Case Description—A 2-year-old Griffon Vendéen was examined because of a 1-month history of right hind limb lameness after a traumatic injury.
Clinical Findings—Neurologic examination revealed monoplegia and anesthesia of the right hind limb distal to the stifle (femorotibial) joint except for the area supplied by the cutaneous saphenous nerve. Results of electromyographic testing were consistent with a severe lesion of the tibial and peroneal nerves at the level of the stifle joint.
Treatment and Outcome—Exploratory surgery revealed an 80-mm-long gap in both the peroneal and tibial branches of the right sciatic nerve. A section of the left cutaneous saphenous nerve was interposed to graft the nerve defects. The dog received joint mechanotherapy and electrophysiologic therapy during the reinnervation process. Ten months after surgery, the dog had recovered almost completely. Neurologic examination revealed diminished flexion of the tarsal and digital joints. Repeat electromyographic testing revealed no abnormal spontaneous electrical activity in the right hind limb musculature, and small compound muscle action potentials were recorded in the right interosseous and cranial tibial muscles.
Clinical Relevance—Without surgical treatment, neurotmesis injury results in poor recovery of motor and sensory functions and may result in amputation. If a nerve defect exists, nerve grafting should be considered, even if the procedure is delayed until well after the injury. The sensory portion of the cutaneous saphenous nerve is a potential source of peripheral nerve for grafting in dogs. Reinnervation is a long-term process and physiologic support and owner involvement are necessary, but nearly complete functional recovery is possible.
A 4.5-year-old neutered male domestic ferret (Mustela putorius furo) was examined because of clinical signs compatible with neuromuscular disease.
Results of electrophysiologic assessment, including measurement of compound muscle action potentials following repetitive nerve stimulation, and measurement of the anti–acetylcholine receptor antibody titer were consistent with a diagnosis of acquired myasthenia gravis.
TREATMENT AND OUTCOME
Medical treatment with pyridostigmine and prednisolone was instituted. The first signs of clinical improvement were observed 2 months later, followed by a slow but steady improvement over the next months. Anti–acetylcholine receptor antibody titer was measured 10 months after initiation of treatment and was markedly decreased, compared with the initial titer. Pyridostigmine and prednisolone dosages were tapered over the following 4 months without any evidence of recurrence of clinical signs. Thirty months after initial examination, the ferret was clinically normal and not receiving any treatment. A follow-up anti–acetylcholine receptor antibody titer was similar to previously published values for healthy ferrets.
Findings indicated that clinical and serologic remission can be achieved in ferrets with myasthenia gravis. However, owner willingness to provide extensive supportive care was vital to the outcome for this patient, as was the owner's decision to not euthanize the ferret despite an initial lack of response to treatment.
Objective—To evaluate the prevalence of congenital sensorineural deafness (CSD) and its association with phenotypic markers in client-owned ferrets.
Animals—152 healthy European pet ferrets.
Procedures—Brainstem auditory evoked response tests were recorded in ferrets during general anesthesia. Phenotypic markers such as sex, coat color and pattern, coat length (Angora or not), and premature graying trait were assessed.
Results—Overall, 44 of the 152 (29%) ferrets were affected by CSD; 10 (7%) were unilaterally deaf, and 34 (22%) were bilaterally deaf. There was no association between CSD and sex or Angora trait, but a strong association between CSD and white patterned coat or premature graying was identified. All panda, American panda, and blaze ferrets were deaf.
Conclusions and Clinical Relevance—The ferrets in this study had a high prevalence of CSD that was strictly associated with coat color patterns, specifically white markings and premature graying. This seemed to be an emerging congenital defect in pet ferrets because white-marked coats are a popular new coat color. Breeders should have a greater awareness and understanding of this defect to reduce its prevalence for the overall benefit of the species. (J Am Vet Med Assoc 2014;244:1047–1052)