EHV-1—Equine herpes virus 1

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Equine Herpesvirus 1

Related terms:

Equine Influenza

Polymerase Chain Reaction

Equine Herpesvirus

Equine Protozoal Myeloencephalitis

Foals

Fetus

Proteins

Central Nervous System

Equus

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Disorders of the Neurologic System

Monica Aleman, ... Stephen M. Reed, in Equine Internal Medicine (Fourth Edition), 2018

Epidemiology and Immunity

EHV-1 and EHV-4 are enzootic in most horse populations, and the majority of horses show serologic evidence of exposure to these viruses. Most horses become infected via the respiratory tract with EHV-1 or EHV-4 (or both) during the first year of life. After an incubation period of 2 to 10 days, clinical signs of respiratory disease of variable severity develop and resolve within 1 to 2 weeks in uncomplicated cases.374-376 Resolution of clinical signs is coincident with development of virus-specific neutralizing antibody directed primarily against surface viral glycoproteins. The development of cell-mediated responses is probably critical for recovery.403 Resistance to reinfection with homologous virus is demonstrable after recovery but generally persists for only 3 to 4 months. Subsequent infections typically induce milder clinical signs or subclinical infection, although virus shedding from the nasopharynx occurs.374,375 The immune response frequently is not successful in clearing herpesviral infection, and the majority of clinically recovered horses remain latently (asymptomatically) infected with EHV-1 or EHV-4 (or both) for life.374,375,404,405 EHV-1 has been shown to evade the host immune system in part by downregulating major histocompatibility complex class I expression at the cell surface. This process may be a prerequisite to the establishment of latency.406

Recrudescence of latent infection is important in the epidemiology of EHV-1 and EHV-4 and explains why these diseases can occur in closed populations without the introduction of new horses.374,375,405,407 Signs of EHV-1 infection may occur in the horse in which stress-associated recrudescence of infection has occurred, or the horse may remain asymptomatic but shed infectious virus in nasal secretions to infect other horses. Natural infection with EHV-1 occurs by inhalation or ingestion of aerosolized infective virus or by direct contact with virus shed in the products of abortion or in the nasal and ocular discharges and saliva of horses with overt clinical disease, subclinically infected horses, or shedding carrier horses.374,375,394 Infectious EHV-1 virus was detected in the feces of experimentally infected foals that developed diarrhea, suggesting that fecal spread is a possibility.408 Virus may be shed by clinically affected and inapparently infected horses for 3 weeks or more, and EHV-1 may remain infective in the environment for up to 14 days and on horse hair for 35 to 42 days.375,409,410

The first definitive association between EHV-1 and myeloencephalopathy was made in 1966 in Norway with the isolation of the virus from the brain and spinal cord of a horse that showed signs of severe neurologic dysfunction.411 The myeloencephalopathic form of EHV-1 infection now is considered to have a worldwide distribution, having been recognized in Denmark, The Netherlands, Germany, Sweden, Austria, Britain, Ireland, Australia, India, the United States, and Canada.382,383,387,398,412,413 In view of the ubiquitous occurrence of EHV-1 infection in horse populations, outbreaks of EHV-1 myeloencephalopathy are rare. In many instances, cases of neurologic EHV-1 infection occur in association with outbreaks of abortion or respiratory disease, although some outbreaks occur in the absence of other manifestations of EHV-1 infection and without the introduction of new horses into the group.394,407,414,415

The myeloencephalopathic form of EHV-1 infection may occur as sporadic individual cases or, more often, as outbreaks involving multiple individuals over a period of several weeks on one or more premises within a limited geographic region. Secondary or tertiary waves of clinical disease may occur as previously unexposed horses become infected from a common source over a short period.383,394,416,417 There has been an increased reporting of occurrences of EHV-1 myeloencephalopathy418 in congregations of horses around the United States. Most of these outbreaks have been associated with a mutant strain of herpesvirus, which appears to replicate rapidly, leading to a very high level of viremia and an apparent increased incidence of neurologic manifestations of this disease.400,401,419 Morbidity rates ranging from less than 1% to almost 90% of exposed individuals and mortality rates ranging from 0.5% to 40% of in-contact horses have been reported. Neurologic EHV-1 infection can occur at any time of year, but the highest incidence is in the late winter, spring, and early summer, perhaps reflecting the seasonal occurrence of abortigenic EHV-1 infections during the same months.219

