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    Admissions with a diagnosis of fish poisoning to the Northern District and Lolowi Hospitals in Vanuatu, 1986–1995.

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    Monthly admission patterns with a diagnosis of fish poisoning to the hospitals on Santo and Ambae, Vanuatu, 1986–1995.

  • 1

    Cameron J, Flowers AE, Capra MF, 1991. Effects of ciguatoxin on nerve excitability in rats (Part I) and man (Part II). J Neurol Sci 101 :87–97.

    • Search Google Scholar
    • Export Citation
  • 2

    Bagnis R, Kuberski T, Laugier S, 1979. Clinical observations on 3,009 cases of ciguatera (fish poisoning) in the South Pacific. Am J Trop Med Hyg 28 :1067–1073.

    • Search Google Scholar
    • Export Citation
  • 3

    Morris JG, Lewin P, Smith CW, Blake PA, Schneider, R, 1982. Ciguatera fish poisoning epidemiology of the disease on St. Thomas, U.S. Virgin Islands. Am J Trop Med Hyg 31 :574–578.

    • Search Google Scholar
    • Export Citation
  • 4

    Glaziou P, Legrand AM, 1994. The epidemiology of ciguatera fish poisoning. Toxicon 32 :863–873.

  • 5

    Quod JP, Turquet J, 1996. Ciguatera in Reunion Island (SW Indian Ocean): epidemiology and clinical patterns. Toxicon 34 :779–785.

  • 6

    Vogt RL, 1986. Ciguatera fish poisoning - Vermont. MMWR Morb Mortal Wkly Rep 35 :263–264.

  • 7

    Frenette C, MacLean JD, Gyorkos TW, 1988. A large common-source outbreak of ciguatera fish poisoning. J Infect Dis 158 :1128–1131.

  • 8

    Moulignier A, Binet D, Frottier J, 1995. Ciguatera fish poisoning: Europe. J Neurology, Neurosurg Psychiatry 59 :192–199.

  • 9

    Barton ED, Tanner P, Turchen CL, Manoguerra A, Clark RF, 1995. Ciguatera fish poisoning. A southern California epidemic. West J Med 163 :31–35.

    • Search Google Scholar
    • Export Citation
  • 10

    Lewis RJ, 2001. The changing face of ciguatera. Toxicon 39 :97–106.

  • 11

    Tosteson TR, Ballantine DL, Tosteson CG, Bardales AT, Durst HD, Higerd TB, 1986. Comparative toxicity of gambierdiscus toxicus, ostreopsis lenticularis and associated microflora. Marine Fish Rev 48 :57–59.

    • Search Google Scholar
    • Export Citation
  • 12

    Benoit E, Legrand AM, Dubois JM, 1986. Effects of ciguatoxin on current and voltage clamped frog myelinated nerve fibre. Toxicon 24 :357–364.

    • Search Google Scholar
    • Export Citation
  • 13

    Bidard JN, Vijverberg HPM, Frelin C, Chungue E, Legrand AM, Bagnis R, Lazdunski M, 1984. Ciguatoxin is a novel type of sodium channel toxin. J Biol Chem 259 :8353–8357.

    • Search Google Scholar
    • Export Citation
  • 14

    Warrell DA, 1996. Injuries, envenoming, poisoning and allergic reactions caused by animals. Weatherall, DJ, Ledingham, JGG, Warrell, DA, eds. Oxford Textbook of Clinical Medicine. Third edition, Oxford: Oxford University Press, 1142–1143.

  • 15

    Vanuatu Government, 1991. Vanuatu National Population Census, 1989. Port Vila, Vanuatu: Statistics Office.

  • 16

    Vanuatu Government, 1992. Statistical and Epidemiological Report 1989–1991. Port Vila, Vanuatu: Health Planning Unit.

  • 17

    David P, Cillauren E, 1988. A Survey of Village Subsistence Fishing in Vanuatu. Paper presented at the 26th Congress of the International Geographic Union.

  • 18

    Glaziou P, Martin PMV, 1993. Study of factors that influence the clinical response to ciguatera fish poisoning. Toxicon 31 :1151–1154.

