Equine Herpesviruses 1 And 4 (EHV-1/EHV-4) - IDEXX
Diagnostic UpdateEquine Herpesviruses 1 and 4(EHV-1/EHV-4)EHV-1 and EHV-4 are ubiquitary double-stranded DNA viruses of the Alphaherpesvirinae family. Hallmark ofthese viruses is the establishment of a lifelong infection (carrier status). A virus reactivation and sheddingin latent-infected horses with or without clinical signs is possible. Three main syndromes are described inconnection with both viruses: rhinopneumonitis, late abortion/neonatal death, and myeloencephalopathy.EHV-4 is mostly responsible for upper respiratory airway diseases in young horses, whereas EHV-1 is mainlyresponsible for rhinopneumonitis, abortion, and myeloencephalopathy.PathogenesisInfection occurs through inhalation of viral particles or contactwith contaminated tissue (e. g. abortion material), saliva, nasalor ocular discharge, and probably feces from virus-sheddingcarriers and horses with an active subclinical or clinicalinfection. Infection may be spread by contaminated handsand fomites (water, feeding bucket). Following inhalation, thevirus replicates in the upper respiratory tract epithelial cells,producing death of cells and epithelial erosion. The virusspreads from cell-to-cell reaching the respiratorytract-associated lymph nodes within 24–48 hours. Followinginfection of leukocytes, a leukocyte-associated viremia isestablished, and it is responsible for the systemic spread of thevirus to the central nervous system (CNS) and the pregnantuterus, among other tissues. Viremia persists for a week orlonger and due to its high tropism for lymphocytes, the viruscan also lead to immunosuppression.Pathogenesis of EHV-related myeloencephalopathy andabortion is most likely related to the cell-associated viremiaand its resulting infection of the endothelium. This in turn leadsto vasculitis and reactive thrombosis, producing a generalderangement of the microcirculation, local hypoxia—andconsequently neuron death—and partial or absolutedetachment of the placenta.First-time infection occurs mostly within the very first weeks ormonths of life. Probably in almost all cases, a lifelong state oflatency is established within the lymphoreticular system andtrigeminal ganglion. Latently infected horses play a major rolein the epidemiology of EHV-1 and EHV-4 infections: in stressfulsituations, such as transport, disease, and weaning, theseanimals may experience a viral reactivation, shedding the virusinto their environment, thus enabling the outbreak of clinicaldisease without the introduction of new horses into the group.It is worth mentioning that the virus can be shed by horsesshowing clinical signs of disease or by asymptomatic cases.The virus can be shed for up to 2–3 weeks after infection orreactivation. In cases of EHV-1 neurologic disease, the viruscan be shed for an even longer period of time. Virus survival inthe environment is estimated to be of about 14 days in mostconditions.Nasal discharge in a case of EHV-1 rhinopneumonitisCourtesy of Equine Hospital Kottenforst/GermanyThe virus has been isolated in semen of clinically healthystallions. Although transmission through semen has not beendocumented, stallions may show scrotal edema, lower qualityof semen and a lack of libido during EHV outbreaks.After infection, immunity toward new infections is short (3–5months). During this period, horses do not shed the virus andno viremia occurs after viral contact.Respiratory tract diseaseClinical signs are observed between 2–10 days after infectionor after a recrudescence episode in latent carriers. In mostcases, infection is self-limiting and horses show mild clinicalsigns, if any (however, asymptomatic horses may still shed thevirus into the environment). Most common clinical signs includepyrexia, depression, coughing, and serous to mucoid nasaldischarge (mucopurulent in cases with secondary bacterialinfection). Pharyngitis and tracheitis may also be present.