The neurologic form of EHV-1 infection has been observed in pregnant mares, barren mares, geldings, stallions, and foals, although foals frequently do not show neurologic manifestations of infection during outbreaks that involve severe neurologic disease in adult horses.382,416 The disease also appears to less commonly affect pony breeds. Pregnant mares and mares nursing foals appear be at increased risk for developing neurologic manifestations of EHV-1 infection, and the stage of gestation may be important in determining the outcome of infection in pregnant mares.377,382,416,420,421 Mares infected during the first 2 trimesters of gestation appear to be more likely to develop neurologic signs without abortion, whereas mares infected during the last trimester are more likely to abort without showing neurologic signs.377,394,420,422,423

All breeds of horses are susceptible to the neurologic form of EHV-1 infection, and other Equidae also may be affected. EHV-1 was the suspected cause of myeloencephalopathy that developed in a zebra 1 week after an in-contact onager (Equus hemionus onager) aborted an EHV-1 infected fetus.424 The authors are unaware of reports of neurologic EHV-1 affecting donkeys and mules, although donkeys and mules have shown seroconversion indicating infection with EHV-1 while in contact with affected horses during outbreaks.425-427 Indeed, donkeys and mules returning from a show were thought to be responsible for dissemination of EHV-1 and propagation of multiple outbreaks of neurologic EHV-1 infection in Southern California in 1984 (and in several subsequent years), suggesting that a donkey-adapted variant of EHV-1 with an increased neuropathogenicity for horses may have been involved.427

A modified live EHV-1 vaccine of monkey cell line origin was associated with neurologic disease in 486 of 60,000 recipients, prompting its withdrawal from the U.S. market in 1977.406 No reports of EHV-1 myeloencephalopathy have been associated with use of the modified live vaccine currently approved for use in horses in the United States.

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Herpesviruses of Horses

D.J. O'Callaghan, N. Osterrieder, in Encyclopedia of Virology (Third Edition), 2008

Defective Interfering Particles and Persistent Infection

EHV-1, EHV-2, and EHV-5 have been shown to mediate persistent infection. In the case of EHV-1, defective interfering particles (DIPs) have been shown to initiate and maintain this outcome. EHV-1 DIPs have been generated in vivo in the Syrian hamster model, and therefore may be relevant during EHV-1 infection of the natural host. DIPs are replication defective and require standard EHV-1 as a helper. The overwhelming majority of EHV-1 DNA sequences are absent from DIPs. The packaged DIP DNA molecule is a concatamer of EHV-1 sequences ranging in size from 5.9 to 7.3 kbp, repeated head to tail until it is approximately the size of the standard viral genome. DNA sequencing has revealed that sequences from three regions of the EHV-1 genome are conserved in DIPs: (1) the L terminus, including genes UL3, UL4 and the 3′ portion of UL5; (2) the junction between UL and the internal IR; and (3) the central portion of IR, including ORI and the 5′ portion of gene IR4. The UL3 and UL4 genes in DIP genomes are 100% identical to those of infectious virus, but their functions in virus replication remain to be elucidated. The DIP genome also contains a perfectly conserved cleavage/packaging signal. The sequences at the L terminus and IR are joined by a homologous recombination event mediated by a conserved 8 bp sequence present at both the L terminus and within the IR4 gene to generate a unique ORF present only in DIPs. This ORF is expressed as a 31 kDa 'hybrid protein' comprising the N-terminal 196 amino acid residues of the IR4 protein (the homolog of HSV-1 ICP22) linked in frame to the C-terminal 68 amino acids of the UL5 protein (the homolog of HSV-1 ICP27). Unique to EHV-1 persistently infected cells (not detected in EHV-1 cytolytic infection) is a 2.2 kbp transcript that maps to the UL/IR junction and is antisense to the IE mRNA. Interestingly, this transcript exhibits significant homology to the latency associated transcripts of HSV-1, which appear to be associated with HSV-1 reactivation rather than establishment of latency.

