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PFIESTERIA AND RELATED DINOFLAGELLATES

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Pfiesteria piscicida and related dinoflagellates are one-celled microorganisms with a diverse array of morphological forms. Pfiesteria has the ability to release exotoxins which can result in the killing of large numbers of fish. Human exposure to the toxin has been associated with a variety of symptoms.

Specific Substances

    1) Pfiesteria piscicida
    2) Dinoflagellates

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Pfiesteria piscicida and related dinoflagellates are one-celled microorganisms with a diverse array of morphological forms. They have 2 flagella that have the ability to secrete 2 harmful exotoxins. These exotoxins are presumed to be a water-soluble neurotoxin that can rapidly kill fish and a lipid-soluble toxin that can initiate epidermal necrosis in fish. The etiology of these fish ulcerations remains unknown.
    B) TOXICOLOGY: There is no available evidence to explain the toxic mechanism in humans or animals.
    C) EPIDEMIOLOGY: Possible estuary-associated syndrome (PEAS) has mostly been described in people along the eastern seaboard, especially in the Chesapeake Bay. Although Pfiesteria piscicida can tolerate varying salinities, the most toxic forms are most prevalent at salinities of 15 parts per thousand (ppt) and temperatures of greater than or equal to 26 degrees C.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Possible estuary-associated syndrome (PEAS) has been used to describe persons with any of the following symptoms within 2 weeks of exposure to estuarine water: intense memory loss, confusion, disorientation, limited ability to learn new information following exposure, peripheral neuropathy, headaches, acute skin burning, skin rash, eye irritation, upper respiratory irritation, muscle cramps, and gastrointestinal complaints (eg, nausea, vomiting, abdominal pain, or diarrhea). There appears to be dose-response relationship between exposure and neuropsychological clinical events. Acute effects of exposure appear to resolve within a few days to a week.
    2) SEVERE TOXICITY: To date, no deaths have been associated with PEAS. The most severe effects include profound memory loss, confusion, difficulty learning new information and disorientation. These effects resolve spontaneously in 1 to 6 months.

Laboratory Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    C) Monitor mental status in symptomatic patients. Neuropsychological tests may be indicated in symptomatic individuals exposed to Pfiesteria toxin.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. In an uncontrolled case series, cholestyramine plus sorbitol appeared to have beneficial effects in patients exposed to Pfiesteria toxin. The proposed mechanism of action was binding of the toxin in the small intestine with subsequent excretion. Neuropsychological tests may be indicated in symptomatic individuals.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended.
    2) HOSPITAL: Consider activated charcoal if the exposure is recent, the patient is not vomiting, and is able to maintain airway. However, the utility of gastric decontamination after ingestion of contaminated material is unknown.
    D) AIRWAY MANAGEMENT
    1) Airway management is very unlikely to be necessary.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION PROCEDURE
    1) It is unknown if hemodialysis would be effective.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Most patients with mild symptoms can be managed at home.
    2) OBSERVATION CRITERIA: Patients with severe gastrointestinal symptoms may need to be monitored for several hours to assess electrolyte and fluid balance. There is no evidence to suggest that asymptomatic patients are likely to develop symptoms and would benefit from observation.
    3) ADMISSION CRITERIA: Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities. A patient with comorbidities that put them at risk for decompensation from the symptoms of PEAS may benefit from admission for IV hydration and further support.
    4) CONSULT CRITERIA: Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    H) PITFALLS
    1) Symptoms are self-limited. Missing an ingestion of a chemical (eg, heavy metal toxicity) or other possible etiologies for a patient’s symptoms. Failure to obtain adequate history of exposure.
    I) DIFFERENTIAL DIAGNOSIS
    1) In patients in whom a source of exposure can be identified, consider heavy metal toxicity. Carbon monoxide poisoning may also present with similar acute symptoms.

Range Of Toxicity

    A) TOXICITY: No specific data exist regarding the concentration or amount of Pfiesteria or related dinoflagellate necessary to cause human symptoms. No deaths have been associated with Pfiesteria exposure in humans.
    B) High concentrations of dinoflagellates may occur during "fish kills", when large numbers of dead fish are found on the surface or underwater due to dinoflagellate toxicity.

