Scott G. Nachbar, DVM
Summary
A sixteen year old female Atlantic bottlenose dolphin was euthanized
following an eight week struggle to diagnose and treat a severe hepatopathy. She had been
wild-caught at approximately 3 years of age in the Gulf of Mexico and had resided at the Aquarium
of Niagara since capture. She had been generally healthy during that time. Approximately eight
months previously, this animal had shown signs of decreased appetite and elevated serum
transaminases, but had eventually responded to oral tetracycline. Routine complete blood counts,
serum chemistry profiles, and erythrocyte sedimentation rates were normal in the interim
period.
Clinical signs began with lethargy and decreased appetite, which progressed to
total anorexia, intermittent vomiting, and cachexia. Routine blood profiling revealed progressive
marked elevations of serum transaminases ALT, AST, and LDH indicating acute severe hepatocellular
damage. Associated hematologic parameters revealed elevated erythrocyte sedimentation rate and
fibrinogen, lymphopenia, and mild anemia. Total white blood cell counts were never elevated.
Prothrombin time gradually increased until bleeding was noted clinically from mild abrasions.
Vitamin K1 supplementation reversed this trend.
The following diagnostic tests were performed (with results):
Serum
Bile Acids: (87.0)
Serum
protein electrophoresis: (no monoclonal bands noted)
LDH
isoenzymes: (increased LD 4 - consistent with liver isoenzyme)
Serum
Iron profile: (One week into disease: Fe 1197 ug/dl, TIBC 1318 ug/dl, %sat 91)
(Five
weeks into disease: Fe 1500 ug/dl, TIBC 1681 ug/dl, %sat 89)
Plasma
Zinc: (1483 ug/L; Human ref range (550 - 1400))
Blood
Lead: (< 2 ug/dl)
Serum
ceruloplasmin - indicator of Copper storage disease in humans: (<2 mg/dl)
Blood
Copper: (normal)
Abdominal radiography: (non-diagnostic with field equipment used)
Abdominal ultrasonography: (no focal liver lesions, borders fairly sharp, parenchymal
echogenicity uniform)
Upper
gastric endoscopy: (no evidence of ulceration or foreign material)
Human
Hepadenavirus screen for hepatitis A, B, and C: (negative)
Serum
neutralization titer to Canine Distemper virus: (neg at 1:4)
Morbillivirus titer: (neg)
Fungal
serology: (Blastomyces, Coccidioides, Histoplasma, Aspergillus, Candida, Cryptococcus all
negative)
Trypsin-like Immunoreactivity: (2.51 ng/ml) Canine reference 5 - 25 ng/ml
Attempts to maintain hydration and decrease catabolic rate by forced
feeding or stomach tubing two to four times daily for five weeks with a mixture of fish gruel,
water, electrolyte solution, and a commercial enteral protein/carbohydrate product (TwoCal) only
helped slow the progression of emaciation.
Medications used during part or all of treatment included antibiotics
(tetracycline, cephalexin, amikacin), antifungals (itraconazole, nystatin), gastrointestinal
support (cimetidine, carafate, pink bismuth, DiGel simethicone, metoclopramide), appetite
stimulants (megesterol acetate, prednisolone, diazepam), and multiple vitamins and mineral
supplements (including folic acid, ferrous gluconate, and Vit K1).
Despite intensive efforts to support the animal and correct the liver disease,
the anorexia never resolved and weight loss became extreme (114 lbs over 8 wks, approx 30% of
normal body wt). Depression and malaise became critical when the dolphin could no longer swim to
the surface to breathe. Humane euthanasia was elected when final blood work suggested impending
septicemia. Final blood cultures revealed many and pure Shewanella putrefaciens.
Post mortem examination failed to identify an etiologic agent but revealed
vacuolar, diffuse, moderate hepatopathy, moderate biliary hyperplasia, and moderate extramedullary
hematopoiesis. Lymphoid depletion; chronic, non-ulcerative, multifocal gastroenteritis; chronic,
multifocal interstitial pneumonia; and mild to moderate generalized inflammation were also
reported. Virus isolation attempts from frozen tissue samples were unrewarding. Bacterial culture
from liver tissue revealed Shewanella efaciens and Vibrio fluviafis.