, EHV-4, or EIV on arrival, or 2-4 days later, and whether shedding was associated with identifiable risk factors. Real-time polymerase chain reaction assays were used to detect EHV-1, EHV-4, and EIV nucleic acid in nasal swabs obtained from 369 horses at the four events. In response to evidence of clinical disease, 82 additional horses were sampled at two farms providing horses for one of the sales. On arrival at the events, shedding of EHV-1 was detected in 3.3%, EHV-4 in 1.1%, and EIV in 0.8% of horses. EHV-1 was detected at low levels, and EHV-1 and EHV-4 detection was not associated with clinical disease. EIV was detected only in horses at a Thoroughbred sale, in association with an outbreak of respiratory disease traced back to regional farms. On arrival at events, horses younger than 2 years had a significantly greater risk of shedding EHV-1 compared with older horses; no other significant risk factors associated with viral shedding were identified. Thus, there is a risk of exposure to EIV, EHV-1, and EHV-4 at equine events, and horses and events should be managed to mitigate this risk.     

Serological markers of Bornavirus infection found in horses in Iceland

Background

In a stable of eight horses in Northern Iceland, six horses presented with clinical signs, such as ataxia and reduced appetite, leading to euthanasia of one severely affected horse. Serological investigations revealed no evidence of active equine herpes virus type 1 infection, a common source of central nervous system disease in horses, nor equine arteritis virus and West Nile virus. Another neurotropic virus, Borna disease virus, was therefore included in the differential diagnosis list.

Findings

Serological investigations revealed antibodies against Borna disease virus in four of five horses with neurological signs in the affected stable. One horse without clinical signs was seronegative. Four clinically healthy horses in the stable that arrived and were sampled one year after the outbreak were found seronegative, whereas one of four investigated healthy horses in an unaffected stable was seropositive.

Conclusions

This report contains the first evidence of antibodies to Borna disease virus in Iceland. Whether Borna disease virus was the cause of the neurological signs could however not be confirmed by pathology or molecular detection of the virus. As Iceland has very restricted legislation regarding animal imports, the questions of how this virus has entered the country and to what extent markers of Bornavirus infection can be found in humans and animals in Iceland remain to be answered.     

Outbreak of equine herpesvirus type 1 myeloencephalitis: new insights from virus identification by PCR and the application of an EHV-1-specific antibody detection ELISA

Five of 10 pregnant, lactating mares, each with a foal at foot, developed neurological disease. Three of them became recumbent, developed complications and were euthanased; of the two that survived, one aborted an equine herpesvirus type 1 (EHV-1)-positive fetus 68 days after the first signs were observed in the index case and the other gave birth to a healthy foal on day 283 but remained ataxic and incontinent. The diagnosis of EHV-1 myeloencephalitis was supported by postmortem findings, PCR identification of the virus and by serological tests with an EHV-1-specific ELISA. At the time of the index case, the 10 foals all had a heavy mucopurulent nasal discharge, and PCR and the ELISA were used to detect and monitor EHV-1 infection in them. The status of EHV-1 infection in the five in-contact mares was similarly monitored. Sera from three of the affected mares, taken seven days after the index case were negative or had borderline EHV-1-specific antibody titres. In later serum samples there was an increase in the titres of EHV-1-specific antibody in two of the affected mares. In contrast, sera from the five unaffected in-contact mares were all EHV-1-antibody positive when they were first tested seven or 13 days after the index case.     

Equine Herpesvirus-I Infection in Horses: Recent Updates on its Pathogenicity,Vaccination, and Preventive Management Strategies

Equine herpesvirus-1 (EHV-1) is one of the most common and ubiquitous viral pathogens infecting equines, particularly horses worldwide. The EHV-1 is known to induce not only humoral but also cellular immune responses in horses. Respiratory distress, abortion in pregnant mares, neurological disorders, and neonatal foal deaths represent EHV-1 infection. Despite the limited success of inactivated, subunit, live, and DNA vaccines, over the past few decades, vaccination remains the prime preventive option to combat EHV-1 infection in horses. However, current vaccines lack the potentiality to protect the neurological form of infections in horses. There is desperate necessity to search effectual EHV-1 vaccines that may stimulate not only mucosal and systemic cellular immunity but also humoral immunity in the horses. This review highlights the state of knowledge regarding EHV-1 biology, EHV-1 pathogenesis, and disparate vaccines studied in the past to prevent EHV-1 infection. The review also underlines the best management strategies which certainly need to be adopted by veterinarians in order to avoid and prevent EHV-1 infection and outbreak in horses in the future.     

