Lessons from a Case of Capture Myopathy in a Pelagic Silky Shark (Carcharhinus falciformis)
American Association of Zoo Veterinarians Conference 2003
Natalie D. Mylniczenko1, DVM, MS; Michael Kinsel1, DVM, DACVP; Forrest Young3; Rachel Wilborn1
1John G. Shedd Aquarium, Chicago, IL, USA; 2Zoological Pathology Program, Loyola University Medical Center, University of Illinois, Maywood, IL, USA; 3Dynasty Marine Associates, Inc., Gulf, Marathon, FL, USA


Public aquaria and zoos have historically had difficulty maintaining elasmobranchs, particularly pelagic sharks. This difficulty is often attributed to “poor acclimatization.” Numerous factors play a part in this poor adaptation to captivity: transportation, exhibit design, lack of established normal biologic parameters in husbandry and medicine, and poor medical databases of diseases and treatments. Additionally, these animals may begin disadvantaged due to capture stress and possibly capture myopathy (CM). A case of exertional myopathy in a silky shark (Carcharhinus plumbeus) and the critical care and treatment options pursued is described.

Case Report

In summer 2002, a 5.56-kg, juvenile, female pelagic silky shark was caught by hook and line with gear designed to ensure a brief capture with minimal stress. The animal was immediately put into a circular live well (within five minutes of initial contact time with capture gear) and transported to a local holding facility. The animal had adjusted well to captivity and remained at the facility for five months. There was no additional handling of the animal because the basic philosophy of the capture group is to minimize handling and intervention. The animal was apparently healthy prior to shipment. After a four-day fast, the animal was transported in a semi-truck fashioned with a specialized fiberglass tank and an oxygenated filtration system.13 Ammonia, pH, dissolved oxygen, and temperature were repeatedly evaluated during the transport and stayed within acceptable ranges. Total transport time was 36 hours; anticipated transport time was 24 hours but due to vehicle mechanical problems, was delayed.

On arrival at the Shedd Aquarium, the animal was assessed in the transport container and deemed normal. Transport water quality was also normal. Due to the fractious nature of pelagic sharks and the lengthy transport event, the animal was anesthetized (to reduce further capture stress) in the transport container with 100 ppm tricaine methane sulfonate (MS222, Argent Chemical Laboratories, Inc., Redmond, WA) then moved to a maintenance dose of 50 ppm. The anesthetic was buffered with an equal weight of sodium bicarbonate (Dwight and Church, Co., Princeton, NJ). Induction was approximately six minutes in duration and uneventful. A physical exam (PE) was performed, morphometric measurements taken, and blood was collected.

Nothing unusual was found on PE except for myosis of the left eye secondary to trauma sustained during shipment. A water pump attached to an oxygen source was placed in the oral cavity. Standard blood processing for elasmobranchs at the aquarium includes i-STAT (cartridges EC8+ and EC7+, Heska Corporation, Fort Collins, CO), blood culture, CBC, and serum chemistries (IDEXX laboratories, Elmhurst, IL). Total anesthesia time was 13 minutes and recovery was normal in the animal’s quarantine tank by 20 minutes after initial contact with anesthetic. At this time blood gas parameters were considered normal in comparison to in-house data from black tip reef sharks (Carcharhinus melanopterus), another pelagic species.

At nine hours post-arrival, an abnormal, wobbly swimming gait was noted, and the shark would not maintain a normal swim-glide pattern despite being housed in a tank appropriately designed for the animal.

