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Epidemiologic Notes and Reports Fish Botulism --- Hawaii, 1990

On July 22, 1990, the Hawaii Department of Health (HDH) was notified that three adults from the same family had been hospitalized July 20--22 with clinical manifestations consistent with botulism. The first patient, a Hawaiian woman of Filipino origin, had onset on July 18 of double vision, difficulty swallowing and speaking, and muscle weakness. When admitted to the hospital on July 20, she had bilateral ptosis, extraocular movement dysfunction, absence of gag reflex, and prominent muscle weakness. During the next 3 days, she developed progressive respiratory impairment and respiratory acidosis. On July 21, her mother was hospitalized with similar manifestations but without respiratory difficulty. On July 22, the index patient's husband was hospitalized with transient ptosis, blurred vision, and dysphonia. All patients were treated with botulinal antitoxin on July 23 and survived. Serum specimens obtained from all three patients after initiation of antitoxin therapy were negative for botulinal toxin. However, stool cultures obtained from the index patient and her mother yielded type B Clostridium botulinum. A common meal of palani (surgeon fish) had been prepared and eaten at home on the evening of July 17. Samples of leftover fish were tested at CDC and contained type B C. botulinum toxin; culture of the samples yielded type B C. botulinum.

The palani, a reef scavenger fish eaten by local residents, had been purchased fresh and cleaned at a retail fish market on July 17, the day of the meal; the index patient's husband cooked the palani directly on the grill at home. After grilling the palani on both sides, he opened the fish with his fingers and noted remnants of the intestines inside the fish. Both the index patient and her mother ate the palani's intestines and the meat around it; the index patient's husband used his fingers to eat the meat near the head and tail, but avoided the intestines. A fourth family member present at the same meal ate meat from the back of the palani only and had no symptoms.

The palani had been sold to the market by local fishermen sometime during July 2--13; the length of time the palani had been held by the market could not be determined. An inspection of the market on August 7 found that fish were kept on ice in a display freezer case with nonfunctional cooling equipment; the internal temperature of the fish on top of the ice in the display freezer was 52 F (11 C). The HDH instructed the market to properly refrigerate the fish and recommended that fish be thoroughly cleaned and rinsed at the market when requested by customers; otherwise, customers should be clearly instructed to clean the fish thoroughly and dispose of all internal organs. Reported by: P Kershaw, MD, Maui Memorial Hospital, Wailuku; M Dioso, MD, B Wong, MD, Kaiser Clinic, Wailuku; C Ibara, D Robertson, MN, W Tamao, M Sugi, MPH, EW Pon, MD, State Epidemiologist, Hawaii Dept of Health. Enteric Diseases Br, Div of Bacterial and Mycotic Diseases, Center for Infectious Diseases; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note:

Foodborne botulism is caused by consumption of a neurotoxin produced by C. botulinum. Illness is characterized by cranial nerve dysfunction and descending muscle paralysis, which can progress to respiratory compromise. In the United States, most cases are associated with home-canned or preserved products. The diagnosis of botulism can be confirmed by detection of neurotoxin in serum samples collected before antitoxin administration, by demonstration of neurotoxin in samples of stool or food, or by isolation of C. botulinum from a patient's stool. Because antitoxin may prevent progression of paralysis if administered shortly after onset of symptoms, clinicians should not wait for laboratory confirmation to consider antitoxin administration. Careful monitoring of respiratory function and intubation, if necessary, can be lifesaving. Testing of clinical or food specimens and acquisition of antitoxin can be arranged through state health departments.

The association between botulism and consumption of contaminated fish has been well established. From 1950 through 1989, 48 (13%) of 365 foodborne outbreaks of botulism in the United States were associated with consumption of fish (1; CDC, unpublished data). In all of these incidents, the fish had been processed and held before consumption. However, this report of fish-associated botulism from Hawaii is unusual because fresh (unpreserved and unfermented) fish was implicated as the source; this appears to be the first report in the United States of botulism caused by consumption of apparently fresh fish. This report is also unusual because most fish-associated cases of botulism are caused by type E C. botulinum; only three of the previous fish-associated outbreaks in the United States were caused by type B C. botulinum (1; CDC, unpublished data).

C. botulinum spores are common in marine sediments (2) and are frequently detected in fish intestines (3). Previous outbreaks of botulism in California, New York, and Israel were associated with consumption of kapchunka, an uneviscerated, freshwater fish soaked in brine and air-dried (4--8). In these outbreaks, salt concentrations, adequate to inhibit growth of C. botulinum in the flesh of the kapchunka, were considered to have been lower in the intestines, allowing C. botulinum organisms to produce toxin (4). In Hawaii, clinical manifestations were most severe in the two persons who ate fish intestines. Localization of toxin within the fish may be important because the consumption of fish intestines may be common in some ethnic groups.

Because refrigeration had been inadequate at the market, the internal temperature of the fish may have been elevated for lengthy periods. The conditions around the retained gut may have facilitated an anaerobic environment, allowing production of toxin. Although botulinal toxin is heat labile, cooking was insufficient to inactivate the toxin.

Because ethnic foods, such as kapchunka and possibly other ungutted fish, may continue to be rare sources of botulism in the United States, public health measures to prevent this problem must take into account local cultural practices. When botulism is suspected, state health departments should be contacted immediately, as rapid intervention may prevent additional cases and prompt administration of antitoxin may halt progression of symptoms.


  1. Feldman RA, Morris JG Jr, Pollard RA. Epidemiologic characteristics of botulism in the United States, 1950--1979. In: Lewis GE Jr, ed. Biomedical aspects of botulism. New York: Academic Press, 1981:271--84.

  2. Hauschild AHW. Clostridium botulinum. In: Doyle MP, ed. Foodborne bacterial pathogens. New York: Marcel Dekker, Inc., 1989:112--89.

  3. Ward BQ, Carroll BJ, Garrett ES, Reese GB. Survey of the U.S. gulf coast for the presence of Clostridium botulinum. Appl Microbiol 1967;15:629--36.

  4. Slater PE, Addiss DG, Cohen A, et al. Foodborne botulism: an international outbreak. Int J Epidemiol 1989;18:693--6.

  5. Telzak EE, Bell EP, Kautter DA, et al. An international outbreak of type E botulism due to uneviscerated fish. J Infect Dis 1990;161:340--2.

  6. California Department of Health Services. Alert: botulism associated with commercially produced, dried salted whitefish. California Morbidity 1981;(Nov 6; suppl 43).

  7. CDC. Botulism associated with commercially distributed kapchunka---New York City. MMWR 1985;34:546--7.

  8. Badhey H, Cleri DJ, D'Amato RF, et al. Two fatal cases of type E adult food-borne botulism with early symptoms and terminal neurological signs. J Clin Microbiol 1986;23:616--8.

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