Clinical observations and management of a severe equine herpesvirus type 1 outbreak with abortion and encephalomyelitis
© Walter et al.; licensee BioMed Central Ltd. 2013
Received: 15 October 2012
Accepted: 25 February 2013
Published: 5 March 2013
Latent equine herpesvirus type 1 (EHV-1) infection is common in horse populations worldwide and estimated to reach a prevalence nearing 90% in some areas. The virus causes acute outbreaks of disease that are characterized by abortion and sporadic cases of myeloencephalopathy (EHM), both severe threats to equine facilities. Different strains vary in their abortigenic and neuropathogenic potential and the simultaneous occurrence of EHM and abortion is rare. In this report, we present clinical observations collected during an EHV-1 outbreak caused by a so-called “neuropathogenic” EHV-1 G2254/D752 polymerase (Pol) variant, which has become more prevalent in recent years and is less frequently associated with abortions. In this outbreak with 61 clinically affected horses, 6/7 pregnant mares aborted and 8 horses developed EHM. Three abortions occurred after development of EHM symptoms. Virus detection was performed by nested PCR targeting gB from nasal swabs (11 positive), blood serum (6 positive) and peripheral blood mononuclear cells (9 positive) of a total of 42 horses sampled. All 6 fetuses tested positive for EHV-1 by PCR and 4 by virus isolation. Paired serum neutralization test (SNT) on day 12 and 28 after the index case showed a significant (≥ 4-fold) increase in twelve horses (n = 42; 28.6%). This outbreak with abortions and EHM cases on a single equine facility provided a unique opportunity for the documentation of clinical disease progression as well as diagnostic procedures.
KeywordsEquine herpesvirus type 1 Neuropathogenicity Stud Treatment Recovery rate Pregnancy rate
Equine herpesvirus type 1 (EHV-1) is ubiquitous in horse populations worldwide. Many horses are latently infected with EHV-1 and reactivation of the virus can occur under stress, upon which latently infected carriers start to shed infectious virus that may spread to in-contact horses [1, 2]. Clinical EHV-1 infection can manifest itself in the form of three different clinical syndromes: respiratory disease, usually mild, in horses under 2 years of age; abortions, typically in the last trimester of pregnancy; and equine herpesvirus myeloencephalopathy (EHM) [1–3]. Different strains vary in their abortigenic potential [4, 5] as well as in neuropathogenicity . A single nucleotide polymorphism (SNP) in the viral DNA polymerase (Pol) gene (ORF30) is considered one major marker for the neuropathogenic potential of EHV-1 strains [7, 8]. The A2254/N752 and G2254/D752 Pol variants apparently differ in their capability of causing EHM [6, 8, 9]. A2254/N752 (non-neuropathogenic) viruses are mainly isolated from cases of abortion and less frequently from horses with EHM. On the other hand, the G2254/D752 Pol variant (neuropathogenic) is found predominantly associated with EHM outbreaks [10, 11]. The estimated prevalence of latent EHV-1 infection varies between 54% and 88%, depending on the population sampled and the method of virus detection used [3, 12]. In the last decades, the prevalence of the G2254/D752 EHV-1 genotype in EHV-1 positive horses in the United States has apparently increased from 3.3% in the 1960s to 19.4% at the beginning of this century [13–15]. This may indicate a selective advantage of the neuropathogenic strain, which also could increase prevalence of EHM in the future.
Simultaneous latent infection in lymphoid tissues with both A2254/N752 and G2254/D752 EHV-1 genotypes was documented in some studies [12, 16, 17]. Parallel reactivation of both genotypes was not addressed in these studies. In contrast, no dual infection with A2254/N752 and G2254/D752 EHV-1 was detected in 419 fetal isolates . However, 2 EDTA blood samples of febrile horses tested positive for both genotypes in another study on one farm (n = 23; 20 abortion outbreaks, 3 EHM outbreaks) with EHM cases .
Detection of the D752 Pol variant in outbreaks without EHM cases is rare and occurred in only 5% of the cases in a retrospective worldwide study . In a 23-year retrospective analysis, 11% (19/176) of isolates carried the G2254/D752 allele, of which 84% (16/19) were collected from EHM cases and only 16% (3/19) from respiratory or abortion cases . A combination of abortions with EHM was documented in 3 of the sampled farms . In Argentina, 7% (4/54) of the abortion outbreaks were induced by the G2254/D752 variant, and in 2 of these simultaneous neurologic disease occurred . Two outbreaks with abortion and EHM cases caused by the neuropathogenic strain were recently documented in Croatia with breed-dependent clinical signs: a high incidence of abortion (53.1%) was described in Lippizaner mares compared to a lower incidence (10%) in Quarter horses infected with the identical virus .
Various reports with clinical data are available for outbreaks either with neurological cases or abortion storms [19–22]. This case report documents for the first time the clinical data collected during an EHV-1 outbreak with an uncommon combination of abortion and EHM on a single facility in Germany.
