I received the following information via e-mail this past spring.  I was wondering if Roxy would in fact like to include it on their website so I forwarded her a copy in asking.  Her response was,

"Kim - this might be something to put on info under the Bellvet site - with
the proviso that it is a sporadic disease that has been recognized a LONG
time - there is a current push to generate funds to study it in more detail.
The trouble with testing the vaccines (there is insufficient evidence either
way as to efficacy of the current vaccines - mostly because there is no way
to consistently (that is, deliberately) produce the disease experimentally -
which is what is necessary to test the efficacy of a vaccine.
We would see sporadic individual cases and I know of 2 incidences of
multiple horses affected with neurological herpes disease with down/dead
horses (correctly diagnosed) while we were working with the PMU barns"

 Equine Herpesvirus-1: Mutant Strain an Emerging Problem
 by: Stacey Oke, DVM, MSc March 14 2008


Scientists from the Gluck Equine Research Center and the Livestock
Disease
Diagnostic Center at the University of Kentucky recently reported that a
particular mutant form of equine herpesvirus-1 (EHV-1) that causes
 myeloencephalopathy (a degenerative disease of the brain and spinal
cord)
 in horses has the potential to pose serious health and economic threats
to
 the North American horse industry.
Like other herpes viruses, EHV-1, including the encephalopathy-causing
 mutant strain, can lay dormant in previously infected horses.

 "Latently infected horses are at risk for re-activation of the dormant
 mutant virus and can serve as a virus reservoir to potentially infect
 other horses," explained George Allen, PhD, a professor at the
University
 of Kentucky and a co-author on the study.

 Since EHV-1 myeloencephalopathy is currently considered a potentially
 emerging disease, this study was designed to determine the prevalence of
 the mutant EHV-1 in the Thoroughbred broodmare population in central
 Kentucky.

 DNA was extracted from submandibular lymph nodes from 132 broodmares and
 was analyzed by a polymerase chain reaction (PCR) test to determine if
EHV-1 and/or mutant EHV-1 were present.

 "Over half of the horses examined were latently infected with EHV-1, and
 18% of these horses harbored the mutant form of EHV-1 that causes
myeloencephalopathy," said Allen.

These results show that the mutant strain of EHV-1 has already become
established in Central Kentucky horses. Considering that EHV-1
 neurological disease is most common where large numbers of horses are
 stabled together, the spread of this virus via latently infected horses
is
 becoming an important consideration.

 Further research on preventative and therapeutic strategies for control
of
 the EHV-1 neurologic disease is clearly warranted.

The study, "Prevalence of latent neuropathogenic equine herpesvirus-1 in
 the Thoroughbred broodmare population of central Kentucky" will be
 published in an upcoming edition of the Equine Veterinary Journal.
Additional information is available at articles (see below) #9689  and
 #9378.

 --------------------------

 Awakening the Dormant Dragon: The Neurological Form of EHV-1
 by: Center for Equine Health Horse Report
May 27 2007, Article # 9689

 Recently, a number of racetracks, private veterinary clinics, and
 university teaching hospitals outside of California were shut down to
 limit the spread of the neurological form of equine herpesvirus-1
(EHV-1)
 infection.

 California had at least four reported cases of EHV-1 in 2006 and another
 four cases so far in 2007, but no facilities have been shut down. In
 preceding years--with the exception of 2003, when there was a large
 outbreak at a riding school in Ohio--few and sporadic cases were seen in
 the United States until 2005, when seven cases in the eastern part of
the
country were reported.

 Why has there been such a sudden increase in the number of EHV-1 cases?
Many questions including this one remain unanswered. More research is
 needed and is currently being conducted to understand the factors
involved
 in the emergence of the neurological form of EHV-1. The April edition of
 the Horse Report presents the information UC Davis has to date.

 Equine herpesvirus-1 is one of a large group of viruses that causes
 potentially serious disease in horses. EHV-1 has two forms. One causes
abortion in mares, while the other causes respiratory infection and
 neurological problems or myeloencephalopathy--damage to the brain and/or
 spinal cord. This latter form is of particular concern because it
results
 in a high death rate, it is resistant to prevention by vaccination, and
it
affects horses of all breeds, ages and vaccination status. It has the
potential to cause catastrophic losses to both the health of horses and
 the economy of the horse industry.

