Abstract
Marine mammals in the United States that are deemed non-releasable due to physical or behavioral issues may be permanently placed in a public display or research facility by the National Marine Fisheries Service.1 One hundred seventy-one California sea lions (Zalophus californianus; CSL) placed in a managed care facility between January 2000 and December 2016 were included in a study investigating clinical outcomes. A survey requesting information about neurologic signs, diagnostic imaging, treatment, and disposition was sent to 60 U.S. holding institutions, and full medical and pathology records were reviewed for animals exhibiting neurologic signs or death.
A total of 25 neurologic cases (15% of all cases) exhibited clinical signs or abnormal behavior during the study period. Of those 25 cases, fourteen developed neurologic signs after placement. Animals that stranded as neonates comprised 44% of the neurologic cases (n=11), though they comprised only 27% of total cases. Of the 171 animals, 26 (15%) were deceased at the time of the study. A perimortem seizure without evidence of conclusive neurologic disease (n=7) and acute, unexplained death (n=5) accounted for 46% of deaths. Fourteen of the neurologic cases (56%) died. Nine of these cases either experienced chronic seizures, sudden death following a seizure, or perimortem illness with neurologic signs. None of the nine cases had any significant findings in the brain or meninges on histopathology.
Neurologic disease appears to play an important role in non-releasable CSLs. The most common cause of acute neurologic signs in CSLs undergoing rehabilitation is domoic acid (DA) toxicosis.2,3 Because neonate CSLs have been linked with known DA dams, and because previous studies have shown that animals with chronic DA show minimal or no typical DA-related lesions in the hippocampus,4 further systematic investigation is required to understand the role that DA plays in non-releasable CSLs.
Clinicians should strive to characterize neurologic changes with MRI for any animals that develop neurologic signs after placement. Animals that die unexpectedly should receive an MRI within 48 hours postmortem.5 Histopathologic evaluation of the brain, in particular the hippocampus, not only provides information about disease in the individual animal, but also helps to answer questions about how DA affects the CSL brain.6 Multi-institutional collaboration is vital to improve patient care and further knowledge of marine mammal neurologic disease.
Acknowledgements
The authors wish to thank the 60 institutions caring for sea lions in the United States that participated in the study, as well as all of the organizations within the Marine Mammal Health and Stranding Response Program that rescue and rehabilitate marine mammals across the country.
* Presenting author
Literature Cited
1. Protected Resources Management Marine Mammal Health and Stranding Response Program. 2012. NMFS Placement Process for Non-releasable Marine Mammals. National Marine Fisheries Service Instruction 02-308-02, 9 pp.
2. Greig D, Gulland F, Kreuder C. 2005. A decade of live California sea lion (Zalophus californianus) strandings along the central California coast: causes and trends, 1991–2000. Aquat Mamm. 31(1):11–22.
3. Simeone CA, Gulland FMD, Norris T, Rowles TK. 2015. A systematic review of changes in marine mammal health in North America, 1972–2012: the need for a novel integrated approach. PLoS One. 10(11):e0142105. doi:10.1371/journal.pone.0142105.
4. Goldstein T, Mazet JAK, Zabka TS, Langlois G, et al. 2008. Novel symptomatology and changing of domoic acid toxicosis in California sea lions (Zalophus californianus): an increasing risk to marine mammal health. Proc Royal Soc B: Biol Sci. 1632:267–276.
5. Montie E, Wheeler E, Pussini N, Battey TWK, et al. 2010. Magnetic resonance imaging quality and volumes of brain structures from live and postmortem imaging of California sea lions with clinical signs of domoic acid toxicosis. Dis Aquat Organ. 91:243–256.
6. Buckmaster PS, Wen X, Toyoda I, Gulland FMD, Van Bonn W. 2014. Hippocampal neuropathology of domoic acid-induced epilepsy in California sea lions (Zalophus californianus). J Comp Neurol. 522(7):1691–1706.