Gudu Kwini Kwini A Tough Meal, No Matter How You Slice It
ABSTRACT & COMMENTARY
Synopsis: Because victims of tetrodotoxin may not be physically able to give a history of ingestion of exotic delicacies by the time they are brought to medical attention, it is important for clinicians to actively ask about foods, especially seafood or marine products, even certain shellfish eggs or seaweed.
Source: Trevett AJ, et al. Tetrodotoxic poisoning from ingestion of a porcupine fish (Diodon hystrix) in Papua New Guinea: Nerve conduction studies. Am J Trop Med Hyg 1997;56:30-32.
A fisherman, working south of port moresby, New Guinea, brought home his catch. Within hours two family members and their pet dog had collapsed and died. A younger daughter survived, after requiring mechanical ventilation for 24 hours. In this recent report by Trevett et al, the pathophysiology of severe tetrodotoxin poisoning is further defined using nerve conduction studies obtained in a survivor of this disease, which accounts for at least 50 deaths annually in Japan from puffer fish (fugu) poisoning. The current report clearly illustrates that other species of edible fish can be just as deadly.
Gudu kwini kwini is the local name in Roku Village, 20 miles from Port Moresby, for the porcupine fish, as distinguished from gudu kopa kopa, the puffer fish, classically associated with tetrodotoxic poisoning. This fresh fish meal was apparently well-cooked by steaming it in creamed coconut milk. Within half an hour of eating the meal, the fisherman’s mother became weak, then experienced widespread prickling, tingling, and numbness. Gait became unsteady, she hypersalivated and sweated profusely, collapsed, and died. Her daughter followed soon after. A 23-year-old younger sister was admitted to Port Moresby General Hospital, three hours after the meal, having experienced weakness, excess salivation, sweating, headache, and chest pain. Her most prominent and terrifying symptoms were the generalized prickling sensation, numbness, and ensuing paralysis.
The patient was cyanotic but conscious, bradycardic, convulsing at times, and exhibiting generalized muscle twitching. She was hypothermic (35.6° C), with a pulse rate of 60 (but increasing to 102/min over time), blood pressure of 110/70, and shallow respirations, constricted pupils responsive to light, tremors, incoordination, and limb weakness with areflexia. Mechanical ventilation was required for 24 hours, with full recovery by day 10. The family dog also ate the remainder of the fish, promptly died, and the village attributed the whole series of catastrophic events to "puri puri," or witchcraft.
Laboratory evaluation of hematological and biochemical parameters was unremarkable. Sinus bradycardia was evident on electrocardiogram. Nerve conduction studies were performed; these included compound muscle action potential amplitudes with both sensory and motor nerve conduction velocities. Conduction velocities in sensory and motor nerves were reduced by as much as 50% from the subsequent baseline levels achieved after 10 days of recovery. The median sensory nerve appeared to have had more severely affected conduction velocities than either the median or ulnar motor nerves. In addition, sensory nerve action potentials were less than 20% of levels achieved at the time of recovery. Compound muscle action potentials were approximately one-third the values later observed at recovery.
COMMENT BY CATHERINE HARDALO, MD, AND FRANK J. BIA, MD, MPH
Tetrodotoxin is an amino perhydroquinazoline, nonprotein, neurotoxin that is extremely potent. The 50% lethal dose in mice is only 8 mcg/kg, and, as illustrated in the unfortunate family described above, the toxin is heat stable. Action potentials are markedly inhibited because the toxin binds to voltage-gated sodium channels, particularly at nodes of Ranvier, where most are situated. With the flow of sodium ions blocked, the time for nerve excitation is prolonged; depolarization thresholds may not be reached, and the consequent decreases in both sensory and motor conduction velocities and evoked amplitudes result.
The conduction blocks seem to be non-focal and diffuse, and the toxin appears to cross the blood-brain barrier. Cranial diabetes insipidus, brainstem areflexia, and even a reversible locked-in syndrome have been attributed to tetrodotoxic poisoning. When investigated experimentally, tetrodotoxin paralyzes the autonomic nervous system. The affected members of the family reported above demonstrated the hypersalivation, sweating, and other clinical manifestations of cholinergic autonomic stimulation, but these are not always observed, and dosage of the toxin may be important. In this case, all parts of the fish were consumed, including skin, ovaries, and liver, which contain the highest concentrations of toxin. Symptoms may begin within minutes of ingestion, and death can occur within an hour, as it did in these cases.