The first reported outbreak of equine herpesvirus myeloencephalopathy in New Zealand

CASE HISTORY AND CLINICAL FINDINGS: On 9 January 2014 (Day 0) a mare from a stud farm in the Waikato region presented with urinary incontinence without pyrexia. Over the following 33 days 15 mares were clinically affected with neurological signs. All but one mare had a foal at foot. The most commonly observed clinical signs were hind limb paresis and ataxia. In some cases recumbency occurred very early in the course of disease and seven mares were subject to euthanasia for humane reasons.

LABORATORY FINDINGS: Equid herpesvirus (EHV) type 1 was detected using PCR in various tissues collected post mortem from two mares with neurological signs. DNA sequencing data from the DNA polymerase gene of the virus showed a nucleotide transition at position 2254, a mutation encoding amino acid D₇₅₂ that is highly associated with the neuropathogenic genotype of EHV-1. In total 12/15 mares were confirmed positive for EHV-1 on PCR. Results from a virus neutralisation test and ELISA on paired serum samples, and PCR on whole blood and nasal swabs, indicated that of four paddocks in a high-risk area where a cluster of cases had occurred, 20/21 (95%) horses were likely to have been exposed or were confirmed infected with EHV-1. Subsequent to the outbreak two mares aborted, one at 9 months and one at 10 months of gestation. The cause of abortion was confirmed as EHV-1 with the same genotype as that involved in the outbreak.

DIAGNOSIS: Equine herpesvirus myeloencephalopathy.

CLINICAL RELEVANCE: The outbreak described shows the considerable impact that can occur in outbreaks of equine herpesvirus myeloencephalopathy in New Zealand. Early biosecurity controls not only reduced the effect on the farm but mitigated the potential for the virus to spread to other horse enterprises.     

Surveillance programme for important equine infectious respiratory pathogens in the USA

The prevalence and epidemiology of important viral (equine influenza virus [EIV], equine herpesvirus type 1 [EHV-1] and EHV-4) and bacterial (Streptococcus equi subspecies equi) respiratory pathogens shed by horses presented to equine veterinarians with upper respiratory tract signs and/or acute febrile neurological disease were studied. Veterinarians from throughout the USA were enrolled in a surveillance programme and were asked to collect blood and nasal secretions from equine cases with acute infectious upper respiratory tract disease and/or acute onset of neurological disease. A questionnaire was used to collect information pertaining to each case and its clinical signs. Samples were tested by real-time PCR for the presence of EHV-1, EHV-4, EIV and S equi subspecies equi. A total of 761 horses, mules and donkeys were enrolled in the surveillance programme over a 24-month study period. In total, 201 (26.4 per cent) index cases tested PCR-positive for one or more of the four pathogens. The highest detection rate was for EHV-4 (82 cases), followed by EIV (60 cases), S equi subspecies equi (49 cases) and EHV-1 (23 cases). There were 15 horses with double infections and one horse with a triple infection. The detection rate by PCR for the different pathogens varied with season and with the age, breed, sex and use of the animal.     

Quantification by real-time PCR of the magnitude and duration of leucocyte-associated viraemia in horses infected with neuropathogenic vs. non-neuropathogenic strains of EHV-1

REASONS FOR PERFORMING STUDY: Neurological disease in horses caused by infection with certain 'paralytic' strains of equine herpesvirus-1 (EHV-1) is a potentially devastating condition the pathogenesis of which is poorly understood. Preliminary observations in both experimentally induced and naturally occurring cases of the central nervous system disease have revealed a more robust cell-associated viraemia in horses infected with paralytic isolates of EHV-1, relative to horses infected with abortigenic isolates. To investigate further this pathogenesis-relevant question, the present study was performed using a greater number of horses and a more precise method for quantification of EHV-1 DNA present in viraemic leucocytes. OBJECTIVE: To compare the magnitude and duration of leucocyte-associated viraemia in seronegative, age-matched foals following infection with paralytic vs. abortigenic isolates of EHV-1. METHODS: Peripheral blood mononuclear cells (PBMC) were collected from 20 weanling foals at 2, 4, 7, 9, 11, 14 and 21 days after intranasal inoculation with either paralytic or abortigenic isolates of EHV-1. The amount of EHV-1 DNA present in each PBMC sample was measured by real-time quantitative PCR. RESULTS: Foals inoculated with paralytic strains of EHV-1 developed both a greater magnitude and longer duration of PBMC-associated viraemia than foals inoculated with abortigenic strains of the virus. CONCLUSIONS: Both the higher magnitude and longer duration of cell-associated viraemia contribute to the risk for development of neurological signs in horses infected with paralytic strains of EHV-1. POTENTIAL RELEVANCE: Our results provide empirically derived, scientific data that contributes to a better understanding of the pathogenetic basis for the differing abilities of paralytic and abortigenic strains of EHV-1 to cause post infection central nervous system disease in the horse. The findings identify the importance of minimising the quantitative burden of viraemic leucocytes that follows exposure to the virus, by the use of effective therapeutic antiviral drugs and efficacious prophylactic vaccines that stimulate cytotoxic immune responses against EHV-1 infected cells.     