EHV-1 occurs throughout the world and indeed almost all horses older
than
 2 years of age have been exposed to it, similar to the herpes simplex
type
 1 virus in humans, which affects about 85% of the world population
sometime during childhood.

 Following initial exposure, EHV-1 has the ability to develop into an
 inapparent, latent infection--that is, it remains in a dormant state and
 does not produce any clinical signs. This ability to reside as a silent
 and persistent infection in horses provides a reservoir of virus that
may
 play a role in transmission.

 According to the U.S. Department of Agriculture's Animal and Plant
Health
 Inspection Service (APHIS), the clustering of outbreaks in certain
regions
 of the country--primarily the eastern United States--
 could be related to where high-level performance horses are located or
where they tend to travel.

 However, since this disease is not well understood, other factors could
also play a role in these outbreaks.

 The neurological form of EHV- 1 is not a new disease, but the evidence
currently supports the observation that it is emerging as a more
virulent
 strain than in the past. It is possible that a strain of EHV-1 has a
 mutation that allows the virus to reproduce rapidly to create very high
 levels of EHV- and with great intensity) that rapidly leads to death.
 However, in other individuals--even in the face of outbreaks--the virus
 appears to be restricted to latency, much like the herpes simplex type 1
 virus in humans.

 How Horses Become Sick

 EHV-1-induced neurological injury occurs when large numbers of the virus
damage small blood vessels in the brain and spinal cord. This leads to
 inflammation of the blood vessels and the formation of clots that
obstruct
 the flow of blood through the circulatory system or hemorrhages into the
 nervous tissue. Ultimately, this results in tissue infarct (tissue that
is
 dead or dying because of a lack to tissues. This is not unlike what
happens when cardiac blood supply is impaired in human heart attack.

 EHV-1 is contagious and is spread by direct horse-to- horse contact, by
contaminated hands, equipment and tack, and for a short time, through
 aerosolization of the virus within the environment of the stall and
 stable. Therefore, to prevent the spread of infection, it is essential
to
 institute isolation and quarantine measures immediately.

 It is also possible that stress factors may reactivate the virus and
 elicit the onset of clinical signs. These stress factors may include
 stress from transport, strenuous physical exercise, suppressed immune
 system, and excessive fatigue.

 Clinical Signs of EHV-1

 The initial clinical signs of EHV-1 infection may be nonspecific and
 include fever of 102°F or greater. Fever may be the only abnormality
 observed. Other signs may be combinations of fever and respiratory
 symptoms of nasal discharge and cough. Some horses may have reddish
mucous
membranes, puffy and red eyes, and swollen legs.

 Horses with the neurological form of EHV-1 can soon become uncoordinated
 and weak and have difficulty standing. They may also experience
difficulty
 in urinating and defecating. Often the hindlimbs are more severely
 affected than the forelimbs. Hence, "dog-sitting" is not uncommon in
sick
 horses (see photo on previous page). Signs of brain dysfunction may
occur
as well, including extreme lethargy and a coma-like state.

 The incubation period for infection is from 2 to 8 days. Once a fever
 occurs, clinical signs can progress to nervous system involvement over
the
next 1 to 7 days.

Vaccinations

While several vaccines are available for protection against the
 respiratory and abortogenic forms of EHV-1, at this time there is no
 equine vaccine that has a label claim for protection against the
neurological strain of the virus.

 More details about the current status of EHV-1 vaccination are presented
 in a later section of this Horse Report.

 Until such time as a vaccine is developed to protect horses from the
 neurological form of EHV- 1, the best way to prevent the spread of
disease
 is through isolation, quarantine and the practice of biosecurity--a
series
 of management steps taken to prevent the introduction of infectious
agents
 into a herd.

----------------------------------------

Demystifying Neurologic Herpes
 by: Equine Disease Quarterly
 April 16 2007, Article # 9378

 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_bi
osecurity.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.