Gas Embolism-Associated Mortality in Captive Chinese (Andrias davidianus) and Japanese (Andrias japonicus) Giant Salamanders
American Association of Zoo Veterinarians Conference 2002
Kenneth N. Cameron1, DVM; Michael M. Garner2, DVM, DACVP; Mark K. Campbell1, DVM; Katherine L. Duffey3†, BS
1Veterinary Services Department and 3Herpetology Department, Cincinnati Zoo and Botanical Garden, Cincinnati, OH, USA; 2Northwest ZooPath, Snohomish, WA, USA; Current Address: Herpetology Department, Cleveland Metroparks Zoo, Cleveland, OH, USA


The aquatic salamanders of the suborder Cryptobranchoidea occur in both North America (genus Cryptobranchus) and Asia (genus Andrias). The Japanese giant salamander (Andrias japonicus) and the Chinese giant salamander (Andrias davidianus) are the largest salamander species, reaching a length of up to 144 cm (A. japonicus) to 152 cm (A. davidianus), and are among the longest-lived.4 Three animals (two A. japonicus and one A. davidianus) held at the Cincinnati Zoo and Botanical Garden became ill and died within a 40-day period. Though multiple factors were found to be involved, the cause of death was attributed to gas embolism.

Animals of both species were housed in a shared closed filtration system, consisting of four large, insulated fiberglass tanks linked in series by polyvinylchloride (PVC) pipes. Biologic filtration was provided by under-gravel filters in each tank, a single sand filter, and a carbon filter. The pump produced a pressure gradient of 25–30 psi between suction and discharge sides of the system. Water return to tanks was carried by overhead PVC pipes to allow splash for aeration and gas dissipation.

Animals were housed individually, two per tank; each tank was divided into two chambers by a fenestrated plexiglass barrier which allowed water flow, but prevented direct physical contact between animals. Water was maintained at a depth of 18–24 inches in all tanks. Substrate consisted of 8 inches of ¼ inch pea gravel and a slate shelter was provided for each animal.

In April 2000, a 25-yr-old male A. davidianus was observed during mid-morning venturing from the safety of the shelter and roaming the tank; behaviour considered unusual by the keeper. The animal appeared somewhat agitated. Within 3 h, signs had progressed to include reddening of the skin, small bubbles or vesicles on the limbs, floating above the gravel substrate and listing to one side. Signs progressed rapidly to include axial muscle fasciculations, agonal thrashing and death. Simultaneous with this animal’s agonal behavior, and in another tank in the shared system, a 14-yr- old A. japonicus was observed floating above the gravel substrate and listing slightly. Numerous 5–10-mm diameter clear vesicles or “bubbles” covered most of the body, including torso, tail and limbs. A patchy reddening of the skin developed, the animal became lethargic and assumed a contorted ‘C-shaped’ posture. Empirical treatment with amikacin sulfate was initiated for suspected bacterial infection. Signs progressed rapidly over the next few hours; the animal became moribund, exhibited agonal thrashing, and cardiac activity ceased. Blood was collected aseptically by cardiocentesis for bacterial culture. Postmortem exams were performed on both animals.

Antibacterial treatment with amikacin sulfate was begun empirically on all remaining animals in the affected system. Water quality testing was performed and water was collected for coliform count. The sand filter was back-washed and a 50% water change performed. Initial testing indicated acceptable levels of ammonia and nitrite, but high levels of nitrate (≥100 ppt). Coliform count of system water (received the following day) was 2700 colony-forming units/100 ml, much higher than USDA limits for marine mammals.

For several days following the initial event, other animals in the affected system exhibited a variety of clinical signs, including venturing from their shelters, assuming a ‘hunched’ posture, lethargy, inappetence, and periodic ‘C-shaped’ lateral curvature of the body. These signs seemed to resolve over the following several days and animals appeared normal within eight to ten days. Forty days after the initial event, one of those animals, a 19-yr-old female A. japonicus, died with no further observed clinical signs. A postmortem examination was performed.

Aeromonas sp. was isolated from blood culture of the second animal to die. Gross postmortem findings on the first two animals included cutaneous emphysema and varying degrees of reddening, hepatopathy, congestion and hemorrhage of colonic and rectal mucosa, serosanguineous coelomic fluid, serositis, inflammation and hemorrhage within urinary bladder and discoloration of skeletal muscles, mucopurulent pulmonary fluid and renal cysts. Gross postmortem findings on the third animal which died included cutaneous reddening and emphysema, foam within the cardiac ventricle, myocardial hemorrhage and/or congestion, inflammation and hemorrhage in urinary bladder, uterine and splenic abscessation and cloudy coelomic fluid.

