Infectious diseases of the nervous system are relatively uncommon compared to other neurological abnormalities in adult animals. However, infectious diseases should be placed high on the differential diagnosis list in puppies and kittens. Poor suckling leading to malnutrition and incomplete transfer of maternal antibodies, difficult parturition, environmental stresses and concurrent disease processes such as Parvo virus can weaken the immune system increasing the chance of bacterial meningoencephalitis. Puppies with bacterial meningoencephalitis may have a fever or leukocytosis. CSF results with bacterial meningoencephalitis are neutrophilic. However, severe neutrophilic pleocytosis can also be seen with non infectious inflammatory diseases such as steroid responsive meningitis arteritis. Culturing the CSF and or urine may help identify a bacterial cause. Visualization of bacteria in the CSF allows for a more definitive diagnosis of bacterial meningoencephalitis. Staphylococcus, E. Coli and Streptococcus and various anaerobes are typically present in bacterial meningoencephalitis.¹ CNS penetration is typically a consideration when choosing an antibiotic. Initially the blood brain barrier is compromised allowing better penetration into the CNS. Once the blood barrier is intact antibiotic penetration may be more difficult. Thus, a longer course of antibiotic therapy, higher dosages or choosing an antibiotic that more reliably penetrates the CNS may be required. Chloramphenicol reaches high CNS concentrations, however is not typically used due to the potential adverse effects. Doxycycline also penetrates the CNS, however its bacteriostatic nature and concerns for its use in young animals should be considered. Trimethoprim/sulfa also reaches relatively high CNS concentrations, but concerns regarding potential adverse effects have limited its use. Amoxacillin/clavulanic acid is broad spectrum, but reaches low CSF concentrations when the blood brain barrier is intact. Fluoroquinilones are good choices for Staphylococcus and E. Coli, however have variable affects on Streptococcus and also reach low CSF concentrations.²

Canine distemper virus (CDV), a single stranded RNA morbillivirus, is typically spread through an aerosol route. CDV is epitheliotropic. The respiratory system is initially infected, but spreads to the CNS, integument, bladder and intestinal tract. CDV crosses the blood brain barrier via infected mononuclear cells. Multifocal lesions are common. Primary demyelination often occurs in the white matter, although gray matter can also be affected. Commonly affected areas of the brain include the cerebellum, periventricular white matter, optic pathways and spinal cord.^3,4

Clinical signs are typically seen in dogs less than 3 year of age. Persistent viral infection can lead to a chronic form, "old dog distemper." Outbreaks may be seen in animal shelters. Vaccination has reduced the incidence of infection, however 30% of cases occur in vaccinated dogs.⁵ Clinical signs are typically focal, despite multifocal lesions. Seizures and myoclonus are the most common neurological signs. Cerebellar and myelopathic signs may also be seen.³ Myoclonus may be due to hyperexcitability of the lower motor neuron. It may persist during sleep, but disappears with anesthesia.⁶

The prognosis for distemper infections is variable. Severely affected dogs will likely die, while mildly affected dogs may recover. Supportive care is the mainstay of therapy. Anticonvulsants should be used to treat seizures, antibiotics for pneumonia and intravenous fluids to maintain hydration. Concurrent toxoplasma infection may occur and if present should be treated.³