Lastly, in EHV-1 persistently infected cells, transcription of certain viral genes appears delayed compared with cytolytically infected cells. Recent findings reveal that expression of the 31 kDa IR4/UL5 hybrid protein downregulates expression of specific EHV-1 promoters. Moreover, altered forms of the EHV-1 IE polypeptides have been observed only in persistently infected cells. Taken together, these studies indicate that altered or aberrant viral regulatory mechanisms may be involved in establishing or maintaining persistent infection. Ongoing studies with recombinant forms of the DIP genome indicate that the hybrid gene is not essential for DIP replication, but is important in the ability of EHV-1 DIPs to establish persistent infection.

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Viral Infections of the Equine Respiratory Tract

James Wood, ... J Richard Newton, in Equine Respiratory Medicine and Surgery, 2007

Virology

EHV-1 and EHV-4 are alphaherpesviruses of the varicellovirus subfamily, being most closely related to the virus that causes chickenpox and shingles in people. The virus particle consists of an inner crystalline DNA nucleocapsid, surrounded by an amorphous tegument layer composed of structural and trans-activating proteins, and an outer envelope bearing major immunogenic glycoproteins (Fig. 22.7). In common with other enveloped viruses such as influenza, EHV-1 and EHV-4 are quickly inactivated in the environment by sunlight and disinfectants (Allen et al 1986, Crabb & Studdert 1995).

Both EHV-1 and EHV-4 have been completely sequenced (Telford et al 1992, 1998). Each virus has 76 genes, and there is considerable sequence homology between the two viruses, with the degree of amino acid identity for individual viral proteins ranging from 55 to 96%. This has two important practical outcomes: diagnostic tests for EHV-1 and EHV-4 often cross-react, and there is immunological cross-protection between the two viruses.

Recent exploitation of sequence data for EHV-1 by workers in Newmarket (Nugent et al, submitted) has enabled grouping of EHV-1 strains into six major strain groups (Fig. 22.8) on the basis of sequence variability of a single gene (ORF68). The six major strain groups show a degree of geographical restriction, with group 2 viruses being the most widespread, and occurring in North and South America, Europe and Australia. Group 5 viruses predominantly occur in North America, and viruses in groups 3, 4, and 6 predominantly occur in Europe. Furthermore, molecular epidemiological studies for additional variable genes has shown a significant association between a particular genetic mutation (of the DNA polymerase) and strains of EHV-1 isolated from outbreaks of neurological disease. These are important breakthroughs, which will revolutionize our understanding of EHV-1 molecular epidemiology, pathogenesis, and prevention, as well as facilitating more targeted diagnostic tests and control procedures.

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Equine Herpesviruses

Josh Slater, in Equine Infectious Diseases (Second Edition), 2014

Virology Overview

EHV-1 and EHV-4 are alpha herpesviruses (members of the Alphaherpesvirinae subfamily) and belong, along with bovine herpesvirus-1, suid herpesvirus-1, canine herpesvirus-1, felid herpesvirus-1, and Marek's disease virus (MDV), to the Varicellovirus genus, the prototypic virus of which is the human pathogen varicella-zoster virus (VZV).29 The varicelloviruses share some similarities with the herpes simplex viruses (HSV-1 and HSV-2), the cause of cold sores and genital herpes, respectively, but are genetically and phenotypically distinct. Indeed, the varicelloviruses are sufficiently different to merit care in extrapolation of data from the simplex viruses to the EHVs, as with the use of the antiviral agent acyclovir to treat EHV-1 neurologic disease (see section on Treatment).

