Wen discussing chemicals hazards in food, we often mention ciquatoxin, a natural toxin found in tropical predator fish such as grouper and barracuda. CDC’s MMWR (Feb 1, 2013), Ciguatera Fish Poisoning - New York, 2010-2011, is a case study that looks at 28 cases of ciguatera fish poisoning (CFP) in 28 individuals that occurred in a one year period, from August, 2010 to July 2011. 13 people became ill after eating barracuda, and 15 after eating grouper.
The toxin originates as a precursor in dinoflagellates (microalgae) which live in coral reef areas. These algae are eaten by smaller fish and the precursor toxin is converted to the toxic form. Predator fish such as barracuda, grouper, snapper, amberjack and surgeonfish eat these small fish, and over time, this toxin accumulates in the larger fish’s body. People eat these larger fish and then suffer the symptoms of CFP. “CFP is characterized by various gastrointestinal, cardiovascular, and neurologic symptoms. A prolonged period of acute illness can result, and the neurologic symptoms can last months, with variable asymptomatic and symptomatic periods.” Typical symptoms include diarrhea, abdominal cramps, dizziness, headache, faintness, nausea, vomiting and tingling in the extremities (fingers and toes).
Two interesting points made in this report:
- “CFP is considered a highly underreported illness, with only an estimated 10% of cases reported to health authorities (7). Increasing awareness among health-care providers might improve reporting and investigation. However, CFP prevention is complicated by difficulty in identifying high-risk fishing grounds and inadequate industry knowledge and compliance with the FDA seafood Hazard Analysis and Critical Control Point (HACCP) regulations.† Premarket testing of fish for CTX is not feasible because of the lack of rapid field methods and the sporadic distribution of toxic fish, even in endemic areas. Coordinated tracebacks of implicated fish by federal and state agencies to specific fishing grounds remains the primary strategy for managing CFP.”
- “This investigation demonstrates the value of CFP-implicated fish traceback along with updated information on emerging CFP risks, including new harvest areas and species. Prevention through education alone might be limited by seafood mislabeling.”
Ciguatera Fish Poisoning — New York City, 2010–2011
February 1, 2013 / 62(04);61-65
On August 6, 2010, an adolescent female aged 16 years, and her mother aged 47 years went to a hospital emergency department (ED) with diarrhea, light-headedness, and perioral tingling after eating barracuda purchased at a fish market in Queens, New York. Hours later, an additional four family members (three males and one female) who had eaten the same fish, reported tingling in their extremities. Two of the four also visited the ED. Later, the four who had gone to the ED experienced abdominal cramps, dizziness, headache, faintness, nausea, and vomiting. Hypotension and bradycardia persisted, despite volume resuscitation with normal saline. The treating physician suspected a link between the barracuda consumption and neurologic and gastrointestinal symptoms (
Table 1), subsequently diagnosed CFP,* and contacted the NYC Poison Control Center (PCC). The PCC reported the incident to DOHMH, and a DOHMH inspector collected samples of barracuda from the fish market and the patients' home. The inspector also embargoed barracuda sale at the fish market.
Samples were analyzed for CTX at the Gulf Coast Seafood Laboratory of the Food and Drug Administration (FDA) using methods developed by FDA to confirm CFP cases. These methods included an in vitro mouse neuroblastoma cell assay for sodium channel toxins to provide a semiquantitative measure of composite ciguatoxicity in fish (1). Extracts that were positive by this method were subsequently analyzed by liquid chromatography–tandem mass spectrometry for unequivocal confirmation of ciguatoxins (1). One meal remnant was confirmed to contain Caribbean CTX-1 and -2 at a toxicity level of 1.1 µg/kg total C-CTX-1 equivalents, more than 10 times the FDA guidance level of 0.1 µg/kg total C-CTX-1 equivalents. The patients reported that some of their neurologic symptoms persisted for 2–5 months (Table 1).
During August–September 2010, an additional seven CFP cases were reported to DOHMH. These consisted of two outbreaks (outbreaks 2 and 3; Table 1) and a single case. All patients experienced symptoms consistent with CFP after eating barracuda purchased from fish markets in three different NYC boroughs and one restaurant (Table 2). On the evening of November 19, 2010, after reading the health alert about CFP, a physician reported a suspected CFP outbreak in Queens (outbreak 4). This new outbreak involved 11 persons from three families who had eaten fish labeled as grouper that was purchased from a Queens supermarket. Five hours after eating the fish, one family member visited the ED with vomiting, nausea, hypotension, and leg cramping. Shortly thereafter, other members of the family reported experiencing numbness and tingling, and two had bradycardia diagnosed several days after fish consumption. In contrast with previously reported cases, four patients experienced tooth pain or paradoxical dysesthesias (Table 1). New York State Department of Agriculture and Markets completed their traceback investigation and identified the same distributor involved in the barracuda-related CFP outbreak reported earlier that year.
On July 12, 2011, two separate outbreaks and an additional four cases that were associated with eating grouper at Manhattan restaurants were reported to DOHMH. One of the patients was a physically active man who swam >2 miles per day before his illness. After the onset of acute CFP symptoms, he had difficulty walking that persisted for several months. A sample of leftover fish was confirmed by FDA to contain 1.9 µg/kg total C-CTX-1 equivalents, exceeding the FDA guidance level by almost 20 times. Before this most recent outbreak, the implicated vendor was inspected by FDA and issued a warning letter detailing violations.
