Difference between revisions of "Equine Togaviral Encephalitis"

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Also known as: '''''Alphaviral encephalitis — Alphaviral encephalitides —  Eastern equine encephalitis — Eastern equine encephalomyelitis — EEE — Western equine encephalitis — Western equine encephalomyelitis — WEE — Venezuelan equine encephalitis — Venezuelan equine encephalomyelitis — VEE
  
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{| cellpadding="10" cellspacing="0" border="1"
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==Introduction==
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| Also known as:
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'''NOTIFIABLE''' and '''ZOONOTIC''' OIE List B, infectious, mosquito-borne diseases of equidae affecting the central nervous system (CNS).  They include:
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|'''Alphaviral encephalitis, Alphaviral encephalitides<br>
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*Eastern Equine Encephalitis (EEE)
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'''Eastern equine encephalitis, Eastern equine encephalomyelitis, EEE<br>
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*Western Equine Encephalitis (WEE)
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'''Western equine encephalitis, Western equine encephalomyelitis, WEE<br>
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*Venezuelan Equine Encephalitis (VEE) - '''reportable''' in the USA<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>
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'''Venezuelan equine encephalitis, Venezuelan equine encephalomyelitis, VEE'''
 
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|-}
 
  
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==Aetiology==
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See this page for details of the [[Equine Encephalitis Virus|equine encephalitis causal pathogens]].  Some of the virus strains can infect swine<ref>Karsted, L, Hansen, R.P (1959) Natural and experimental infections in swine with the virus of eastern equine encephalomyelitis, ''J Infect Dis'' 105:293-296.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>, poultry and other farmed birds including quail and ratites.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Isolated cases have also been noted in cattle<ref>Pursell, A.R, Mitchell, F.E, Seibold, H.R (1976) Naturally occurring and experimentally induced eastern encephalomyelitis in calves, ''J Am Vet Med Assoc'', 169:1101-1103.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>, sheep and non-domestic ungulates.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Some strains are potential agents of biowarfare or bioterrorism<ref>Steele, K.E, Twenhafel, N.A (2010) Review Paper: Pathology of Animal Models of Alphavirus Encephalitis. ''Vet Pathol.'' Jun 15. [Epub ahead of print].</ref>.
  
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====Description====
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==Epidemiology==
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'''NOTIFIABLE''' and '''ZOONOTIC''' infectious mosquito-borne disease of equidae affecting the central nervous system (CNS).
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===Distribution===
 +
Togaviral encephalitis in equids is largely confined to the Western Hemisphere.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Venezuelan EEV can cause large outbreaks of disease over extensive geographical areas in both humans and horses.  Spread of this virus into Central America has had disasterous consequences with epidemics as far north as Texas.<ref name="duplicate">http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/viralenceph/index.htm, accessed July 2010</ref> Climatic conditions and interventions that support vector populations, such as irrigation, greatly influence the geographical spread of the disease.<ref name="duplicate">http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/viralenceph/index.htm, accessed July 2010</ref>  EEE has been recorded across the United States, but mostly in the Southeastern States.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  As its names suggests, WEE has a predilection for the Western states which have been subject to significant outbreaks in the past.  A regional alteration in virulence has been proposed for the steep decline in clinical case numbers observed in this area.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  A lag phase of 2-5weeks is commonly observed between horse and human cases of WEE in a given locus.<ref>McLintock, J (1980) The arbovirus problem in Canada, ''Can J Public Health'', 67(Suppl 1):8-12.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Both are dead-end hosts for the virus.    A subtype of Western EEV, Highlands J virus, was isolated from the brain of a horse with encephalitis in Florida.<ref>Karabatsos, N, Lewis, A.L, Calisher, C.H, Hunt, A.R, and Roehrig, J.T (1988). Identification of Highland J virus from a Florida horse. ''Am J Trop Med Hyg'', 39, 603-606. In: ''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>
  
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====Aetiology====
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===Transmission===
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[[Equine Encephalitis Virus|see this page for details of the causal pathogens]].  The same virus strains can infect poultry and other farmed birds including quail and ratites.  Some strains are potential agents of biowarfare or bioterrorism (Steele and Twenhafel, 2010).
+
Transfer is '''vector'''-mediated, primarily via '''[[Culicidae|mosquito]]''' salivary transfer.  WEE and VEE may also be transmitted horse to horse through nasal secretions.  This mode of transmission is less likely, despite the fact that high concentrations of VEE virus are found in ocular and nasal discharges from infected horses.<ref>Kissling, R.E, Chamberlain, R.W (1967) Venezuelan equine encephalitis, ''Adv Vet Sci Comp Med'', 11:65-84.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> The viraemic phase ends when nervous signs develop<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> and is important for disease amplification.  Amplification from horses is likely only with VEE virus, in association with a relatively high and potentially persistent viraemia.<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref>  Similarly, zoonotic spread is unlikely for Eastern and Western equine encephalitis, but has been noted with VEE.
  
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====Epidemiology====
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===Seasonal Incidence===
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Disease associated with EEE, WEE and VEE is largely restricted to the Western Hemisphere, ranging from temperate to desert climates.  EEE in the United States is mainly seen in the Southeastern United States but has been detected in all states east of the Mississippi River and some Western states.  Large outbreaks of WEE have been described in California and other Western states but the incidence of clinical disease in these areas has experienced a dramatic decrease. The reason for this unknown but may be due to geographical variation in virulence. Equine disease associated with WEE is rare on the Eastern seaboard ofthe United States. VEE  virus is a very important human andveterinary pathogen in the Western Hemipshoere that can cause large outbreaks of disease in humans and horses over large geopgrahic areas. VEE has spread into Central America, causing devastating epidemics as far north as Texas. The disease distribution is determined by climatic conditions as well as agricultural practices, such as irrigation, which favour the life cycle and spread of mosquitoes. Transfer is via '''vector''': mostly through '''[[Culicidae|mosquito salivary transfer]]'''. WEE and VEE may also be transmitted via nasal secretions but this is less likely.  Disease amplification occurs during the viraemic phase which lasts until nervous signs develop.  Amplification from horses is unlikely with EEE and WEE but occurs with VEE in association with a relatively high viraemia. Ocular and nasal discharges from infected horses cotnain high concentrations of VEE. Zoonotic spread has been noted with VEE but is unlikely for the other two serotypes. Horse to horse spread of EEE is possible. Humans and horses are terminal hosts for WEE.  Horses with WEE are sentinels for humans in a given area.
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The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref> Case numbers peak in June to November in temperate climates.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> The vector season is longer in warmer climates, where the disease period is prolonged.  Global warming may promote more outbreaks in historically colder climates.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
  
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Highlands J virus, antigenically related to WEE virus, has been isolated in eastern USA. Although it is generally believed not to cause disease in mammals, it has been isolated from the brain of a horse dying of encephalitis in Florida (4).WEE virus infection in horses is often observed over a wide geographical area, e.g. sporadic cases over 1000 square miles. EEE virus infections are usually observed in limited geographical areas.  
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===Epidemics===
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Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  However, some epidemic requirements are beyond question.  Adequate amounts of infective virus, sufficent vectors, infected sylvatic hosts and susceptible terminal hosts, and finally, appropriate reservoirs, are all crucial.<ref>Sellers, R.F (1980) Weather, host and vector: their interplay in the spread of insect-borne animal virus diseases, ''J Hyg (Lond)'', 85:65-102.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
  
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=====Seasonal Incidence=====
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==Pathogenesis<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>==
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The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.  In temperate climates, case numbers peak in June to November.  In warm climates, where the vector season is longer, the disease period is prolonged.  Global warming may promote more cold climate outbreaks.
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Upon entry to the host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  In macrophages and neutrophils viral replication leads to shedding and significant clearance of viral particles.  No further clinical signs develop if this clearance is successful.  Erythrocyte and leukocyte absorption are used to circumvent the immune defences of the host.  After incomplete elimination, residual virus infects endothelial cells and accumulates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus and a second viraemic period, typically associated with early clinical signs.  Neuroinvasion and replication occurs within a week.<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref>  An incubation period of 7-21days has been demonstrated after experimental infection with Eastern or Western EEV, but the incubation is often shorter for EEE compared with that of WEE.
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=====Epidemics=====
 
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Prerequisites for epidemics to occur include adequate and adjacent numbers of reservoir animals, sufficient quantities of virulent virus, infected intermediate hosts, insect vectors and susceptiple horse and human populations.  Outbeak prediction has been inaccurate, implyingf that other, unidentified factors may be important.
 