Each of the Alphaherpesvirinae has a restricted host range, typically infecting a single target species, although laboratory animal models have been employed to study many of these viruses, including EHV-1, -2, and -5, with varying success. The varicelloviruses all share common genome structure and are of broadly similar genome size.

EHV-1 and EHV-4 are closely related30,31 but genetically and antigenically distinct with different disease profiles. EHV-1 is principally a pathogen of the domestic horse, but there is serologic evidence of occasional infection of domestic cattle and captive camelids and cervids. In contrast, EHV-4 is an exclusive pathogen of the domestic horse. In the laboratory, some aspects of EHV-1 pathogenesis can be modeled with limited success in mice32-34 and hamsters,35,36 but this has not proved possible for EHV-4.

Within the Varicellovirus genus, there is a spectrum of cellular tropism from principally neurotropic viruses (e.g., VZV) to viruses that are principally lymphotropic (e.g., MDV). EHV-1 and -4 lie midway along this spectrum, being both neurotropic and lymphotropic during their life cycle (see section on Pathogenesis). A key feature of the life cycle of EHV-1, distinguishing it from EHV-4, is that it efficiently infects a variety of cell types,37 including respiratory epithelial cells,38 endothelial cells,39 neuronal cells,40 and lymphoid cells.41,42 The EHV-4 virus, on the other hand, has a tropism principally restricted to epithelial and neuronal cells and has limited potential for infection of endothelial and lymphoid cells.

The gamma herpesviruses EHV-2 and EHV-5 are primarily lymphotropic, establishing functional latency in these cells.43,44 Although viral deoxyribonucleic acid (DNA) has been detected in trigeminal ganglia,45 reactivation from this site has not been demonstrated. EHV-2 and EHV-5 have typical Gammaherpesvirinae genome structures, with close similarity to saimiri and Epstein-Barr viruses.46 They have different disease profiles from EHV-1 and EHV-4 and share no cross-protective antigens with these viruses.

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Nervous System1

Andrew D. Miller, James F. Zachary, in Pathologic Basis of Veterinary Disease (Sixth Edition), 2017

Herpesviruses

Equine Herpesvirus 1 Myeloencephalopathy.

Equine herpesvirus 1 (EHV-1) (an alphaherpesvirus) is an important cause of equine abortion and perinatal foal infection and death, in addition to myeloencephalitis. EHV-1 can also cause rhinopneumonitis. EHV-1 does not appear to be neurotropic, which is in contrast to some herpesvirus encephalitides of other species in which the virus replicates in neurons (herpes simplex viral infection in the human, infectious bovine rhinotracheitis viral infection in calves, and pseudorabies viral infection in pigs). In addition to vasculitis being the principal lesion, the infection in the horse also differs somewhat from most other herpetic infections of the CNS in being primarily a disease of the adult, although young animals can be affected.

Equine herpesvirus myeloencephalopathy begins with inhalation of the EHV-1. The virus infects epithelial cells of the nasopharynx and spreads to local lymphoreticular tissue, where it infects lymphocytes and macrophages (monocytes). Through trafficking by monocytes, EHV-1 is transferred to endothelial cells of the CNS. The virus, which is endotheliotropic, even though infection of neurons and astrocytes can occur, localizes in small arteries and capillaries of the CNS and some other tissues after direct spread from the circulating infected cells. Inflammation of endothelial cells then results in vasculitis, leading to thrombosis and infarction of the neural tissue supplied by the thrombosed vessel. Latent infection of the trigeminal ganglion and lymphoid tissues can also occur. Although viral infection can be identified in neurons, the virus is not neurovirulent and has no effect on neural cells; thus the gross and histologic lesions noted in this disease are entirely related to vasculitis.

