Abstract

On February 17, 2003, a young female juvenile sea otter, "Venus", was rescued from mud flats in Seward, Alaska. She was estimated to be approximately 4-6 months of age and a physical exam revealed her to be weak, lethargic, disoriented and dehydrated. Her coat was in poor condition and contaminated with mud. Her initial blood work revealed a profile of a sea otter that has not eaten recently, which included a mildly low glucose and an increased PCV/TS. WBC, serum chemistries and electrolytes were all within normal limits, with the exception of a slightly increased LDH. Radiographs of the chest and abdomen did not reveal any abnormalities. Signs of weakness were attributed to the low glucose and the initial plan was to initiate supportive care with fluids, glucose, vitamins, anti-ulcer medication, food and warm water baths to decontaminate fur and instigate grooming behavior. Video monitoring via infrared camera was set up in her enclosure and she was monitored hourly throughout the night. Serology for Morbillivirus, Leptospirosis, Toxoplasmosis, Sarcocystis and Seal Herpes Type 1 were sent out for analysis.

The first time food was offered, the otter did not seem to visualize the food. When food was placed on her nose, she began to eat ravenously. She appeared to visualize the food intermittently during feeds. She was placed in baths with warm non-chlorinated fresh water mixed with salt water twice daily. At times, she appeared uncoordinated and disoriented with daily efforts, such as eating, grooming and swimming. Caretakers reported episodes of severe aggression, dementia and hyper responsiveness, as well as periods of lethargy and unresponsiveness, along with episodes of normal behavior. Antibiotic therapy was instituted to treat a possible bacterial meningoencephalitis. Her appetite remained essentially normal and she was consuming between 29-32% of her body weight daily. Three days after she arrived, she began to have mild seizure like episodes. Full blood panels were repeated several times and all results were within normal ranges. Serology results for Sarcocystis revealed a weak positive titer. Treatment for a possible protozoal encephalopathy was started with diclazuril. Seizures and neurological behaviors progressed despite treatments. Blood was analyzed for heavy metal levels and liver was tested to assess function, both of which appeared within normal ranges.

Venus was found dead on the morning of March 10th and a full necropsy was performed. Gross necropsy revealed congested lungs, parasites in the GI tract, mild congestion of the kidneys, jejunum, and bladder and a significant cystic swelling at the base of the cerebrum on the left side. Histopathology described significant lesions that included porencephaly of the pyriform lobe, meningitis of the spinal cord, pulmonary edema, organ congestion and drainage of acute and subacute hemorrhage form the right sublumbar lymph node. Considering the history, the most likely cause of death was continued seizure activity leading to hyperthermia and pulmonary edema, along with organ congestion.

Differential diagnosis of seizures and altered mentation should include: extra cranial causes such as metabolic abnormalities, toxicities and nutritional deficiency; intra cranial causes can include degenerative disease, neoplasia, infectious disease, inflammatory, immune-mediated, idiopathic, trauma, vascular disorders, and congenital and familial disorders. Malformation of the CNS is common in domestic animals. The malformation in this animal is most consistent with porencephaly, which is characterized by cystic cavities in the cerebral cortex. The cavities can communicate with the lateral, ventricle or subarachnoid space. They can be bilateral, multiple or individual cavities, and focal lesions most often affect the temporal lobe. Many malformations remain unexplained, although most are caused by heredity or intrauterine exposure to infectious agents and teratogens. Most common causes of infectious agent exposure are less likely in this case. Most likely, this is a sporadic developmental defect.

Acknowledgements

Special thanks goes to Dr. Kathy Burek, who provided the histopathology review and pictures on this case. Also, thanks to Tim Lebling, Millie Gray and the ASLC Rescue and Rehabilitation staff, interns and volunteers for their many hours spent for the care of this animal.