Signalment: 4.5 year old MC Shepherd Mix
Clinical history: The dog had a 3 week history of left unilateral temporalis muscle atrophy when I met him. Hyporexia and nasal hemorrhage from the right nostril were noted when the signs first started, but they had improved by our consult. The atrophy, however, continued to progress.
Physical and Neurologic Examination:
The physical exam was normal.
Mentation: BAR
Cranial nerves: moderate left temporalis muscle atrophy, otherwise normal. No sensory abnormalities noted.
Gait: Ambulatory, no evidence of lameness, weakness or ataxia
Reflexes: normal all limbs
Postural reactions: Normal all limbs
Palpation: Non-painful spinal palpation and normal CROM
Neuroanatomic Lesion Localization?
Let's walk this through. First, what nerve innervates the temporalis muscles? (CN 5: trigeminal) So, our problem is a) peripheral trigeminal b) brainstem at the trigeminal motor nucleus or c) muscle. How do you sort between these? Right! Let's rule out the easy one first. Signs of brainstem disease include changes in mentation, paw replacement deficits (ipsilateral to the atrophy) and/or hemiparesis. Any one of these three abnormalities is present and voila! it is a brainstem lesion until otherwise discovered. We ruled out brainstem disease in this dog. Is this, then, peripheral trigeminal nerve (motor portion) or muscle? This differentiation can be hard on the neurologic examination so I actually included both of these possibilities on this dog's final neuroanatomic lesion localization. However, without a sensory deficit (he didn't have one) a trigeminal neuropathy is less likely. That said, if the CK is normal, it's hard to make a story for a myopathy. His was normal. So...I left both on the final list. You could have said "neuromuscular" and you would have been correct because that localization includes peripheral neuropathy, neuromuscular junction and myopathy.
Differential Diagnoses?
Neuropathy: Neoplasia, neuritis (infectious or non-infectious), hypothyroidism and trauma.
Myopathy: Masticatory muscle myositis (3M), infectious myositis (toxoplasma and Neospora caninum are most common causes of infectious myositis.)
Diagnostic Results
CBC, serum biochemistry: unremarkable.
T4: normal
Neospora antibody M titer: > 1:200 (positive!)
Toxoplasma IgG/IgM titer: Negative
3M antibody titer: < 1:100 (negative)
Conclusion
This patient was diagnosed with a Neospora myositis based on positive titers. We placed him on sulfa antibiotics and tracked the titers. Clindamycin is also an acceptable antibiotic choice for fighting protozoa myositis.
2 months later: 1:200
4 months later: 1:100
1.5 months later: negative.
Unfortunately, this patient developed an adverse reaction from the sulfa that included blood dyscrasias and hypothyroidism 5.5 months from the original diagnosis. The sulfa-based antibiotic was discontinued and clindamycin was started. My goal is to have 2 negative Neospora titers before discontinuing antibiotics but we will have to see if we get to meet that goal with this guy!
Key Points:
1. Muscle atrophy (especially unilateral) should prompt a toxoplasma (cat) and toxoplasma and Neospora titer (dog). This is a lesser known infection in Wisconsin dogs!
2. Treat with either a sulfa antibiotic or clindamycin to the point of two consecutive negative titers to ensure clearance of the infection. Titers are typically checked every 4-8 weeks.
This was a very interesting case and a great one to remind us all about protozoal infections in house pets. Remember - when we work together, we all learn!
I look forward to working with you soon.