  
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====Pathogenesis====
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==Signalment==
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After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles.  No further clinical signs develop if clearance is successful but neutralizing Abs are still produced.  Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption.  After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus.  The second viraemic period is typically associated with early clinical signs.  CNS infection occurs within 3-5 days.
+
Unvaccinated adult horses and other equids ([[Venezuelan Equine Encephalomyelitis (VEE) - Donkey|'''VEE in donkeys''']]) are at risk in areas with suitable vectors.  Vaccinated horses can still develop the disease, particularly if they are young or old.
  
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Viraemia during the acute phase of EEE and WEE.  Incubation period of 1-3weeks after experimental infection with EEE or WEE.  Incubtion often shorter with EEE.  Central nervous system (CNS) replication within a week
+
==Clinical Signs==
  
 +
Worse in unvaccinated horses.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Neurological signs may be assymmetrical.<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref> 
  
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3 key phases of the pathogenesis of alphavirus encephalitis. These are the early extraneural phase, the process of neuroinvasion itself, and virus and host factors related to neurovirulence.
+
===EEE and WEE===
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Following an incubation period of up to 21days<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>, an initial pyrexia and mild depression are short-lived and often missed.  The acute phase of the disease presents with mild to severe pyrexia, anorexia and stiffness, lasting up to 5 days. During this time, the horse is viraemic and capable of amplifying the disease. The fever may then fluctuate with neurological derangements appearing a few days post-infection.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref> These changes indicate disease progression, which occurs more frequently with EEE (the most virulent of the three serotypes).  Any of the following may be observed<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>:
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====Signalment====
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*conscious proprioceptive deficits
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Unvaccinated adult horses '''[[Venezuelan Equine Encephalomyelitis (VEE) - Donkey|and other equids]]''' are at risk in areas with suitable vectors.  Vaccinated horses can still develop the disease, particularly if they are young or old.
 
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====Clinical Signs====
 
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The incubation of the disease after infection with the virus is from 1 to 3 weeks. In the initial stage there is fever, which may be accompanied by depression, and loss of appetite, but the reaction may be so mild it goes unnoticed. The virus causing Eastern Equine Encephalomyelitis (EEE) is the most virulent of the three types and the symptoms produced are the most severe, with a case fatality rate of up to 90%. The viraemia (level of virus in the blood) may be so high with this strain that horse to mosquito to horse cycling can occur.
 
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The nervous signs, when they appear, are hypersensitivity to sound and touch with periods of excitement and restlessness with apparent blindness. Affected horses may walk blindly into objects or walls. Muscle twitchings may occur in the face and shoulder muscles. A period of severe depression follows. Affected horses stand with their heads hung low and may have a half-chewed mouthful of feed hanging from their lips. The animal appears to be asleep and is unable to hold up his head and often rests it on some solid object.
 
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Although VEE does not cause as high a mortality as WEE/EEE, the clinical signs are similar. However, a second generalised infection may be caused by the virus causing fever, depression, colic and diarrhoea.
 
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Worse in unvaccinated animals.  Acute signs of EEE and WEE are nonspecific, last up to 5 days and include:
 
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*mild to severe pyrexia
 
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*anorexia
 
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*stiffness
 
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Early signs transient and often missed:
 
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*pyrexia
 
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*mild depression
 
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Disease progression occurs more frequently with EEE than WEE:
 
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*fever may rise and fall sporadically
 
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Cerebral signs often occur a few days post-infection (but can occur at any time.  In the acute phase the following may be noted:
 
 
*propulsive walking
 
*propulsive walking
 
*depression
 
*depression
 
*somnolence
 
*somnolence
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*hyperaesthesia
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*aggression
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*agression
 
 
*excitability
 
*excitability
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*frenzy in response to sensory stimulation
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*restlessness
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*conscious proprioceptive deficits
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*hypersensitivity to sound and touch
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With progression, worsening cerebral cortical and cranial nerve dysfunction may result in:
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Worsening neurological deficits may result in<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>:
 
*head pressing
 
*head pressing
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*propulsive walking
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*head tilt
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*blindness
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*ataxia
 
*circling
 
*circling
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*head tilt
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*apparent blindness
 
*facial and appendicular muscle fasciculations
 
*facial and appendicular muscle fasciculations
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*paralysis of pharynx, larynx and tongue
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*pendulous lower lip<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>
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*recumbency for 1-7 days followed by death
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*pharynx, larynx and tongue paralysis
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VEE may have similar or different clinical presentations to WEE and EEE, which may relate to a persistently hightitre viraemia with VEE and differences in strain pathogenicity:
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*seizures<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>
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*pyrexia peaks early and remains high throuhgout the disease course
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*recumbency for 1-7 days followed by death<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>
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*mild fever and leukopenia associated experimentally with endemic strains
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*severe pyrexia and leukopenia associated with epidemic strains
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===VEE===
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*diarrhoea, severe depression recumbency and death may precede neurological signs
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Clinical signs may resemble those of WEE and EEE or may vary<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>:
 +
*pyrexia peaks early and persists throughout the disease course
 +
*mild pyrexia and leukopenia with endemic strains  
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*severe pyrexia and leukopenia with epidemic strains
 
*neurological signs around 4 days post-infection
 
*neurological signs around 4 days post-infection
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*other associated signs: abortion, oral ulceration, pulmonary haemorrhage, epistaxis
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*diarrhoea, severe depression, recumbency and death may precede neurological signs
 +
*other signs: abortion, oral ulceration, pulmonary haemorrhage, epistaxis
  
 +
==Diagnosis==
 +
Presumptive based on history, epidemiology and clinical signs.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>  Definitive diagnosis requires virus identification, serological tests and/or post-mortem examination. 
  
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*Paralysis of the lips
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===Laboratory Tests===
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*Drooping eyelids
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====[[Equine Encephalitis Virus#Virus Identification|Virus Identification]]====
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*Incoordination
 
  
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====Diagnosis====
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====Serology====
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Presumptive based on clinical signs and epidemiological features.  Definitive diagnosis requires serological tests and/or post-mortem examination.  Virus isolation can be performed from blood or spinal fluid samples
 
  
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=====Laboratory Tests=====
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Ab titre increases sharply within 24 hours of the initial viraemia, before clinical signs are apparent.  It then deteriorates over 6 months.  Samples taken when clinical signs appear are likely to miss the Ab peak and will demonstrate a decreasing titre.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Thus, serological confirmation of Eastern or Western EEV infection requires a four-fold or greater increase<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref> OR decrease in Ab titre in paired serum samples taken 10-14 days apart.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>  A presumptive diagnosis can be made on a single sample if an unvaccinated horse with suggestive clinical signs has Ab against only Eastern or Western EEV.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>  Colostral-derived Ab has a serum half-life of around 20days and may interfere with diagnosis in foals.<ref name="repeat"> Ferguson, J.A, Reeves, W.C, Hardy, J.L (1979) Studies on immunity to alphaviruses in foals, ''Am J Vet Res'', 40:5-10.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
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A combination of complement fixation (CF), haemagglutination inhibition (HAI) and cross-serum neutralization assays supports the acquisition of a positive diagnosis.  A 4-fold increase in antibody (Ab) titre in convlescent sera is quoted for diagnosis but this test lacks sensitivity.  The presence of viral Abs within 24hours of the initial viraemia typically precedes clinical signs.  Ab titre increases sharply then deteriorates over 6 months.  Samples taken when clinical signs appear are likely to miss the Ab peak and may thus demonstrate a decreasing titre. A single sample demonstrating an increased titre using HAI, CF and neutralizing Ab can provide a presumptive diagnosis.
 
