Pathogenesis:
How Does WNV Develop?

         The exact pathogenesis of WNV derived encephalomyelitis has not yet been determined, but it’s mechanism if likely similar to that found for equine encephalomyelitis viruses. 
         The primary target for infection and injury is most likely the neuron and possibly microglial cells.  It has been found that viral-induced apoptotic cell death is the mechanism  
          responsible for neuronal injury in experimental West Nile Viral infections.  The fatality rate for animals with WN encephalomyelitis is roughly 30-40%.  Mortality jumps to 60-80%
          for those animals that develop complete paralysis of one or more limbs.  These animals are often euthanised for humane reasons [6].

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     In Horses:

      Gross Lesions: involve the grey matter and include hyperemia and petechiation – discolouration and prominent hemorrhage involving the lower brainstem and ventral horns of the   
        thoracolumbar spinal cord [4, 5].

      Microscopic Lesions: nonsuppurative (lymphocytic/histiocytic) polioencephalomyelitis and hemorrhage of the CNS (degree of severity may vary).  Perivascular cuffing of 
       lymphocytes and monocytes is also often present [1, 9].