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Of six members of the family who ate the same barracuda, one was asymptomatic and two only experienced nausea, vomiting, and mild abdominal pain. The other three members of the family developed nausea, vomiting, watery diarrhea, and myalgias about 1 hour after eating three to ten eggs of the fish.
Case 1. A 47-year-old previously healthy female was brought to the emergency department (ED) due to nausea, vomiting, watery diarrhea, and myalgias about 1 hour after ingestion of about 10 barracuda eggs. Numbness and tingling of the lips and all four limbs followed the gastrointestinal symptoms about 2 hours after ingestion. Severe headache and dizziness were also present. She was treated with intravenous fluids (normal saline), as well as 5 mg atropine and a dopamine infusion due to bradycardia and hypotension. Abdominal discomfort, vomiting, and diarrhea improved, but bradycardia persisted for several days, and she required a continuous intravenous infusion of atropine totaling 40 mg totally over 2 days. Because of continued paresthesias of the extremities, electromyelography and nerve conduction studies were performed and were negative. Her perioral numbness and paresthesia in the extremities had fully resolved about 26 months later.
Case 2. A 71-year-old male was admitted due to dyspnea. He had a medical history of diabetes mellitus. Severe nausea, vomiting, watery diarrhea, and myalgias began about 1 hour after eating eight eggs of the barracuda fish. Headache, dizziness, weakness, dysuria, perioral paresthesia, and paresthesia of the extremities developed later. Sinus bradycardia was accompanied by hypotension with BP 90/56 mm of Hg. He was treated with intravenous fluids (normal saline), atropine (5 mg), and dopamine infusion. The gastrointestinal symptoms improved 1 day later; however, bradycardia persisted, which required a continuous infusion of atropine with a total dose of 30 mg over 2 days. His perioral paresthesia and paresthesia of the extremities had resolved 2 months later.
Case 3. A 45-year-old previously healthy female came to the emergency department due to dizziness, nausea, vomiting, watery diarrhea, perioral paresthesia, and myalgias about 1 hour after eating three eggs of the barracuda fish. After treatment with intravenous fluids (normal saline), she was discharged from the ED 4 hours later.
The remaining eggs from leftover raw barracuda that was eaten were recovered from cold storage and then tested for ciguatoxin using a bioassay at the Department of Food Science, National Taiwan Ocean University. The bioassay for ciguatera toxin was based on previous studies.8,9 From the bioassay method, we estimated a content of 0.05 MU of ciguatoxin per gram of barracuda egg.
Ciguatera toxins are produced by dinoflagellates, which herbivorous fish consume. These fish are then eaten by larger, predatory reef fish (e.g., barracuda, grouper, and amberjacks), which appear to be unharmed by the toxin; because the toxins are lipid-soluble, they accumulate in fish upward through the food chain. The toxin may be most concentrated in the head, viscera, and eggs.5 The concentration of ciguatoxin in the fish depends on the fishing area and depth, the fish size and tissues, and climatic disturbances.7 More than 400 species of fish can be vectors of ciguatoxins, but generally only a relatively small number of species are regularly incriminated in ciguatera.
Ciguatoxins activate sodium ion channels, causing cell membrane excitability and instability.10 There is no immunity, and the toxins are cumulative.10 Ciguatera fish poisoning produces gastrointestinal, neurologic, and cardiovascular symptoms that usually begin developing within 12 to 24 hours of eating contaminated fish.5,6,11 Initially, gastrointestinal symptoms of diarrhea, abdominal pain, nausea, and vomiting occur, followed by neurologic symptoms of numbness and tingling of hands and feet, dizziness, altered hot/cold perception, muscle aches, and low heart rates and blood pressure. In rare cases, death occurs through respiratory failure.11,12 The largest series of cases examined in the literatures was from the South Pacific.6 Clinical observations on ciguatera were collected between 1964 and 1977 on 3,009 patients from several South Pacific island groups. The distribution by sex was 59.3% in males and 40.7% in females, with 49.7% of cases occurring in the third and fourth decades of life. Common symptoms or signs included circumoral paresthesis (89%), paresthesias of the extremities (89%), burning or pain to skin on contact with cold water (87.6%), arthragias (85.7%), myalgias (81.5%), diarrhea (70.6%), asthenia (60%), headache (59.2%), chills (59%), abdominal pain (46.5%), pruritis (44.9%), vomiting (37.5%), dysuria (18.7%), dyspnea (16.1%), bradycardia (13.4%), and hypotension (12.2%). The duration of the illness in patients in this study was usually 1–2 days, but residual weakness and sensory changes can persist for weeks, even years in severe cases.6,10
Because there is no approved human assay for ciguatoxin, the diagnosis is based on clinical findings and by the detection of toxin in samples of fish.13 As in this outbreak, ciguatera fish poisoning is diagnosed by the characteristic combination of acute gastrointestinal and neurologic symptoms in persons who eat large, predatory barracuda fish. The bioassay for ciguatera toxin is the only available method in Taiwan.
There is no known antidote for ciguatoxin poisoning, and treatment is primarily supportive.6,12,13 Intravenous mannitol may be effective early in the course of illness, and recently the results of a randomized, placebo-controlled trial of mannitol therapy were reported to have improved the neurologic but not gastrointestinal symptoms.3
In conclusion, in two patients with ciguatoxin poisoning after barracuda fish egg ingestion, persistent bradycardia required prolonged atropine infusion.
Received February 26, 2004. Accepted for publication July 27, 2005.
Acknowledgment: The authors deeply thank Professor Kent R. Olson for his valuable comments and grammatical revision of this manuscript.
* Address correspondence to Yao-Min Hung, Division of Nephrology, Department of Medicine, Kaohsiung Veterans General Hospital, 386 Ta-Chung 1st Road, Kaohsiung 813, Taiwan. E-mail: ymhung1{at}doctor.com 
Authors’ addresses: Yao-Min Hung, Kang-Ju Chou, Neng-Chyan Huang, Chung-Ni Tung, and Hsiao-Min Chung, Kaohsiung Veterans General Hospital, 386 Ta-Chung 1st Road, Kaosiung 813, Taiwan, Telephone: 886-7-3422121, ext. 2050, Fax: 886-7-3455412, E-mail: ymhung1{at}doctor.com. Shih-Yuan Hung, E-Da Hospital, 1 Eda Road, Yanchou Hsiang, Kaohsiung County 824, Taiwan. Deng-Fwu Hwang, National Taiwan Ocean University, 2 Pei-Ning Road, Kee-lung 202, Taiwan.
Reprint requests: Yao-Min Hung, Division of Nephrology, Department of Medicine, Kaohsiung Veterans General Hospital, 386 Ta-Chung 1st Road, Kaohsiung 813, Taiwan. Telephone: 886-7-3422121 ext 2050, Fax: 886-7-3455412, E-mail: ymhung1{at}doctor.com.
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