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Viral-specific IgM to the surface glycoprotein of Venezuelan EEV may be detected by ELISA, from 3 days post-onset of clinical signs up to 21 days post-infection.  The ELISA is useful in acute VEE infections where convalescent serum samples are unobtainable.  Viral culture may also be useful for acute VEE.  Virus may be isolated from the CSF of acutely infected horses.  Virus may be found in brain tissue using fluorescent Ab, ELISA and virus isolation.
 
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Maternal-derived Ab may interfere with diagnosis in foals.  The serum half-life of colostral Ab in foals is around 20days.
 
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The virus is identified by complement fixation (CF), immunofluorescence, or plaque reduction neutralisation (PRN) tests. EEE and WEE viral RNA may also be detected by reverse-transcription polymerase chain reaction methods
 
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1.  Identification of the agent
 
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    The most definitive method for diagnosis of EEE or WEE is the isolation of the viruses. EEE virus can usually be isolated from the brains of horses, unless more than 5 days have elapsed between the appearance of clinical signs and the death of the horse. EEE virus can frequently be isolated from brain tissue even in the presence of a high serum antibody titre. WEE virus is rarely isolated from tissues of infected horses. Brain is the tissue of choice for virus isolation, but the virus has been isolated from other tissues, such as the liver and spleen. It is recommended that a complete set of these tissues be collected in duplicate, one set for virus isolation and the other set in formalin for histopathological examination. Specimens for virus isolation should be sent refrigerated if they can be received in the laboratory within 48 hours of collection; otherwise, they should be frozen and sent with dry ice. A complete set of tissues will allow the performance of diagnostic techniques for other diseases. For isolation, a 10% suspension of tissue is prepared in phosphate buffered saline (PBS), pH 7.8, containing bovine serum albumin (BSA) (fraction V; 0.75%), penicillin (100 units/ml), and streptomycin (100 µg/ml). The suspension is clarified by centrifugation at 1500 g for 30 minutes.
 
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    The newborn mouse is considered to be a sensitive host system. Inoculate intracranially one or two litters of 1-4-day-old mice with 0.02 ml of inoculum using a 26-gauge 3/8 inch (9.3 mm) needle attached to a 1 ml tuberculin syringe. The inoculation site is just lateral to the midline into the midportion of one lateral hemisphere. Mice are observed for 10 days; dead mice are collected daily and frozen at -70°C. Mouse brains are harvested for virus identification by aspiration using a 20-gauge 1 inch (2.5 cm) needle attached to a 1 ml tuberculin syringe. A second passage is made only if virus cannot be identified from mice that die following inoculation.
 
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    The chicken embryo is considered to be less sensitive than newborn mice when used for primary isolation of EEE and WEE viruses. Tissue suspensions can be inoculated by the yolk-sac route into 6-8-day-old embryonating chicken eggs. There are no diagnostic signs or lesions in the embryos infected with these viruses. Inoculated embryos should be incubated for 7 days, but deaths usually occur between 2 and 4 days post-inoculation. Usually only one passage is made unless there are dead embryos from which virus cannot be isolated. Newly hatched chickens are susceptible and have been used for virus isolation. If this method is used, precautions must be taken to prevent aerosol exposure of laboratory personnel, as infected birds can shed highly infectious virus.
 
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    EEE and WEE viruses can also be isolated in a number of cell culture systems. The most commonly used cell cultures are primary chicken or duck embryo fibroblasts, continuous cell lines of African green monkey kidney (Vero), rabbit kidney (RK-13), or baby hamster kidney (BHK-21). Isolation is usually attempted in 25 cm2 cell culture flasks. Confluent cells are inoculated with 1.0 ml of tissue suspension.
 
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    Following a 1-2-hour absorption period, maintenance medium is added. Cultures are incubated for 7 days, and one blind passage is made. EEE and WEE viruses will produce a cytopathic change in cell culture. Cultures that appear to be infected are frozen. The fluid from the thawed cultures is used for virus identification.
 
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    When the complement fixation (CF) test is used, EEE or WEE viruses can be identified in infected mouse or chicken brains, cell culture fluid, or amnionic-allantoic fluid. A 10% brain suspension is prepared in veronal (barbitone) buffer; egg and cell culture fluids are used undiluted or diluted 1/10 in veronal buffer. The fluid or suspension is centrifuged at 9000 g for 30 minutes, and the supernatant fluid is tested against hyperimmune serum or mouse ascitic fluid prepared against EEE and WEE viruses using a standard CF procedure (13). The CF test requires the overnight incubation at 4°C of serum-antigen with 7 units of complement. Virus can be identified in cell culture by direct immunofluorescent staining. The less commonly used method of virus identification is the neutralisation test, as outlined below.
 
−
 
−
    EEE virus nucleic acid in mosquitoes and tissues has been identified by the polymerase chain reaction (PCR) using primers selected from the capsid gene (15). RNA is extracted using guanidium iso-thiocyanate-acid phenol. Forty repetitions of the three-step amplification cycle of nucleic acid denaturisation, primer annealing and primer extension are used. Temperature and duration of each step are optimised for the specific primer pair, reagents and thermal cycler used in the PCR cycles. Reaction products or their fragments are analysed on 2.0-2.6% agarose gels that have been stained with 1 µg/ml of ethidium bromide. An alternate identification procedure is by hybridisation with an oligonucleotide probe. A reverse-transcription PCR method for detection of WEE RNA and alternative methods for EEE RNA detection have also been described (5, 7).
 
−
 
−
    Antigen-capture enzyme-linked immunosorbent assay (ELISA) has been developed for EEE surveillance in mosquitoes. This can be used in countries that do not have facilities for virus isolation or PCR (1).
 
−
 
−
2.  Serological tests
 
−
 
−
    Serological confirmation of EEE or WEE virus infection requires a four-fold or greater increase or decrease in antibody titre in paired serum samples collected 10-14 days apart. Most horses infected with EEE and WEE virus have a high antibody titre when clinical disease is observed. Horses infected with EEE or WEE virus usually have antibody titres in the acute stage of the disease. Consequently, a presumptive diagnosis can be made if an unvaccinated horse with appropriate clinical signs has antibody against only EEE or WEE virus. The detection of IgM antibody by the ELISA can also provide a presumptive diagnosis of acute infection (11). The plaque reduction neutralisation (PRN) test or, preferably, a combination of PRN and haemagglutination inhibition (HI) tests is the procedure most commonly used for the detection of antibody against EEE and WEE viruses. There are cross-reactions between antibody against EEE and WEE virus in the CF and HI tests. CF antibody against both EEE and WEE viruses appears later and does not persist; consequently, it is less useful for the serological diagnosis of disease.
 