Haematological changes in two thoroughbred horses in training with confirmed equine herpesvirus 1 infections

An outbreak of respiratory disease among thoroughbred horses in training in Hong Kong was caused by equine herpesvirus 1 (EHV-1) subtype 1 (abortion strain). Two of the horses affected by EHV-1 were serially blood sampled over a period of several weeks and their haematological values measured. There was an increase in monocyte count in the first few days which steadily decreased in one horse, but the other had a second monocyte peak after a period of exercise, thus demonstrating the importance of not working animals in the early stages of the disease.     

Viruses associated with outbreaks of equine respiratory disease in New Zealand

AIM: To identify viruses associated with respiratory disease in young horses in New Zealand. METHODS: Nasal swabs and blood samples were collected from 45 foals or horses from five separate outbreaks of respiratory disease that occurred in New Zealand in 1996, and from 37 yearlings at the time of the annual yearling sales in January that same year. Virus isolation from nasal swabs and peripheral blood leukocytes (PBL) was undertaken and serum samples were tested for antibodies against equine herpesviruses (EHV-1, EHV-2, EHV-4 and EHV-5), equine rhinitis-A virus (ERAV), equine rhinitis-B virus (ERBV), equine adenovirus 1 (EAdV-1), equine arteritis virus (EAV), reovirus 3 and parainfluenza virus type 3 (PIV3). RESULTS: Viruses were isolated from 24/94 (26%) nasal swab samples and from 77/80 (96%) PBL samples collected from both healthy horses and horses showing clinical signs of respiratory disease. All isolates were identified as EHV-2, EHV-4, EHV-5 or untyped EHV. Of the horses and foals tested, 59/82 (72%) were positive for EHV-1 and/or EHV-4 serum neutralising (SN) antibody on at least one sampling occasion, 52/82 (63%) for EHV-1-specific antibody tested by enzyme-linked immunosorbent assay (ELISA), 10/80 (13%) for ERAV SN antibody, 60/80 (75%) for ERBV SN antibody, and 42/80 (53%) for haemagglutination inhibition (HI) antibody to EAdV-1. None of the 64 serum samples tested were positive for antibodies to EAV, reovirus 3 or PIV3. Evidence of infection with all viruses tested was detected in both healthy horses and in horses showing clinical signs of respiratory disease. Recent EHV-2 infection was associated with the development of signs of respiratory disease among yearlings [relative risk (RR)=2.67, 95% CI=1.59-4.47, p=0.017]. CONCLUSIONS: Of the equine respiratory viruses detected in horses in New Zealand during this study, EHV-2 was most likely to be associated with respiratory disease. However, factors other than viral infection are probably important in the development of clinical signs of disease.     

Equid herpesvirus (EHV-1) live vaccine strain C147: efficacy against respiratory diseases following EHV types 1 and 4 challenges

