Electroencephalographic Findings Associated with Domoic Acid Poisoning in California Sea Lions
IAAAM Archive
D. Colette Williams1; Martin Haulena2; Sophie Dennison2; Kenneth D. Laxer3; Barry Tharp4; Tracey Goldstein2; Frances M.D. Gulland2
1Veterinary Medical Teaching Hospital University of California-Davis, Davis, CA, USA; 2The Marine Mammal Center, Sausalito, CA, USA; 3Pacific Epilepsy Program, California Pacific Medical Center, San Francisco, CA, USA; 4MIND Institute, University of California (Davis) Medical Center, Sacramento, CA, USA


Strandings of California sea lions (Zalophus californianus) associated with harmful algal blooms have been increasingly reported over the last decade. Strandings were due to toxicosis with domoic acid, produced by a number of diatoms including Psuedo-nitzschia australis, that is transferred to sea lions through a fish vector. Clinical signs associated in acute mortality events of sea lions include seizures and ataxia. Since 2000, sea lions have been observed with other clinical signs including loss of appetite, aggression, abnormal behavior and intermittent seizures that are suspected as resulting from previous domoic acid exposure.

Between August 2004 and November 2005, electroencephalograms (EEGs) were performed on 24 animals suspected of surviving previous domoic acid poisoning and 6 control animals which presented to The Marine Mammal Center for other reasons (e.g., trauma). For this procedure sea lions were sedated with medetomidine at 0.07 mg/kg, given intramuscularly (IM). In the initial studies, butorphanol (0.1 mg/kg, IM) was also given but was discontinued due to muscle fasciculations in some animals. Fifteen EEG, 4 EOG, 2 EKG and a ground electrode were placed for each recording. Placement of electrodes was based on a standard canine diagnostic system. Recording lengths varied, depending on patient cooperation and time constraints, with a minimum duration of 10 minutes. All but two of the suspect domoic acid cases received at least one course of anticonvulsant treatment (Phenobarbital 2 mg/kg PO BID) prior to recordings. These ranged from a single dose in one case to 23 days in another. Four animals had repeat EEGs at least one week after the initial recording took place.

Epileptiform activity, consisting of spikes, sharp waves and spike-and-waves, was noted in EEGs obtained from sea lions suspected of previous exposure to domoic acid. These events were generalized and multifocal in most patients, though in a few cases, were more prominent in one hemisphere. No such changes were observed in the EEGs recorded from control animals.

These findings are supportive of a diagnosis of secondary epilepsy as the result of domoic acid exposure in these California sea lions.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Colette Williams

MAIN : Clinical Advances II : Domoic Acid Poisoning
Powered By VIN