−
 
−
    a)   Complement fixation
 
−
 
−
        The CF test is frequently used for the demonstration of antibodies, although the antibodies detected by the CF test may not persist for as long as those detected by the HI or PRN tests. A sucrose/acetone mouse brain extract is commonly used as antigen. The positive antigen is inactivated by treatment with 0.1% beta-propiolactone.
 
 
   
 
   
−
        In the absence of an international standard serum, the antigen should be titrated against a locally prepared positive control serum. The normal antigen, or control antigen, is mouse brain from uninoculated mice similarly extracted and diluted.
+
*Complement fixation (CF): to avoid anti-complementary effects, serum should be separated from blood as soon as possible.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref> CF Ab against both Eastern and Western EEV is less useful for serological diagnosis because it appears relatively late and does not persist.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>
−
+
*Haemagglutination inhibition (HAI): titres of 1/10 and 1/20 are indicative, titres of 1/40 and above are positive.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>
−
        Sera are diluted 1/4 in veronal buffered saline containing 1% gelatin (VBSG), and inactivated at 56°C for 30 minutes. Titrations of positive sera may be performed using additional twofold dilutions. The CF antigens and control antigen (normal mouse brain) are diluted in VBSG to their optimal amount of fixation as determined by titration against the positive sera; guinea-pig complement is diluted in VBSG to contain 5 complement haemolytic units-50% (CH50). Sera, antigen, and complement are reacted in 96-well round-bottom microtitre plates at 4°C for 18 hours. The sheep red blood cells (SRBCs) are standardised to 2.8% concentration. Haemolysin is titrated to determine the optimal dilution for the lot of complement used. Haemolysin is used to sensitise 2.8% SRBCs and the sensitised cells are added to all wells on the microtitre plate. The test is incubated for 30 minutes at 37°C. The plates are then centrifuged (200 g), and the wells are scored for the presence of haemolysis. The following controls are used: (a) serum and control serum each with 5 CH50 and 2.5 CH50 of complement; (b) CF antigen and control antigen each with 5 CH50, and 2.5 CH50 of complement; (c) complement dilutions of 5 CH50, 2.5 CH50, and 1.25 CH50; and (d) cell control wells with only SRBCs and VBSG diluent. These controls test for anticomplementary antigen, anticomplementary serum, activity of complement used in the test, and integrity of the SRBC indicator system in the absence of complement, respectively.
+
*ELISA may be used to detect viral-specific IgM to the surface glycoprotein of Venezuelan EEV, from 3 days post-onset of clinical signs up to 21 days post-infection. This is useful in acute infections where convalescent serum samples are unobtainable.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
−
+
 
−
        To avoid anticomplementary effects, sera should be separated from the blood as soon as possible. Positive and negative control sera should be used in the test.
+
*The plaque reduction neutralization (PRN) test is very specific and can differentiate EEE and WEE infections. It is performed in duck embryo fibroblast, Vero, or BHK-21 cell cultures. Serum is tested against 100 plaque-forming units of virus. Endpoints are based on a 90% reduction in the number of plaques compared with the virus control.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>
−
 
−
    b)  Haemagglutination inhibition
 
−
 
−
        The antigen for the HI test is the same as described above for the CF test. The antigen is diluted so that the amount used in each haemagglutinating unit (HAU) is from four to eight times that which agglutinates 50% of the RBCs in the test system. The haemagglutination titre and optimum pH for each antigen are determined with goose RBCs diluted in pH solutions ranging from pH 5.8 to pH 6.6, at 0.2 intervals.
 
−
 
−
        Sera are diluted 1/10 in borate saline, pH 9.0, and then inactivated at 56°C for 30 minutes. Kaolin treatment is used to remove nonspecific serum inhibitors. Sera should be absorbed before use by incubation with a 0.05 ml volume of washed packed goose RBCs for 20 minutes at 4°C.
 
−
 
−
        Following heat inactivation, kaolin treatment and absorption, twofold dilutions of the treated serum are prepared in borate saline, pH 9.0 with 0.4% bovalbumin. Serum dilutions (0.025 ml/well) are prepared in a 96-well round-bottom microtitre plate in twofold dilutions in borate saline, pH 9.0, with 0.4% bovalbumin. Antigen (0.025 ml/well) is added to the serum. Plates are incubated at 4°C overnight. RBCs are derived from normal white male geese (RBCs from adult domestic white male geese are preferred, but RBCs from other male geese can be used. If cells from female geese are used, there may be more test variability. It has been reported that rooster RBCs cause a decrease in the sensitivity of the test) and washed three times in dextrose/gelatin/veronal (DGV), and a 7.0% suspension is prepared in DGV. The 7.0% suspension is then diluted 1/24 in the appropriate pH solution, and 0.05 ml per well is added immediately to the plates. Plates are incubated for 30 minutes at 37°C. Positive and negative control sera are incorporated into each test. A test is considered to be valid only if the control sera give the expected results. Titres of 1/10 and 1/20 are suspect, and titres of 1/40 and above are positive.
 
−
 
−
    c)  Enzyme-linked immunosorbent assay
 
−
 
−
        The ELISA is performed by coating flat-bottomed plates with anti-equine IgM capture antibody (11). The antibody is diluted according to the manufacture's recommendations in 0.5 M carbonate buffer, pH 9.6, and 50 µl is added to each well. The plates are incubated at 37°C for 1 hour, and then at 4°C overnight. Prior to use, the coated plates are washed twice with 200 µl/well of 0.01 M PBS containing 0.05% Tween 20. After the second wash, 200 µl/well of PBS/Tween/5% nonfat dried milk is added and the plates are incubated at room temperature for 1 hour. Following incubation, the plates are washed again three times with PBS/Tween. Test and control sera are diluted 1/100 and 1/1000 in 0.01 M PBS, pH 7.2, containing 0.05% Tween 20, and 50 µl is added to each well. The plates are incubated at 37°C for 2 hours and then washed three times. Next, 50 µl of viral antigen is added to all wells. (The dilution of the antigen will depend on the source and should be empirically determined.) The plates are incubated overnight at 4°C, and washed six times. Then, 50 µl of horseradish-peroxidase-conjugated monoclonal antibody (MAb) to encephalitis virus (available from: Centers for Disease Control and Prevention, Biological Reference Reagents, 1600 Clifton Road NE, Mail Stop C21, Atlanta, Georgia 30333, United States of America) is added. The plates are incubated for 60 minutes at 37°C and then washed three times. Finally, 50 µl of freshly prepared ABTS (2,2'-Azino-bis-[3-ethylbenzo-thiazoline-6-sulphonic acid]) substrate + hydrogen peroxidase is added, and the plates are incubated at room temperature for 15-40 minutes The absorbance of the test serum is measured at 405 nm. A test sample is considered to be positive if the absorbance of the test sample in wells containing virus antigen is at least twice the absorbance of negative control serum in wells containing virus antigen and at least twice the absorbance of the sample tested in parallel in wells containing control antigen.
 
−
 
−
    d)  Plaque reduction neutralisation
 
−
 
−
        The PRN test is very specific and can be used to differentiate between EEE and WEE virus infections. The PRN test is performed in duck embryo fibroblast, Vero, or BHK-21 cell cultures. The sera can be screened at a 1/10 and 1/100 final dilution. Endpoints can be established using the PRN or HI test. Serum used in the PRN assay is tested against 100 plaque-forming units of virus. The virus/serum mixture is incubated at 37°C for 75 minutes before inoculation on to confluent cell culture monolayers in 25 cm2 flasks. The inoculum is adsorbed for 1 hour, followed by the addition of 6 ml of overlay medium. The overlay medium consists of two solutions that are prepared separately. Solution I contains 2 x Earle's Basic Salts Solution without phenol red, 6.6% yeast extract lactalbumin hydrolysate, 4% fetal bovine serum, 800 units/ml penicillin, 400 µg/ml streptomycin, 200 µg/ml nystatin, 6% of a 7.5% solution of sodium bicarbonate, and 3.3% of a 1/1500 dilution of neutral red (1/8000). Solution II consists of 2% Noble agar that is sterilised and maintained at 47°C. Equal volumes of solutions I and II are adjusted to 47°C and mixed together just before use. The test is incubated for 48-72 hours, and endpoints are based on a 90% reduction in the number of plaques compared with the virus control flasks, which should have about 100 plaques.
 
