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ACUTE EXPOSURE INFORMATION

1. WITH POISONING/EXPOSURE
   1. CDC CASE DEFINITIONS
      1. BACKGROUND
         1. Harmful algal blooms (HABs) are fast growing algae that are found worldwide, which can have a negative impact on the environment, as well as the health and safety of humans and animals. As part of the ongoing efforts of the Centers for Disease Control and Prevention (CDC), the Harmful Algal Bloom-related Illness Surveillance System (HABISS) collects data on the effects to human and animal health due to the potential environmental impact of HABs. The CDC has developed case definitions for HABs toxin-related disease as part of their national surveillance efforts to support public health decision-making. The following information has been created to identify pertinent information related to a potential exposure to HABs. For further information regarding the reporting of suspected human illness due to HABs, please contact: Lorraine C. Backer, PhD, MPH, Senior Scientist and Team Lead, National Center for Environmental Health, CDC, Atlanta, GA at lfb9@cdc.gov or Rebecca LePrell, MPH, HABISS Coordinator, National Center for Environmental Health, CDC, at gla7@cdc.gov.
      2. ACUTE SYMPTOMS
         1. Hypothermia, hypotension due to vasodilation, bradycardia, dysrhythmias, and asystole can occur. Hypertension has also been reported. Nausea, vomiting, diarrhea, salvation and diaphoresis may occur. Death is typically caused by respiratory depression and respiratory muscle paralysis. Cyanosis and depression of the cough reflex can also occur. Vertigo, dizziness, headache and blurred vision are common. Generalized weakness in the limbs with ascending onset, paresthesias (particularly perio-oral), ataxia, and areflexia may occur. Seizures are rare. Victims may appear comatose with pinpoint or dilated fixed pupils, but they are actually completely aware as long as ventilation is provided.
      3. CHRONIC SYMPTOMS
         1. At present time, no data available regarding chronic symptoms.
      4. FATALITY RATE
         1. Fatality rates can vary and are dependent on the correct diagnosis and treatment (including life support and ICU facilities availability). The reported fatality rates have varied from 13% to 60%.
      5. ONSET OF SYMPTOMS
         1. Symptoms can present in minutes to hours. Death may occur within the first 6 to 24 hours, and prognosis is good if patient survives the first 24 hours.
      6. DURATION
         1. Recovery is usually seen within days, but there has been no formal follow-up beyond days to weeks.
      7. ROUTE OF EXPOSURE
         1. Consumption of the flesh, viscera, ovaries, or skin of contaminated fish. The musculature is usually free of toxin.
      8. CAUSATIVE ORGANISMS
         1. Recent evidence suggests that the tetrodotoxin may be produced by bacteria in the implicated fish, rather than by the fish themselves. The following organisms have been implicated: Epiphytic bacteria (Aleromonas spp.), Vibrio spp., Psuedomonas spp., and Dinoflagellate Alexandrium tamarense.
      9. TOXIN
         1. Tetrodotoxin
         2. Pufferfish poisoning with saxitoxins, not tetrodotoxins, have been reported; therefore although the clinical presentation and symptoms are similar, confirmatory laboratory testing must be performed for both saxitoxins and tetrodotoxins.
      10. DOSE
          1. A dose of approximately 10 mcg/kg is thought to be a serious toxic dose for humans based on extrapolated mouse data. Oral LD50 for mice is 334 mcg/kg.
      11. VECTOR
          1. Tetradontiformes: balloon fish, blow-fish, globe fish, swellfish, toad fish, "fugu" in Japan (Speroides vermicularis, Speroides rubripes, Takifugu oblongus), and other pufferfish varieties from the coasts of Japan, Thailand, Bangladesh, the Phillipines and southeastern US Atlantic coast.
          2. Levels of tetrodotoxin are particularly high in the gonads and viscera of the pufferfish. In Japan, licensed chefs with special training prepare the "fugu" as a soup or sashimi to avoid tetrodotoxin contamination of the muscle by the viscera and gonads.
          3. Tetrodotoxins can be accumulated in the following: blue-ringed octopus (Haplochlaena maculosa), salamanders and newts (Tarichatorosa), crab (Xanthid), starfish (Astropecten latespinosus, A. Scoparius, A. polyacanthus), flatworms, ribbonworms, arrowworms, annelids, red calcareous alga (Jania spp.), gastropod mollusks and Gobius criniger.
      12. MECHANISM
          1. Tetrodotoxin is a potent neurotoxin which blocks sodium ion channels in nerves, particularly skeletal muscles, causing paralytic poisoning through blockade of both action potential generation and impulse conduction.
      13. LIKELY GEOGRAPHIC DISTRIBUTION
          1. It is most common in subtropical and tropical marine waters, although tetrodotoxins have been reported in freshwater pufferfish as well.
      14. DIFFERENTIAL DIAGNOSIS
          1. Other marine toxin poisonings (primarily neurotoxic shellfish poisoning), brevetoxicosis in the food web, scombroid fish poisoning, ciguatera fish poisoning, pesticide poisoning including organophosphate poisoning, cholinesterase inhibitor poisoning, microbial food poisonings, botulism, guillain-barre.
      15. DIAGNOSIS
          1. May be based on all of the following: history of consuming pufferfish and subsequent onset of gastrointestinal and neurologic symptoms or detection of tetrodotoxin in meal remnant or clinical specimen (urine or blood) by HPLC. Urine HPLC can be utilized up to 5 days after exposure.
      16. SUSPECT CASE
          1. History of consuming pufferfish and very rapid onset of symptoms.
          2. Victims can present much like victims of PSP and may even be suffering from saxitoxin contaminated pufferfish poisoning; therefore both toxins must be tested for in any specimens.
      17. CONFIRMED CASE
          1. Suspect cases along with laboratory confirmation of toxin in meal remnants or clinical specimen.
      18. REFERENCES
          1. (HABISS Work-Group et al, Jan 12, 2009).

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