Demystifying Neurologic Herpes

Our attention has recently been captured by reports of numerous outbreaks of equine herpesvirus-1 (EHV-1) neurologic disease at racetracks, show venues, clinics, and boarding stables across the country. Questions about the neuropathogenic herpesvirus are the buzz of the industry. The intent here is to address several misconceptions about neurologic herpes in response to questions most frequently put to investigators at the Maxwell H. Gluck Equine Research Center.

The neuropathogenic strain of EHV-1 is not a "business-as-usual" equine herpesvirus. Although only a single, tiny mutation within its genome has been revealed by comparative DNA sequence analysis, that small genetic change has huge consequences for the virus's behavior in the horse. The fateful mutation has turned the microbe into one with enhanced replicative powers and as a consequence increased pathogenic potential. The mutant (neuropathogenic) strain of EHV-1 replicates to very high levels--tenfold higher than the wild type strain--in the upper respiratory tract, blood leukocytes, and vascular endothelium of the infected horse. Its pathogenic hallmark is a shift toward more severe morbidity and greater mortality. This is the result of ischemic damage to the horse's central nervous system ignited by a widespread and intense inflammation of virus-infected, blood vessel endothelium.

Because of its replication-facilitated increase in the level of nasal shedding, the mutant EHV-1 strain has also acquired the ability to spread more efficiently, another essential feature of epidemic strains of viruses. Other than its exaggerated replicative capacity, however, no additional attributes distinguish the mutant strain of EHV-1 from its wild-type parent. The two genetic strains of EHV-1 exhibit no known differences in their antigenic composition, susceptibility to disinfectants, or tropism for nervous tissue of the horse.

The horse has no hiding place from neurologic EHV-1! Circulating within the world's horse population at least since the time of its first isolation in 1966, neuropathogenic strains comprise 15% of the current biological reservoir of latent EHV-1. The mutation event has occurred on multiple occasions and in each of the six evolutionary branches of the virus. Recent surveillance studies at the University of Kentucky Livestock Disease Diagnostic Center indicate that approximately 6% of today's horses are latently infected with a neuropathic genotype of EHV-1. With such compelling statistics, it is apparent that there is no justification for culling or quarantining latent carriers of the mutant herpesvirus or for any differential treatment of survivors of EHV-1 neurologic disease.

More worrisome is that vaccination, the cornerstone for prevention of infectious diseases, offers little assistance for controlling outbreaks of neurologic EHV-1. Limited scientific evidence exists that any currently marketed vaccine for EHV-1 will provide significant protection against the neurologic manifestation of infection. None of the licensed products carries a label claim for efficacy in preventing central nervous system disease from infection by EHV-1. Efforts at further vaccine development for the disease are conceptually behind, and much catching up is required. Without an efficacious vaccine, an epidemic of EHV-1 paralytic disease could be a scary and potentially devastating scenario.

Furthermore, the most effective strategy for curtailing the spread of the neurologic herpesvirus and blunting its epidemic mortality--keeping horses minimally stressed and physically segregated--does not fit well into the densely populated, heavily intermingling, high-stress environments of racetracks, show events, training centers, or boarding/riding stables. And, finally, efforts at pharmaceutical intervention via antiviral treatment of neurologic herpes have shown little immediate promise. The unsettling consequence of such a triad of management failures (ineffective segregation, vaccination, and antiviral therapy) is that there is currently no foolproof method for either prevention or treatment of neurologic EHV-1, and its threat for disruption of large equestrian events is therefore likely to continue.

The only remaining weapon in our arsenal against infectious diseases is containment and elimination of the viral infection at its point of origin by the practices of isolation, quarantine, and testing. This containment effort will be facilitated by a recent, novel test procedure for rapid identification of horses infected with the neuropathogenic strain of EHV-1. However, random application of the PCR diagnostic procedure to test for the presence of neuropathogenic EHV-1 DNA in the blood of asymptomatic horses not associated with an ongoing disease outbreak represents an inappropriate use of the procedure. The precise interpretation of positive test results in such instances would not be possible due to issues of latency, silent reactivation, residual dead virus, vaccination, etc.

Overall, the prevailing situation with neurologic EHV-1 highlights the importance for all facilities in which large numbers of horses of diverse origin congregate for purposes of shows, racing, training, sales, etc., to have established and well-rehearsed plans as well as the necessary physical facilities for

1. defining the requirements for entry of horses into the facility,

2. temporary isolation of new arrivals during an observation period,

3. rapid infectious disease control responses in the face of an EHV-1 neurologic outbreak.

Useful information on the establishment of such contingency plans can be found at the following Web sites (pdf files):

www.aaep.org/pdfs/control_guidelines/Biosecurity_instructions%201.pdf  

www.aphis.usda.gov/vs/ceah/ncahs/nahms/equine/equine05/equine05_infosheet_biosecurity.pdf  

www.usef.org/documents/competitions/2007/ehV.pdf  

Contact: Dr. George Allen, 859/257-4757, gallen@uky.edu, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky.

This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd's, London, brokers, and their Kentucky agents.

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Equine Disease Quarterly

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