At 16 hours the shark’s swimming slowed and it began bumping into the tank walls. A mild water current was noticed in the tank and flow rate was decreased but resulted in no improvement. The patient was removed from the exhibit for supportive care and blood gas assessment under 50 ppm buffered MS-222. Capture stress and myopathy were strongly suspected. Blood gas analysis indicated a slight metabolic acidosis (compared to entry values) and decreased oxygen saturation. Hematocrit indicated anemia. Supportive treatment was initiated. A 150 ml bolus of 0.9% NaCl (Baxter Health Care Corporation, Deerfield, IL) with 40 mg sodium acetate (anhydrous, Fisher Biotec, Fairland, NJ) and 5% dextrose (50%, Burns Veterinary Supply, Westbury, NY) added, and 3 mg/kg sodium prednisolone succinate (500 mg, Pharmacia and Upjohn, Kalamazoo, MI) were given intravenously; 30 mg/kg ceftazidime (Fortraz, 100 mg/ml, Glaxo, RTP, NC), and 2 IU vitamin E (Compounded as vitamin ND/Eat Martin Ave Pharmacy, Naperville, IL) were given intramuscularly. Normal cardiac contractility and heart rate (70 beats/min) were noted with cardiac ultrasound. Recovery was rapid and the shark was re-released to the enclosure.

At 18 hours the shark was unresponsive to her environment, had postural abnormalities (tail down) and appeared ataxic. Additional critical care was initiated. There was no resistance to restraint, and anesthesia was unnecessary. Cardiac ultrasonography revealed poor contractility and bradycardia. Repeat blood gas analysis and ionized calcium were monitored. Acidosis progressed, ionized calcium fell, and oxygen saturation was reduced despite oxygenated water flow over the gills. Treatments over a three-hour period included repetitive doses of 0.1 mg/kg IV calcium gluconate (10%, American Regent Labs, Inc., Shirley, NY) administered slowly, 1 mEq/ml IV sodium bicarbonate (8.4%, American Regent Labs, Inc., Shirley, NY), 0.1 mg/kg IV atropine sulfate L.A. (15 mg/ml Neogen Corporation, Lexington, KY), and 20 ml/kg IV hetastarch (6% in 0.9% NaCl, Abbott Laboratories) mixed with additional IV fluids.

Response to treatment in the first hour was initially positive. Blood gas values improved, calcium increased, heart rate increased, and contractility improved. The shark began exhibiting swimming motion and an increased awareness of her environment. Despite initial stabilization, the patient ceased all independent swimming behavior by the second hour of supportive care and continued to decline over the next two hours. Cardiac arrhythmias ensued, pH continued to drop, and oxygen saturation could no longer be maintained. Euthanasia was elected. Serial bloodwork (Table 1) was obtained.

Table 1. Select blood chemistry values for (Carcharhinus falciformis) with capture myopathy




16-hours post














Ca (mg/di)




K (mEq/L)





A complete necropsy examination was performed. There were no gross lesions. Histologically, there was moderate, multifocal ventricular myocardial contraction band necrosis, and mild, multifocal rhabdomyolysis of skeletal muscle. Additional incidental lesions were mild, multifocal, lymphocytic meningitis and minimal lymphocytic perivascular cuffing in the olfactory bulb. The final diagnosis was exertional rhabdomyolysis.


Rhabdomyolysis was probably a function of stress and overexertion during confinement in-transit and was exacerbated by conditions in the holding tank. Despite novel transport techniques13,14 and efforts to provide the correct environment, the mild current in the tank likely resulted in additional exertional effort by an already compromised individual, as the shark persistently swam against the current, perhaps in an effort to increase exposure to oxygenated water. The tank design lent itself to a swim/glide pattern, but the shark never established this pattern, critical for a normal ‘rest’ phase in the swimming cycle.

Marked increases in CPK and LDH were present at the time of entry, indicating myocellular necrosis had occurred prior to arrival at the aquarium. Only mild skeletal muscle necrosis was noted histologically, possibly a function of sampling, as lesions with rhabdomyolysis can be sporadic in distribution. Muscle enzyme levels were indicative of moderate skeletal muscle damage and thought to be higher than would have been expected from myocardial necrosis alone. Notably, cardiac contractility and heart rate declined during clinical course, and myocardial necrosis secondary to physiologic stress, acidosis, and possibly anoxia could have been a secondary sequela of rhabdomyolysis, though cardiac necrosis as a primary lesion of capture myopathy has been described.