Nathan Graber, MD, Faina Stavinsky, MS, Robert Hoffman, MD, Jessica Button, Nancy Clark, MA, New York City Dept of Health and Mental Hygiene; Scott Martin, MD, Stony Brook Univ Medical School, Stony Brook, New York. Alison Robertson, PhD, Food and Drug Administration. John Hustedt, MPH, Public Health Prevention Svc, CDC. Corresponding contributor: John Hustedt, firstname.lastname@example.org, 212-788-4290.
CTX are naturally occurring toxins that can accumulate in commonly consumed coral reef fish (e.g., barracuda, grouper, snapper, amberjack, and surgeonfish). Precursors of CTX are derived from marine dinoflagellates (microalgae) that live on the surfaces of seaweeds and denuded corals. These microalgae are consumed by herbivorous fish and undergo bioconversion to the more potent CTX as they move through the food chain. CTX can accumulate in reef fish that eat other fish, reaching levels that can cause CFP among humans when consumed. The toxins are colorless, odorless, tasteless, and temperature-stable, making them difficult to detect or destroy. Consequently, CFP occurrence is not attributable to incorrect food handling, storage, preparation, or procurement methods. The attack rate can be 80%–90% among persons who have eaten a toxic fish, depending on the concentration of CTX in the fish, the total amount of fish consumed, and the consumer's body weight and health status (2). As in the outbreaks described in this report, symptomatology is variable.
Initial treatment options for CFP are limited and supportive only. The majority of patients experience symptoms within 6–48 hours after eating contaminated fish. In an acutely symptomatic patient, any vital sign instability or electrolyte imbalance should be treated in accordance with the normal standard of care (3). Administration of intravenous mannitol was thought to reduce neuronal edema; however, a randomized double-blind, clinical trial found no evidence of mannitol being superior to normal saline, and mannitol can cause additional side effects, including hypotension, requiring caution during administration (4–6). Treatment of CFP symptoms (e.g., neuropathy, fatigue, and headache) with amitriptyline, sodium channel blockers, and pain medications all have been tried with variable success (4). Consultation with the local PCC is recommended and in NYC fulfills the reporting requirement.
This report reflects the importance of surveillance and outreach networks in responding to patients' histories, including food consumption, that are indicative of CFP, and highlights prevention challenges. Reports made to the NYC PCC allowed expeditious and effective action when the first cases of CFP were reported. Investigators notified other jurisdictions, consulted local health departments with expertise in CFP prevention and case management, and conducted outreach to NYC health-care providers. In southern Florida, where CFP is endemic, 68% of physicians who were presented with a typical case of CFP diagnosed it correctly (7). As a result of considerable education and outreach efforts by the Florida Department of Health during the past decade, accuracy of CFP diagnosis in that state has improved. However, in other nonendemic regions, diagnostic recognition remains low.
An interstate comparison of reports to PCCs revealed additional trends, beyond the increased number of NYC CFP cases. Unpublished data from CFP-related calls to the American Association of Poison Control Centers during 2000–2010 were analyzed for trends and changes in geographic distribution. The data revealed that the rate of CFP-related calls per capita during 2010, compared with the previous 10 years, was 55% higher in NYC but 44% lower in Florida. Although this data set might not be representative of individual state CFP records, the rate per capita of U.S. cases remained relatively constant throughout the preceding 11 years. This increase of reported cases in NYC might reflect changing sources and diversity of fish species marketed in NYC and elsewhere. The increase might also indicate improved awareness and capacity for investigation by the medical and public health community. The decrease in CFP reports from Florida likely was the result of improved awareness of CFP after extensive long-term outreach and education efforts and specific guidance on the harvest of high-risk fish in this endemic region.
CFP is considered a highly underreported illness, with only an estimated 10% of cases reported to health authorities (7). Increasing awareness among health-care providers might improve reporting and investigation. However, CFP prevention is complicated by difficulty in identifying high-risk fishing grounds and inadequate industry knowledge and compliance with the FDA seafood Hazard Analysis and Critical Control Point (HACCP) regulations.† Premarket testing of fish for CTX is not feasible because of the lack of rapid field methods and the sporadic distribution of toxic fish, even in endemic areas. Coordinated tracebacks of implicated fish by federal and state agencies to specific fishing grounds remains the primary strategy for managing CFP.
The findings in this report are subject to at least three limitations. First, meal remnant samples were available only in three of the six CFP outbreaks. Second, where physician reports to the PCC were unavailable, the symptoms were based entirely on self-report or secondhand reports from family members. Finally, additional cases might have occurred but were unrecognized because of lack of physician awareness to make an appropriate diagnosis and the need to report.
This investigation demonstrates the value of CFP-implicated fish traceback along with updated information on emerging CFP risks, including new harvest areas and species. Prevention through education alone might be limited by seafood mislabeling. Reports indicate that 20%–25% of all seafood products are mislabeled (8). A recent assessment of seafood purchased at retail stores and restaurants in New York, New Jersey, and Connecticut indicated that >20% of 190 specimens were mislabeled, incompletely labeled, or misidentified by employees (8). Methods for fish species identification using DNA barcoding have been validated (9) and are being implemented in several U.S. state and federal laboratories, as well as academic institutions. These methods have been applied to multiple CFP cases. Ongoing collaborative efforts with federal, state, and local agencies tasked with consumer protection and food safety might be useful in controlling CFP and mislabeling of fish (10). Until accurate and cost-effective means of premarket testing become available, prevention of additional cases will continue to be dependent on HACCP compliance by the seafood industry and CFP diagnosis and reporting by health-care providers, warranting additional outreach and education.
Munerah Ahmed, MPH, New York City Dept of Health and Mental Hygiene, New York.
Additional information - http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6204a1.htm?s_cid=mm6204a1_x