  • 19

    Blythe DG, De Silva DP, 1990. Mother’s milk turns toxic following fish feast (letter). JAMA 265 :2339.

  • 20

    Katz AR, Terrell-Perica S, Sasaki DM, 1993. Ciguatera on Kauai: investigation of factors associated with severity of illness. Am J Trop Med Hyg 49 :448–454.

    • Search Google Scholar
    • Export Citation
  • 21

    Tosteson TR, Ballantine DL, Durst HD, 1988. Seasonal frequency of ciguatoxic barracuda in southwest Puerto Rico. Toxicon 26 :795–801.

  • 22

    Blythe DG, De Sylva DP, Fleming LE, Ayyar RA, Baden DG, Shrank K, 1992. Clinical experience with IV mannitol in the treatment of ciguatera. Bull Soc Pathol Exot 85 :425–426.

    • Search Google Scholar
    • Export Citation
  • 23

    Palafox NA, 1992. Review of the use of intravenous mannitol with ciguatera fish poisoning from 1988 to 1992. Bull Soc Pathol Exot 85 :423–424.

    • Search Google Scholar
    • Export Citation

 

 

 

 

 

CIGUATERA POISONING IN VANUATU

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  • 1 Department of Paediatrics, St. Mary’s Hospital, Imperial College, London, United Kingdom

Ciguatera poisoning is endemic in many tropical and subtropical countries. We conducted a retrospective study of admissions to two hospitals on the islands of Vanuatu in the southwestern Pacific region. We estimated the annual hospital admission rate for fish poisoning to be 65 (95% confidence interval [CI] = 55–75)/100,000 population on the island of Santo and 29 (95% CI = 19–43)/100,000 population on the island of Ambae. Hospital admission was more common in males 20–29 years old. Death was a rare complication. In the face of increases in both tourism and in the global trade in tropical and exotic fish, physicians in both endemic and non-endemic areas should be familiar with the epidemiology and clinical features of this important condition.

INTRODUCTION

It has been estimated that ciguatera toxin is the most common cause of fish poisoning worldwide.1 To date, however, few reports have been published describing its public health impact in at-risk communities.2–5 Moreover, the increasing global trade in tropical and exotic fish, coupled with increasing tourism to endemic areas, makes research into the epidemiology of fish poisoning a subject of increasing public health relevance.6–9

Ciguatera fish poisoning is endemic throughout much of the tropics and sub-tropics.10 It is caused by ciguatoxins that originate in dinoflagellate organisms, including Gambierdiscus toxicus.11 Such toxins lead to increased nerve membrane excitability through their action on voltage-gated sodium channels.12,13 The clinical manifestations of ciguatera fish poisoning vary widely; however, the usual presentation is with gastrointestinal, neurologic, or cardiovascular symptoms beginning 1–6 hours after the ingestion of fish containing the toxins.14 Features of peripheral neuropathy including paresthesia, dental pain, and paradoxical disturbance of thermal sensation, are the hallmarks of this condition. Nevertheless, except in severe cases, the results of electrophysiologic studies are usually normal.1

In this paper, we describe the epidemiology of ciguatera fish poisoning on two of the northern islands of the archipelago of Vanuatu in the southwestern Pacific region.

MATERIALS AND METHODS

Study area and population.

The islands of Vanuatu (formerly known as The New Hebrides) form a chain of 80 islands situated between the Solomon Islands and New Caledonia. The climate is tropical, with a long wet or summer season (November-May) and a shorter dry or winter season (June-October). Indigenous Melanesians (Ni-Vanuatu) constitute 98% of the population, with the remainder consisting mainly of Chinese, Vietnamese, and Europeans. In 1989, the national census estimated the population of Santo and Ambae to be 25,581 and 8,583, respectively.15 The demographic characteristics of Vanuatu are similar to those of many developing nations, with 17.5% of the population less than five years old and 55% less than 20 years old. More than 75% of the adult population work in subsistence farming, a category that includes fishing.15 A single hospital in Luganville, Santo, in the Northern District Hospital (NDH) serves as a referral center for the Northern District; however, more than 95% of the admissions to the NDH are from Santo alone. Lolowi Hospital is the only hospital on the island of Ambae. Most admissions to both hospitals are self-referred. Hospital-based studies were conducted in the Northern District and Lolowi Hospitals.

