Captive Environmental Conditions Disrupt Reproduction and Effect Mortality in Dungeness Crab, Cancer magister
IAAAM Archive
Jamie D. Thomton1; Shannon Atkinson1; Sherry Tamone2; Pam Tuomi3
1University of Alaska Fairbanks, Fairbanks, AK, USA and Alaska SeaLife Center, Seward, AK, USA; 2University of Alaska Southeast, Juneau, AK, USA and University of Alaska Fairbanks, Fairbanks, AK, USA; 3Alaska SeaLife Center, Seward, AK, USA

Abstract

On July 23, 2003, 73 adult female Dungeness crabs were collected from Port Frederick, Alaska and transported to the Alaska SeaLife Center, in Seward, Alaska to facilitate a captive molting and reproductive biology study. The research objective was to extract hemolymph monthly from captive female crabs during an annual growth and reproductive cycle. Subsequently, concentrations of the molting hormone, ecdysteroid, and reproductive protein, vitellogenin, were quantified via ELISA and SDS-PAGE techniques respectively.

In Alaskan waters, Dungeness crabs predominantly inhabit protected inshore habitats with frequent exposure to temperature and salinity fluctuations. The currently accepted reproductive cycle of Alaskan Dungeness crabs maintains that females molt and mate during summer months, extrude their eggs with simultaneous fertilization to the abdominal pleopods in the fall, and incubate eggs through the winter until larval hatching in May/June.1,2,4

The crabs collected for this study were maintained in three individual 500 gallon flow-through tanks. Monthly hemolymph samples were withdrawn throughout a molting and/or extrusion cycle. Extrusion of eggs in Alaskan Dungeness crabs typically occurs between September and November.5 Captive crabs began to extrude eggs on September 8th with 29% of the crabs spawning by October 9th, after which all egg extrusion ceased. Coincidently, on September 23rd the incoming seawater temperature began to fluctuate between 7° and 12°C due to unusual oceanographic conditions in Resurrection Bay and continued until October 9th. During this time, crab extrusions ceased and significant crab mortality began. Between September 23rd and October 29th, 25% of the crabs died; 61% of these crabs had developed ovaries ready for egg extrusion. It appeared that an unspecified physiological stress interrupted extrusion and precipitated death. In November an additional 15% died; 91% of these crabs had mature ovaries but failed to extrude, the other 9% had extruded successfully the previous month yet still died. Another 15% died during December; 55% had developed ovaries, 27% had extruded eggs, and 18% had immature ovaries. In brief, there was an increase in autotomy of appendages during this period, vitellogenin discolored hemolymph in the absence of extrusion (due to egg resorption), and significant mortality, predominantly in the non-ovigerous female group.

Hemolymph samples from two crab mortalities were analyzed at the Veterinary Medical Teaching Hospital, University of California, Davis; no organisms were detected on the direct smear, no growth or anaerobes observed in the culture, and the fungal culture was negative.

Tissues collected from freshly dead crabs were analyzed at the Alaska Department of Fish and Game Pathology Laboratory. No systemic pathogens were reported. Hematopoietic tissues had a high frequency of mitotic figures and pyknotic cells suggestive of abnormal mitoses, and indicative of physiological stress. Colonies of bacterial rods were also present in autolytic skeletal muscle and clotted hemolymph, most likely due to necrosis of autotomized appendages.

Crabs continued to die in the following eight months at a much slower rate of 2% per month. Shell disease caused by chitinolytic bacteria became predominant in the remaining crabs, which is a common outcome of chronic physiological stress.3 Ultimately, shell disease became systemic and resulted in severely diseased crabs. In summary, 52 of the original 73 females died over 11 months due to physiological stress induced by captive environmental conditions; the remaining 21 shell diseased crabs became moribund and were euthanized for necropsy.

Acknowledgements

The authors are grateful to the aquarium and research departments at the Alaska SeaLife Center for husbandry and research assistance. The University of Alaska Fairbanks Foundation funded this project.

References

1.  Jaffe LA, CF Nyblade, RB Forward, SD Sulkin. 1987. Reproduction and development of marine invertebrates of the northern Pacific coast. Data and methods for the study of eggs, embryos and larvae. In: M. F. Strathmann (eds.). Phylum or subphylum Crustacea, class Malacostraca, order Decapoda, Brachyura. University of Washington Press. Pp. 451-465.

2.  Scheding K, TC Shirley, CE O'Clair, SJ Taggart. 2001. Critical habitat for ovigerous Dungeness crabs. Spatial Processes and Management of Marine Populations, 17th Lowell Wakefield Fisheries Symposium. Fairbanks, AK. 431-455.

3.  Sindermann CJ, A Rosenfield. 1967. Principal diseases of commercially important bivalve Mollusca and marine Crustacea. Fishery Bulletin. 66: 335-385.

4.  Stone RP, CE O'Clair. 2001. Seasonal movements and distribution of Dungeness crabs Cancer magister in a glacial southeastern Alaska estuary. Marine Ecology Progress Series. 214: 167-176.

5.  Swiney KM, TC Shirley. 2001. Gonad development of southeastern Alaskan Dungeness Crab, Cancer magister, under laboratory conditions. Journal of Crustacean Biology. 21: 897-904.

Speaker Information
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Jamie D. Thomton


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