Some horses develop the so-called “poor performancesyndrome” after infection with EHV-1/EHV-4, which ispresumably attributable to a nonspecific bronchialhypersensitivity. Young naive foals are more clinically affectedthan older horses and develop a biphasic pyrexia for 8–10days, nasal discharge, conjunctivitis, serous ocular dischargeand progressive lymphadenopathy. In more serious cases,foals may experience respiratory distress and death. Duringperinatal infections, foals may show weakness and respiratorydistress, and the infection may be fatal.AbortionPregnant mares may experience a clinical or subclinicalinfection. The occurrence of viremia is the most importantcondition for uterus infection and placenta detachment.Therefore, a virus reactivation episode in latent-infected maresmay probably also lead to abortion as well as a new viralinfection or reinfection.As a result of viremia, mares may experience an infectionof endothelial cells leading to vasculitis, deranged placentamicrocirculation, and transplacental virus spread. Fetalinfection occurs in the course of virus translocation throughoutthe uterine-placental barrier, through blood-passage in theumbilical circulation, or by inhalation of infected amniotic fluid.Aborted fetuses are usually virus positive. Fetuses may bevirus negative if placental necrosis/separation occurredbefore transplacental infection of the fetus.EHV-1 abortion may occur at any stage of pregnancy.However, a virus-induced vasculitis seems to be morepronounced between the fifth and the ninth months ofgestation, and 95 % of abortions caused by EHV-1 occur inthe last trimester of pregnancy. This probably relates to ahormone-induced expression of virus adhesion moleculesin the endothelium and leukocytes within the pregnant uterus.The aborted fetus is usually fresh, while minimal signs ofautolysis can be present in some cases. A pronounced icterusis frequently observed and some foals may also havepetechiation in the oral mucosa and nostrils. Placentae areoften fresh but may show light edema. Increased fluid in thepericardial, thoracic, and abdominal cavities may be found,as well as mucosal hemorrhage of internal organs. Liver andspleen are frequently swollen with a brown or dark red color.Aborted foals, fetal membranes, and related tissues are arich source of infectious virus.Near-term infections may result in acute foal death after a fewdays due to fulminant viral pneumonia, hepatitis (icterus), anddestruction of bone marrow.Abortion may occur shortly after infection or some timethereafter, and mares usually do not show any premonitoryclinical signs; nowadays, presentation as sporadic cases ismore common but epidemic abortions still occur. It is importantto note that abortion may also occur in regularly vaccinatedmares. The virus remains within the genital tract shortly afterabortion and in most cases the future fertility of the mareremains intact.MyeloencephalopathyThe EHV-1 induced myeloencephalopathy is rather anuncommon manifestation and may be observed in horsesof different ages, in both males and females of any breed,as well as in barren or pregnant mares. However, some hostfactors like age, sex, pregnancy status, immunocompetence,and previous contact with the virus—as well as environmentaland viral factors, like duration of viremia, viral load, andgenetic variation of the virus—probably influence the clinicalmanifestation. The epidemiological presentation of diseasemay be sporadic or epidemic, and most cases are observedin late winter, spring, and early summer. The questionsregarding why and when this cell-associated viremia leads tomyeloencephalopathy have not been answered yet. A geneticstrain of EHV-1 has been identified that contains a mutationthat is highly associated with neurologic clinical signs. Thisneuropathogenic EHV-1 strain is detected more frequently incases of myeloencephalopathy than in cases presenting withother clinical manifestations.D etection of the mutated neuropathogenic strainindicates a significantly increased risk of developingmyeloencephalopathy. However, the nonmutatedwild-type strain can occasionally lead to EHV-1 inducedmyeloencephalopathy. Generally speaking, the clinicaland epidemiological approach in isolated neurologicalcases and outbreaks should be the same, independentof the strain identified.Infection of endothelial cells within the CNS appears to resultin vasculitis, microthrombosis and migration of mononuclearcells with perivascular infiltration and local hemorrhage. Thisin turn leads to a disseminated ischemic necrosis of the spinalcord with degeneration and necrosis of the white matter and, toa lesser extent, the gray matter. The brain stem usually remainsunaffected. Clinical signs are caused by ischemic lesions ofCNS tissue and are not due to viral infection of CNS tissue;the correct term for this condition is thereforemyeloencephalopathy and not encephalomyelitis. Morbidityof neurological cases in EHV-1 outbreaks varies greatly, but isusually about 10%.Clinical signs appear 6–10 days after infection or reactivationof infection in latent carriers but can also present later on inthe course of infection. Clinical signs may present withoutpremonitory fever or signs of respiratory disease. Fever mayappear but it goes usually unnoticed unless horses arechecked on a regular basis. Most horses are normothermicand some may even be hypothermic. The severity ofneurological clinical signs depends on the number, size, andlocation of neurologic lesions. Usually, a sudden onset ofbilaterally symmetrical or asymmetrical ataxia of variableseverity is observed, together with weakness of the fore- orhindlimbs, hypotonia of tail and anus, and a lack of perinealsensitivity. In general, pelvic limbs are affected earlier and moreseverely than the forelimbs. In mild cases, a proprioceptiveinsufficiency reflected in circumduction in one or several limbs,clumsiness, stumbling, toe dragging, and unwillingness tomove are observed. Bladder atony with incontinence anddifficulties to urinate may also be present. In more severecases, horses may show a profound weakness of the limbsand even full paresis (with dog-sitting position), tetraparesis,and recumbency.
