Case study: meningoencephalitis in a young Staffordshire bull terrier

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meningoencephalitis
Above (1 and 2): MRI scans revealed patchy asymmetric hyperintensities on T2 and FLAIR sequences. Six months after treatment (images 3 and 4) all abnormalities had resolved.

MUO is thought to represent an idiopathic immune-mediated condition, and as such diagnosis requires exclusion of other differential diagnoses, such as protozoal infection, disseminated fungal disease, other infectious agents, and neoplasia. The typical signalment for dogs with MUO such as GME are small breed dogs with a mean age of five years, and a reportedly higher prevalence in females.

The prognosis for affected individuals is variable. Initial publications reported that most dogs with GME die or are euthanased within six months of diagnosis, with median survival time (MST) of eight days for disseminated disease, and 114 days for focal GME. More recent studies still report MST around six months for dogs with focal lesions. However, it is the perception among many specialists that dogs who respond to treatment have a more favourable outcome, with the longer survivals reported in small numbers of dogs treated with aggressive treatment protocols.

In this clinical case, a Staffordshire bull terrier was admitted to the Internal Medicine service of Western Australian Veterinary Emergency and Specialty (WAVES) for investigation of seizures. One generalised seizure episode had been witnessed six weeks prior to presentation, with further seizure activity developing 24 hours prior to presentation, progressing to cluster seizures. Small-intestinal type diarrhoea was also noted. There was no history of interstate or overseas travel and vaccinations were current. The dog had been treated with phenobarbitone and levetiracetam overnight at the primary care practice prior to referral.

The initial clinical examination revealed quiet mentation and marked ptyalism. The dog had a normal gait but was pacing compulsively and showed faecal incontinence. Neurological examination was difficult due to post-ictal status and recent phenobarbitone administration, but cranial nerve reflexes were intact and, although slow, conscious proprioceptive reflexes were present. Intermittent facial twitching and tremors were persistent. Based on the signalment, history, and examination findings, differential diagnoses included idiopathic epilepsy, sterile or infectious inflammatory CNS disease, or neoplasia.

Results of blood tests submitted prior to referral revealed no significant haematological or biochemical abnormalities. Cryptococcal antigen titre was negative. Antibody titres for Neospora canine and Toxoplasma were not supportive of infection. A faecal sample was submitted for PCR testing given the diarrhoea, with a positive result (low level) for Clostridium perfringens alpha toxin gene, and negative results for all other pathogens tested including Canine Distemper Virus.

The dog was anaesthetised for cross-sectional imaging of the brain. Magnetic resonance imaging (MRI) was performed which revealed patchy asymmetric hyperintensities on T2 and FLAIR sequences. This was present in both temporal lobes (worse on the left), and extended to the piriform lobes. There was no meningeal enhancement and no other structural abnormalities identified. A CSF sample was obtained using aseptic technique from the cerebromedullary cistern with no immediate complications. Cytology of this CSF revealed mild mixed pleocytosis with predominately large mononuclear cells. 

Pleocytosis of CSF is seen with inflammatory conditions such as GME, disc disease, trauma, haemorrhagic myelomalacia, infarction, as well as neoplasia. There was no evidence of trauma, disc disease, haemorrhage or infarction clinically and the hyperintensities on MRI were consistent in appearance with inflammation or neoplasia. No evidence of infectious disease was noted on blood samples. Based on the results, a presumptive diagnosis of MUO was made.

The dog was initially hospitalised on IV fluids until the diarrhoea resolved. Immunosuppressive treatment was started parenterally in case of reduced intestinal absorption given diarrhoea. Dexamethasone was started at 0.4mg/kg IV q24h. Four SC doses of cytosine arabinoside 50mg/m2 q12h. Anti-seizure medications were continued with levetiracetam 30mg/kg IV q8h and phenobarbitone 3mg/kg IM q12h.

Over the following three days the dog slowly improved, although the facial twitching persisted for 36 hours before resolution and demeanour remained subjectively lethargic. The dog was discharged after five days on oral medications, including prednisolone 2mg/kg (50mg) PO q24h, levetiracetam 40mg/kg (1000mg) PO q8h, phenobarbitone 3mg/kg (75mg) PO q12h. Ten days later the dog was presented for reassessment. Marked improvement was noted in mentation, with normal interaction with the owners. Intermittent episodes of facial twitching were persistent but no generalised seizures had been witnessed. Medication was continued unchanged.

Three weeks after the initial cytosine arabinoside dose the dog was reassessed again, having discontinued levetiracetam five days prior to this recheck. All neurological abnormalities had resolved with no further twitching or tremors, although these had been intermittent until a few days prior to this reassessment. No generalised seizures had been seen. Cytosine arabinoside was repeated using the same protocol and prednisolone was reduced to 40mg PO q24h. Phenobarbitone was tapered and discontinued after two months. Over the following four months the dog was reassessed monthly with a cytosine arabinoside repeated at each visit. The final dose was administered five months after clinical signs originally developed.

Six months after diagnosis the dog was reassessed again and remained asymptomatic at home. The only treatment at this stage was prednisolone 0.2mg/kg PO daily. MRI and CSF analysis was repeated to confirm full remission prior to discontinuing corticosteroid. This revealed complete resolution of the previous hyperintensities, and CSF analysis was unremarkable. The prednisolone was discontinued, and the dog remains asymptomatic nine months after initial seizure signs developed.


Dr Jenny Ellis European Specialist in Small Animal Internal Medicine
MA BVM&S GPCert (FelP) DipECVIM MRCVS

meningoencephalitis

Dr Ellis completed a Biological Natural Sciences degree (immunology and virology) at the University of Cambridge in 2005, followed by graduation from the Royal (Dick) School of Veterinary Studies at the University of Edinburgh in 2010. She initially worked in small animal general practice in the UK for three years, during which she completed a GP Certificate in Feline Practice. This was followed by a rotating internship at Dick White Referrals, Cambridgeshire, UK.

Having developed an interest in Internal Medicine during general practice and internship, Dr Ellis returned to Dick White Referrals in 2014 for a residency program. She achieved specialty status in Europe in 2018 through the European College of Veterinary Internal Medicine (Diploma in Internal Medicine). Dr Ellis moved from the UK to Western Australia in late 2018 and currently works at WAVES, a multidisciplinary specialist hospital near Perth. Special interests include immunology and oncology, and all things feline. Dr Ellis lives on the Fremantle coastline. In her spare time she enjoys surfing, running and anything in the Aussie sun!

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