A 6-week-old Clydesdale filly presented to Cornell's Large Animal Internal Medicine Service for acute progressive ataxia, decreased suckling, weakness and inappetence. The day prior to presentation the owner noticed that the filly was ataxic and febrile (102.6F). Three weeks prior to presentation, lameness and swelling over the left carpus were noted however she improved shortly after. Two weeks prior to presentation, a deep abrasion on the lateral surface at the level ofleft tarsus was noted but was healing well. On presentation, the patient was dull, quiet and responsive. She was moderately ataxic and occasionally knuckling over on all 4 limbs with thoracic limbs worse than pelvic limbs. All of her vital parameters were within normal limits. The physical examination revealed increased bronchovesicular sounds on both craniovcntral lung fields. The menace response was absent bilaterally with an intact PLR (pupillary light reflex) OU(both eyes). Warm, mildly painful soft tissue swellings were noted bilaterally at the level of C2. Joint effusion was noted on both tarsi and the left carpus. Palpation of the patient's umbilicus revealed a slightly enlarged umbilical remnant compared to the filly's age, however there was no discharge. Thoracic ultrasound was performed which showed mild comet tail artefacts on both cranial lung fields, supportive of mild pneumonia. The absent menace OU with apparently intact vision and PLRs (pupillaiy light reflex) and no other signs of forebrain disease, the lesion was localised to cerebellum/thalamus; the severe ataxia on all four legs without hypermetria suggested Cl­CS myelopathy and the dullness could be from the brainstem or from the severe systemic disease. Therefore a multi focal neurolocalisation was present with Cl-CS and thalamus or cerebellum. The history suggested septicemia and a septic CNS ( central nervous system) focus was suspected. To further assess the CNS involvement cervical radiographs were obtained which revealed a round soft tissue opacity structure at the atlanto-axial joint region. Complete blood count and chemistry panel showed moderate neutrophilia, mild hyperfibrinogenemia (supporting chronic inflammation with a possible septicemia), severe increased liver enzymes (GLDH, GGT), and moderate metabolic acidosis. The primary differentials were infectious prioritizing bacterial infection, viral infection, trauma or congenital defect. A nasal swab was used to rule out EHV (Equine Herpesvirus)-1 & -4. Blood culture later revealed gram positive rods. A cervical Computed Tomography (CT) revealed a severely bilaterally distended ventrolateral aspect of the atlanto-axialjoint, which resulted in spinal cord compression at that level. Erosive arthropathy with osteomyelitis of Cl& C2 was also noted. A spinal tap showed meningoencephalomyelitis. Due to the meningitis and septic arthritis with osteomyelitis the prognosis was poor and euthanasia was elected.