A 3-year-old 77-lb (35-kg) neutered male collie was presented to the Veterinary Teaching Hospital at the Virginia-Maryland
Regional College of Veterinary Medicine for evaluation of an acute onset of progressive ataxia, tetraparesis, a single tonic-clonic
seizure, vomiting, and ptyalism. The owner reported that the signs had started as intermittent periods of excessive anxiety
and dementia and had rapidly progressed over the previous four days despite supportive care (140 ml/hr intravenous Normosol-R
[Abbott Laboratories]; no oral food or water) administered by the referring veterinarian. The results of a complete blood
count, serum chemistry profile, and abdominal radiographic examination performed before referral had been unremarkable. Pertinent
history included administration of heartworm prophylaxis (ivermectin with pyrantel) orally the day before the onset of the
clinical signs. The dog had received the monthly preventive since 6 months of age. In addition, the dog had been allowed to
roam unsupervised and had had access to carrion the week before the clinical signs developed. Its vaccination status was current.
Physical and neurologic examinations
On presentation, the dog was obtunded and in lateral recumbency with marked extensor rigidity involving all four limbs. In
addition, the patient demonstrated continuous ptyalism and persistent bradycardia (heart rate = 40 to 50 beats/min).
We detected several abnormalities on neurologic examination. When allowed to ambulate without assistance, the dog circled
to the right and had severe truncal ataxia and asymmetric tetraparesis. We noted postural reaction deficits in all four limbs,
but the right side was more severely affected. The cranial nerve examination revealed a right head tilt and bilateral mydriasis
with normal pupillary light responses. Pathological, positional rotary nystagmus was present when the dog was placed in dorsal
recumbency, as was a ventrolateral strabismus in the right eye. Segmental spinal reflexes were normal in all four limbs. Because
of these neurologic examination findings, we suspected that a lesion was affecting the central portion of the vestibular system,
although after considering the historical evidence of seizure activity, we could not exclude multifocal intracranial disease.
The patient's initial problems included ptyalism, bradycardia, vomiting, and central vestibular (or possibly multifocal intracranial)
disease. Our differential diagnoses for the ptyalism included metabolic disorders, neurologic diseases, toxicoses, gastrointestinal
disorders, and salivary gland diseases. Potential causes of bradycardia include excess vagal tone secondary to gastrointestinal
or respiratory disease, hyperkalemia, increased intracranial pressure, endocrinopathies, sick sinus syndrome, and a drug reaction.
Acute vomiting can be associated with many systemic diseases, neurologic disorders, toxin exposures, and gastrointestinal
diseases. Our primary differential diagnoses for the central nervous system signs included toxin exposure, infectious meningoencephalitis,
After considering the cumulative clinical signs, we thought polysystemic metabolic (hepatic disease, hypoadrenocorticism),
toxic (bacterial toxins, ivermectin, lead, organophosphates), and infectious conditions (canine distemper, rickettsial diseases,
rabies) or multiple concurrent diseases were the most likely differential diagnoses.
Initial diagnostic tests and therapy
At admission, we performed a complete blood count, serum chemistry profile, and urinalysis. The results of the complete blood
count and urinalysis were unremarkable (Table 1). Hypokalemia may have resulted from the ptyalism, vomiting, inappetence, previous administration of potassium-deficient
fluids, or a combination of these. We attributed the mild elevations in protein to dehydration.
Table 1 : Results of Initial Laboratory Tests
We submitted additional blood samples for a tick-borne disease panel and measurement of whole blood cholinesterase activity
and lead concentration as well as plasma ivermectin concentration. The results of six-lead electrocardiography confirmed a
sinus bradycardia (heart rate = 42 beats/min). We also performed thoracic radiographic and abdominal ultrasonographic examinations,
and the results were unremarkable.