  
−
=====Clinical Pathology=====
+
Most commonly, the PRN test or a combination of PRN and HAI tests is used to detect Ab against Eastern and Western EEV. Cross-reactivity occurs between Ab against these viruses in the CF and HAI tests.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>
−
Changes in cerebrospinal fluid (CSF) include increased cellularity (50-400 mononuclear cells per microlitre) and protein concentration (100-200mg/dl)
 
  
−
=====Post-mortem findings=====
+
====Clinical Pathology====
−
'''''PRECAUTION'': infective viral particles may be present in CNS and other tissues'''.
+
CSF samples demonstrate increased cellularity (50-400 mononuclear cells/µl) and protein concentration (100-200mg/dl).<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
−
The brain and spinal cord are typically grossly normal, but vascular congestion and discolouration of the CNS may be seen.  Histologically the entire brain is affected by nonseptic mononuclear cell and neutrophilic inflammation. Severe lesions are noted in the cerebral cortex, thalamus and hypothalamus. Mononuclear meningitis, neuronal degeneration, gliosis and perivascular cuffing with mononuclear cell and neutrophilic infiltration are evident. Immunohistochemistry can be diagnostic. Liquefactive necrosis and haemorrhage of the cerebral cortex, atrophy of the pancreatic acinar cells and hyperplasia of the pancreatic duct cells commonly occur with VEE.
 
  
−
IN VEE there may be damage to other organs such as the pancreas, liver and heart.
+
===Post-mortem findings===
−
 
+
'''''PRECAUTION'': infective viral particles may be present in CNS and other tissues'''.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
−
Gross pathological lesions are rarely observed in horses and, if present, consist only of the congestion of the brain and meninges. Ecchymotic haemorrhages of traumatic origin may be observed. Microscopic lesions are usually found throughout the central nervous system and can be diagnostic. There is widespread evidence of a severe inflammatory response involving the grey matter. Neuronal degeneration with infiltration by polymorphonuclear leukocytes, diffuse and focal gliosis, and perivascular cuffing with lymphocytes and neutrophils are seen. Also observed are neuronophagia and liquefaction of the neuropil. The extent of the lesions depends on the severity of the infection and the duration of the neurological involvement (16).
+
Gross pathological lesions of the brain and spinal cord are rarely seen in horses, although traumatic ecchymotic haemorrhages and vascular congestion of the CNS may be evident.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref> The extent of microscopic lesions is dictated by the severity of infection and duration of neurological involvement.<ref>Walton T.E (1981) Venezuelan, eastern, and western encephalomyelitis. In: ''Virus Diseases of Food Animals. A World Geography of Epidemiology and Control''. Disease Monographs, Vol. 2, Gibbs E.P.J, ed. Academic Press, New York, USA, 587-625.</ref>  Such lesions with or without immunohistochemistry may be diagnostic.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>  The cerebral cortex, thalamus and hypothalamus are often severely affected. Mononuclear meningitis, neuronal degeneration, diffuse and focal gliosis and perivascular cuffing are also seen.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>  Histological lesions of EEE are usually present throughout the CNS, with widespread and severe neutrophilic inflammation of the grey matter. Lesions caused by Western EEV infection are more focal and lymphocytic in nature.<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref>  VEE cases often exhibit haemorrhage and liquefactive necrosis of the cerebral cortex, but lesions are not restricted to the CNS.  In the pancreas, acinar cells atrophy and duct cells undergo hyperplasia.<ref>Monlux, W.S, Luedke, A.J (1973) Brain and spinal cord lesions in horses inoculated with Venezuelan equine encephalomyelitis virus (epidemic American and Trinidad strains), ''Am J Vet Res'', 34:465-473.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  There may also be damage to the liver and heart.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> 
−
Brain lesions caused by WEE virus infection are focal and have lymphocytic infiltrations. Brain lesions caused by EEE virus infection are more severe and are found throughout the grey matter. They are characterised by a larger number of neutrophils among the inflammatory cells.
 
  
 
[[Image:Venezuelan_equine_encephalitis_virus.jpg|300px|thumb|right|''' (Photomicrograph of mouse brain tissue after dying of Venezuelan Encephalitis. Reveals neural necrosis and edema.  ''Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Public Health Image Library (PHIL) Image #2809, 2006)'' ''']]
 
[[Image:Venezuelan_equine_encephalitis_virus.jpg|300px|thumb|right|''' (Photomicrograph of mouse brain tissue after dying of Venezuelan Encephalitis. Reveals neural necrosis and edema.  ''Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Public Health Image Library (PHIL) Image #2809, 2006)'' ''']]
  
−
====Differential diagnosis====
+
==Differential diagnoses<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>==
 
*Other togaviral encephalitides
 
*Other togaviral encephalitides
 +
*Other [[Equine Viral Encephalitis|viral encephalitides]]
 
*Trauma
 
*Trauma
−
*Hepatic encephalopathy
+
*[[Equine Herpesvirus 1|Equine herpesvirus 1]] infection
−
*Rabies
+
*[[Hepatic Encephalopathy|Hepatic encephalopathy]]
 +
*[[Rabies]]
 +
*Botulism
 
*Leukoencephalomalacia
 
*Leukoencephalomalacia
 
*Bacterial meningoencephalitis
 
*Bacterial meningoencephalitis
−
*Equine protozoal myeloencephalitis (EPM)
+
*[[Equine Protozoal Myeloencephalitis|Equine protozoal myeloencephalitis]] (EPM)
 
*Verminous encephalomyelitis
 
*Verminous encephalomyelitis
−
*West Nile Virus (WNV) infection
+
*[[West Nile Virus|West Nile Virus (WNV)]] infection
 
*Toxicosis
 
*Toxicosis
  
−
====Treatment====
+
==Treatment<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>==
−
No effective, specific treatment is available.  Supportive management includes:
+
No effective, specific treatment is available.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref> Supportive management includes:
 
*NSAIDs (phenylbutazone, flunixin meglumine) to control pyrexia, inflammation and discomfort
 
*NSAIDs (phenylbutazone, flunixin meglumine) to control pyrexia, inflammation and discomfort
 
*DMSO IV in a 20% solution to control inflamation, provide some analgesia and mild sedation
 
*DMSO IV in a 20% solution to control inflamation, provide some analgesia and mild sedation
−
*Pentobarbital, diazepam IV, phenobarbital PO or phenytoin IV to control convulsions
+
*Pentobarbital, diazepam IV, phenobarbital PO or phenytoin IV to control seizures
 
*Antibiotic therapy in cases with secondary bacterial infection
 
*Antibiotic therapy in cases with secondary bacterial infection
 
*Balanced fluid solutions IV or PO as necessary to correct hydration status
 
*Balanced fluid solutions IV or PO as necessary to correct hydration status
−
*Dietary supplementation (enteral or parenteral if anorexia persists more than 48 hours)
+
*Dietary supplementation (enteral, or parenteral if anorexia persists more than 48 hours)
−
*Laxatives to minimize the risk of impaction
+
*Laxatives to reduce the risk of impaction
−
*Protection of areas susceptible to self-induced trauma and provision of deep bedding
+
*Protection of body regions susceptible to self-induced trauma and provision of deep bedding
−
*Sling support if the horse is recumbent
+
*Sling support for recumbent horses
  
