A 49-year-old woman developed nausea, vomiting, and diarrhea 4 hours after she ate at a local Memphis restaurant. Her dinner consisted of a salad and broiled grouper. She remained nauseated the next day, but diarrhea stopped, and she had no fever. Two days later, she developed burning of the lips, tongue, fingers, and toes and pain in the teeth. She had a sensation of burning in the limbs when exposed to cold temperatures, and both drinking and washing her hands with fresh and warm tap water produced a burning sensation. The patient received ciprofloxacin and cimetidine for 3 days without help, and both were discontinued. She was placed on gabapentin 300 mg three times a day for 3 days with minimal improvement. Other symptoms included muscle aches, hypersomnia, increased sensitivity to light, and watery eyes, but no headaches.
She had a history of hepatitis A 15 years before without sequelae. Family history was noncontributory. The patient drank alcohol occasionally and stated that drinking wine made her symptoms worse.
Physical examination revealed normal vital signs and general physical examination, except that her distal limbs felt cold to the examiner. She had normal pulses. Mentation and cranial nerves were also normal. Muscle strength and reflexes were normal and symmetrical. There were no pathologic reflexes. Sensory examination was unremarkable, except that she described aching and burning sensations when the examiner touched her with a cold tuning fork. Gait and coordination were normal, and there was no myotonia.
An Emg Test was Performed
| Nerve and Site | Latency (ms) | Amplitude (mV) | Conduction Velocity (m/s) |
|---|---|---|---|
| Peroneal Nerve R. | Normal ≤ 5.7 | Normal ≥ 3 | Normal ≥ 40 |
| Ankle | 4.2 | 11 | – |
| Fibular head | 9.8 | 10 | 47 |
| Knee | 11.7 | 10 | 47 |
| Nerve | Latency (ms) | Normal Latency ≤ (ms) |
|---|---|---|
| Peroneal nerve R. | 45 | 54 |
| H-reflex R. | 32 | 34 |
| Nerve | Peak Latency (ms) | Normal Peak Latency ≤ (ms) | Amp (μV) | Normal Amp ≥ (μV) |
|---|---|---|---|---|
| Sural nerve R. | 3.8 | 4 | 32 | 13 |
| Rt. hand—normal |
| Rt. foot—normal |
| Muscle | Insrt Activity | Fibs | Pos Waves | Fasc | Amp | Dur | Poly | Pattern |
|---|---|---|---|---|---|---|---|---|
| Vastus lateralis R. | Norm | None | None | None | Norm | Norm | None | Full |
| Tibialis anterior R. | Norm | None | None | None | Norm | Norm | None | Full |
| Gastrocnemius R. | Norm | None | None | None | Norm | Norm | None | Full |
What were the EMG Findings?
The nerve conduction tests and needle EMG were normal in the arm and leg including the sympathetic skin responses.
Complete blood count and chemistry profile, including liver enzymes, serum creatine kinase, and erythrocyte sedimentation rate, were normal.
What is the Most Likely Diagnosis?
This patient presented with a history of paresthesias with burning sensations and paradoxical sensations to cold and heat after a gastrointestinal illness which occurred 4 hours after the ingestion of seafood, suggesting seafood poisoning.
The initial gastrointestinal symptoms could have been caused by a bacterial infection such as Salmonella or Escherichia coli . She, however, never had fever, and her gastrointestinal symptoms disappeared, while her neurologic symptoms persisted, which is not characteristic of these infections.
Botulism could also present with gastrointestinal symptoms, but this produces paralysis and ophthalmoplegia, and patients are usually constipated.
Scombroid fish poisoning is caused by eating tuna and mackerel that are infested with Proteus morganii bacteria containing high levels of histamine and a substance called saurine . The symptoms include coryza, flushing, headaches, and dry mouth. This patient had none of these symptoms; rather, her presentation suggested ciguatera poisoning. She was treated with intravenous mannitol 25% with marked improvement.
What is Ciguatera Poisoning?
Ciguatera is the most common fish poisoning in the world; it is caused by certain strains of a Benthic dinoflagellate which was initially isolated in the Gambier Islands and is called Gambierdiscus toxicus . The incidence of the disease is about 25,000 cases annually, which is higher in warmer climates, particularly in the Caribbean. The poison is acquired by eating tropical or subtropical fish, such as barracuda, eels, mackerel, amberjack, snapper, and grouper.
The name ciguatera comes from Turbo pica , a marine snail called “ cigua ” in Spanish. The term was later applied to poisoning by fish.
