Abstract
In October 2014, four Orinoco crocodiles (Crocodylus intermedius) at Tampa's Lowry Park Zoo were found demonstrating varying degrees of neurological clinical signs. These ranged from abnormal buoyancy in the water to marked ataxia on land, with difficulty hauling out and exaggerated tail and limb movements. Exophthalmos was present in two out of four individuals. Differential diagnoses for the acute neurological presentation included infectious causes such as West Nile Virus,1 water quality abnormalities in particular cyanobacteria, harmful algal bloom (HAB), thiamine deficiency, dietary contamination such as ciguatoxin, domoic acid toxicity and heavy metal toxicity.
Blood samples were taken for CBC, biochemistry, arbovirus panel, and heavy metal screening. Atropine was administered at 0.22 mg/kg total dose, ¼ IV, ¾ IM, as well as vitamin E at 5 IU/kg IM. The pool was drained, cleaned and refilled. The following day one individual was found floating dorsally in the pool minimally responsive. This individual received additional atropine, dexamethasone (0.25 mg/kg IV/IM) and enrofloxacin (5 mg/kg IV) to treat secondary aspiration pneumonia. Radiographs ruled out foreign body metal ingestion. This individual was isolated in an indoor heated dry docked enclosure. Over the next 24 h, this animal remained minimally responsive while the conspecifics gradually improved. All bloods were within normal limits including arsenic, lead, cadmium, mercury and thallium.
Over the next week, 3 individuals continued to show an improvement, but one was still minimally responsive. Repeat bloods showed a high CK of > 75,000 IU/L. Following a third round of atropine, additional fluids, dexamethasone, ceftiofur (4 mg, IV), dantrolene (120 mg, IV), and selenium (2.2 mg, IM), we began to see some small improvements to stimuli. This individual had a plasma level of brevetoxin of 1.3 ng/ml whereas the other three individuals were negative. In manatees with brevetoxicosis, we rarely see correlation of clinical signs and plasma brevetoxin levels. This individual potentially had the greatest exposure and the other individuals had returned to baseline prior to sampling. Within the following month all animals were classed as clinically normal.
This is a case report of a severe neurological presentation in a critically endangered species. We do not have a definitive diagnosis in this case. Water testing close to the time of onset of the acute neurological signs showed no evidence of harmful algal toxins, but the sampling was less than ideal. Arbovirus panel was negative for WNV, WEE, VEE and EEE. No specific therapy was given for potential thiamine deficiency and recovery would argue against this as the etiology. The individuals were fed barracuda the week prior to presentation, which could have been a source of toxicosis; however, this same fish was fed out to other animals which showed no clinical signs. The barracuda was eviscerated and fed out, making ciguatoxins less likely to be the source. Testing of brevetoxin in the barracuda returned as negative. Our most likely explanation currently lies within inadequate chlorination of the pool resulting in a HAB confirmed by raised brevetoxin levels in one individual. To the authors' knowledge this is the only report of this species surviving such severe neurological symptoms.
Acknowledgements
The authors wish to thank Mr. Dan Costell and his department staff as well as Dr Bryan Vorbach, and the Veterinary Clinic staff Michelle Devlin and Heather Henry. The authors thank FWC for their technical assistance with samples.
* Presenting author
+ Student presenter
Literature Cited
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