Abstract

Over a period of nine months, a number of jellies from a mixed species gallery at the Aquarium of the Pacific presented to the veterinary department with irregular, damaged, torn, and ulcerative lesions of the umbrellar epidermis¹ of the bell. Affected jellies were wild-caught, housed in groups by species, and included West Coast Sea Nettles (Chrysaora fuscescens), East Coast Sea Nettles (Chrysaora quinquecirrha), lagoon jellies (Mastigias papua), blubber jellies (Catostylus mosaicus), Sandaria jellies (Sandaria malayensis), moon jellies (Aurelia aurita; Aurelia labiata), and white-spotted jellies (Phyllorhiza punctata).

All jellies were kept in recirculating kreisel-type tanks with oval to round shapes and smooth Plexiglas walls containing approximately 200-800 L. Types of filtration varied between tanks and included protein skimmers and bio-towers. Water supply for the jelly exhibits consisted of natural seawater conditioned by sand and ozone filtration prior to use within the exhibit gallery. Water quality parameters (ammonia, nitrates, nitrites, salinity, pH) were checked weekly and found to be within normal limits. Jellies were fed a variety of diet items, including nauplii (brine shrimp, adult and juvenile), Aurelia aurita slurry, cyclopeeze (zooplankton derived from the copepod), blood worms, and small krill.

Physical examination was performed by isolating each jelly into a small, round, glass container of tank water and assessing lesions visually for depth and severity. We identified a range of lesions, including erosions and ulcers of the peripheral edges and dorsal surfaces of the bell, and full-thickness tears of the bell with secondary internal organ herniation. Jellies with severe "bell rot" and/or herniation were culled and euthanized by hypothermia (placement into a refrigerated container at approximately 5°C). Jellies with lesions of approximately less than three cm in diameter were isolated into hospital tanks for treatments and observations.

Treatment for "bell rot" consisted of precise removal of the necrotic, damaged tissue (with 0.5 cm margins of healthy tissue) using sharp dissection, achieved best with Brown-Adson forceps to stabilize and ophthalmic (iris) scissors to trim. Based on the lack of adverse responses by any jellies to superficial excisional procedures, no anesthesia was deemed necessary in these cases. Care was taken to keep dissection and trimming techniques as superficial as possible. After affected bell tissue was removed, representative biopsies were preserved in 10 percent neutral buffered formalin for histopathologic evaluation.

Biopsies of the umbrella (bell) from several specimens were embedded in paraffin, sectioned at 5.0 µm, and stained with Hematoxylin and eosin (H&E stain). Biopsies from affected jellies showed moderate to marked multifocal coalescing necrosis of the epidermis (ectoderm) covering the exumbrella. The epidermis lining the subumbrella was less severely affected. There was multifocal sloughing and loss of the epithelium (ulcers). The necrotic epidermis was covered by cell debris and few degenerate, necrotic hemocytes. The necrosis extended deep into the underlying mesoglea. The mesoglea was multifocally infiltrated by granulated and ungranulated hemocytes. Two of the jellies had many, 10-20 µm, round, algal-like organisms with a thick, refractile cell wall on the surface of the exumbrella that infiltrated into areas of epidermal and mesogleal necrosis. Two other jellies had rod-like to undulating filamentous bacteria infiltrating the areas of epidermal necrosis. A Sandaria jelly with bell necrosis had neither bacteria nor algal-like organisms evident within the lesions.

After excisional treatment, some of the jellies were treated with antibiotics topically via nitrofurazone baths (10 mg/L for one to two hours, followed by two mg/L continuous immersion until healed or improved, usually four to five days). Several jellies treated by tissue removal and antibiotic immersion regenerated bell tissue within eight to twelve weeks and were returned to their exhibits; however, a few individuals sustained permanent superficial scarring of the bell following the procedure and were no longer of exhibit quality. Nerve function following excision therapy remained intact^2,3 based on observed ability of the bell to continue propulsion movements in a normal manner.

The following hypothesis is proposed. Traumatic bell lesions were sustained by jellies colliding with tank walls, either accidentally or because of irregular currents induced by water flow within the kreisel tanks. Damaged ectodermis supported invasion by opportunistic bacteria and algal-like organisms, leading to inflammation (hemocytic infiltration) and necrosis. In some tanks, hydroid colonies present on exhibit walls may have contributed to damage of bell surfaces coming into contact with them.

The algal-like organisms associated with moderate to marked epidermal and mesogleal necrosis were more abundant and microscopically different from commensal algae (zooxanthellae) naturally found in jellies living higher in the water column.¹ Possible sources of these algal-like organisms include: addition of newly acquired wild-caught jellies without adequate quarantine, contaminated water supply, equipment, or food source, and suboptimal water quality leading to overgrowth of opportunistic non-commensals. Further evaluation of the algal-like organisms by electron microscopy is warranted to help determine treatments or management techniques indicated in the prevention of this syndrome.

Efforts should be made to maintain proper husbandry for captive jellies. Ultraviolet filtration, timed lighting cycles, and dilution by water changes may help reduce presence or numbers of microorganisms. The live food sources should be examined for possible hydroid contamination within the exhibit. In addition, water flow within jelly tanks must be frequently monitored and adjusted to regulate currents and prevent erratic swimming patterns in the jellies.

To our knowledge, this is the first report documenting necrotic dermatitis in captive jellies associated with algal-like organisms. Excision of the affected tissue, followed by topical anti-bacterial therapy, may improve healing and appearance of the bell. Frequency of necrotic dermatitis syndrome in jellies from this collection prompted re-evaluation of water flow in each system in order to prevent tank wall contact and subsequent damage to delicate ectodermal layers.

Acknowledgements

We thank Mr. Mark Loos of the Aquarium of the Pacific for jelly husbandry expertise.

References

1.  Brusca RC, GJ Brusca. 1990. Invertebrates. Sinauer Associates, Inc. Publishers, Sunderland, Massachusetts, Pp. 228-229.

2.  Lin Y-CJ, NG Grigoriev, AN Spencer. 2000. Wound Healing in Jellyfish Striated Muscle Involves Rapid Switching between Two Modes of Cell Motility and a Change in the Source of Regulatory Calcium. Developmental Biology 225:87-100.

3.  Sparks AK. 1972. Invertebrate Pathology: Noncommunicable Diseases. Academic Press. London, Pp. 32-36.