Data collection.

We conducted a retrospective descriptive study at the Northern District and Lolowi Hospitals. Ward registers were examined for the 10-year period January 1, 1986 to December 31, 1995 to identify patients admitted with a diagnosis of either fish or ciguatera poisoning. The hospital notes for cases were traced and information on clinical symptoms was recorded onto a standard form. Where notes were not available, limited information regarding age, date of admission, and outcome (discharged or died) was recorded from the ward register. Some adults did not know their ages and were classified as more than 20 years old. Although the study was conducted in January 2000, the study period was chosen because a national strike caused a severe disruption in record keeping during the intervening years.

Data processing.

Data were collected onto a standardized form and entered onto a computer spreadsheet (Excel®; Microsoft, Inc., Redmond, WA). A case of fish poisoning was defined as a patient admitted to hospital with a diagnosis of either fish or ciguatera poisoning recorded in the ward register. An outbreak was defined as two or more cases presenting on the same day from the same area. The drainage populations for each hospital were estimated using figures from the 1989 national census, which was inflated by 2.8% per year to account for population growth.15 The mid-study (1990) populations were thus estimated at 26,297 (14,463 < 20 years old and 11,834 ≥ 20 years old) for the NDH and 8,823 (4,853 < 20 years old and 3,970 ≥ 20 years old) for Lolowi Hospital. Crude and age-adjusted rates of hospital admission with fish poisoning were then calculated.

RESULTS

Between January 1, 1986 and December 31, 1995, 198 cases of fish poisoning were admitted to the Northern District and Lolowi Hospitals. Of the 171 cases admitted to the NDH, 148 (86.5%) subjects were Ni-Vanuatu and 23 (13.5%) were Oriental. Seventy-two of these cases presented in 24 outbreaks. The type of fish consumed was recorded in only 11 cases (reef fish, 4; barracuda, 2; and eel, 5). One patient was recorded as having eaten the liver of the fish. Six cases were admitted with additional diagnoses, including upper respiratory tract infection, malaria, hypertension, and diabetes mellitus. One patient died during admission and another developed an organic psychosis. Although the latter case was thought to be exacerbated by diabetes mellitus, neuropsychiatric disorders are a recognized feature of ciguatera poisoning.11

Twenty-seven cases of fish poisoning were admitted to Lolowi Hospital during the study period. All patients were Ni-Vanuatu. Two individuals were admitted more than once. Another individual was diagnosed with post-ciguatera/malaria. No deaths were recorded. Five cases occurred in two outbreaks.

Crude annual admission rates with fish poisoning (95% confidence interval) to the Northern District and Lolowi Hospitals were 65 (55–75) and 29 (19–43)/100,000 population, respectively.

Age and sex.

The age and sex of the cases is shown in Table 1. Fish poisoning was more common in adults than in children, and the age distribution was similar in both hospitals. Among adults, males were more frequently admitted to the hospital than females (Table 1), with a male: female ratio of 4:1. This marked sex difference was not seen in children < 10 years old: however, the numbers in this age group were limited. This imbalance was not seen in those admitted with other diagnoses.16

Temporal and seasonal patterns.

Figures 1 and 2 show the variation of admissions by year and month. The apparent peak of cases in 1992 included several small clusters of 4–5 cases presenting to the NDH. In 1988, a large outbreak of fish poisoning occurred when 13 Vietnamese fisherman were admitted on the same night in July. This outbreak accounts for the apparent peak in the month of July (Figure 2).

Clinical data.

Hospital records were available for 95 (48%) of 198 patients. The availability of information from patients admitted with fish poisoning was similar to that of information for individuals admitted with other diagnoses (Goodman A, unpublished data) and was not believed to represent a systematic bias. The clinical data are shown in Table 2. Although the onset of symptoms occurred shortly after the consumption of the suspected fish in all cases, the length of time to hospital presentation was variable. Most patients presented within three hours to nine days; however, in one patient, presentation was delayed for one month.

