Hepatopathy in a Captive Black Sea Bottlenose Dolphin with Mixed Bacterial and Fungal Infection: Case Report
IAAAM 2009
Vasily V. Romanov; Maria B. Chelysheva
Utrish Dolphinarium Ltd, Moscow, Russian Federation

Abstract

Hepatic disorders are fairly common in marine mammals.1,3,7 Cetaceans kept in captivity frequently experience asymptomatic or mildly, symptomatic hepato-biliary disorders associated with a variety of underlying causes such as reactions to hepatotoxic medications, unbalanced diets, fluctuations in water quality, etc. Removal or correction of these factors in most cases leads to normalization of liver function as evidenced by a return to normal serum chemistry indices. Severe, life-threatening hepatopathies appear to be less frequent. The etiology of these conditions often remains unknown even after autopsy.2,5 The present communication focuses on a case of severe hepatopathy which developed in a Black Sea bottlenose dolphin (Tursiops truncatus ponticus Barabash-Nikiforov, 1940) with mixed bacterial and fungal infection.

The seven-year-old male bottlenose dolphin, captured in 2001 in the Taman Gulf of the Black Sea, was successfully kept for 5 years in pools with chlorinated sea water in different facilities of the Utrish Dolphinarium Ltd. Over this period, there were no substantial deviations in the condition of the animal and hematological parameters were within the species reference values. In December 2007, the 170 kg dolphin showed a gradual decrease, over 4 days, in locomotion, playing, and eating. The dolphin was sluggish and depressed. The hematological examination revealed signs of an acute infectious-inflammatory process: neutrophilic leucocytosis with eosinopenia; a considerable increase in ESR; decrease in ALP activity and albumin content; and an increased level of globulins (Table 1, 5th day). The dolphin was put on amikacin (14 mg/kg IM SID) with ceftriaxone (20 mg/kg IM SID) and rehydration therapy (5% dextrose and half-strength Rehydron solution through the stomach tube).

Despite therapy, the dolphin's condition progressively deteriorated over the week and became critical by day 9. Sluggishness and adynamia progressed in combination with total anorexia and severe weight loss. Tachypnea, hypopnea, and signs of hemorrhagic diathesis appeared. Hematological studies revealed marked elevations in serum ALT, AST, GGT, total and direct bilirubin content as well as pronounced thrombocytopenia (Table 1; 9th and 11th days) indicating disease progression. Based on culture sensitivities of bacteria isolated from the blowhole (Pseudomonas aeruginosa and Staphylococcus aureus), the antibiotics were changed to impinem (11.7 mg/kg IM BID). In addition, the dolphin was put on a 5 day course of decreasing doses of dexamethasone, beginning at 0.12 mg/kg, and vitamin K (0.5 mg/kg SID) supplementation. Within 6 hours after steroid administration, the dolphin showed some minor improvement in locomotor activity and responsiveness to the presence of personnel. In the following 2 hours, the animal showed minor interest in food.

In the subsequent week, the general condition of the dolphin remained stable with a slow increase in food intake. During this period, clinical signs of hepatic dysfunction appeared including icteric mucous membranes in the mouth cavity and acholic feces. Dense, ring-like, gray-yellowish lesions with a sharp obnoxious odor were clearly visible through the opened blowhole. Cytological examination of the smears taken from the upper airways revealed pseudomycelium formed by budding yeasts. Candida spp. and Pseudomonas aeruginosa were cultured from the blowhole upon repeat microbiological examination. The results of the blood tests performed on the 16th day of clinical signs (Table 1) testified to the minimal positive dynamics of the inflammatory process indicators against the background of serious deviation of biochemical indices for liver function. Serological tests on viral hepatitis markers turned to be negative.

A strict low fat diet (hake and pollack up to 3.5 kg per day) combined with rehydration (6-9 liters of liquid per day) and vitamin therapy were administered to the animal. Amikacin (14 mg/kg IM SID) and fluconazole (2 mg/kg PO BID) were initially added to the impinem, which was subsequently dropped.