The temperature sensitive and host range mutant clone 147 of equine herpesvirus 1 (EHV-1) was assessed for its ability to protect conventional, susceptible adult horses against respiratory infection by EHV-1 and equine herpesvirus 4 (EHV-4).Intranasal (IN) vaccination with 5.2 log(10) TCID(50) did not cause adverse clinical reactions although a limited virus shedding and viraemia (leukocytes) was observed in 11 of 15 and 10 of 15 vaccinated horses respectively. All 15 vaccinated horses showed a significant seroresponse to both EHV-1 and EHV-4 for virus neutralising (VN) antibody. None of 14 control horses shed virus or became viraemic or seroconverted prior to challenge. EHV-1 challenge (dose 6.0 log(10)) 6 weeks after vaccination resulted in pyrexia in all eight control horses while eight vaccinated horses remained unaffected. Six control horses developed nasal discharge, five of which were mucopurulent nasal discharge (mean duration 3.2 days) which also occurred in four vaccinated horses for 1 day. All eight control horses shed challenge EHV-1 at a significantly higher level (group mean titre 2.6+/-0.4 log(10) TCID(50) per sample) and for much longer (mean duration 4.8+/-1.5 days) than that (group mean titre 1.4+/-0.8 log(10) TCID(50) per sample and mean duration 1.5+/-0.5 days) in six vaccinated horses. Furthermore, all eight control horses became viraemic (mean duration 2.9 days) but viraemia did not occur in eight vaccinated horses. Following EHV-1 challenge, all eight control horses showed a significant VN antibody rise to both EHV-1 and EHV-4 but this occurred in only one vaccinated horse and to EHV-4 only. In EHV-4 challenge (dose of 4.2 log(10) TCID(50)) of a separate pair of seven vaccinated and six control horses, 6 weeks after EHV-1 vaccination resulted in pyrexia (mean duration 2.3 days) and nasal discharge (mean duration 1.8 days) in three and five control horses respectively but the only reaction observed in the vaccinated group was nasal discharge for 1 day in one animal. All six control animals shed virus (mean titre 2.5+/-0.6 log(10) TCID(50) per sample and mean duration 2+/-0.6 days) compared to one vaccinated animal. Although EHV-4 viraemia is rare, 3 of 6 control horses became viraemic after EHV-4 challenge but this was not observed in vaccinated horses. After EHV-4 challenge 3 and 5 of 6 control horses seroconverted for VN antibody to EHV-1 and EHV-4 respectively; a non-responsive control horse had high level of pre-existing VN antibody to EHV-4. However, only 1 of 7 vaccinated horses showed a significant antibody rise and only to EHV-4.     

Equine Multinodular Pulmonary Fibrosis in association with asinine herpesvirus type 5 and equine herpesvirus type 5: a case report

A standardbred gelding with a history of 10 days pyrexia and lethargy was referred to the Equine Hospital at the Swedish University of Agricultural Sciences in Uppsala, Sweden.The horse had tachypnea with increased respiratory effort and was in thin body condition. Laboratory findings included leukocytosis, hyperfibrinogenemia and hypoxemia. Thoracic radiographs showed signs of pneumonia with a multifocal nodular pattern, which in combination with lung biopsy findings indicated Equine Multinodular Pulmonary Fibrosis (EMPF). EMPF is a recently described disease in adult horses with clinical signs of fever, weight loss and respiratory problems. The pathological findings include loss of functional pulmonary parenchyma due to extensive nodular interstitial fibrosis which has been related to infection with the equine herpesvirus type 5 (EHV-5). In this case, lung biopsy and tracheal wash samples tested positive for both asinine herpesvirus type 5 (AHV-5) and EHV-5 using PCR assays. The horse failed to respond to treatment and was euthanized for humane reasons. Postmortem examination confirmed the diagnosis of EMPF. This case suggests that not only EHV-5 alone should be considered in association with the development of this disease.     

马疱疹病毒1型感染马疾病模型的建立及评价

试验旨在建立马疱疹病毒1型（Equine herpesvirus type1,EHV-1）人工发病模型,确定EHV-1感染马的半数感染量（ID₅₀）及感染发病的判定标准,为该病的预防与治疗药物的研发奠定基础。以新疆伊犁地区某发病马场流产胎儿中分离的EHV-1 XJ2015株为研究对象,设立4组不同病毒剂量感染组及对照组,经鼻内喷雾感染马,5 mL/匹,每天观察试验马的临床症状和发病情况,14 d后进行剖检,观察各组织脏器病理变化并应用实时荧光定量PCR方法检测鼻腔排毒及病毒分布情况。结果显示,EHV-1 XJ2015株感染马的ID₅₀为10^-6.67/5 mL,其病毒含量为10^4.33 TCID₅₀/mL。与对照组相比,1×10⁶和1×10⁵ TCID₅₀/mL感染组马临床评分显著升高,主要表现为体温升高（高达39.5 ℃,一般持续2~6 d）、食欲不振、流浆液性鼻液和下颌淋巴结肿大;且1×10⁶和1×10⁵ TCID₅₀/mL感染组试验马均表现出不同程度的排毒,肺脏及脑组织中可检测出大量病毒,与对照组相比极显著或显著升高（P<0.01;P<0.05）;病理学检查发现,患马脑组织出现非化脓性脑炎及神经元水肿,肺脏组织出现间质性肺炎、嗜中性粒细胞、炎性细胞浸润、出血和肺泡间隔增厚。以上结果表明,EHV-1 XJ2015株对马具有较强的致病性,患病马临床症状典型,病毒主要随鼻液排出,并富集在肺脏及脑组织,通过上述指标确定EHV-1感染马发病的判定标准,本试验成功建立EHV-1感染本体动物疾病模型。     