−
====Prognosis====
+
==Prognosis==
−
Comatose animals rarely survive.  Survivors exhibit functional improvement over weeks to months, but complete recovery from neurological deficits is rare.  Residual ataxia, depression and abnormal behaviour is often seen with EEE, less commonly with WEE.  The mortality rates for neurological equine viral encephalitis are reportedly:
+
Comatose animals rarely survive.  Survivors exhibit functional improvement over weeks to months, but complete recovery from neurological deficits is rare<ref>Patterson, J.S, Maes, R.K, Mullaney, T.P, Benson, C.L (1996) Immunohistochemical diagnosis of eastern equine encephalomyelitis, ''J Vet Diagn Invest'', 8(2):156-160.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Residual ataxia, depression and abnormal behaviour is often seen with EEE, but less so with WEE.  The mortality rates for neurological equine viral encephalitis are reportedly:
 
*EEE 75-100%
 
*EEE 75-100%
 
*WEE 20-50%
 
*WEE 20-50%
 
*VEE 40-80%
 
*VEE 40-80%
−
It is generally assumed that infection does not provide protective immunity, however, protection for up to 2 years has been noted.
+
It is generally assumed that infection does not provide protective immunity, however, protection for up to 2 years has been noted.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>
−
====Control====
+
 
−
=====Vaccination=====
+
==Control==
−
Vaccinate susceptible horses annually.  Vaccinate horses in the face of an outbreak.  Vaccinate mares one month prior to foaling.  Colostral-derived Ab persists for 6-7 months.  Although folas ca be vaccinated at any time, they should be re-vaccinated at 6 months and at one year if they were vaccinated early.  Most vaccines are killed (produced in cell culture and inactivated with formalin) and elicit significant increases in Ab titre after 3 days.  Protective titres last for 6-8 months.  Some cross-protection is seen between the serotypes but not between WEE and EEE.  Monovalent, divalent and trivalent vaccines are available but the response to VEE vaccination alone is decreased in horses previously vaccinated against WEE and EEE.  Susceptible horses should be vaccinated annually in late spring or several months before the high risk season.  Biannual or triannual vaccination is recommended in regions where the mosquito season is prolonged. Vaccination does not interfere with the ELISA assay for VEE.  '''''PRECAUTION'': human vaccination recommended for vets in endemic areas'''.
+
=== Vaccination===
 +
Most vaccines are killed (produced in cell culture and inactivated with formalin)<ref name="manual">''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref> and elicit significant increases in Ab titre after 3 days.<ref name="attenuated">Ferguson, J.A, Reeves, W.C, Milby, M.M, Hardy, J.L (1978) Study of homologous and heterologous antibody responses in California horses vaccinated with attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83), ''Am J Vet Res'', 39:371-376.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Protective titres last for 6-8 months.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Some cross-protection is seen between the serotypes but not between Western and Eastern EEV.<ref>Jochim, M.M, Barber, T.L (1974) Immune response of horses after simultaneous or sequential vaccination against eastern, Western and Venezuelan equine encephlaomyelitis, ''J Am Vet Med Assoc'', 165:621-625.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Monovalent, divalent and trivalent vaccines are available but the response to monovalent VEE vaccination is decreased in horses previously vaccinated against WEE and EEE.<ref>Calisher, C.H, Sasso, D.R, Sather, G.E (1973) Possible evidence for interference with Venezuelan equine encephalitis virus vaccination of equines by pre-existing antibody to eastern or western equine encephalitis virus, or both, ''Appl Microbiol'', 26:485-488.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> The current recommendation is to vaccinate susceptible horses annually in late spring or several months before the high risk season.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref> Biannual or triannual vaccination should be employed in regions where the vector season is prolonged.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Susceptible horses should also be vaccinated in the face of an outbreak.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Mares should be vaccinated one month prior to foaling to boost colostral-derived Ab<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref>, which persists for 6-7 months.<ref name="repeat"> Ferguson, J.A, Reeves, W.C, Hardy, J.L (1979) Studies on immunity to alphaviruses in foals, ''Am J Vet Res'', 40:5-10.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Although foals can be vaccinated at any time, early vaccination should be followed by boosters at 6 months and at one year.  Vaccination does not interfere with the ELISA assay for VEE.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> '''NOTE''': Formalin-treated preparations of virulent epizootic VEE virus should never be used in equids as residual virulent virus can result in severe illness.  Instead, the attenuated vaccine, strain TC-83<ref name="attenuated">Ferguson, J.A, Reeves, W.C, Milby, M.M, Hardy, J.L (1978) Study of homologous and heterologous antibody responses in California horses vaccinated with attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83), ''Am J Vet Res'', 39:371-376.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>, or an inactivated preparation created from that strain should be used. <ref>Walton, T.E, Grayson, M.A (1989)Chapter 46, Venezuelan equine encephalomyelitis. In: ''The Arboviruses: Epidemiology and Ecology'', Vol. 4, Monath T.P., ed. CRC Press, Boca Raton, Florida, USA, 203-231.  In:''Manual of Diagnostic Tests and Vaccines for Terrestrial Animals'' found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.</ref> '''''PRECAUTION'': human vaccination is recommended for vets in endemic areas'''.
 +
 
 +
===Vector control===
 +
Responsible use of insecticides and repellents<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>, elimination of standing water, and stable screening will all help to reduce viral transmission.  Environmental application of insecticides may be useful in endemic areas or during an outbreak.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  Horses infected with Venezuelan EEV should be isolated for 3 weeks after complete recovery.<ref name="same">Pasquini, C, Pasquini S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, p266, SUDZ publishing.</ref>
 +
 
 +
 
 +
{{Learning
 +
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Responsible use of insecticides and repellents, elimination of standing water and stable screening will all help to reduce viral transmission. Environmental application of insecticides may be useful in endemic areas or during an outbreak. Horses infected with Venezuelan EEV should be isolated for 3 weeks after complete recovery.
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====References====
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==References==
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Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) ''Equine Internal Medicine'', Third Edition, Saunders, Chapter 12.
 
  
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Manual of Diagnostic Tests
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and Vaccines for Terrestrial Animals http://www.oie.int/eng/normes/mmanual/A_00081.htm
 
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4.    Karabatsos N., Lewis A.L., Calisher C.H., Hunt A.R. & Roehrig J.T. (1988). Identification of Highland J virus from a Florida horse. Am. J. Trop. Med. Hyg., 39, 603-606.
 
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Walton T.E. (1981). Venezuelan, eastern, and western encephalomyelitis. In: Virus Diseases of Food Animals. A World Geography of Epidemiology and Control. Disease Monographs, Vol. 2, Gibbs E.P.J., ed. Academic Press, New York, USA, 587-625.
 
  
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http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/viralenceph/index.htm
 
  
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Vet Pathol. 2010 Jun 15. [Epub ahead of print] Review Paper: Pathology of Animal Models of Alphavirus Encephalitis.
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Steele KE, Twenhafel NA.
 