Treatments prescribed included atropine for bradycardia and intravenous fluids for hypotension or dehydration. Promethiazine hydrochloride (an antihistamine) was commonly prescribed for pruritus. Other treatments included anatacids, hyoscine butylbromide (to reduce gut motility and gastric secretions), codeine preparations (for diarrhea), and oral rehydration solution and prochlorperazine (for nausea and vomiting). Mannitol was not prescribed in this series.

DISCUSSION

Our report confirms that fish poisoning is an important cause of morbidity in Vanuatu. Although fish poisoning is widely viewed as a health problem in tropical and sub-tropical countries, remarkably few incidence studies have appeared in the published literature. On the basis of the few studies that have used hospital-based case detection, the incidence varies widely from 7.8/100,000 per year in Reunion Island5 to 360/ 100,000 in St. Thomas in the United States Virgin Islands.3 We estimate hospital admission rates of 29 and 65/100,000 population in the communities studied. These incidence figures represent a minimum estimate of the true burden of disease attributable to fish poisoning in Vanuatu for two reasons. First, we made no attempt in our study to identify cases of fish poisoning that had been misclassified under other diagnoses such as neurologic or gastrointestinal illnesses. Second, we anticipated that patients presenting to hospital represented only a small proportion of all cases of fish poisoning. This conclusion is supported by a recent community survey conducted in coastal areas in Vanuatu that estimated an incidence of 460/100,000 population/year.17

Previous studies have found little evidence for a sex difference in the incidence of fish poisoning, although one study conducted in Tahiti found an increased risk in males (risk ratio = 1.6).18 Nevertheless, in the current study 80% of the cases admitted to hospital were male. Since previous studies have failed to find an association between the severity of the disease and sex, we believe that the sex bias seen in the current study may be attributable to behavioral factors. For example, in Vanuatu it is traditional for men to eat before the rest of the family, and nutritional interviews have shown that Ni-Vanuatu males eat more fish than other members of the family (Phelps L, unpublished data). Moreover, men are more likely to eat the head and entrails of the fish when sharing it with their families (Phelps L, 1997, The Aetiology and Prevalence of Malnutrition in Children in Vanuatu, MSc thesis, Leeds Metropolitan University). Conversely, women traditionally avoid fish during pregnancy or while breastfeeding (Phelps L, 1997, The Aetiology and Prevalence of Malnutrition in Children in Vanuatu, MSc thesis, Leeds Metropolitan University), a practice that may prevent cases in infants, since the transfer of ciguatera toxin via breast milk has been reported.19

More than 40% of patients admitted to the hospital with fish poisoning in our study were in their third or fourth decade, an observation that is consistent with data from previous studies.3,18,20 A number of explanations may account for this. First, children may be less susceptible to the toxin or, for cultural reasons, may be exposed less often. Second, eating fish with low levels of toxin over many years may lead to accumulation of or sensitization to the toxin in older patients, a hypothesis supported by the worsening of symptoms with repeated episodes of ciguatera poisoning.3,18,20 Therefore, the explanation for the increased incidence of fish poisoning in this age group remains unresolved. Previous studies have shown some evidence for seasonality of fish poisoning, which has been ascribed to fluctuations in the abundance of dinoflagellate organisms.421 In the current study we found little evidence of seasonality of fish poisoning in Vanuatu.

Of the patients hospitalized with a diagnosis of fish poisoning in our study, common clinical features included gastrointestinal disturbance, hypotension, and bradycardia (Table 2). Paresthesia or neurologic sequelae occurred in only 18% and mortality was negligible. Mannitol, an osmotic diuretic found by other investigators to be effective in the treatment of ciguatera poisoning,22 was not used on the islands of Santo or Ambae. Whether this reflects limited drug availability, a lack of awareness of its possible benefits, or a belief that it is ineffective, the limited use of mannitol in the Pacific has been previously noted.23

In conclusion, ciguatera fish poisoning causes considerable morbidity in Vanuatu. However, most communities continue to consume fish, which remains an important source of dietary protein. Although we were unable to detect any appreciable acute mortality, the long-term effects on survival are unknown. Two factors argue for an increased awareness regarding the features and management of fish poisoning outside endemic areas. First, the growth in global tourism puts travelers at potential risk. Second, the increasing global trade in tropical fish, in conjunction with the absence of wide-scale testing for the toxin, makes ciguatera poisoning a potential risk in parts of the world where there is little experience of the disease. Both travelers to high-risk areas and their physicians should be aware of the risks and manifestations of fish poisoning.

