Abstract

A two-year-old, intact male, semi-domesticated, California sea lion (Zalophus californianus), housed in an open ocean pen, presented with two, isolated, generalized seizures, which occurred almost one year apart from each other. Aggressive anti-seizure therapy (diazepam, dexamethasone, antibiotics, and subcutaneous fluid therapy) was used in the first, but not the second, event. Ultimately, both seizures were self-limiting with no abnormal neurological signs reported by training staff between events. Aside from the occasional bite wound from a pen mate requiring antibiotic therapy, the animal's clinical history was otherwise unremarkable.

Hematology after each event was unremarkable. Paired sera from prior to and immediately after the first event were submitted to the Oklahoma Animal Disease Diagnostic Laboratory (OADDL) for Leptospirosis (L. canicola, L. grippo, L. hardjo, L. ictero, L. pomona, L. bratislava) antibody (all negative), morbillivirus (CDV, DMV, PDV, PMV) serum neutralization (negative), and Toxoplasma antibody (negative). After the second event, paired (acute and three months post) sera were submitted to OADDL for fungal serology (Aspergillus, Blastomyces, Coccidioides, Cryptococcus, and Histoplasma), and to UC Davis for protozoal serology (Toxoplasma, Sarcocystis, and Neospora), again with negative results.

Three months after the second seizure, an MRI was performed under general anesthesia. After 15 mg oral diazepam premedication the animal was induced to general anesthesia with 72 mg of a 1:1 solution of tiletamine and zolazepam (Telazol^TM) and 5 mg of Medetomidine (Dormitor^TM) in a single intramuscular injection.¹ The animal was intubated and allowed to breathe room air until supplemental anesthesia was required, at which time he was maintained on isoflurane (Isoflo^TM) in 100% oxygen. Upon completion of the MR exam, anesthesia was reversed with 12.5 mg atipamezole and the animal recovered uneventfully.

MR images revealed dramatic, intracranial, structural pathology. A neuroradiologist familiar with sea lion brain MRIs interpreted the images as showing a right-sided, right ventricular mass effect. The extra-axial (not parenchymal) mass appears chronic and slowly progressive as evidenced by a lack of cytotoxic or vasogenic edema. There is a large fluid pocket consistent with secondary hydrocephalus, not cystic development. Differential diagnoses include: Indolent, chronic infection vs. primary or metastatic neoplasia.

The animal had a third seizure event one week after the MRI. This time seizures were serial in nature, and were eventually controlled with 30 mg intramuscular diazepam. Long-term seizure control had not been implemented up to this point because of the infrequent incidence of seizures. Given the new MRI evidence for progressive disease, and the recent change in seizure severity, the animal was started on oral, once daily phenobarbital (4 mg/kg). No additional seizures have occurred since initiation of phenobarbital therapy. As of the submission of this abstract, a surgical venture for diagnosis and potential therapy is being planned.

While it may not be uncommon for an animal with severe intracranial pathology to appear outwardly normal ², we believe this case is interesting both in the clinical presentation, as well as the diagnostic approach. To the best of our knowledge, this is the first time an antemortem diagnosis of gross, intracranial, structural pathology has been reported in this species.

References

1.  Haulena M, Gulland FM. 2001 Use of medetomidine-zolazepam-tiletamine with and without atipamezole reversal to immobilize captive California sea lions. J Wildl Dis. Jul; 37(3): 566-73.

2.  McKnight CA, Haulena M, Gulland FM, Reynolds TL. 2003. Hemi-cerebral agenesis in a stranded pacific harbor seal (Phoca vitulina richardsi). Proc. of the International Assoc. for Aquatic Animal Medicine: 34th Annual Conference. May 9-14, Waikoloa, HI; 166-67.