  
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[[Category:Togaviridae]]
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[[Category:Expert_Review]]
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[[Category:Horse]]
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[[Category:Zoonoses]]
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[[Category:To_Do_-_Viruses]]
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[[Category:Neurological Diseases - Horse]]
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[[Category:To_Do_-_Nina]]
 

Latest revision as of 15:24, 6 July 2012


Also known as: Alphaviral encephalitis — Alphaviral encephalitides — Eastern equine encephalitis — Eastern equine encephalomyelitis — EEE — Western equine encephalitis — Western equine encephalomyelitis — WEE — Venezuelan equine encephalitis — Venezuelan equine encephalomyelitis — VEE

Introduction

NOTIFIABLE and ZOONOTIC OIE List B, infectious, mosquito-borne diseases of equidae affecting the central nervous system (CNS). They include:

  • Eastern Equine Encephalitis (EEE)
  • Western Equine Encephalitis (WEE)
  • Venezuelan Equine Encephalitis (VEE) - reportable in the USA[1]

Aetiology

See this page for details of the equine encephalitis causal pathogens. Some of the virus strains can infect swine[2], poultry and other farmed birds including quail and ratites.[3] Isolated cases have also been noted in cattle[4], sheep and non-domestic ungulates.[3] Some strains are potential agents of biowarfare or bioterrorism[5].

Epidemiology

Distribution

Togaviral encephalitis in equids is largely confined to the Western Hemisphere.[3] Venezuelan EEV can cause large outbreaks of disease over extensive geographical areas in both humans and horses. Spread of this virus into Central America has had disasterous consequences with epidemics as far north as Texas.[6] Climatic conditions and interventions that support vector populations, such as irrigation, greatly influence the geographical spread of the disease.[6] EEE has been recorded across the United States, but mostly in the Southeastern States.[3] As its names suggests, WEE has a predilection for the Western states which have been subject to significant outbreaks in the past. A regional alteration in virulence has been proposed for the steep decline in clinical case numbers observed in this area.[3] A lag phase of 2-5weeks is commonly observed between horse and human cases of WEE in a given locus.[7] Both are dead-end hosts for the virus. A subtype of Western EEV, Highlands J virus, was isolated from the brain of a horse with encephalitis in Florida.[8]

Transmission

Transfer is vector-mediated, primarily via mosquito salivary transfer. WEE and VEE may also be transmitted horse to horse through nasal secretions. This mode of transmission is less likely, despite the fact that high concentrations of VEE virus are found in ocular and nasal discharges from infected horses.[9] The viraemic phase ends when nervous signs develop[3] and is important for disease amplification. Amplification from horses is likely only with VEE virus, in association with a relatively high and potentially persistent viraemia.[10] Similarly, zoonotic spread is unlikely for Eastern and Western equine encephalitis, but has been noted with VEE.

Seasonal Incidence

The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.[1] Case numbers peak in June to November in temperate climates.[3] The vector season is longer in warmer climates, where the disease period is prolonged. Global warming may promote more outbreaks in historically colder climates.[3]

Epidemics

Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation.[3] However, some epidemic requirements are beyond question. Adequate amounts of infective virus, sufficent vectors, infected sylvatic hosts and susceptible terminal hosts, and finally, appropriate reservoirs, are all crucial.[11]

Pathogenesis[3]

Upon entry to the host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes. In macrophages and neutrophils viral replication leads to shedding and significant clearance of viral particles. No further clinical signs develop if this clearance is successful. Erythrocyte and leukocyte absorption are used to circumvent the immune defences of the host. After incomplete elimination, residual virus infects endothelial cells and accumulates in highly vascular organs such as the liver and spleen. In these organs, viral replication produces circulating virus and a second viraemic period, typically associated with early clinical signs. Neuroinvasion and replication occurs within a week.[10] An incubation period of 7-21days has been demonstrated after experimental infection with Eastern or Western EEV, but the incubation is often shorter for EEE compared with that of WEE.

Signalment

Unvaccinated adult horses and other equids (VEE in donkeys) are at risk in areas with suitable vectors. Vaccinated horses can still develop the disease, particularly if they are young or old.

Clinical Signs

Worse in unvaccinated horses.[3] Neurological signs may be assymmetrical.[10]

EEE and WEE

Following an incubation period of up to 21days[3], an initial pyrexia and mild depression are short-lived and often missed. The acute phase of the disease presents with mild to severe pyrexia, anorexia and stiffness, lasting up to 5 days. During this time, the horse is viraemic and capable of amplifying the disease. The fever may then fluctuate with neurological derangements appearing a few days post-infection.[1] These changes indicate disease progression, which occurs more frequently with EEE (the most virulent of the three serotypes). Any of the following may be observed[3]:

  • conscious proprioceptive deficits
  • propulsive walking
  • depression
  • somnolence
  • aggression
  • excitability
  • restlessness
  • hypersensitivity to sound and touch

Worsening neurological deficits may result in[3]:

  • head pressing
  • head tilt
  • ataxia
  • circling
  • apparent blindness
  • facial and appendicular muscle fasciculations
  • pendulous lower lip[1]
  • pharynx, larynx and tongue paralysis
  • seizures[1]
  • recumbency for 1-7 days followed by death[1]

VEE

Clinical signs may resemble those of WEE and EEE or may vary[3]:

  • pyrexia peaks early and persists throughout the disease course
  • mild pyrexia and leukopenia with endemic strains
  • severe pyrexia and leukopenia with epidemic strains
  • neurological signs around 4 days post-infection
  • diarrhoea, severe depression, recumbency and death may precede neurological signs
  • other signs: abortion, oral ulceration, pulmonary haemorrhage, epistaxis

Diagnosis

Presumptive based on history, epidemiology and clinical signs.[1] Definitive diagnosis requires virus identification, serological tests and/or post-mortem examination.

Laboratory Tests

Virus Identification

Serology

Ab titre increases sharply within 24 hours of the initial viraemia, before clinical signs are apparent. It then deteriorates over 6 months. Samples taken when clinical signs appear are likely to miss the Ab peak and will demonstrate a decreasing titre.[3] Thus, serological confirmation of Eastern or Western EEV infection requires a four-fold or greater increase[1] OR decrease in Ab titre in paired serum samples taken 10-14 days apart.[12] A presumptive diagnosis can be made on a single sample if an unvaccinated horse with suggestive clinical signs has Ab against only Eastern or Western EEV.[12] Colostral-derived Ab has a serum half-life of around 20days and may interfere with diagnosis in foals.[13]

  • Complement fixation (CF): to avoid anti-complementary effects, serum should be separated from blood as soon as possible.[12] CF Ab against both Eastern and Western EEV is less useful for serological diagnosis because it appears relatively late and does not persist.[12]
  • Haemagglutination inhibition (HAI): titres of 1/10 and 1/20 are indicative, titres of 1/40 and above are positive.[12]
  • ELISA may be used to detect viral-specific IgM to the surface glycoprotein of Venezuelan EEV, from 3 days post-onset of clinical signs up to 21 days post-infection. This is useful in acute infections where convalescent serum samples are unobtainable.[3]
  • The plaque reduction neutralization (PRN) test is very specific and can differentiate EEE and WEE infections. It is performed in duck embryo fibroblast, Vero, or BHK-21 cell cultures. Serum is tested against 100 plaque-forming units of virus. Endpoints are based on a 90% reduction in the number of plaques compared with the virus control.[12]

Most commonly, the PRN test or a combination of PRN and HAI tests is used to detect Ab against Eastern and Western EEV. Cross-reactivity occurs between Ab against these viruses in the CF and HAI tests.[12]

Clinical Pathology

CSF samples demonstrate increased cellularity (50-400 mononuclear cells/µl) and protein concentration (100-200mg/dl).[3]