Severe acute rhabdomyolysis associated with Streptococcus equi infection in four horses

Four Quarter Horses (9 months to 7 years of age) with submandibular lymphadenopathy and firm muscles (palpation of which elicited signs of pain) were evaluated; in general, the horses had a stiff gait, and 3 horses became recumbent. Streptococcus equi was cultured from aspirates of lymph nodes or samples of purulent material collected from the auditory tube diverticula. Once the horses were recumbent, their condition deteriorated rapidly despite aggressive antimicrobial and antiinflammatory treatment, necessitating euthanasia within 24 to 48 hours. One horse did not become recumbent and recovered completely. Among the 4 horses, common clinicopathologic findings included neutrophilia, hyperfibrinogenemia, and high serum activities of creatine kinase and aspartate aminotransferase. Necropsies of the 3 euthanatized horses revealed large, pale areas most prominent in the semimembranosus, semitendinosus, sublumbar, and gluteal muscles that were characterized histologically by severe acute myonecrosis and macrophage infiltration of necrotic myofibers. Streptococcus equi was identified in sections of affected muscle by use of immunofluorescent stains for Lancefield group C carbohydrate and S. equi M protein. In the 4 horses of this report, acute severe rhabdomyolysis without clinical evidence of muscle atrophy or infarction was associated with S. equi infection; rhabdomyolysis was attributed to either an inflammatory cascade resembling streptococcal toxic shock or potentially direct toxic effects of S. equi within muscle tissue.     

Viruses associated with outbreaks of equine respiratory disease in New Zealand

AIM: To identify viruses associated with respiratory disease in young horses in New Zealand.

METHODS: Nasal swabs and blood samples were collected from 45 foals or horses from five separate outbreaks of respiratory disease that occurred in New Zealand in 1996, and from 37 yearlings at the time of the annual yearling sales in January that same year. Virus isolation from nasal swabs and peripheral blood leukocytes (PBL) was undertaken and serum samples were tested for antibodies against equine herpesviruses (EHV-1, EHV-2, EHV-4 and EHV-5), equine rhinitis-A virus (ERAV), equine rhinitis-B virus (ERBV), equine adenovirus 1 (EAdV-1), equine arteritis virus (EAV), reovirus 3 and parainfluenza virus type 3 (PIV3).

RESULTS: Viruses were isolated from 24/94 (26%) nasal swab samples and from 77/80 (96%) PBL samples collected from both healthy horses and horses showing clinical signs of respiratory disease. All isolates were identified as EHV-2, EHV-4, EHV-5 or untyped EHV. Of the horses and foals tested, 59/82 (72%) were positive for EHV-1 and/or EHV-4 serum neutralising (SN) antibody on at least one sampling occasion, 52/82 (63%) for EHV-1-specific antibody tested by enzyme-linked immunosorbent assay (ELISA), 10/80 (13%) for ERAV SN antibody, 60/80 (75%) for ERBV SN antibody, and 42/80 (53%) for haemagglutination inhibition (HI) antibody to EAdV-1. None of the 64 serum samples tested were positive for antibodies to EAV, reovirus 3 or PIV3. Evidence of infection with all viruses tested was detected in both healthy horses and in horses showing clinical signs of respiratory disease. Recent EHV-2 infection was associated with the development of signs of respiratory disease among yearlings [relative risk (RR)=2.67, 95% CI=1.59-4.47, p=0.017].

CONCLUSIONS: Of the equine respiratory viruses detected in horses in New Zealand during this study, EHV-2 was most likely to be associated with respiratory disease. However, factors other than viral infection are probably important in the development of clinical signs of disease.