The dolphin's general condition greatly improved over the following 2 months. Behavior, appetite and physical activity returned to normal. The clinical manifestations of candidiasis disappeared within one week; icterus of the oral mucosa remained for two weeks and discolored stool for more than a month. The restoration of hematological indices lagged behind the clinical dynamics (Table 1). Gradual normalization of the inflammatory disease indicators combined with continuous increase and subsequent stabilization (at the raised levels) of biochemical parameters, characterizing hepatic function, were noted during the period of 0.5-1.5 months from the onset of clinical signs. Stepwise restoration of the liver's enzymatic activity was seen during the period of 1.5-3 months. The return of total and direct bilirubin, ALT, AST and GGT to normal values was reached by the end of third month. However, anemia and moderate deviations of the leukogram persisted for more than a year of supervised follow-up.

Concurrently, with the improvement of the animal's general condition and restoration of biochemical indices of hepatic function, the diet was changed. The amount of fish fed was slowly increased, and the composition of the ration expanded. Therapy with antibiotics continued over a period of 3.5 months and with antifungal medications for 2 months. The replacement of antibiotics and antifungal agents, selection of their optimal combinations and schemes of administration were made based upon clinical and laboratory data and sensitivity of the cultured microorganisms. Several courses of therapy with hepatoprotectors, e.g., ademetionine, were administered for 3 months during the period of liver function restoration. After completion of the described treatments, the dolphin showed clinical manifestations of nephrolithiasis for which it is receiving therapy at the present time.

The etiology of the hepatopathy in this dolphin is not completely understood. In our opinion, the most probable explanation is a secondary pathological process to a severe, mixed microbial infection. This assumption can be supported by clinical and laboratory data: 1) initially the disease developed like an acute infectious-inflammatory process with typical deviation of hematological indices and changes in the microflora of the upper airways characteristic of an acute infection; 2) results of serological tests for viral hepatitis were negative; 3) the positive dynamics of the biochemical indicators of hepatic function appeared only after the successful suppression of the bacterial-fungal infection. Such cases, normally accompanied by high mortality, are known in medical practice and described in patients with sepsis and other severe infections as "ischemic" hepatitides.4,6

Table 1. Results of hematological examinations

Parameters

Units

Time since the onset of clinical signs

Days

Months

5

9

11

16

0.5-1.5; X±m (lim); n=7

1.5-3; X±m (lim); n= 9

3-4.5; X±m (lim); n=11

RBC

1012/l

4.0

4.3

3.0

3.9

3.4 ± 0,1 (3.2-3.9)

3.3 ± 0.1 (2.9-3.6)

3.2 ± 0,1 (2.9-3.5)

Hb

g/l

157

169

119

154

134 ± 3.5 (126-153)

128 ± 1.9 (117-136)

127 ± 2.4 (113-135)

Reticulocytes

%

1.1

1.4

6.6

7.4

10.0 ± 1.2 (5.4-15.0)

7.7 ± 0.6 (5.1-10.7)

6.1 ± 0.5 (4.5-9)

ESR

mm/h

39

43

65

58

39 ± 0.6 (30-46)

35 ± 3.4 (22-48)

15 ± 1.4 (8-25)

WBC

109/l

16.9

25.6

34.8

21.5

14.3 ± 1.4 (9.1-21.5)

13.0 ± 1.2 (8.2-18.3)

12.7 ± 0.7 (8.8-15)

Neutrophils (bands)

%

2

2

0

5

0.9 ± 0.7 (0-5)

0.3 ± 0.2 (0-2)

0.4 ± 0.2 (0-2)

Neutrophils (mature)

%

71

69

67

83

83.3 ± 1,8 (76-90)

77.7 ± 1.6 (71-86)

75.6 ± 0.8 (72-80)

Eosinophils

%

4

3

7

1

1.6 ± 0.6 (0-4)

8.2 ± 1.7 (2-18)

5.7 ± 1.1 (1-10)

Lymphocytes

%

21

24

24

8

14.1 ± 2.3 (8-24)

13.0 ± 1.3 (6-17)

17.7 ± 1,3 (12-24)

Monocytes

%

2

2

2

1

0.1 ± 0.1 (0-1)

0.8 ± 0.4 (0-3)

0.7 ± 0.2 (0-2)

Platelets

109/l

88

17

61

233

384 ± 73 (168-617)

324 ± 35.3 (181-549)

233 ± 16.4 (181-318)

ALT

IU/l

28

506

740

1076

443 ± 45 (268-620)

144 ± 23.6 (58-292)

51 ± 14.6 (24-164)