Table 1

Admissions to the hospital with fish poisoning in Vanuatu, stratified by age and sex

Age group (years)Males no. (%)Females no. (%)Total (%)
0–98 (4.0)6 (3.0)14 (7.1)
10–1919 (9.6)5 (2.5)24 (12.1)
20–2945 (22.7)7 (3.5)52 (26.3)
30–3924 (12.1)2 (1.0)26 (13.1)
40–4914 (7.1)0 (0.0)14 (7.1)
50–597 (3.5)2 (1.0)9 (4.5)
60–695 (2.5)5 (2.5)10 (5.1)
Adults (age unknown)39 (19.7)10 (5.1)49 (24.7)
    Total161 (81.3)37 (18.7)198 (100)
Table 2

Clinical information on a subset of 95 patients presenting to the hospitals on Santo and Ambae, Vanuatu in whom clinical features were available

Clinical dataNo. with dataNo. with clinical feature (%)
* Blood pressure was not recorded in 16 patients.
† Heart rate was not recorded in 17 patients.
‡ These included confusion (1), paresthesia (7), pruritus (4), temperature perception reversal (2), numbness of the mouth (1), and dental pain (2).
§ These included dysuria and difficulty in passing urine.
Abdominal pain9530 (32.6)
Diarrhea9564 (67.4)
Vomiting9559 (62.1)
Hypotension*7934 (43.0)
Bradycardia†7836 (46.1)
neurologic symptoms‡9517 (17.8)
Urinary symptoms§957 (7.4)
Joint pain9515 (15.7)
Figure 1.
Figure 1.

Admissions with a diagnosis of fish poisoning to the Northern District and Lolowi Hospitals in Vanuatu, 1986–1995.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 68, 2; 10.4269/ajtmh.2003.68.263

Figure 2.
Figure 2.

Monthly admission patterns with a diagnosis of fish poisoning to the hospitals on Santo and Ambae, Vanuatu, 1986–1995.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 68, 2; 10.4269/ajtmh.2003.68.263

Authors’ addresses: Anna Goodman, 13 Ringley Drive, Whitefield, Manchester M45 7DR, United Kingdom. Thomas N. Williams, Department of Paediatrics, St. Mary’s Hospital, Imperial College, London W2 1NY, United Kingdom. Kathryn Maitland, Kenya Medical Research Institute, PO Box 230, Kilifi, Kenya, Fax: 254-1-252-2390, E-mail: kmaitland@kilifi.mimcom.net.

Acknowledgments: We thank the staff of the Northern District and Lolowi Hospitals for their help with this study, and Dr. Tim Vocor for his encouragement and support.

Financial support: Anna Goodman was supported by funds from the University of London. Thomas N. Williams and Kathryn Maitland were supported by the Wellcome Trust.

Disclaimer: None of the authors have any conflicts of interests.

REFERENCES

  • 1

    Cameron J, Flowers AE, Capra MF, 1991. Effects of ciguatoxin on nerve excitability in rats (Part I) and man (Part II). J Neurol Sci 101 :87–97.

    • Search Google Scholar
    • Export Citation
  • 2

    Bagnis R, Kuberski T, Laugier S, 1979. Clinical observations on 3,009 cases of ciguatera (fish poisoning) in the South Pacific. Am J Trop Med Hyg 28 :1067–1073.

    • Search Google Scholar
    • Export Citation
  • 3

    Morris JG, Lewin P, Smith CW, Blake PA, Schneider, R, 1982. Ciguatera fish poisoning epidemiology of the disease on St. Thomas, U.S. Virgin Islands. Am J Trop Med Hyg 31 :574–578.