Post-mortem findings

PRECAUTION: infective viral particles may be present in CNS and other tissues.[3] Gross pathological lesions of the brain and spinal cord are rarely seen in horses, although traumatic ecchymotic haemorrhages and vascular congestion of the CNS may be evident.[12] The extent of microscopic lesions is dictated by the severity of infection and duration of neurological involvement.[14] Such lesions with or without immunohistochemistry may be diagnostic.[12] The cerebral cortex, thalamus and hypothalamus are often severely affected. Mononuclear meningitis, neuronal degeneration, diffuse and focal gliosis and perivascular cuffing are also seen.[12] Histological lesions of EEE are usually present throughout the CNS, with widespread and severe neutrophilic inflammation of the grey matter. Lesions caused by Western EEV infection are more focal and lymphocytic in nature.[12] VEE cases often exhibit haemorrhage and liquefactive necrosis of the cerebral cortex, but lesions are not restricted to the CNS. In the pancreas, acinar cells atrophy and duct cells undergo hyperplasia.[15] There may also be damage to the liver and heart.[3]

(Photomicrograph of mouse brain tissue after dying of Venezuelan Encephalitis. Reveals neural necrosis and edema. Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Public Health Image Library (PHIL) Image #2809, 2006)

Differential diagnoses[3]

Treatment[3]

No effective, specific treatment is available.[1] Supportive management includes:

  • NSAIDs (phenylbutazone, flunixin meglumine) to control pyrexia, inflammation and discomfort
  • DMSO IV in a 20% solution to control inflamation, provide some analgesia and mild sedation
  • Pentobarbital, diazepam IV, phenobarbital PO or phenytoin IV to control seizures
  • Antibiotic therapy in cases with secondary bacterial infection
  • Balanced fluid solutions IV or PO as necessary to correct hydration status
  • Dietary supplementation (enteral, or parenteral if anorexia persists more than 48 hours)
  • Laxatives to reduce the risk of impaction
  • Protection of body regions susceptible to self-induced trauma and provision of deep bedding
  • Sling support for recumbent horses

Prognosis

Comatose animals rarely survive. Survivors exhibit functional improvement over weeks to months, but complete recovery from neurological deficits is rare[16] Residual ataxia, depression and abnormal behaviour is often seen with EEE, but less so with WEE. The mortality rates for neurological equine viral encephalitis are reportedly:

  • EEE 75-100%
  • WEE 20-50%
  • VEE 40-80%

It is generally assumed that infection does not provide protective immunity, however, protection for up to 2 years has been noted.[3]

Control

Vaccination

Most vaccines are killed (produced in cell culture and inactivated with formalin)[12] and elicit significant increases in Ab titre after 3 days.[17] Protective titres last for 6-8 months.[3] Some cross-protection is seen between the serotypes but not between Western and Eastern EEV.[18] Monovalent, divalent and trivalent vaccines are available but the response to monovalent VEE vaccination is decreased in horses previously vaccinated against WEE and EEE.[19] The current recommendation is to vaccinate susceptible horses annually in late spring or several months before the high risk season.[1] Biannual or triannual vaccination should be employed in regions where the vector season is prolonged.[3] Susceptible horses should also be vaccinated in the face of an outbreak.[3] Mares should be vaccinated one month prior to foaling to boost colostral-derived Ab[10], which persists for 6-7 months.[13] Although foals can be vaccinated at any time, early vaccination should be followed by boosters at 6 months and at one year. Vaccination does not interfere with the ELISA assay for VEE.[3] NOTE: Formalin-treated preparations of virulent epizootic VEE virus should never be used in equids as residual virulent virus can result in severe illness. Instead, the attenuated vaccine, strain TC-83[17], or an inactivated preparation created from that strain should be used. [20] PRECAUTION: human vaccination is recommended for vets in endemic areas.

Vector control

Responsible use of insecticides and repellents[1], elimination of standing water, and stable screening will all help to reduce viral transmission. Environmental application of insecticides may be useful in endemic areas or during an outbreak.[3] Horses infected with Venezuelan EEV should be isolated for 3 weeks after complete recovery.[1]



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References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 Pasquini, C, Pasquini S, Woods, P (2005) Guide to Equine Clinics Volume 1: Equine Medicine, third edition, p266, SUDZ publishing.
  2. ↑ Karsted, L, Hansen, R.P (1959) Natural and experimental infections in swine with the virus of eastern equine encephalomyelitis, J Infect Dis 105:293-296. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25 3.26 3.27 Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  4. ↑ Pursell, A.R, Mitchell, F.E, Seibold, H.R (1976) Naturally occurring and experimentally induced eastern encephalomyelitis in calves, J Am Vet Med Assoc, 169:1101-1103. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  5. ↑ Steele, K.E, Twenhafel, N.A (2010) Review Paper: Pathology of Animal Models of Alphavirus Encephalitis. Vet Pathol. Jun 15. [Epub ahead of print].
  6. ↑ 6.0 6.1 http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/viralenceph/index.htm, accessed July 2010
  7. ↑ McLintock, J (1980) The arbovirus problem in Canada, Can J Public Health, 67(Suppl 1):8-12. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  8. ↑ Karabatsos, N, Lewis, A.L, Calisher, C.H, Hunt, A.R, and Roehrig, J.T (1988). Identification of Highland J virus from a Florida horse. Am J Trop Med Hyg, 39, 603-606. In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.
  9. ↑ Kissling, R.E, Chamberlain, R.W (1967) Venezuelan equine encephalitis, Adv Vet Sci Comp Med, 11:65-84. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  10. ↑ 10.0 10.1 10.2 10.3 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010
  11. ↑ Sellers, R.F (1980) Weather, host and vector: their interplay in the spread of insect-borne animal virus diseases, J Hyg (Lond), 85:65-102. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 Manual of Diagnostic Tests and Vaccines for Terrestrial Animals found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.
  13. ↑ 13.0 13.1 Ferguson, J.A, Reeves, W.C, Hardy, J.L (1979) Studies on immunity to alphaviruses in foals, Am J Vet Res, 40:5-10. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  14. ↑ Walton T.E (1981) Venezuelan, eastern, and western encephalomyelitis. In: Virus Diseases of Food Animals. A World Geography of Epidemiology and Control. Disease Monographs, Vol. 2, Gibbs E.P.J, ed. Academic Press, New York, USA, 587-625.
  15. ↑ Monlux, W.S, Luedke, A.J (1973) Brain and spinal cord lesions in horses inoculated with Venezuelan equine encephalomyelitis virus (epidemic American and Trinidad strains), Am J Vet Res, 34:465-473. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  16. ↑ Patterson, J.S, Maes, R.K, Mullaney, T.P, Benson, C.L (1996) Immunohistochemical diagnosis of eastern equine encephalomyelitis, J Vet Diagn Invest, 8(2):156-160. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  17. ↑ 17.0 17.1 Ferguson, J.A, Reeves, W.C, Milby, M.M, Hardy, J.L (1978) Study of homologous and heterologous antibody responses in California horses vaccinated with attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83), Am J Vet Res, 39:371-376. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  18. ↑ Jochim, M.M, Barber, T.L (1974) Immune response of horses after simultaneous or sequential vaccination against eastern, Western and Venezuelan equine encephlaomyelitis, J Am Vet Med Assoc, 165:621-625. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  19. ↑ Calisher, C.H, Sasso, D.R, Sather, G.E (1973) Possible evidence for interference with Venezuelan equine encephalitis virus vaccination of equines by pre-existing antibody to eastern or western equine encephalitis virus, or both, Appl Microbiol, 26:485-488. In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 12
  20. ↑ Walton, T.E, Grayson, M.A (1989)Chapter 46, Venezuelan equine encephalomyelitis. In: The Arboviruses: Epidemiology and Ecology, Vol. 4, Monath T.P., ed. CRC Press, Boca Raton, Florida, USA, 203-231. In:Manual of Diagnostic Tests and Vaccines for Terrestrial Animals found at http://www.oie.int/eng/normes/mmanual/A_00081.htm, accessed July 2010.


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