Nonspecific changes on initial diagnosticsCBCIn an active viral infection, there are mostly nonspecificchanges. A transient leukopenia (lymphopenia) is observedwithin the very first days of infection. As infection progresses,a leukocytosis (lymphocytosis) may develop.Cerebrospinal fluid (CSF)In an active EHV-1 infection, CSF total protein may beincreased with or without a concomitant increase of the totalnucleated cell concentration. Moreover, xanthochromia maybe present as a result of altered endothelial properties.Specific diagnostic testingDiminished proprioception in a case of EHV-1myeloencephalopathyCourtesy of Equine Hospital Kottenforst/GermanyNasal discharge, limb edema, colic, and anorexia can beconcomitant clinical signs. Nasal discharge and coughingmay appear days or even weeks before the presentation oftypical CNS-related signs. Other abnormalities like mydriasis,hypopyon, uveitis, and optic neuritis have also beendescribed. Signs related to cranial nerves dysfunction, likeseizures, blindness, vestibular signs, and lingual, mandibular,and pharyngeal paresis (dyspaghia), are rare. Depression is inmost cases secondary to complications related to the overallinfection process and not due to brain involvement. Signs ofbrain damage, like aberrant behavior and a low sensorium,are very rare.EHV-1 myeloencephalopathy should always be considereda potential diagnosis if in the short-term several cases withweakness, ataxia, pyrexia, respiratory disease, or abortion areobserved. It should be noted that clinical signs may greatlyvary. Horses with mild neurological signs tend to stabilize withinhours or a few days and usually show a complete recovery.Recumbent horses may develop secondary complications(myopathy, pneumonia, colic, bladder rupture, etc.) with apoor prognosis.DiagnosisDiagnosis of EHV-1/EHV-4 infections should be based ona complete history, the epidemiological hallmarks of eachcase, physical examination, and laboratory tests. The choiceof the correct test in the right stage of disease is of paramountimportance for an accurate diagnosis.RealPCRReal-time PCR detecting viral DNA in respiratory specimens,whole blood, CSF fluid, or reproductive/abortion specimensoffers a reliable, sensitive, and rapid diagnostic tool. A positiveequine herpesvirus (EHV-1 or EHV-4) RealPCR result canhelp you confidently: Diagnose horses exhibiting clinical signs consistentwith EHV disease. Diagnose horses exposed to confirmed EHV cases. Isolate infected or exposed horses from other susceptiblehorses in a timely manner. Identify mutated EHV-1 strains that are more likely toresult in neurological clinical manifestations.Respiratory specimensIn respiratory disease, abortion and myeloencephalopathy,the virus is usually shed for about 10 days (seldom for up to3 weeks) after infection or reactivation of virus in latent carriers.The specimen should be obtained in the early stages ofdisease. A negative result does not rule out an EHV infection.The highest virus shedding from the nasal mucosa usuallyoccurs during the first fever peak.EDTA whole bloodA positive EHV result in a whole blood specimen is indicative ofan EHV-related viremia. The specimen should be taken duringa fever episode (viremia) or shortly thereafter. A positive resultis indicative of viral infection in a patient with clinical signs.Viremia usually occurs during the second fever peak in thecourse of infection.The submission of both whole blood in EDTA and a nasalswab is recommended.