The characteristic lesion in the CNS caused by EHV-1 infection is a vasculitis affecting endothelial cells of small blood vessels with thrombosis and resulting in focal CNS necrosis (infarction). Lesions occur in both the gray and white matter of the spinal cord, medulla oblongata, mesencephalon, diencephalon, and cerebral cortex (Fig. 14-80, A). The endothelium appears to be the initial site of involvement (see Fig. 14-80, B), with the subsequent intimal and medial degeneration resulting in hemorrhage, thrombosis, extravasation of plasma proteins into the perivascular space, axonal swelling with ballooning of the myelin sheath and degeneration of the cell body, and variable mononuclear cell cuffing. Other lesions include cerebrospinal ganglioneuritis and vasculitis in nonneural tissues, including the endometrium, nasal cavity, lungs, uvea of the eye, hypophysis, and skeletal muscle. Inclusion bodies are not observed in CNS lesions.

The neurologic form of EHV-1 infection has a worldwide distribution and affects other Equidae, including zebras in addition to the horse, but appears to be relatively uncommon when compared with the incidence of abortion and upper respiratory tract disease caused by EHV-1. The neurologic disease may accompany or follow outbreaks of respiratory disease or abortion. An outbreak of epizootic acute encephalitis in Thomson's gazelle (Gazella thomsoni) was reported in 1997 from a zoologic garden in Japan. That disease resembled equine herpesvirus encephalitis, and the virus, named gazelle herpesvirus 1, was serologically related to EHV-1 and had a strong tropism for endothelium.

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Ocular Manifestations of Systemic Disease

Jennifer L. Davis, in Equine Ophthalmology (Second Edition), 2011

Equine Herpesvirus

Equine herpesvirus 1 (EHV-1) is a common cause of upper respiratory tract infection, abortion, and neurologic disease in horses. Respiratory signs are more common in young horses and show horses and include fever, cough, and a mucoid nasal discharge that may progress to mucopurulent discharge with secondary bacterial infections. Abortions tend to occur after the seventh month of gestation and are sudden, without premonitory signs.84 Stillbirths may also occur, and foals born alive are often weak, have severe interstitial pneumonia, and typically die within the first few days of life. The neurologic form of EHV-1 frequently presents with hindlimb ataxia, decreased tail and anal tone, and fecal and urinary retention. Signs may progress to the forelimbs, and horses may eventually become recumbent, which indicates a poor prognosis.

Ocular signs associated with EHV-1 or EHV-4 include hyperemia of the conjunctiva or sclera. Experimental infection of a foal with EHV-1 led to signs of severe visual dysfunction and chorioretinitis 28 days after exposure.85 Ophthalmic exam revealed severe degeneration of the neurosensory retina, retinal pigmented epithelium, and choroidal layers, with EHV-1 DNA present in the ocular tissues. This lesion has not been reported in naturally occurring infection. Infection with the neuropathic strain of EHV-1 may result in diffuse cerebral dysfunction and cranial nerve involvement.

Treatment with the antiviral drug valacyclovir has been evaluated, but its benefits are questionable, and it remains cost prohibitive at this time.86 Supportive care including antiinflammatory treatments, stall rest, and adequate nursing for horses with the neurologic form of the disease is recommended. Commercial vaccines against EHV-1 and EHV-4 are available, although protection is only short lived, and the vaccines may not protect against the neurologic form of the disease.

EHV-2 is a cytomegalovirus not known to cause disease by itself but considered important in the pathogenesis of other diseases through immunosuppression or possible transactivation of EHV-1.87-89 The virus has been detected in pulmonary macrophages of up to 90% of horses with chronic pulmonary disease.90 There are numerous reports of ocular signs associated with EHV-2, including serous to mucopurulent ocular discharge, conjunctival hyperemia and chemosis, superficial dendritic-type corneal lesions, which may be linear or punctate, and corneal edema and vascularization (Fig. 13-11).7,91 Response to topical antiviral medications is often favorable.92,93 Topical application of interferon and oral administration of l-lysine may be helpful (see Chapter 5 for more information).