This report is an account of an acute outbreak of EHV-1 in a mixed horse operation. Consequently, all clinical decisions and laboratory diagnostic procedures were initiated during the course of the outbreak. The documented outbreak occurred on an equine riding and breeding facility in southern Germany in early 2009. The stud includes different areas for sport and breeding horses. Broodmares and breeding stallions were kept separate from the sports horses. Breeding stallions were attended by grooms, which did not enter the broodmare or sport horse facilities as required for a European Union accredited breeding facility. In the sports horse section, horses were brought onto the premise without quarantine prior to entering the facility.
Description of horse populations in the different barns on the stud
No. of horses
Same staff as horses of other barns
BM; 1 foal
The index case of the outbreak was an abortion in the broodmare barn 7. The day of the abortion is referred to as day 1 of the outbreak. Sixty-one clinical cases (77.2%) were detected during the outbreak and cases were identified over a period of 44 days. Onset, type and duration of clinical signs were documented for all individuals and are documented in the following sections.
In 71 horses, housed in barns 1 to 7, body temperatures were taken twice daily, starting on day 5 after the first abortion (index case). In the remaining 8 horses of the stabled population, control of body temperature as a routine procedure was practically impossible. Fever was defined as a body temperature of 38.1°C or higher (≥ 100.6°F).
Clinical and laboratory data in individual horses with EHM (n = 8) and/or abortion (n = 6)
Day of Onset of Fever/EHM/Abortion b (EHM grade) c
Fever Max/Duration d
PCR e D12
SNT f D12/D28
Fetus Cell Culture/PCR g
Eight of the 61 clinically affected horses (13.1%) developed neurological signs, which we all attributed to EHV-1 infection. Neurological symptoms were graded according to Reed and Andrews . Fever was detected before onset of clinical signs of EHM in 3 of the 8 cases. In 5 horses, EHM symptoms became evident between day 5 and 9 of the outbreak without a preceding fever period, which could be the result of the delayed implementation of regular body temperature measurements. The incubation period for EHM symptoms in experimental and natural infected horses was previously described to range between 6 and 8 days . In this outbreak EHM symptoms developed 5 (two horses) or 9 (one horse) days after the first fever, and 1, 2 and 4 days after the last fever (Table 2). As reported previously by other authors, all horses developing EHM were non-febrile at the onset of neurologic disease .
In three horses, neurological signs were restricted to mild ataxia of the hind limbs (grade 2). Four other horses suffered from more severe ataxia and upper motor neuron (UMN) symptoms as evidenced by an inability to open the urethral sphincter for autonomous urination (grade 4). One horse became temporarily recumbent (grade 5) . The “UMN bladder” was observed between 2 and 13 days after onset of ataxia (2, 4, 10, 12 and 13 days in grade 4 and 5 horses). The average age of the eight EHM cases was 7.8 ± 4.5 years with a range of 4 to 16 years. In other studies, horses under five years of age had a decreased risk to develop EHM [19, 20, 22]. This outbreak included 4 EHM horses (50%) that were only 4 years old, with 3 of these younger horses developing grade 2 neurological signs. Just one horse with grade 4 neurological signs was 4 years old and the 3 other horses suffering from neurological signs grade 4 were over 9 years of age. Other authors also described a more severe clinical presentation in older horses. It was recently shown that the amount of virus in biological samples was not systematically related to the intensity of clinical signs observed . During the outbreak described here, we too were unable to correlate virus detection and development of EHM (Table 2).
The 13.1% incidence of EHM observed in this outbreak appears relatively low. A cumulative analysis of records from the United States showed a 26% incidence of EHM in 452 EHV-1 infected horses, out of which 29% required euthanasia . A recent report described a case fatality rate for EHV-1 of 71.4% (5 out of 7) . The high mortality associated with EHM is at odds with our observations, where all 8 EHM cases survived and returned to their former level of activities, regardless of the severity of the disease. How the low EHM incidence and mortality were influenced by the implemented heparin treatment or supportive veterinary care remains speculative. Other reports document factors beside the neuropathogenicity of the virus (breed, sex, age or vaccination) that may contribute to the risk to develop severe EHM after EHV-1 infection and may be also responsible for the good outcomes in this outbreak [6, 26, 27].
The laboratory results confirmed the clinical diagnosis “EHV-1 infection” that was based on the typical clinical course with fever (n = 55), abortions (n = 6) and neurological deficits (n = 8).
Gross pathology and histopathology were performed on all abortions. An ORF30 (Pol)-specific polymerase chain reaction (PCR) was used for detection of viral nucleic acid in fetal lung, liver and fetal membranes. Typical lesions in spleen and liver, with necrosis and intranuclear inclusion bodies, were detected in all 6 aborted fetuses. In 4 of the aborted fetuses, cell culture isolation of the virus was successful and in all 6 fetuses EHV-1-specific PCR amplification was positive. Sequencing of the amplification product was performed after digestion with restriction enzyme Sal I to identify the EHV-1 Pol D752 genotype .