Common symptoms include abdominal pain, diarrhea, vomiting, myalgia, paradoxical reversal of temperature sensations, paresthesias, mood disorders, ataxia, dental pain, tremors, stiffness, and increased salivation. These start 20 minutes to over 24 hours after the ingestion of contaminated fish. Patients might also develop fatigue, flaccidity, skin rash, and autonomic dysfunctions, such as hypertension, brachycardia or tachycardia, and orthostatic hypotension. Rarely, they develop a polyneuropathy or a myositis. Cigua toxins activate voltage-sensitive sodium channels, causing hyperparalyzation-shifts and spontaneous repetitive nerve discharges. Excessive activation of small myelinated and unmyelinated fibers could cause the symptoms.
Electrophysiologic tests in ciguatera poisoning could be normal or could show slowing of motor and sensory conduction velocities.
The diagnosis is purely clinical, although an enzyme-linked immunosorbent assay (ELISA) test can be done in serum; this is not commercially available.
The treatment of ciguatera poisoning consists of infusions, 1 g/kg, of 25% mannitol intravenously over 3–6 hours. Benefits in more chronic cases have also been reported. For maximum benefit the treatment should be given within 72 hours of toxin ingestion. A recent report indicated that mannitol is not superior to normal saline infusions. Other treatments include antihistaminics, sodium channel blockers, and gabapentin.
The prognosis of ciguatera poisoning is usually good, although the disease can last for months. Fatalities are rare but do occur.
Food poisoning such as this could be an important public health problem, particularly as the contaminated fish are not identified and because the toxin is heat-resistant and not eliminated by common cooking. It is recommended that fish poisoning should be reported to the public health services. For further information, one can refer online to http://www.csfan.fda.gov .
What are Other Ingestible Seafood Toxins?
Maitotoxin is another toxin that can produce symptoms similar to ciguatera; it comes from a dinoflagellate present in the gut of sturgeon that causes increased calcium accumulation in nerves and endocrine glands. Prominent muscle spasms also occur. Palytoxins are also biotoxins from tropical fish that can cause muscle spasms, seizures, and elevated serum creatine kinase levels.
Another important toxin that was unlikely in this case is tetrodotoxin , caused by ingestion of puffer-fish, producing paresthesias and paralysis which could be lethal. In that condition the poison blocks sodium channels. (The recent novel by Robin Cook, Crisis , provides an entertaining reading on tetrodotoxin poisoning and of concierge medicine.)
Shellfish poisoning by molluscs, such as mussels infected by the dinoflagellate that causes “red tides,” produces paresthesias and reverse cold/hot temperature sensations but can also cause ataxia and other neurologic symptoms. Amnestic shellfish poisoning is caused by cultured blue mussels that contain the domoic toxin, a glutamate antagonist similar to kainic acid. It usually causes muscle cramps and diarrhea, and, later, neuropathy, seizures, and memory loss. Similar contaminations have been reported in crabs and clams. Hallucinating mullet poisoning from ingesting that contaminated fish causes delirium and hallucinations. This poison is likely a variant of ciguatera.
Clupeotoxin is another toxin present in contaminated herring and anchovies. It causes headaches, convulsions, and even coma. A more severe paralytic shellfish poisoning that develops within hours of ingestion of shellfish is caused by a mixture of toxins including saxitoxins that block voltage-dependent sodium channels in nerve and muscle; its symptoms include paresthesias, dysphagia, weakness, and respiratory failure.
A lipid-soluble toxin, called carchatoxin , which infects sharks’ flesh, has similar symptoms to ciguatera but could be much more severe and even lethal.
Some Historical Aspects of Seafood Poisoning
It appears that Egyptians knew that puffer-fish could be poisonous, as a puffer-fish drawing is shown in a tomb of the Fifth Dynasty during 2500 BCE. Knowledge of poisoning by eating puffer-fish was introduced to Western Civilization by Kaempfer in the History of Japan in 1727. Puffer-fish is a delicacy in Japan where the fish is prepared by expert cooks in licensed restaurants; these cooks are able to carefully remove the liver and roe which are highly toxic.
The awareness of symptoms that appear to be ciguatera poisoning is also described during the T’ang Dynasty in CE 618–907, and sailors with the explorer Fernandez de Quiroz, who became sick after eating pargo (red snapper) in 1600, likely had ciguatera poisoning.
The great explorer Captain James Cook ( Fig. 42-1 ) traveled extensively in the South Pacific, and during his second journey in the HMS Resolution, he apparently ate a piece of puffer-fish liver and became acutely ill in New Caledonia in 1774. During this voyage, he also reported more episodes of sea poisoning from eating two other types of fish. He described paradoxical sensations from seafood poisoning as follows:
We found ourselves seized with an extraordinary weakness and numbness all over our limbs attended with numbness of sensation like to that caused by exposing one’s hands and feet to a fire after having been pinched much by frost. I had almost lost the sense of feeling; nor could I distinguish between light and heavy bodies, of such as I had the strength to move, a quart pot full of water and feather being the same in my hand.