Another report published in 1996 highlighted the dangers associated with classic puffer fish ingestion, even for expert epicures. Signs and symptoms were reviewed for this marine toxin ingestion to assist the clinician in recognizing a syndrome that may be obscure but is life- threatening.1 Three cases of tetrodotoxin poisoning due to the ingestion of imported fugu, a Japanese delicacy prepared from puffer fish, involved expert sushi chefs from California, well-versed in the preparation of the potentially poisonous delicacy, who were served a pre-packaged, ready-to-eat form imported by a coworker. Luckily, their knowledge of symptoms alerted them to seek medical attention immediately. The relatively small amounts eaten (0.25-1.5 oz) may seem to clinicians to be a minor, unrelated exposure. However, the short onset of symptoms (3-20 minutes after eating) is typical of tetrodotoxin poisoning.
Tetrodotoxin causes a flaccid, ascending paralysis by blockade of neuronal sodium fast-channels and also interferes with central brain receptors regulating respiratory drive, causing respiratory failure.2 Dilation of the pupils and bradycardia with hypotension seen with tetrodotoxin poisoning are symptoms of preganglionic interference with the sympathetic and parasympathetic pathways. Higher brain functions are spared, so that the victim remains conscious and alert despite the ensuing paralysis and respiratory failure. A 59% fatality rate has been reported in a large Japanese study of more than 6300 cases of tetrodotoxin ingestion, most of them from fugu.3 Tetrodotoxin occurs naturally in other animals, such as the blue-ringed octopus, certain species of salamanders and newts, and in horseshoe crabs.2,3 A report from Thailand details the epidemic of 71 persons, including two fatal cases, affected by tetrodotoxin from ingestion of horseshoe crab eggs.4 Another report from Taiwan reports tetrodotoxin poisoning from mollusks, with hypertension as an unusual clinical feature.5 All patients presented with a classic picture of numbness or paresthesias, followed by vomiting, ascending paralysis, and fixed, dilated pupils in the most severe cases.
There are no specific antidotes for tetrodotoxic poisoning. Fish remnants should be removed by gastric lavage with 2% sodium bicarbonate and activated charcoal. Intravenous fluids, pressors, cysteine, atropine, and anticholinesterases may have a role in therapy.
Hence, treatment of tetrodotoxin consists of supportive therapy, with early intubation and mechanical ventilation playing the major role in saving lives. In anecdotal reports, administration of edrophonium 10 mg had apparent success in two cases with severe paralysis.2 Prognosis for recovery is good if the patient survives the initial 18-24 hours.2 An excellent table summarizing the features of other marine toxin syndromes was published in the same issue of Morbidity & Mortality Weekly Report and accompanies this case report. Because victims may not be physically able to give a history of ingestion of exotic delicacies by the time they are brought to medical attention, it is important for clinicians to actively ask about foods, especially seafood or marine productseven certain shellfish eggs or seaweed.
References
1. Centers for Disease Control and Prevention. Tetrodotoxin poisoning associated with puffer fish imported from JapanCalifornia, 1996. Morb Mortal Wkly Rep 1996;45:389-391.
2. Brown CK, Sheperd SM. Marine trauma, envenomations, and intoxications. Emerg Med Clin N Am 1992;10:385-408.
3. Eastaugh J, Sheperd S. Infectious and toxic syndromes from fish and shellfish consumption. A review. Arch Intern Med 1989;149:1735-1740.
4. Kanchanapongkul J, Krittayapoositpot P. An epidemic of tetrodotoxin poisoning following ingestion of the horseshoe crab Carcinscorpius rotundicauda. Southeast Asian J Trop Med Pub Health 1995;26:364-367.
5. Yang CC, et al. An outbreak of tetrodotoxin poisoning following gastropod mollusk consumption. Hum Exper Toxicol 1995;14:446-450.
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