    • Search Google Scholar
    • Export Citation
  • 4

    Glaziou P, Legrand AM, 1994. The epidemiology of ciguatera fish poisoning. Toxicon 32 :863–873.

  • 5

    Quod JP, Turquet J, 1996. Ciguatera in Reunion Island (SW Indian Ocean): epidemiology and clinical patterns. Toxicon 34 :779–785.

  • 6

    Vogt RL, 1986. Ciguatera fish poisoning - Vermont. MMWR Morb Mortal Wkly Rep 35 :263–264.

  • 7

    Frenette C, MacLean JD, Gyorkos TW, 1988. A large common-source outbreak of ciguatera fish poisoning. J Infect Dis 158 :1128–1131.

  • 8

    Moulignier A, Binet D, Frottier J, 1995. Ciguatera fish poisoning: Europe. J Neurology, Neurosurg Psychiatry 59 :192–199.

  • 9

    Barton ED, Tanner P, Turchen CL, Manoguerra A, Clark RF, 1995. Ciguatera fish poisoning. A southern California epidemic. West J Med 163 :31–35.

    • Search Google Scholar
    • Export Citation
  • 10

    Lewis RJ, 2001. The changing face of ciguatera. Toxicon 39 :97–106.

  • 11

    Tosteson TR, Ballantine DL, Tosteson CG, Bardales AT, Durst HD, Higerd TB, 1986. Comparative toxicity of gambierdiscus toxicus, ostreopsis lenticularis and associated microflora. Marine Fish Rev 48 :57–59.

    • Search Google Scholar
    • Export Citation
  • 12

    Benoit E, Legrand AM, Dubois JM, 1986. Effects of ciguatoxin on current and voltage clamped frog myelinated nerve fibre. Toxicon 24 :357–364.

    • Search Google Scholar
    • Export Citation
  • 13

    Bidard JN, Vijverberg HPM, Frelin C, Chungue E, Legrand AM, Bagnis R, Lazdunski M, 1984. Ciguatoxin is a novel type of sodium channel toxin. J Biol Chem 259 :8353–8357.

    • Search Google Scholar
    • Export Citation
  • 14

    Warrell DA, 1996. Injuries, envenoming, poisoning and allergic reactions caused by animals. Weatherall, DJ, Ledingham, JGG, Warrell, DA, eds. Oxford Textbook of Clinical Medicine. Third edition, Oxford: Oxford University Press, 1142–1143.

  • 15

    Vanuatu Government, 1991. Vanuatu National Population Census, 1989. Port Vila, Vanuatu: Statistics Office.

  • 16

    Vanuatu Government, 1992. Statistical and Epidemiological Report 1989–1991. Port Vila, Vanuatu: Health Planning Unit.

  • 17

    David P, Cillauren E, 1988. A Survey of Village Subsistence Fishing in Vanuatu. Paper presented at the 26th Congress of the International Geographic Union.

  • 18

    Glaziou P, Martin PMV, 1993. Study of factors that influence the clinical response to ciguatera fish poisoning. Toxicon 31 :1151–1154.

  • 19

    Blythe DG, De Silva DP, 1990. Mother’s milk turns toxic following fish feast (letter). JAMA 265 :2339.

  • 20

    Katz AR, Terrell-Perica S, Sasaki DM, 1993. Ciguatera on Kauai: investigation of factors associated with severity of illness. Am J Trop Med Hyg 49 :448–454.

    • Search Google Scholar
    • Export Citation
  • 21

    Tosteson TR, Ballantine DL, Durst HD, 1988. Seasonal frequency of ciguatoxic barracuda in southwest Puerto Rico. Toxicon 26 :795–801.

  • 22

    Blythe DG, De Sylva DP, Fleming LE, Ayyar RA, Baden DG, Shrank K, 1992. Clinical experience with IV mannitol in the treatment of ciguatera. Bull Soc Pathol Exot 85 :425–426.

    • Search Google Scholar
    • Export Citation
  • 23

    Palafox NA, 1992. Review of the use of intravenous mannitol with ciguatera fish poisoning from 1988 to 1992. Bull Soc Pathol Exot 85 :423–424.

    • Search Google Scholar
    • Export Citation
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