Abortion specimensDifferential diagnosisIn cases of abortion, fetal and placental tissue should besubmitted in addition to reproductive tract swabs and wholeblood from the affected mare.All other forms of respiratory disease, including viral (e.g.,influenza virus, viral arteritis) and bacterial infections arepotential differential diagnoses. The same applies for othercauses of neurological impairment, like cervical vertebralinstability, stenotic myelopathy, cervical vertebral or CNStrauma, polyneuritis equi, aberrant parasite migration,degenerative myelopathy, intoxications, botulism, etc. Otherinfectious causes of abortion, like leptospirosis, viral arteritis,and others should also be considered. In foals, otherdifferential diagnoses are neonatal septicemia, viral arteritis,neonatal maladjustment syndrome, and neonatal nutritionalmyodegeneration syndrome. I n some cases, clinical signs are observed several daysafter infection. In these cases, viral DNA may not bedetected in nasopharyngeal swabs or blood at the timeof presentation of clinical signs (e.g., in cases ofabortion). The virus may be shed in cases of otherdiseases not related to these viruses.SerologyQuantitative detection of antibodies by virus neutralizationoffers a retrospective diagnostic tool but may not be positiveearly in infection. Paired serum specimens taken 2–3 weeksapart are recommended, and the first specimen must beobtained in the early stages of disease. Ideally, bothspecimens should be tested at the same time. For thispurpose, keep the first serum specimen frozen and sendit together with the second specimen to be analyzed.Recent contact with the virus is suspected with seroconversionor if at least a four-fold increase of antibodies is detected.A positive titer in a single specimen indicates merely aprevious exposure to the virus and/or that the horse has beenvaccinated. The antibody titer does not correlate to the degreeof protection against infection nor to the degree of viremia. In cases of abortion, viral infection may have occurredweeks or even months before onset of clinical signs. Inthese cases, no significative antibody increase will bedetected in the paired serum specimens, as serum isobtained at the time of presentation of clinical signs.TreatmentThere is no specific treatment available for EHV-1/EHV-4infections, only supportive symptomatic alternatives.Respiratory disease is often self-limiting and requires mostlygeneral nursing support. It is important to note that affectedhorses are a source of infectious virus and should, therefore,be housed and managed individually.In cases of myeloencephalopathy, therapeutic options areunfortunately quite limited. Recumbent patients should haveenough bedding in the stable, which should be in a quiet area.Sedation, IV fluid therapy, and parenteral nutrition may benecessary. Special care should be taken to avoid decubitalulcers and impaction colic. Regular bladder and rectalevacuation may be necessary. In cases of impaired bladderfunction, an indwelling Foley catheter may be needed. Itis important to keep it under aseptic conditions to avoidsecondary infections. Skin-protective ointments (e.g.,petroleum jelly) should be applied in the perineal area toavoid urine scalding.Horses in the convalescent phase should be rested for about3 weeks after clinical signs subside.The most important medication for the symptomatic treatmentof EHV infections is presented below. Different medicationsmay be used according to the clinical signs and the currentstage of disease.
