Am. J. Trop. Med. Hyg., 73(6), 2005, pp. 1026–1027 Copyright © 2005 by The American Society of Tropical Medicine and Hygiene
SHORT REPORT: PERSISTENT BRADYCARDIA CAUSED BY CIGUATOXIN POISONING AFTER BARRACUDA FISH EGGS INGESTION IN SOUTHERN TAIWAN YAO-MIN HUNG,* SHIH-YUAN HUNG, KANG-JU CHOU, NENG-CHYAN HUANG, CHUNG-NI TUNG, DENG-FWU HWANG, AND HSIAO-MIN CHUNG Division of Nephrology, Department of Medicine, and Department of Pharmacy, Kaohsiung Veterans General Hospital, Kaohsiung; Division of Nephrology, E-Da Hospital, I-Shou University, Kaohsiung; Department of Food Science, National Taiwan Ocean University, Keelung; and National Yang-Ming University, School of Medicine, Taipei, Taiwan
Abstract. We report an outbreak of ciguatoxin poisoning after barracuda fish ingestion in southern Taiwan. Three members of a family developed nausea, vomiting, watery diarrhea, and myalgias about 1 hour after eating three to ten eggs of a barracuda fish. Numbness of the lips and extremities followed the gastrointestinal symptoms about 2 hours after ingestion. Other manifestations included hyperthermia, hypotension, bradycardia, and hyperreflexia. Bradycardia persisted for several days, and one patient required a continuous infusion of intravenous atropine totaling 40 mg over 2 days. Further follow-up of the patients disclosed improvement of neurologic sequelae and bradycardia, but sensory abnormalities resolved several months later. In conclusion, ciguatoxin poisoning causes mainly gastrointestinal and neurologic effects of variable severity. In two patients with ciguatoxin poisoning after barracuda fish egg ingestion, persistent bradycardia required prolonged atropine infusion.
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.
INTRODUCTION Ciguatera fish poisoning (ciguatera), a common poisoning caused by ingestion of certain fish, is common in tropical regions between 35° N and 35° S latitude. In the United States, 90% of cases occur in Hawaii and Florida.1 Ciguatera food poisoning may occur in international travelers exposed to a toxic fish while traveling in a tropical region.2–5 Because of changes in the eating habits of the general population, international trade, an increase in the immigrant population, and a wider geographic distribution of food products, it is reasonable to suppose that this problem will increase. Ciguatera causes a polymorphic syndrome with gastrointestinal, cardiovascular, and neurologic signs and symptoms. Among the toxic manifestations, hypotension and bradycardia occurred infrequently.6,7 An outbreak of ciguatoxin poisoning after barracuda fish ingestion has never been reported in Taiwanese patients before. We report an outbreak of ciguatoxin poisoning in Taiwan after consumption of barracuda fish eggs. Some of the victims had persistent bradycardia and hypotension. This report summarizes the investigation of this outbreak, which occurred among members of the same family residing in Kaohsiung city. CASE REPORT For this investigation, ciguatera food poisoning was defined as a combination of gastrointestinal (nausea, vomiting, diarrhea, or abdominal cramps) and neurologic symptoms (muscular or dental pain, weakness, dizziness, perioral paresthesia or paresthesia of the extremities, or dysesthesia) in patients who had eaten some of the suspected fish. Each reported case was investigated by detailed history-taking using a standard questionnaire and review of their medical records. Of six members of the family who ate the same barracuda,
* 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:
[email protected]
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OUTBREAK OF CIGUATOXIN POISONING
RESULTS Results of cultures of stool samples from two affected family members were negative for Salmonella, Shigella, Campylobacter, Yersinia, and Vibrio. 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. DISCUSSION Ciguatera is an important cause of human poisoning from the consumption of seafood. Ciguatera is an important medical entity in tropical and subtropical Pacific and Indian Ocean regions and in the tropical Caribbean.10 As reef fish are increasingly exported to other areas, it has become a world health problem. However, the disease is underreported and often misdiagnosed.10 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. 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:
[email protected]. 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, Keelung 202, Taiwan. Reprint requests: Yao-Min Hung, Division of Nephrology, Department of Medicine, Kaohsiung Veterans General Hospital, 386 TaChung 1st Road, Kaohsiung 813, Taiwan. Telephone: 886-7-3422121 ext 2050, Fax: 886-7-3455412, E-mail:
[email protected].
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