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Management of the Pregnant Mare

Terry L. Blanchard DVM, MS, Dipl ACT, ... Sherri L. Rigby DVM, PhD, Dipl ACT, in Manual of Equine Reproduction (Second Edition), 2003

Equine Herpesvirus Abortion

Equine herpesvirus type 1 (EHV-1) is the primary form of equine herpesvirus that is associated with abortion. The virus has also been associated with perinatal foal mortality; rhinopneumonitis in foals, growing horses, and some adult horses; and encephalomyelitis in adult horses. The virus is distinct from EHV-4, which is the major cause of rhinopneumonitis in foals and is only rarely isolated from equine abortions.

EHV-1 infection is acquired by inhalation, with the virus attaching to, penetrating, and replicating in upper airway mucosal epithelial cells. If the local immune response fails to overcome the infection, the virus breaches the basement membrane to invade the lamina propria of the respiratory mucosa and infects T lymphocytes and endothelial cells. The resulting viremia disseminates virus throughout the body. Abortion is the result of ischemia caused by vasculitis of uterine vessels that disrupt the uteroplacental barrier. It is also thought that lymphocytes resident within the endometrium may transfer virus directly to uterine endothelium and result in abortion. This latter mechanism has been proposed to explain abortion in single mares in a group and abortions that occur many weeks or months after viremia.

Viral latency also occurs with EHV-1 infection, with periodic reactivation of latent virus resulting in asymptomatic shedding of the virus from the respiratory tract that may cause infection of in-contact horses. If local immunity has waned, reinfection with viremia can occur, again placing the fetus at risk. Although vaccinations do not eliminate preexisting latent EHV-1 infections, if they stimulate a sufficient local immune response to prevent shedding, transmission of virus to other in-contact animals may be prevented.

Timing and efficacy of vaccinations to protect against abortion associated with EHV-1 infection remain controversial. Pneumabort-K +1b (Fort Dodge Laboratories) is a killed-virus preparation approved for use to protect against EHV-1 abortions in mares, with administration recommended during the fifth, seventh, and ninth months of gestation. The vaccine should be administered to pregnant and nonpregnant mares at the same time. Rhinomune (Pfizer) is an attenuated live virus preparation approved for use to aid in preventing respiratory disease caused by EHV-1. Although the product label makes no claim that the drug provides protection against virus-associated abortion, it does state that no adverse reactions have been reported in pregnant mares vaccinated with this product and further recommends vaccination of pregnant mares after the second month of gestation and at 3-month intervals thereafter. Prestige II with Havlogen is a killed-virus preparation (Bayer Corporation) containing EHV-1, EHV-4, and equine influenza subtypes A1 and A2; the product label makes no claims concerning provision of protection against virus-associated abortion. Prodigy (Bayer Corporation) is a killed-virus preparation of EHV-1 labeled for the prevention of virus-associated abortion. Vaccination with this product is recommended at the fifth, seventh, and ninth months of gestation. Recommendations for how often booster vaccines are administered vary with the product used; however, herpesvirus vaccines typically do not stimulate long-lasting immune protection (even immunity resulting from natural infection wanes in 3 to 6 months) and thus boosters should be given at regularly scheduled intervals. Although the efficacy of vaccination in the face of an abortion outbreak caused by rhinopneumonitis is unknown, Pneumabort-K +1b is labeled for this use.

Research on changes in vaccine types/brands during gestation is lacking. Some practitioners feel that switching between different types or brands of vaccines during pregnancy leads to "vaccine breaks" in which EHV-1 infection-associated abortion is more likely. Until this phenomenon is studied, we caution against changing products during pregnancy in gestating mares.