Transporting pelagic sharks is a difficult process and until recently16 rarely resulted in long-term survival post-transport. Silky sharks have been successfully shipped on long-term (>24 hour) transports.14 Nevertheless, as in this case, unforeseen incidents such as equipment failure and obstacles encountered in travel can prolong an already stressful event. Further, many pelagic sharks are fractious in nature which may predispose them to capture myopathy.

Myopathy in elasmobranchs likely occurs more often than previously documented or recognized. This is due largely to the lack of biochemical or necropsy data on captive animals that succumb to ‘poor adaptability.’ At Shedd, clinically inapparent and mild myopathies during short transports between exhibits have been observed, evidenced by moderate elevations of LDH and CPK, as well as prolonged recovery from anesthesia, when compared to less agitated conspecifics.

Diagnostics for Antemortem Evaluation of Capture Myopathy in Elasmobranchs

Shark muscle is comprised of a predominant white portion and a smaller amount of red muscle for bursts of activity. While most muscle uses aerobic glycolysis, shark white muscle predominantly uses anaerobic glycolysis, which means local lactic acid production is higher than in other species.1 In elasmobranchs, lactate dehydrogenase (LDH) and creatinine phosphokinase (CPK) are the enzymes known to seep into the bloodstream in muscle necrosis1 and, thus, are the key enzymes required for antemortem diagnosis of rhabdomyolysis. The published normal values for LDH are no higher than 263 IU/L, comparable to other species.5,6,10 However, limited data precludes determination of levels of prognostic value for recovery or demise. At Shedd, routine use of the i-STAT lactate cartridge in normal animals has recently been implemented with the hope that this will assist with tank-side assessment of elasmobranchs pre, during, and post-shipment. For all elasmobranchs, pre-shipment bloodwork, in-transit tank-side monitoring, and follow-up bloodwork upon arrival are strongly encouraged. Bloodwork should at a minimum include blood-gas analysis, and serum LDH and CPK.


Treatment should be targeted symptomatically. Acidosis occurs frequently when elasmobranchs are handled. Correction of acidosis should be attempted when values drop rapidly; however, it should be noted that most fish that develop mild acidosis resolve spontaneously.12 In CM, hypoxia and shock (hypovolemia) are the most critical conditions to correct. Fluid therapy is essential, but caution must be used with fluids in saltwater elasmobranchs due to the high blood osmolality (secondary to greatly elevated blood urea nitrogen); in this report we used a modified sodium chloride solution and there is an ‘elasmobranch Ringer’s’ recipe available.4 Intravenous calcium supplementation produced favorable clinical responses in critical animals at the Aquarium. Muscle pain is inevitable and use of anti-inflammatories and analgesics could be contemplated. There are no published doses for analgesia in elasmobranchs so, again, caution must be exercised. Steroids are of questionable efficacy but are often used in critical situations. At doses described in this text, there have been no adverse effects. Antioxidants may be useful and are usually not harmful; 0.1 ml/kg IM vitamin A/DIE has been used at the Aquarium without adverse effects, although efficacy in exertional myopathies has been questioned.9,11

Preventive Recommendations

  • During initial capture, ensure all gear is suitable for rapid placement into a stable holding facility; minimize any handling prior to final shipment.
  • Decrease stress before, during and after shipment.
    • Chemically: (1) anesthesia decreases the stress of handling during processing but carries its own risks in compromised individuals. (2) psychotropic drugs are of potential interest in transporting elasmobranchs (azaperone, zuclopenthixol).2,7,8
      Diazepam (1 mg/kg PO) has been used as a premedication at the Aquarium.
    • Behaviorally: condition sharks to transport by desensitizing them over time to nets, capture, and actual transport if possible.
  • Use well-trained staff that can rapidly and safely capture animals.
  • Maintain an oxygenated water pump at all times during transport and handling.
  • Keep out-of-water time minimal; air-exposed, exercised fishes show greater mortality rates.3
  • Use appropriate containers.13
  • Fast animals prior to transport to avoid poor water quality.
  • Once an animal undergoes a stress event, avoid moves/transport for three weeks.
  • Consider antioxidant therapy (vitamin E/selenium, vitamin A).