CorticosteroidsCorticosteroids have strong anti-inflammatory and antioxidanteffects. In cases of myeloencephalopathy, corticosteroidsmay be appropriate, as they may limit the degree ofthromboischaemic lesions caused by infection of endothelialcells. Corticosteroids should be prescribed with caution.However, the risk of a viral reactivation (viremia) due to theadministration of corticosteroids seems to be low. Corticosteroidtreatment for more than 5 days may interfere with the tissueregeneration process.Nonsteroidal anti-inflammatory drugs (NSAIDs)NSAIDs play an important role as antipyretic and prostaglandinblocking agents. Furthermore, they can reduce thrombocyteaggregation during vasculitis at the CNS level. Aspirin shouldnot be administered in cases of myeloencephalopathy, due tothe high risk of hemorrhage associated with its use.AntibioticsDue to immunosuppression, antibiotics may be administeredin cases of secondary bacterial infection of the upperrespiratory tract, when a urinary bladder catheter is placedfor a long period of time, in cases with decubital ulcers, etc.However, antibiotics are not necessary in all cases.Dimethyl sulfoxide (DMSO)DMSO is a free radical scavenger and may inhibitthrombocyte aggregation. Treatment with DMSO infusionhas been described in cases of neurologic disease. Dueto its potential teratogenic effect, DMSO should not be usedin pregnant mares.SympathomimeticsSympathomimetic drugs, like clenbuterol, may increasethe mucociliary clearance and reduce contamination of therespiratory airways.MucolyticsMucolytic agents can be used in cases of rhinopneumonitis.AntioxidantsThe positive effects of vitamin E in inflammatory processes canbe favorable at any stage of disease. However, the necessaryconcentration within CNS tissue may be achieved only afterseveral days.L-LysineL-Arginine is an important amino-acid necessary for herpesviral replication, whereas L-Lysine inhibits intestinal absorptionof L-Arginine. L-Lysine is a component of several food stuffadditives and seems to have a stronger therapeutic effectwithin the very first stages of infection. In cases of neurologicdisease, L-Lysine seems to be of limited efficacy.Antiviral drugsSecond-generation nucleoside analogues, like acyclovir,valacyclovir, or gangaciclovir, have no effect during latentinfections, because of the lack of expression of viral geneticreplication material. Several features related to these drugs,such as their efficacy during an active infection, dose, potentialside effects, and development of resistance require furtherinvestigation before a clear indication for its use can be made.Prevention and controlDue to the characteristics of viral transmission andpathogenesis, prevention and control of infection andoutbreaks are difficult tasks. Equine herpesviruses 1 and 4are enzootic in the equine population worldwide with a veryhigh prevalence. Outbreaks may present a high morbidityand, under certain circumstances, high lethality. Generalcontrol measures have three main aims:1. Prevention of disease entrance onto sites (difficult!).2. Limit dissemination of infection and severity of clinicalcases after the onset of active infections.3. Limit viral spread to other premises.However, good management practices together with stricthygiene measures offer a good basis for disease control.Abortion material is a rich source of infectious virus andshould be collected, dealt with and disposed appropriately.Sick horses should be kept in isolation facilities. Separateequipment and persons should be used for healthy andaffected equines. A regular and consistent vaccinationprogram of all equines within a premises, including pregnantmares, is recommended in order to achieve a high generalimmunity. Combination vaccines can be used in order tocomply with current regulations regarding influenzavaccination. Vaccination does not prevent clinical infectionsin every case, nor does it prevent the establishment ofviremia and latent infections (carriers), but vaccinated horsesseem to have a shorter period of viral shedding after infection.Vaccination in an EHV-1 outbreak is controversial, and manyauthors discourage this practice. Immunostimulants can beadministered to healthy horses in stressful situations or duringoutbreaks.
