A 10.75 years old, male-neutered Australian Shepherd with a 2-day history of progressive gait abnormality and two self-limiting generalized tonic-clonic seizures was presented. Two months before presentation, the dog showed a left sided facial paralysis, which completely resolved after 15 days of prednisolone treatment by the primary veterinarian. The vaccination status was not reported.
At the time of presentation, the dog showed orofacial seizures, which developed into generalized tonic-clonic seizures and could be controlled with diazepam (2 mg/kg i.v.). Rectal body temperature was 39.4  C. Heartbeat was 90 bpm without murmur on auscultation. Breathing pattern was normal, frequency was 40/min with physiological effort. Auscultation revealed mild vesicular lung sounds. Capillary refill time was under 2 s, the mucous membranes were pink and moist. Abdominal palpation was within normal limits. Macroscopical evaluation of eyes, external ears, nose, and skin were unremarkable. Blood examination revealed mildly elevated alanine aminotransferase (102 U/l; reference <50 U/l) and alkaline phosphatase (193 U/l; reference >150 U/l) activity. Clinical signs progressed within 24 hours, and the dog showed severe bradypnea and cyanosis. At neurological examination the dog was in lateral recumbency with generalized increased muscle tone and high-frequency, low-amplitude generalized tremor. He was comatose, showed bilateral absent palpebral reflexes and menace response and decreased pupillary light response on both eyes. Vestibuloocular and spinal reflexes were not tested. Consequently, the dog was intubated and mechanically ventilated.
Subsequent MRI (Figure 4) showed generalized flattened sulci and reduced volume of internal and external CSF space due to swelling of the CNS parenchyma. The FLAIR sequence revealed a subtle, diffuse, increased signal intensity of the internal capsule. There was transtentorial forebrain herniation as well as caudal foraminal herniation of the cerebellum with severe compression of the brainstem. At the site of compression, there was an intraaxial, T2w hyperintense lesion with multifocal signal void in the brainstem. There was no physiological contrast enhancement in the choroid plexus, which was suspected to be secondary to the compressed basilar artery preventing contrast agent to reach the CNS parenchyma.
Due to an infaust prognosis, no further examinations were performed and the dog was euthanized on owner's request.
Necropsy revealed a generalized swelling of the brain with mild herniation of the cerebellar vermis into the foramen occipitale magnum as well as herniation of the occipital lobe underneath the tentorium cerebelli osseum as indicated in the MRI. Furthermore, there was severe, acute hemorrhage and softening of the neuroparenchyma within the brain stem (Figure 5A).
Histologically, the cerebral cortex, cerebellum, brain stem as well as the spinal cord showed severe, lympho-histiocytic and plasmacytic panencephalomyelitis and meningitis with perivascular edema (Figure 5B). Additionally, severe vasculitis with inflammatory infiltrates in the damaged vascular wall (leukocytoclastic vasculitis) and in the perivascular space was found within the brain and the spinal cord, accompanied by moderate to severe hemorrhage. Spinal ganglia displayed mild to moderate infiltration of lymphocytes and macrophages, too. Additionally, the right eye displayed a mild to moderate, lympho-histiocytic to granulomatous neuritis and perineuritis of the optic nerve.
IHC of the CNS (Figures 5C-E) revealed that the majority of inflammatory cells infiltrating the vascular wall as well as the perivascular space were comprised of B- and T-lymphocytes. B-lymphocytes outnumbered T-lymphocytes in most of the investigated areas. Few infiltrating cells represented CD204-positive macrophages in these regions. However, the number of infiltrating macrophages was variably increased in other areas, where less lymphocytes were visible.
Using IHC and histochemistry, no infectious agent or signs of demyelination were detected.
Additionally, the tracheobronchial lymph node showed severe anthracosis. The bone marrow revealed a dominating myeloid cell population. In lungs, heart, gastrointestinal tract, and CNS no parasites were found.