A vaccination program cannot be the sole means relied on for prevention and control of abortion caused by EHV-1 infection because vaccination provides limited protection against viral shedding and the disease, and properly vaccinated mares will occasionally abort. One should use appropriate management procedures in concert with a vaccination protocol to reduce exposure of mares to the virus. Pregnant mares should be separated from the rest of the farm population. Permanent resident mares should not be allowed to have contact with transient boarders that normally reside elsewhere. Stress should be minimized to reduce the risk of activation of EHV-1 that may already be present in the mare. Mares that have aborted as a result of EHV-1 infection should be isolated from the rest of the herd. Additionally, all mares that have been in contact with aborting mares should be segregated from those not yet exposed to the virus, and booster vaccines may be administered to in-contact mares in an attempt to stimulate immunity. Strict hygienic measures should be instituted to minimize spread of infection to the rest of the mares on the premises.

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Infectious Diseases

Thea Brabb, ... Martha Hanes, in The Laboratory Rabbit, Guinea Pig, Hamster, and Other Rodents, 2012

Equid herpesvirus 1 (EHV1) (Also Known As Equine Herpes Virus 1 and Equine Abortion Virus)

Background and Etiology

EHV1 is an equine pathogen that causes a persistent infection in horses with a variety of clinical presentations including respiratory disease, abortion, neonatal death, and neurologic disease (Reed and Toribio, 2004). EHV1 is a species in the genus Varicellovirus of the Alphaherpesvirinae subfamily (Fauquet, 2005). Other members of this genus include the type species Human herpesvirus 3 (varicella-zoster virus or chickenpox) and Bovine herpesvirus 1 (infectious bovine rhinotracheitis virus).

Pathogenesis and Clinical Manifestations

One recent report describes infection with EHV1 resulting in hindlimb paralysis, ataxia, abortion, or stillbirth in 18 of 80 guinea pigs at a European zoo (Wohlsein et al., 2010). In this outbreak, Thomson gazelles (Equus thomsoni) kept in the same building as the guinea pigs were first affected and suffered a short course of fatal neurologic disease. The source of the virus was unclear, although a similar strain of virus was isolated 6 months earlier from affected black bears (Ursus americanus) and clinically unaffected onagers (Equus hemionus kulan). In the second outbreak, a similar strain of virus was also recovered from clinically unaffected zebra (Equius quagga boehmi) housed in the same building as the guinea pigs and gazelles.

Pathology

Lympho-histiocytic meningoencephalitis was seen predominantly in the olfactory bulb and the frontal cortical regions of the brain with neuronal and glial necrosis, gliosis, and intranuclear inclusion bodies (Wohlsein et al., 2010). EHV1 antigen was demonstrated in the neurons, neuronal processes and glial cells by immunohistochemistry and encapsulated herpes viral particles of 120–150 nm were detected by electron microscopy.

Diagnosis

Differentiation from other members of the Herpesviridae is important for diagnosis. Immunohistochemistry, virus isolation, PCR, and DNA sequencing were used in this report to identify the virus involved (Wohlsein et al., 2010).

Prevention and Therapy

EHV1 infection of guinea pigs is an example of the severe disease seen when members of the Alphaherpesvirinae infect unusual hosts similar to Human herpes virus I (herpes simplex virus) which has been shown to infect guinea pigs experimentally (Wohlsein et al., 2010) and has also been reported to cause naturally acquired clinical disease in rabbits (Weissenbock et al., 1997) and chinchillas (Wohlsein et al., 2002). Separation of species, control of fomites, and use of appropriate personal protective equipment can be used to prevent transmission of members of the Alphaherpesvirinae subfamily of viruses to aberrant hosts such as guinea pigs.