AST

IU/l

230

352

852

572

1422 ± 101 (981-1784)

515 ± 87.7 (93-980)

185 ± 10.4 (87-148)

GGT

IU/l

44

112

137

204

339 ± 98.5 (113-712)

126 ± 12.6 (81-174)

51 ± 2.9 (43-71)

ALP

IU/l

266

352

562

688

750 ± 100.7 (428-1218)

412 ± 36.1 (315-660)

336 ± 28.7 (232-512)

Bilirubin total

μmol/l

5,4

133

124

172

174 ± 45.5 (22.3-340)

11,0 ± 2.5 (6.8-30.7)

7.0 ± 0,5 (5.1-10.2)

Bilirubin dir.

μmol/l

3,4

111

117

159

116.3 ± 37.1 (17-266)

5.5 ± 0.7 (3.2-10.2)

3.1 ± 0.4 (1.7-5.4)

Creatinine

μmol/l

88

53

53

44

52 ± 3.1 (44.2-62)

86 ± 7.9 (62-140)

113 ± 3.4 (97.2-132)

Glucose

mmol/l

10.1

6.9

6.3

4.95

4.6 ± 0,3 (3,6-5,4)

5,3 ± 0,24 (4,3-6,4)

4,8 ± 0,3 (3,0-6,6)

Serum proteins

g/l

67

69

72

80

78 ± 2.4 (70-87)

80 ± 0.9 (76-86)

78 ± 2,0 (68-87)

Albumins

g/l

28

37

24

40

39 ± 2.6 (25-46)

44 ± 1.2 (37-49)

43 ± 1.5 (37-52)

Globulins

g/l

39

3.2

46

40

39 ± 2.14 (32-46)

36 ± 1.2 (28-43)

35 ± 2.4 (22-50)

Sodium

mmol/l

154

152

154

158

156 ± 0.7 (155-160)

159 ± 0.4 (158-161)

159 ± 0.3 (158-161)

Potassium

mmol/l

4.7

3.4

3.6

4.2

4.1 ± 0.2 (3.3-4.7)

4.5 ± 0.1 (4.3-4.7)

4.5 ± 0.1 (4.2-4.7)

Iron

μmol/l

48.5

36.0

38.6

29.7

49.7 ± 3.5 (29.7-56.2)

48.5 ± 0.7 (44.7-51.0)

49.6 ± 1.5 (37-53)

Comments: X - mean; m - standard error; lim-limits; n-quantity of samples.

References

1.  Bossart G.D., T.H. Reidarson, L.A. Dierauf, and D.A. Duffield. 2001. Clinical pathology. In: L.A. Dierauf and F.M.D. Gulland (eds). CRC Handbook of Marine Mammal Medicine, 2nd edition. Boca Raton, FL: CRC Press; Pp. 383-436.

2.  Gage L.J. 1991. Medical management of liver disease in a captive dolphin and a wild porpoise. Abstr Proc Int Assoc Aquat Anim Med; Pp. 23-24.

3.  Gulland F.M.D., L.J. Lowenstine, and T.R. Spraker. 2001. Noninfectious diseases. In: L.A. Dierauf and F.M.D. Gulland (eds). CRC Handbook of Marine Mammal Medicine, 2nd edition. Boca Raton, FL: CRC Press; Pp. 521-547.

4.  Hickman P.E., and J.M. Potter. 1990. Mortality associated with ischaemic hepatitis. Internal Med J 20(1): 32-34.

5.  Nachbar S.G. 1996. Case report of severe hepatopathy in an Atlantic bottlenose dolphin (Tursiops truncatus). Abstr Proc Int Assoc Aquat Anim Med; Pp. 44-45.

6.  Saenko V.F., V.I. Desjaterik., T.A. Perceva, and V.V. Shapovaljuk. 2005. Sepsis i poliorgannaja nedostatochnost'. Krivoiy Rog: Mineral, 466 s. (In Russian).

7.  Venn-Watson S., C.R. Smith, and E.D. Jensen. 2008. Assessment of increased serum aminotransferases in a managed Atlantic bottlenose dolphin (Tursiops truncatus) population. J Wildl Dis 44(2): 318-330.

 

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

Maria B. Chelysheva
Utrish Dolphinarium Ltd
Moscow, Russian Federation


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