Special thanks to Dynasty Marine, Inc. associates Angus Barnhart, Ben Daughtry, Heath Laetari, and Cory Walter for their diligent and thoughtful work in improving safe transport of pelagic sharks and their continued dedication to ensure post-transport adaptability of these animals. Many thanks to the Aquarium Collections staff at the John G. Shedd Aquarium for their dedication to the elasmobranchs in their care and their proactive endeavors to maintain healthy sharks at the Aquarium.

Literature Cited

1.  Bone Q. Muscular system: microscopic anatomy, physiology, and biochemistry of elasmobranch muscle fibers. In: Hamlett, WC, ed. Sharks, Skates, and Rays. 1999:115–144.

2.  Caulkett MR, McCallister NA. Use of zuclopenthixol acetate to decrease handling stress in wapiti (Cervus elaphus). In: Proceedings from the American Association of Zoo Veterinarians. 2000:115.

3.  Ferguson RA, Tufts BL. Physiological effects of brief air exposure in exhaustively exercised rainbow trout (Oncorhynchus mykiss): implications for “catch and release” fisheries. Can J Fish Aquat Sci. 1992;49:1157–1162.

4.  Greenwell MG, Sherill J, Clayton LA. Osmoregulation in fish: mechanisms and clinical implications. In: Hernandez-Divers, SM and Hernandez-Divers, SJ, eds. Internal Medicine. VCNA. January: 2003:169–190.

5.  Harms C, Ross T, Segars A. Plasma biochemistry reference values of wild bonnethead sharks, Sphyrna tiburo. Vet Clin Pathol. 2002;31(3):111–115.

6.  Jones RT, Andrews JC. Hematologic and serum chemical effects of simulated transport on sandbar sharks, Carcharhinus plumbeus. J Aquar Aquatic Sci. 1999:5(4).

7.  Latas PJ. The use of azaperone in the spiny dogfish (Squalus acanthias). In: Proceedings from the International Association of Aquatic Animal Medicine. 1987.

8.  Read MR, McCorkell RB. Use of azaperone and zuclopenthixol acetate to facilitate translocation of white-tailed deer (Odocoileus virginianus). J Zoo Wild Med. 2002;33(2):163–165.

9.  Spraker TR. Stress and capture myopathy in artiodactylids. In: Fowler ME. Zoo and Wild Animal Medicine. WB Saunders Company; 1993:481–488.

10.  Stoskopf MK. Clinical pathology of sharks, skates, and rays. In: Stoskopf MK, ed. Fish Medicine. WB Saunders; 1993:754–757.

11.  Williams ES, Thome ET. Exertional myopathy (capture myopathy). In: Fairbrother A, Locke LN, Hoff GL, eds. Noninfectious Diseases of Wildlife. Ames, IA: Iowa State University Press; 1996:181–192

12.  Wood CM, Turner JD, Graham MS. Why do fish die after exercise? J Fish Biol. 1983;22:189–201.

13.  Young FA, Kajiura SM, Visser GJ, Correia JPS, Smith MFL. Notes on the long-term transport of the scalloped hammerhead shark (Sphyrna lewini). Zoo Biol. 2002;21:243–251.

14.  Young FA, Powell DC, Lerner R. Long-Distance Transportation of the Silky Shark, Carcharhinus falciformis, Poster Session. In: Proceedings from the American Elasmobranch Society; 2000:Session 959.


Speaker Information
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Natalie D. Mylniczenko, DVM, MS
Lincoln Park Zoo
Chicago, IL, USA

John G. Shedd Aquarium
Chicago, IL, USA

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