From day 1, quarantine was imposed for broodmare barn 7. From day 5, different grooms attended separate barns. Facilities were entered through hygienic barriers in which personnel had to change clothes. Horse movements were prohibited and all horses remained indoors. However, new cases of fever were detected in nearly all barns during the outbreak. We concluded from this observation that quarantine measures were implemented too late and infection had already been fully established in all areas of the premise (except the breeding stallion part). Separation of horses, which were suspected to shed virus based on clinical symptoms such as fever, EHM and/or abortion in the affected barns, was deemed impossible. Isolation facilities were not available and barn construction could not be changed fast enough, so horses were able to maintain nose-to-nose contact. All abortions occurred in the broodmare stall and aborted fetuses and placentas were submitted to pathological examination and taken with precautions in order not to contaminate the environment. The facility imposed on itself a voluntary quarantine and all horse transports on and off the stud were restricted from day 1.
At the beginning of the outbreak, clinically healthy horses (n = 33) received prophylactic IM application of an immunostimulant based on inactivated parapoxvirus ovis (2 mL/horse; IM)c given three times in two-day intervals. However, thirty-one (94%) of the treated horses developed a fever. Administration of a parapoxvirus ovis preparation was previously described as a successful measure to avoid severe clinical consequences of EHV-1 and -4 infection in young horses , but seemed to be not effective in our outbreak.
Horses showing fever as the only symptom received no other medication as long as they maintained good general condition and appetite. Three horses with fever were depressed and received flunixin-meglumined (1.1 mg/kg once daily for 1 – 3 days; IV). Mares that had an abortion also received flunixin-meglumined and were treated with heparinb for laminitis prevention, benzathine-penicilline (10,000 I.U./kg every other day, three times; IM), gentamicinf (4 mg/kg twice daily for 5 days; IV), oxytocing (15 I.U. as necessary; SC) and uterine lavage treatments.
In an attempt to prevent EHM, heparinb (25.000 I.U.) was given twice daily for 3 days to 31 febrile horses from day 10 of the outbreak, while the first 30 horses exhibiting fever did not receive heparin. Horses showing signs of EHM were treated symptomatically . The management was directed towards supportive nursing, nutritional care and reduction of CNS inflammation with non-steroidal anti-inflammatory drugs (flunixin-meglumined,1.1 mg/kg once daily; IV). Generally, EHM horses showed good appetite but had to be fed at head level because uptake of food and water from the ground seemed to be difficult. EHM horses were also treated with flunixin-meglumined, lactated Ringer solution and 5% glucose solution, depending on the horse’s general condition and laboratory results. Patients with UMN bladder were catheterized periodically as was deemed necessary. A combination of sulfamerazin/trimethoprimh (45 mg/kg twice daily; PO) was administered for cystitis prevention until paralysis was resolved.
Horses with fever as the sole clinical sign remained in good general condition over the course of the outbreak and recovered without complication. Fertility of the aborting mares was good, as only 1 of the 6 aborting mares was barren in the following breeding season. All 8 EHM horses survived, ataxia and UMN bladder symptoms improved steadily and was resolved completely in all horses 3 months after infection.
We document a clinical outbreak of EHV-1 caused by a G2254/D752 ORF30 variant virus resulting in 61 clinical cases. Infection caused fever (n = 55), abortion (n = 6) and/or EHM (n = 8) for 44 days in 7 barns. Strict containment procedures employed from day 5 of the outbreak did not prevent spread of virus on the premise. Abortion (n = 6) and EHM (n = 8) cases provided a unique opportunity to collect clinical data about disease progression and prognosis for recovery and fertility. Procedures to prevent EHV-1 outbreaks include in particular proper vaccination for newly introduced horses and the restriction of contact between brood mares, adolescent horses and sport horses with foreign contact [3, 6, 27].
Written informed consent was obtained from the patients for publication of this report and any accompanying images.
aDuvaxyn, Fort Dodge Animal Health
bHeparin-Natrium Braun “Multi”, Braun
cZylexis, Pfizer Animal Health
fGenta 100, CP-Pharma
gOxytocin Albrecht, Albrecht
hTrimetox-Pulver, Veyx-Pharma GmbH.
equine herpesvirus-associated myeloencephalopathy
equine herpesvirus type 1
peripheral blood mononuclear cells
polymerase chain reaction
serum neutralization test
upper motor neuron
The authors highly appreciate support by owners and team of the stud, which enabled collection of clinical data and sample collection. Tierseuchenkasse Baden-Württemberg, a state institution, funded this investigation. Parts of this article were presented at the 16th Annual Conference of the European Society for Domestic Animal Reproduction in Dublin, August 29th to September 1st 2012.
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