Diagnostic optionsWhen to useTest name and componentsTest codeScreening of nonclinical or clinicalhorses with known exposure toequine herpesvirus (EHV)Equine Herpesvirus Types 1 (EHV-1) and 4 (EHV-4) RealPCR Tests2–11 Specimens12 or More Specimens26992669226693Equine herpesvirus type 1 (EHV-1; includes identification of wild-type and mutatedneuropathogenic strains) and equine herpesvirus type 4 (EHV-4) RealPCR testsHorses with neurological clinicalsigns compatible with equineherpesvirus myeloencephalopathy(EHM)Equine Neurologic Disease PanelEquine protozoal myeloencephalitis (EPM) by Western blot (serum), West Nile virus IgM antibodyby capture ELISA, equine herpesvirus type 1 (EHV-1; wild-type and mutated neuropathogenicstrains) RealPCR tests2619Comprehensive testing for horseswith respiratory signs and unknownexposure historyEquine Respiratory RealPCR Panel (Comprehensive)Equine adenovirus, equine influenza virus (EIV/H3N8), equine herpesvirus type 1 (EHV-1;wild-type and mutated neuropathogenic strains), type 2 (EHV-2), type 4 (EHV-4), and type 5(EHV-5); equine rhinitis A virus (ERAV); equine rhinitis B virus (ERBV); Streptococcusdysgalactiae subsp. equisimilis; Streptococcus equi subsp. equi; and Streptococcus equisubsp. zooepidemicus RealPCR tests. Includes culture (organism ID only) on selectivemedia for ß-hemolytic Streptococcus spp.3324Equine Respiratory RealPCR Panel (Standard)Equine influenza virus (EIV/H3N8), equine herpesvirus type 1 (EHV-1; wild-type and mutatedneuropathogenic strains) and type 4 (EHV-4), Streptococcus dysgalactiae subsp. equisimilis,Streptococcus equi subsp. equi, and Streptococcus equi subsp. zooepidemicus RealPCR tests; includes culture (organism ID only) on selective media for ß-hemolytic Streptococcus spp.2740Comprehensive testing forhorses with history of abortionand unknown exposure historyAbortion/Postpartum Sick Mare RealPCR Panel—EquineAmycolatopsis spp., Bartonella spp., Candida albicans, Crossiela equi, equine herpesvirus type 1(EHV-1) and type 4 (EHV-4), Leptospira spp., Salmonella spp., Streptococcus dysgalactiaesubsp. equisimilis, and Streptococcus equi subsp. zooepidemicus RealPCR tests3558Treatment monitoring ofEHV-1 confirmed horsesEquine Herpesvirus Type 1 (EHV-1) RealPCR Test2–11 specimens12 or More Specimens25662566225663Includes identification of wild-type and mutated neuropathogenic strainsSpecimen requirements7 mL EDTA whole blood and/or deep nasopharyngeal swabs; keep refrigerated. Nasal swabs are used to detect animals shedding the virus or thatwere recently exposed to a confirmed case. A whole blood specimen is recommended from a symptomatic animal to detect viremia. Submissionof both specimen types for EHV RealPCR testing is ideal. For nasopharyngeal swabs, please submit dry, plastic-stemmed swabs, without transportmedia, in an RTT or WTT (plain plastic tube); keep refrigerated.For equine neurologic panel submissions, also include 2 mL serum (no hemolysis or lipemia) for serology.For respiratory disease panel submissions, deep nasopharyngeal swabs (one from each nostril) are the preferred specimen type and should becollected prior to antibiotic administration. For culture, please submit an additional culture swab in transport media.For abortion/postpartum mare panel submissions, recommended specimens are the following: endometrial swab or endocervical brush, swabfrom clitoral fossa and sinus, and 2 mL EDTA whole blood (LTT); keep refrigerated. If available, also include 2 mL (0.1 mL minimum) umbilical cord blood(LTT), fresh placental tissue (from cotyledons), fresh fetal spleen, fresh fetal lung, and/or 2 mL fetal stomach contents. Submit tissue, fluids, and dry,plastic-stemmed swabs, without transport media, in RTTs or empty, sterile containers. Submit placental tissue and fetal specimens in separate containersand label as “fetal” or “placental.” Place separate fetal and placental containers together into a single bag and submit with a single requisition form.Collect specimens prior to antibiotic administration.Turnaround time: 1–4 days for RealPCR tests; allow additional time for culture or serologyOrdering your tests onlineDid you know that you can search for diagnostic tests,create requisitions, and review status and results onvetconnectplus.com?Customer support servicesIDEXX supports your practice with our customer support,technical support, and medical consulting services teams,including our diagnostic support veterinarians andboard-certified veterinary specialists.1-888-433-9987Published May 2021. 2021 IDEXX Laboratories, Inc. All rights reserved. 09-2663052-00All /TM marks are owned by IDEXX Laboratories, Inc. or its affiliates in the United States and/or other countries. PCR testing is a serviceperformed pursuant to an agreement with Roche Molecular Systems, Inc. The IDEXX Privacy Policy is available at idexx.com.
Some horses develop the so-called "poor performance syndrome" after infection with EHV-1/EHV-4, which is presumably attributable to a nonspecific bronchial hypersensitivity. Young naive foals are more clinically affected than older horses and develop a biphasic pyrexia for 8-10 days, nasal discharge, conjunctivitis, serous ocular discharge
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