DEPARTMENT OF PATHOLOGY
The Johns Hopkins Medical Institutions

Vol. 17, No. 27

THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Monday, July 13, 1998

  1. Provided by Carmela Groves, R.N., M.S., Chief, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.
From July 6, 1998 to July 10, 1998, 4 outbreaks have been reported to the Maryland Department of Health and Mental Hygiene. Of the 4, 2 were clusters of salmonellosis identified through laboratory surveillance, 1 was salmonellosis associated with a food service facility, and 1 was conjunctivitis associated with a long term care facility. Investigation of the source for the two Salmonella clusters is underway.

From June 19, 1998 to June 25, 1998, 3 outbreaks have been reported to the Maryland Department of Health and Mental Hygiene. Two were foodborne gastroenteritis, one of which was associated with a food service facility and one of which was associated with a party in a private home. The third outbreak was scabies associated with a long term care facility.

  1. The Johns Hopkins Hospital. Information provided by Dr. May Arroyo, Department of Pathology.
Case Presentation: A 53 year old Caucasian female with a past medical history significant for asthma developed watery diarrhea and nausea within 9 hours of eating dinner consisting of fried grouper with onions and peppers. In addition, she developed perioral paresthesia and slurring of her speech. She was admitted to a local hospital where she was managed with intraveous fluids. Stool samples were negative for leukocytes, ova, and paratises. Stool cultures were negative for Campylobacter jejuni, Salmonella, Shigella, Yersinia, Vibrio, and Escherichia coli 0157. . The diarrhea and nausea resolved within two days. During her hospitalization, the patient began complaining of cramping of her hands and calves, chills, sweats, temperature perception reversal, and unsteadiness during walking. Sporadic episodes of hot-cold reversal and muscle cramps continued for 1 year. The symptoms were exacerbated by the ingestion of seafood products or alcohol.

Ciguatera poisoning

Ciguatera poisoning results from the ingestion of a variety of reef-dwelling fishes, including grouper, red snapper, barracuda, seabass, and jack species. The disease is caused by a variety of toxins produced by several photosynthetic marine dinoflagellates (1, 2). The best studied of these is Gambierdiscus toxicus which produces ciguatoxin, maitotoxin, scaritoxin, palytoxin, and okadaic acid. The toxins are produced by only certain toxic strains of these dinoflagellates. The dinoflagellates, living as epiphytes on macroalgae or bio-detritus along a coral reef, are ingested by herbivores, and, in turn, carnivore fish. The toxins concentrate as they move up the food chain. Ciguatoxin, the most active toxin, is a polyether, quaternary ammonium compound which is heat stable and not inactivated by food preparation. Ciguatoxin acts by opening voltage-dependent sodium channels thereby leading to membrane depolarization.

Clinical Manifestations: Symptoms usually begin within 12 hours of ingesting a ciguatoxic fish and are characterized by gastrointestinal, musculoskeletal, neurological, and (less commonly) cardiovascular symptoms (1,2,3). Watery diarrhea, nausea, and abdominal cramping are generally the initial symptoms which resolve in 1 or 2 days. Most patients develop temperature-perception reversal (paradoxical dysesthesiae) and dental pain. Neurological symptoms may last for several months or up to a year and include circumoral paresthesias, paresthesias of the extremities, vertigo, and ataxia. Cardiovascular symptoms include bradycardia and hypotension. Other symptoms include pruritus, myalgias, arthralgias, and chills.

Diagnosis: Ciguatera poisoning is a clinical diagnosis. The constellation of gastrointestinal and neurological symptoms, especially temperature-perception reversal, following the consumption of fish should alert the clinician to this diagnosis. Differential diagnosis includes botulism, organophosphate poisoning, paralytic shellfish poisoning, neurotoxic shellfish poisoning, tetrodotoxin poisoning, palytoxin poisoning, and scombroid poisoning. Several ELISA assays have been developed, albeit not commonly used, for the detection of ciguatoxin on fish tissue.

Treatment: The treatment of ciguatera is mostly supportive. Management includes intravenous fluids for fluid loss, and atropine for episodes of bradycardia. Intravenous mannitol has been shown to diminish or prevent the neurological symptoms if administered within the first 24 hours after the onset of symptoms (1,2,3).

Epidemiology: Ciguatoxic fish are present between the latitudes of 35 degrees north and south (1). Ciguatera is endemic to the Caribbean and South Pacific Islands, where the incidence is approximately 97/100,000 (1). In the United States ciguatoxic fish have been identified as far north as North Carolina. Outbreaks of ciguatera, however, have been reported in Vermont, Canada, Chicago, and California due to the importation of ciguatoxic fish. The mortality rate is 0.1 to 1% of poisonings and is related to heart or respiratory failure (1).

References:

(1) Swift, A.E.B., and Swift, T.R. Ciguatera. Clinical Toxicology 31:1-29;1993.

(2) Mines, D.M., Stahmer, S., and Shepherd, S. Poisonings: Food, Fish, Shellfish. Emergency Medicine Clinics of North America 15:157-177:1997.

(3) Underman, A.E., and Leedom, J.M. Fish and shellfish poisoning. Curr. Clin. Top. in Inf. Dis. 13:203-225;1993.