Page 1089 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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1064                                       CHAPTER 10



  VetBooks.ir  Hyperaesthesia is also reported. Signs associated   and spinal cord. The spinal cord lesions become pro-
                                                          gressively worse caudally. Histopathological changes
           with spinal cord pathology include ataxia (which
           is sometimes asymmetrical and may involve mul-
                                                          unlike other causes of viral encephalitis, WNV has
           tiple limbs), flaccid paralysis (due to LMN disease),   include  monocellular  perivascular cuffing  and,
           paresis and recumbency. Muscle fasciculations (par-  a predilection for the basal ganglia, thalamus, pons
           ticularly of the muzzle) are relatively common in   and medulla. WNV cases have limited viral load in
           affected horses, in comparison with other causes   their neurological tissue, and therefore detection of
           of encephalitis. Some authors also report a stiff   antibody or WNV antigen should focus on the mid-
           gait that may initially be mistaken for lameness.   brain and hindbrain areas to maximise sensitivity of
           Reported CN abnormalities include weakness of   these tests.
           the tongue (CN XII), muzzle deviation (CN VII),
           head tilt/vestibular ataxia (CN VIII) and difficulty  Management
           swallowing (CN IX).                            There are no antiviral therapies licensed for use in
                                                          neuroinvasive flavivirus infections and therefore,
           Differential diagnosis                         as with alphavirus encephalitides, therapy is based
           Other viral causes of encephalitis should be consid-  on supportive care. Anti-inflammatory treatment
           ered, depending on the geographical region and time   such as flunixin meglumine (0.5–1 mg/kg i/v q12 h)
           of year. Other relevant differential diagnoses include   may  be helpful. Corticosteroid  therapy  is contro-
           hepatic encephalopathy, tremorigenic toxicity (rye-  versial, without an evidence-base, and may increase
           grass staggers), hypocalcaemia, head trauma, poly-  peripheral and CSF viral load as has been demon-
           neuritis equi, equine herpes myeloencephalopathy,   strated in other species. Anti-oedema therapy with
           verminous meningomyeloencephalitis and botulism.   mannitol (0.5–1.0 g/kg as a 20% solution i/v via a
                                                          blood filter q12–24 h for 2–3 days) may be benefi-
           Diagnosis                                      cial in cases with rapidly progressing neurological
           WNV encephalomyelitis should be  suspected in   signs. Commercial hyperimmune serum or plasma
           any horse showing signs of neurological disease   products are available. Neutralising antibody is the
           in an area (or in close geographical proximity to   predominant antibody response and appears impor-
           an area) in which WNV activity has been docu-  tant in the blocking of intracellular infection in vitro.
           mented. Definitive diagnosis of a positive case of   At the time of writing, the clinical efficacy of these
           WNV encephalitis is challenging because of the   products had not yet been proven. The hypothesis
           cross-reactivity of antigens and the use of vac-  is that the administration of neutralising antibody
           cines.  An  ante-mortem  diagnosis  usually  depends   against WNV early in the course of the disease will
           on the demonstration of: specific IgM antibod-  reduce the severity and shorten the duration of clini-
           ies  in serum and/or CSF;  a  four-fold  increase in   cal signs in the horse. The use of interferon alpha
           competitive (c)ELISA (IgG) titres (ideally 10 days   (3 million units diluted in 250 ml saline s/c or i/v
           apart);  or  PRNT  (plaque  reduction  neutralisa-  q12 h [recumbent horses] or q24 h [standing horses]
           tion test)-positive serum samples taken during the   for 5–7 days) is based on anecdotal reports in the
           acute phase and convalescent phase. The cELISA   human and veterinary literature.
           and PRNT tests are affected by recent vaccination,   Prevention is based on limiting exposure to mos-
           and although it was initially reported to differenti-  quito vectors and on vaccination. Vaccines licensed
           ate vaccinated from recently infected horses, there   for  prevention  of  WNV  viraemia  include  whole
           is now debate in the literature about the effect of   inactivated virion vaccines, one recombinant inacti-
           vaccination on IgM titres as detected via the IgM   vated vaccine and a canarypox-vectored live recom-
           capture (MAC) ELISA.                           binant vaccine. Protection against WNV lineage 2
             Clinicopathologically, neuroinvasive flaviviruses   is recommended because there has been a surge in
           such as WNV cause a polioencephalomyelitis,    neuroinvasive WNV disease from this lineage in
           mainly involving the grey matter of the hindbrain   recent years.
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