Natalie D. Mylniczenko; Karen S. Kearns
In January 2007, a 20-year-old, captive, female, harbor seal presented with progressively decreased appetite over several days duration. Four days after onset, the animal developed episodic head tremors that progressed over 3 days to generalized body tremors and hyperesthesia. Initial physical and ultrasonographic exam findings were unremarkable; abdominal and thoracic radiography revealed no significant findings. Initial diagnostic samples included a complete blood count (CBC), serum chemistry, aerobic and anaerobic blood and fecal culture, bile acids, electrophoresis (EPH), heavy metal analysis (including lead and zinc), and trace element analysis. Clinically relevant results indicated mild inflammatory disease on the EPH. Serologic testing included: leptospirosis, brucellosis, toxoplasmosis, morbillivirus (phocid, canine, and cetacean distemper virus), phocid herpes virus, West Nile virus (WNV), and rabies virus. All tests were negative except for herpes (no change in titer from previous samples) and a marginal Toxoplasma gondii titer. Empirical oral treatments were initiated on the second day of partial anorexia and included amoxicillin with clavulanic acid, carprofen and omeprazole. The animal became completely anorectic, necessitating regular restraints. A depot ceftiofur, thiamine and vitamin B were initiated; NSAIDS and gastric protectants were continued. With no response over two days to treatment, high dose steroids were administered and antibiotics were changed to florfenicol; steroids were not repeated after the initial dose. On the third day after onset of neurologic signs, an MRI and contrast study were performed and revealed no abnormalities. A cerebrospinal fluid (CSF) sample was obtained and revealed evidence of nonsuppurative inflammatory disease; CSF cultures were negative. Repeated diagnostic samples on blood included: CBC, serum chemistries and T. gondii. Additional testing on this blood sample included: a fungal panel (coccidiomycosis, aspergillosis, histoplasmosis, blastomycosis), Sarcocystis neurona, Neospora hughesi, and N. caninum. CSF was analyzed for T. gondii, S. neurona, N. hughesi, N. caninum, WNV, equine encephalomyelitis virus, western equine encephalitis, and equine herpes virus type 1. S. neurona was diagnosed in both serum and CSF samples.
The animal was dry docked once neurologic signs were persistent. Treatment of this case relied heavily on response to medical treatment since most serologic and CSF diagnostic testing had lag times of 7-14 days. Supportive care was initiated 1 week after initial clinical signs. Due to anorexia and dysphagia, daily or twice daily restraints were instituted and included gavaging of medications and assist feedings (fish gruel then switched to whole fish). Ponazuril at 5 mg/kg PO SID and albendazole (2 doses) were started empirically by daily gavage on the fourth day after the first onset of tremors. Thiamine and vitamin E doses were increased over the animal's normal vitamin supplementation. Two days after initiation of ponazuril treatment, the animal's tremors were less exaggerated, by the third day, hyperesthesia was dramatically reduced and tremors were only observed during intentional movement. The animal improved gradually over the following week until overt cerebellar signs and tremors were no longer present, even with intentional movement. Weekly blood samples were drawn to monitor the animal. Salt supplementation was started after initiation of freshwater fluid gavaging. At the time of this report, the animal was still under treatment with ponazuril and carprofen and had improved to the point of consistently eating on her own. Severe cerebellar signs had not recurred. A repeat titer of S. neurona at two weeks post treatment indicated a rise in titer, prompting an increase in the ponazuril dose to 10 mg/kg. Ponazuril serum levels are being investigated and the long term prognosis of the seal is unknown but at this time appears to be hopeful for recovery. The source of disease is not clear, though S. neurona has been isolated in different areas at the housing institution.
Sarcocystis neurona encephalitis has been reported previously as a cause of death of free range harbor seals along the California coast1,2. Clinical signs included weakness, head tremors, and seizures2. Animals usually died shortly after hospitalization. In one report1, a captive harbor seal was diagnosed post-mortem but details of that case were omitted from the report. Ponazuril therapy has been attempted ante-mortem in harbor seals3 with suspected sarcocystosis but treatments were not successful. It is probable that free range animals that present to rehabilitation facilities have advanced disease that is less likely to respond to treatment.
The authors would like to thank the veterinary and marine mammal staffs and the Brookfield Zoo for their contributions to this case, as well as Patricia Conrad of UC Davis College of Veterinary Medicine and her laboratory staff for helping to clarify the diagnosis via serology and CSF analyses.
1. Lapointe JM, Duignan PJ, Marsh AE, Gulland FM, Barr BC, Naydan DK, King DP, Farman CA, Huntingdon KA, Lowenstine LJ. 1998. Meningoencephalitis due to a Sarcocystis neurona-like protozoan in Pacific harbor seals (Phoca vitulina richardsi) J Parasitol. Dec;84(6):1184-9.
2. Dubey JP, Zarnke R, Thomas NJ, Wong SK, Van Bonn W, Briggs M, Davis JW, Ewing R, Mense M, Kwok OC, Romand S, Thulliez P. 2003. Toxoplasma gondii, Neospora caninum, Sarcocystis neurona, and Sarcocystis canis-like infections in marine mammals. Vet Parasitol. 116(4):275-96. Erratum in: Vet Parasitol. 2006 Feb 18;135(3-4):385.
3. Haulena M. Staff Veterinarian, Vancouver Aquarium, Vancouver, British Columbia, Canada, personal communication