Abstract

From October 2000 through March 2001, 49 debilitated subadult loggerhead sea turtles (Caretta caretta--LST) with clinical signs of neurological disease were recovered from coastal waters of southern Florida, USA. Turtles were found over a large geographic region that spanned from Manatee County on the west coast to Brevard County on the east coast; however, approximately 70% were found in the Florida Keys region. Clinical signs included variable degrees of paresis and the absence of deep pain sensation, menace response and corneal, palpebral and swallowing reflexes. Most of the affected animals died and necropsy was performed on 17 turtles.

For each turtle, the diagnosis of a peripheral demyelinating polyneuropathy and/or neuromuscular junction transmission block was based on results from neurological examination, electrophysiological studies and pathologic examination of peripheral nerve biopsy or necropsy specimens. Additionally, at necropsy, all 17 turtles had variable burdens of spirorchiid trematodes that included both generalized and central nervous system (CNS) infections. In the CNS, spirorchiid ova were within and around blood vessels of the brain and meninges with attending granulomatous or mixed leukocyte inflammation, vasculitis, edema, axonal degeneration and occasional necrosis. In 8 turtles, spirorchiid adults were within meningeal vessels of the brain and/or spinal cord. In 2 LST, adult trematodes were dissected from meningeal vessels and identified as Neospirorchis sp. The CNS burden of spirorchiid adults and ova of this cohort were compared to that of a control cohort (n = 17) that died of various causes prior to 2000, and the turtles from the 2000/2001 mortality event had a relatively greater CNS burden of spirorchiids.

Neurospirorchiidiasis may explain some of the clinical signs exhibited by LST in this mortality event; however, in some cases, burdens were relatively minimal or mild, and there was no clear association between the spirorchiid lesions in the CNS and the electrophysiological abnormalities and demyelinating changes in peripheral nerve specimens. Thus, other primary causes of neurological disease, including biotoxicosis, heavy metal toxicosis and exposure to cholinesterase inhibitors, were investigated. Tissues were analyzed for brevetoxins, ciguatoxins, domoic acid and palytoxin, as well as 15 heavy metals, including arsenic, copper, lead, mercury and selenium. Samples from 8 of 20 LST tested positive for brevetoxins; however, the levels were not indicative of acute toxicity. Also, the LST mortality event did not correlate temporally or geographically with natural (algal blooms) or anthropogenic (pollutant spills) phenomena or die-offs of other marine species. Blood cholinesterase levels in affected turtles were comparable to healthy control LST. Detectable levels of some metals were demonstrated in all turtles; however, there were no trends or excessively high levels to suggest heavy metal toxicosis as a cause of the neurological disease.

The authors hypothesize that the clinical signs and pathological lesions seen in this 2000-2001 LST mortality event were a combined result of CNS infection by spirorchiid trematodes, possibly Neospirorchis sp., and a peripheral demyelinating polyneuropathy and/or neuromuscular junction transmission block due to possible exposure to a novel toxin in the environment or diet.

Acknowledgments

The authors would like to thank Damien Shea, North Carolina State University, Raleigh, North Carolina; Fran Van Dolah and Todd Leighfield, National Ocean Service, Biotoxin Laboratory, Charleston, South Carolina.