Histopathologic diagnoses included gas bubble disease of the liver, lung, kidney, mesentery, intestine, colon, esophagus, heart, intestine, stomach, and the urinary bladder, chronic pulmonary interstitial fibrosis and emphysema, biliary hyperplasia, hepatic fibrosis and melanosis, focal chronic cholecystitis, interstitial pancreatitis, gastric metazoan parasitosis, acute congestion of the intestine, acute renal interstitial edema, mild hepatic vacuolar change, moderate chronic nonsuppurative cholangiohepatitis, chronic gastric and intestinal congestion, and ovarian, oviductal and splenic mycobacteriosis. The cause of death was attributed to gas bubble disease, with other inflammatory findings considered incidental.

Supersaturation of water occurs when the total dissolved gas pressure exceeds the barometric pressure.2 In a captive husbandry situation, it is likely to be the result of problems with the water handling system. Air introduced by leaks into the suction side of the system can be forced into solution when the air/water mixture is pressurized,3 as occurs in the pump. Rapid changes in water temperature can also play a role.7 Dissolved gases cross the respiratory epithelium and endothelium, come out of solution in the blood, forming gas emboli.1 Gas bubbles in the skin or eyes of aquatic species are considered an indicator of supersaturation.8 Clinical signs in amphibians include dermal gas bubbles, which may coalesce, hyperemia, petechial and ecchymotic dermal hemorrhages, and gas emboli of the stomach, mesonephroi, and heart. Dermal pathology allows secondary bacterial infection, such as aeromoniasis.5

In the case reported here, dissolved oxygen levels (and presumably dissolved nitrogen levels) were ≥186% of saturation at the 13°C water temperature, much higher than the 125% nitrogen saturation levels reported to affect adult fish.6 The source of supersaturation was determined to be two-fold. A leak was discovered in the suction side of the water handling system. In addition, an animal keeper not usually associated with the care of these species had been deliberately mixing air into the system in an attempt to improve aeration. Agitation of the water column can help dissipate dissolved gases in the water.9 In this case, the “splash” provided by the overhead water return was evidently not adequate to do so. Complicating factors involved in this event included high water coliform counts, extreme indoor air and water temperature fluctuations, very high ammonia levels in the water system, and possible underlying disease processes.

Literature Cited

1.  Bouck, G.R. 1980. Etiology of gas bubble disease. Trans. Am. Fish Soc. 109:703–707.

2.  Colt, J., G.R. Bouck, L. Fidler. 1986. Review of current literature and research on gas supersaturation and gas bubble trauma. Special Publication No. 1, B.P.A. and Bioengineering Section, American Fisheries Society.

3.  Diana, S.G., V.B. Beasley, K.M. Wright. 2001. Clinical toxicology. In: Whitaker, B.R., and K.M. Wright (eds.). Amphibian Medicine and Captive Husbandry. Krieger Publishing Co., Malabar, Florida. Pp. 223–232.

4.  Duellman, W.E., and D.L. Trueb. 1994. Biology of Amphibians. The Johns Hopkins University Press, Baltimore, Maryland.

5.  Green, D. Earl. 2001. Pathology of amphibia. In: Whitaker, B.R., and K.M. Wright (eds.). Amphibian Medicine and Captive Husbandry. Krieger Publishing Co., Malabar, Florida. Pp. 401–485.

6.  Plumb, J.A. 1993. Toxicology and pharmacology of temperate freshwater fishes. In: Stoskopf, M.K. (ed.). Fish Medicine. WB Saunders Co., Philadelphia, Pennsylvania. Pp. 311–318.

7.  Tomasso, J.R., Jr. 1993. Environmental requirements and disease of temperate freshwater and estuarine fishes. In: Stoskopf, M.K. (ed.). Fish Medicine. WB Saunders Co., Philadelphia, Pennsylvania. Pp. 240–246.

8.  Whitaker, B.R., and K.M. Wright. 2001. Clinical techniques. In: Whitaker, B.R., and K.M. Wright (eds.). Amphibian Medicine and Captive Husbandry. Krieger Publishing Co., Malabar, Florida. Pp. 89–110.

9.  Wood, J.W. 1976. Disease of Pacific Salmon. (2nd ed.). Washington Department of Fisheries. Seattle, Washington.


Speaker Information
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Kenneth N. Cameron, DVM
Veterinary Services Department
Cincinnati Zoo & Botanical Garden
Cincinnati, OH, USA

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