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Equine Herpesviruses and Interspecies Infections

Alex David Greenwood, Klaus Osterrieder, in Fowler's Zoo and Wild Animal Medicine Current Therapy, Volume 9, 2019

Modes of Transmission

EHV-1 and EHV-9 infection is known to be spread from individual to individual as a respiratory smear infection. However, this route of transmission applies to equids and may not be generally applicable to interspecies transmissions. In the majority of observed cross-species transfers, there was no obvious physical contact between equids and non-equids. For example, in a 2010 fatal EHV-1 infection of a polar bear, the zebra enclosure was 200 m from that of the polar bear, and the zookeepers were not shared between the enclosures.10 Nor were the polar bears fed equine meat or carcasses, which could expose them to remaining infectious virus if the culled equids were virus positive at the time of killing. The conditions were similar in a fatal polar bear case in 2009 with involvement of EHV-9.12 Transmission was indirect inasmuch as neither equids nor rhinoceros were co-housed in close proximity. In a recent case, a polar bear and Indian rhinoceros exhibited neurologic signs. The polar bear recovered and was found weakly positive for EHV-1 in nasal swabs.8 Several weeks later, the rhino aborted an 8.5-month-old fetus, exhibited neurologic clinical signs, and was euthanized after failure to respond to treatment. An EHV-1–EHV-9 recombinant very closely related to that found in the 2010 polar bear case was identified in the lung and brain of the rhinoceros. A clear route of spread or connection, if there was any, between the polar bear enclosure and rhino enclosure is not obvious. Clearly, direct respiratory transmission from equid to non-equid has not been likely in the majority of reported cases.

Fomites, defined as nonliving objects (anything from dust to clothing to shared instruments) are often responsible for transfer of pathogens.12 Supporting this mode of transmission, Saklou et al. (2013) demonstrated that in "barn conditions" and at certain temperatures, infectious EHV-1 could persist on a variety of surfaces including stall bedding, shavings, and leather.38

Another potential source of contamination is water. EHV-1 remains stable for several weeks in water, even at high temperature.39,40 Many zoological collections have enclosure-connecting water sources or noncaptive animal populations (rodents, birds) that move among enclosures and/or water sources. Thus, it is possible that water contaminated with the viruses could expose multiple enclosures to various EHVs. Alternatively, secondary reservoirs or fomite carrying rodents and birds could transfer infected materials from one water source to the next.

The mode of transmission from environmental sources or intermediate hosts remains an unsolved mystery and there may be more than one route. This is a critical area of research because, without a clearer picture, developing management strategies will remain difficult. Regardless, stringent hygiene controls should be applied to prevent EHVs from spreading from equid (or rhinoceros) enclosures to other areas of the zoo. Equid meat should be fed only to carnivores naturally sympatric with equids. For example, lions hunt and consume zebras in nature but polar bears do not. Therefore, it is likely less problematic, from a health standpoint, to feed zebra or other equid meat to lions than to non-African carnivores. This applies to mixed species enclosures where natural sympatry should be considered when placing species together.

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Female Reproductive System and Mammae1

Robert A. Foster, in Pathologic Basis of Veterinary Disease (Sixth Edition), 2017

Equine Herpesvirus.

Equid herpesvirus 1 (EHV-1) (family Alphaherpesvirinae, genus Varisellovirus) is an important cause of failure of pregnancy in mares. EHV-1 infects respiratory epithelium, and after lymph node involvement, the virus is transported to the uterus (and other tissues) in leukocytes where infection of uterine arteriolar endothelial cells occurs. The resultant microvascular damage leads to thrombosis, edema, hemorrhage, and infarction. The endometrium has perivascular lymphocytes, neutrophils, and histiocytes. Fluid that escapes through the damaged endometrium separates the maternal and fetal layers, thus allowing virus from the endometrium to enter the placenta and then fetus. Fetal endothelial cells and the cells of most organs are then infected with the virus. The classic lesion, as with most herpesviruses, is focal hepatic necrosis. Focal necrosis also occurs microscopically in many other organs. Death of bronchiolar epithelial cells and fibrin exudation produce a diffuse pneumonia. Fibrin casts in the trachea are formed in some cases, and this is a characteristic diagnostic lesion. EHV-3 (equine coital exanthema) and EHV-4 produce a similar lesion but much less frequently.