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NEUROMUSCULAR CASE OF THE MONTH - OCTOBER 2001
Severe generalized paresis/paralysis in subadult Loggerhead turtles
Contributed by Drs. Elliott Jacobson, Cheryl Chrisman, Diane Shelton
University of Florida, Gainesville, FL (Jacobson, Chrisman)
University of California, San Diego, La Jolla, CA (Shelton)
Clinical History
Beginning in October 2000, subadult loggerhead sea turtles (Caaretta caretta) showing clinical signs of a neurological disorder were found in waters off
south Florida. Several other species of sea turtles were in the same waters and only loggerheads had been reported to be affected. Loggerheads feed on mollusks,
crustacea, and fish. The history suggests either a toxin in their prey base or an infectious agent highly specific for loggerheads. Three affected animals were further
evaluated at the University of Florida.
Physical and Neurological Examination
Depressed mentation was present with no menace response in either eye. There was little eye movement in general, a lack of palpebral
reflexes (Figure 1), and reduced jaw tone. The animals could not chew or swallow. There was loss of neck retraction and neck
muscle tone, slight to no response to superficial nociceptive stimuli, and generalized lack of limb movements, muscle tone, and
flexor reflexes. Some tail and cloacal reflexes were present. There was no response to sensory stimuli along the dorsal or ventral
shell, and no righting response could be elicited when turtles were placed on their backs. A generalized lower motor neuron disorder
was suspected including a polyneuropathy (generalized involvement of cranial and spinal nerves), neuromuscular junction blockade,
or polymyopathy (thought to be less likely due to severity of paralysis).
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Figure 1.
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Electrophysiological Evaluation
Prolonged insertional activity was present without positive sharp waves or fibrillation potentials (Fig. 2). There
was little evidence of motor unit action potentials usually found on electromyograms in unanesthetized animals. No evoked
muscle response to stimulation of the sciatic nerve was found on either side. The limb did not move nor did the unanesthetized
turtle act as if it experienced any discomfort. A normal loggerhead turtle was also evaluated. The normal turtle had an evoked
muscle response and a motor nerve conduction velocity of 48.8 m/sec. This animal was anesthetized for the nerve stimulation
due to the discomfort of the procedure. A polyneuropathy associated with axonal degeneration was thought unlikely due to the
lack of fibrillation potentials and positive sharp waves. The lack of evoked muscle responses to nerve stimulation suggested
a neuromuscular junction blockade such as found in tick paralysis, coral snake envenomation, botulism or drugs such as curare.
A last possibility would be a demyelinating polyneuropathy that has spared axons but resulting in a conduction block.
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Figure 2.
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Muscle and Nerve Evaluation
Forelimb and hind limb muscles were collected at necropsy and none showed any abnormalities. This finding would be consistent
with the lack of abnormal electrical activity within the muscles evaluated by electrodiagnostic testing. Evaluation of a nerve
root (Fig. 3) from one of the affected animals showed numerous nerve fibers with ballooning dilatation of myelin, myelin splitting,
abnormally thin myelin sheaths, and endoneurial edema. In two animals evaluated, scattered thinly myelinated or demyelinated
nerve fibers were also observed within the ulnar and sciatic nerves. |
Figure 3.
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Brain and Spinal Cord
Histology revealed a granulomatous meningitis of brain and spinal cord with numerous intravascular spirorchid trematode adults
and eggs present in the meningeal vessels (Figure 4). Collections of eggs were also present in packets scattered throughout
the meninges (Figure 5). |
Figure 4.
Figure 5.
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Conclusion
At this time it is impossible to attribute the illness and epidemic to any one specific pathogen or toxin. However, the neurospirorchidiasis
has many similarities to neuroshistosomiasis reported in humans. Spirorchidae and Schistosomatidae represent sister groups of intravascular
trematodes. Neuroschistosomiasis is well described and a range of neurological defects have been reported in humans. However in the
literature, only one case of polyneuropathy could be found in a patient with neuroschistosomiasis (J Egypt Med Assn 1972;55:44-49).
Areflexic flaccid paraplegia with spincter dysfunction and disturbance of sensation has also been described in CNS Shistosoma infection
(Brain 1985;106:1023-1028). It is possible that an immune response to either the organism itself or to release of previously hidden
self-antigens (ie: myelin) may result in either the observed demyelination or to impairment of neuromuscular junction function. It
is also possible that these parasites may act as vectors for some other pathogen. Algal toxins are known to cause neurologic disorders
in a variety of marine animals and assays are being conducted to determine if any of these toxins are present. However, no fish or
other species of marine turtles are known to be affected within the range of the ill loggerheads. If it is a toxin it would have to
be localized in the prey base of these turtles, or these turtles have to be uniquely sensitive to this toxin. A final consideration
is the possibility of jellyfish toxicosis. Loggerhead have been observed at sea feeding upon large aggregates of jellyfish.
The authors would like to acknowledge the contributions of Drs. Bruce Homer, Ellis Grenier, Nancy Szabo, Paul Klein, and Sadie Coberly (University of Florida, Gainesville);
Drs. Allen Foley, Jan Landsberg, and Leanne Flewelling (Florida Marine Research Institute, Florida Fish and Wildlife Conservation Commission, St. Petersburg, FL);
Dr. Ruth Ewing (National marine Fisheries Service, Miami, FL); And Drs. Ritchie Moretti, Susan Schaff, and Douglas Mader (Sea Turtle Hospital, Marathon, FL).
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