History
A 3-month-old intact female Belgian Malinois was admitted for further investigation of a sudden onset of pelvic limb weakness over the previous 3 days. No trauma was reported; however, the patient was vaccinated 4 days prior to the presentation. Physical examination revealed a bilateral and symmetrical enlargement of both popliteal lymph nodes, moderate muscle atrophy in both pelvic limbs, and asymmetric abrasion of the nails of the second and third digits of both pelvic limbs. The neurological examination revealed marked ambulatory paraparesis, pelvic limb proprioceptive ataxia, and increased muscle tone in both pelvic limbs with absent patellar reflex bilaterally, weak and incomplete withdrawal reflex in both pelvic limbs, reduced perineal reflex, moderate delay of the postural reactions in both pelvic limbs, and lumbar discomfort on spinal palpation.
Assessment
Anatomic diagnosis
A T3-L3 myelopathy was considered most likely to explain the ambulatory paraparesis and the pelvic limb proprioceptive ataxia with increased muscle tone in both pelvic limbs. To account for the absence of the spinal reflexes in both pelvic limbs and the reduced perineal reflex, the L4-S3 spinal cord segments or peripheral nerves were also considered.
Likely location of the lesion
The most likely location to explain all the neurological findings was the L4-S3 spinal cord segments with an associated myopathy to account for the increased muscle tone.
Etiologic diagnosis
An inflammatory disease (infectious vs noninfectious) such as protozoal meningomyelitis, discospondylitis with empyema (bacterial vs fungal), or meningomyelitis of unknown etiology was considered the most likely differential diagnoses in a patient of this age. Less likely differential diagnoses included developmental anomalies.
Further diagnostic testing included a full CBC, serum biochemistry followed by an MRI of the lumbosacral area, and lumbar cerebrospinal fluid collection alongside serology and PCR on CSF for Neospora caninum and Toxoplasma gondii.
Diagnostic test findings
The results of the serum biochemistry and CBC showed a mild microcytic nonregenerative anemia (31% Hct; reference range, 37.3% to 61.7% Hct), moderate basophilia (1.38 M/L; reference range, 0 to 0.1 M/L), and a moderate elevation of the creatine kinase (755 U/L; reference range, 99 to 436 U/L).
The patient was then anesthetized for an MRI. The study was performed with a 1.5-T scanner (PetVet; Hallmarq Veterinary Imaging) with pre- and postcontrast sequences. The study included dorsal, sagittal, and transverse T2-weigthed (T2W) fast spin echo, dorsal STIR, and dorsal, sagittal, and transverse T1-weighted (T1W) spin echo pre- and postcontrast (Gadobutrol; Gadovist).
The MRI showed multiple ill-defined lesions affecting the gluteus muscles of both pelvic limbs, being most severe on the left and the terminal aspects of the left longissimus coli muscle. These lesions were hyperintense on T2W STIR and isointense on T1W relative to gray matter, with moderate contrast enhancement. On the T1W postcontrast sequences, there was strong contrast enhancement of the nerve roots exiting from the L4 to L7 segments (Figure 1).
A—Dorsal STIR at the level of the lumbosacral spine showing an ill-defined muscle lesion involving the left medial gluteal muscle. B—T1-weighted fast spin echo preconstrast and T1-weighted fast spin echo postcontrast at the level of the L4 intervertebral disk space showing a strong contrast enhancement of the nerve roots.
Citation: Journal of the American Veterinary Medical Association 261, 5; 10.2460/javma.22.10.0468
A—Dorsal STIR at the level of the lumbosacral spine showing an ill-defined muscle lesion involving the left medial gluteal muscle. B—T1-weighted fast spin echo preconstrast and T1-weighted fast spin echo postcontrast at the level of the L4 intervertebral disk space showing a strong contrast enhancement of the nerve roots.
Citation: Journal of the American Veterinary Medical Association 261, 5; 10.2460/javma.22.10.0468
A—Dorsal STIR at the level of the lumbosacral spine showing an ill-defined muscle lesion involving the left medial gluteal muscle. B—T1-weighted fast spin echo preconstrast and T1-weighted fast spin echo postcontrast at the level of the L4 intervertebral disk space showing a strong contrast enhancement of the nerve roots.
Citation: Journal of the American Veterinary Medical Association 261, 5; 10.2460/javma.22.10.0468
Post MRI, CSF analysis from lumbar collection showed a moderate eosinophilic pleocytosis with 78 total nucleated cell counts/μL (normal range, 0 to 5 total nucleated cell counts/μL) and a high total protein concentration of 266 mg/dL (normal range, 15.0 to 45.0 mg/dL).
Due to the high suspicion of an infectious etiology, treatment with clindamycin (15 mg/kg, PO, q 12 h) and cotrimoxazole (20 mg/kg, PO, q 12 h) was commenced.
Blood serologies for T gondii and N caninum were both positive with a titer of 1/800 and 1/200 respectively; PCR on CSF was positive for N caninum.
Comments
Neospora caninum has been reported to cause a severe polyradiculoneuritis in young dogs, equally affecting meninges, nerves, and muscles.1
Neosporosis usually affects juveniles under 3 months of age, with an acute progression of paraparesis and spasticity of the hind limbs. The pathogenesis is in the form of vertical transmission from the mother to the juvenile, with selective targeting of the nerve ganglions of the lumbar plexus.2–4 It is not recommended to breed from females that produce affected offspring, as it has been demonstrated there is a higher likelihood of transmission of further disease in these cases.5
Antibiosis is the mainstay in treatment of N caninum, with commonly used antibiotics including clindamycin or sulfonamides. They are often used in combination with intensive physiotherapy.
There are reports in the literature relating to the long-term outcomes of young dogs affected with N caninum; however, anecdotally, the prognosis is considered good to fair if appropriate treatment is commenced quickly. That said, the recovery of normal hind limb function is generally considered unlikely.3
References
- 2.↑
Cummings JF, de Lahunta A, Suter MM, Jacobson RH. Canine protozoan polyradiculoneuritis. Acta Neuropathol. 1988;76(1):46-54.
- 3.↑
Dubey JP, Lindsay DS. A review of Neospora caninum and neosporosis. Vet Parasitol. 1996;67(1-2):1-59.
- 4.↑
Cuddon P, Lin D, Bowman DD, et al. Neospora caninum infection in English Springer Spaniel littermates. J Vet Intern Med. 1992;6(6):325-332.
- 5.↑
Lahunta AD, Glass EN, Kent M. Veterinary Neuroanatomy and Clinical Neurology. Elsevier Health Sciences; 2014.
