MRI changes in dogs with Neosporosis vs Meningoencephalitis of Unknown Origin (MUO)

Well folks, we’re back to talking about Neospora caninum infections this week. BOY have I been seeing a lot of these! Are you holding them special for me or are we seeing a global increase in neosporosis in dogs?

This week, I reviewed an article that was published in the Frontiers Journal (doi.org/10.3389/fvets.2024.1517256) in January 2025. The purpose was to describe the MRI and biochemical findings in dogs diagnosed with Neospora caninum and compare them to those diagnosed with meningoencephalitis of unknown origin (MUO). Quick refresher:

MUO: non-infectious, inflammatory (suspected auto-immune) inflammation in the brain, spinal cord and nerves that can affect dogs or cats. Diagnosis is obtained via a combination of MRI, CSF and clinical history findings in conjunction with negative infectious disease testing.  Treatment is immunosuppression. Not curable.
Neospora caninum: a protozoal parasite that can affect brain, spinal cord, nerves or muscles. Diagnosis is obtained via positive serum titers and/or histopathologic observation of the encysted organism. Treatment is clindamycin or sulfa antibiotics, in most cases. Maybe curable?

Riddle me this: What do you do when you see a dog with multifocal neurological signs, and you’ve identified inflammation on MRI and spinal tap but don’t have the infectious testing back yet? Statistically, about 98% of dogs have MUO… infectious meningoencephalitis is only about 2% of the population. Infectious meningoencephalitis could be caused by fungal, bacterial, protozoal or viral infections. Infectious serology/PCR takes 7-10 days to come back in many cases. So, what do you treat? This article attempted to identify markers of neosporosis on MRI to improve early identification BEFORE serology is available. Here is what they found:

• CSF analysis: no statistical difference between dogs with MUO and those with Neosporosis in WBC or protein.

• CK: Dogs with Neosporosis had significantly higher CK compared to those with MUO. (median 1423 U/L vs 161 U/L).

• MRI: Dogs with neosporosis had inflammation more frequently in the masticatory muscles compared to dogs with MUO. The presence of muscle changes had a sensitivity of 27% and specificity of 96% to predict a diagnosis of neosporosis. The odds ratio was 8.25 but not statistically significant.

Take home message:

• If you have a dog with multifocal neurologic lesion localization, run a CK on your routine biochemistry testing. If it’s pretty darn high, run a Neospora caninum titer on serum (IFA)!

• If I see masticatory muscle inflammation on MRI, I’m going to suggest we treat with clindamycin while awaiting serology results…just..in..case.

• Keep up the good referrals! We’ll keep trying to figure out why Neospora caninum has become so prevalent in Wisconsin.

Thanks for reading! I hope you have a great week!

How do MRI lesions affect survival for MUE?

 
A study was published this week that looked at the survival times between dogs with and dogs without MRI lesions and diagnosed with meningoencephalomyelitis of unknown etiology (MUE). MUE is diagnosed if a dog has evidence of CNS inflammation (meningitis, encephalitis, myelitis or a combination of these) without evidence of infectious etiology. Signs can be focal or multifocal, and age is irrelevant. To make this diagnosis an MRI, CSF tap, and infectious disease testing are performed. There is a subset of dogs that are diagnosed with immune mediated CNS disease that do not show evidence of disease on MRI but have all of the other markers of MUE. The purpose of this paper was to determine if there is a difference in survival between the two groups of dogs.
Results
A total of 73 dogs with MUE were included in the study. This included 19 dogs with a normal MRI and 54 with an abnormal MRI. The survival time was >107 months in both groups with a significantly longer survival in the normal MRI group. Neither group reached median survival in Kaplan-Meier survival, however. Death was secondary to MUE in 1/19 dogs with a normal MRI, and 18/54 in dogs with an abnormal MRI.
Below is the breakdown comparison between the two groups:

• Remission – 68% of the normal MRI group; 53% of the abnormal MRI group.

• Death within 3 months due to disease – 5% in the normal MRI group and 13% in the abnormal MRI group.

No difference was found between dog groups regarding remission, disease-free interval, or relapse while on prednisone. The two groups received similar treatment protocol, for which corticosteroids were included in all dogs and a variation of additional immunosuppression. The total nucleated cell count (TNCC) was higher in the dogs with the abnormal MRI however this did not correlate with higher rates of death after multivariate analysis. The only significant factor associated with death was the presence of an abnormal MRI.

Why don’t they have lesions on MRI?

Perhaps we’re catching these cases early in the course of disease. This would stand to reason why they might have a lower death rate than those with more progressive disease at the time of diagnosis. Another option is that this is a different form of inflammatory brain disease. MUE is a “catch all” for inflammatory brain disease that isn’t infectious, or a specific form such as SRMA or EME. It likely includes all of the previously diagnosed cases of GME and NME.
Take away: If you have a dog with spinal pain, seizures, vestibular signs or multifocal CNS signs remember MUE! This disease can cause all of those signs, and a collection of other signs, in dogs. Early detection may = improved outcomes. So, if your patient is showing neurologic signs, please reach out to get a consult ASAP and to proceed with additional testing when able. We might just save their life!

Thanks for reading! I hope you are scratching out the very best that summer has to offer. I look forward to working with you soon!

Reference: Survival in dogs with meningoencephalomyelitis of unknown etiology with and without lesions detected by magnetic resonance imaging. Ostrager A, Bently, TR, Lewis MJ, Moore GE.