Summary Of Exposure

    A) DESCRIPTION: Pfiesteria piscicida and related dinoflagellates are one-celled microorganisms with a diverse array of morphological forms. They have 2 flagella that have the ability to secrete 2 harmful exotoxins. These exotoxins are presumed to be a water-soluble neurotoxin that can rapidly kill fish and a lipid-soluble toxin that can initiate epidermal necrosis in fish. The etiology of these fish ulcerations remains unknown.
    B) TOXICOLOGY: There is no available evidence to explain the toxic mechanism in humans or animals.
    C) EPIDEMIOLOGY: Possible estuary-associated syndrome (PEAS) has mostly been described in people along the eastern seaboard, especially in the Chesapeake Bay. Although Pfiesteria piscicida can tolerate varying salinities, the most toxic forms are most prevalent at salinities of 15 parts per thousand (ppt) and temperatures of greater than or equal to 26 degrees C.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Possible estuary-associated syndrome (PEAS) has been used to describe persons with any of the following symptoms within 2 weeks of exposure to estuarine water: intense memory loss, confusion, disorientation, limited ability to learn new information following exposure, peripheral neuropathy, headaches, acute skin burning, skin rash, eye irritation, upper respiratory irritation, muscle cramps, and gastrointestinal complaints (eg, nausea, vomiting, abdominal pain, or diarrhea). There appears to be dose-response relationship between exposure and neuropsychological clinical events. Acute effects of exposure appear to resolve within a few days to a week.
    2) SEVERE TOXICITY: To date, no deaths have been associated with PEAS. The most severe effects include profound memory loss, confusion, difficulty learning new information and disorientation. These effects resolve spontaneously in 1 to 6 months.

Heent

    3.4.3) EYES
    A) Eye irritation has been reported following contact with Pfiesteria (Samet et al, 2001; CDC, 1997; Matuszak et al, 1998; Glasgow et al, 1995)

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Shortness of breath was reported in 7 of 22 individuals following a Pfiesteria exposure in an estuary in Maryland (Samet et al, 2001).
    B) IRRITATION SYMPTOM
    1) Upper respiratory tract irritation, including coughing and wheezing, has been reported following Pfiesteria contact (CDC, 1997; Matuszak et al, 1998; Shoemaker, 1998; Morris, 1999). Pneumonia has been reported infrequently (Samet et al, 2001).
    C) SINUSITIS
    1) WITH POISONING/EXPOSURE
    a) Sinusitis was reported 13 of 22 individuals following a Pfiesteria exposure in an estuary in Maryland (Samet et al, 2001).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) Various neuropsychological symptoms, including confusion, disorientation, memory problems, and headache have been reported following Pfiesteria exposure. Cognitive disturbances appear to be temporary and do not last more than 2 to 3 weeks. There appears to be a dose-response relationship between exposure and neuropsychological clinical effects (Grattan et al, 2001).
    2) In a retrospective study of 24 people who had contact with the Pocomoke river and other waters of the Chesapeake Bay during periods with high numbers of fish killed with Pfiesteria-like lesions, people with high exposure were significantly more likely to have neuropsychological symptoms compared to controls. These symptoms included confusion, disorientation, new or increasing forgetfulness, or difficulty concentrating (Grattan, 1998).
    3) Tracy et al (1998) studied the psychological health of symptomatic fishermen exposed to Pfiesteria piscicida and unexposed matched fishermen to determine if an underlying disorder played a role in the symptomatic fishermen's complaints. The exposed fishermen had problems with memory, attention, and psychomotor speed. The study found that both groups scored similarly on a Profile of Mood States (POMS) test, indicating that there was not a preexisting, unusual incidence of mood or personality disorders in the affected fishermen.
    4) In a study of 18 people with documented exposure to estuary waters with Pfiesteria or related organisms who had abnormal performances on standardized neurological tests not explained by any other cause, concentration problems, forgetfulness, prospective memory, and information overload were the most common subjective memory complaints. Exposed cases also reported feeling uneasy and confused more than controls (Grattan et al, 1998a).
    5) In a review of Pfiesteria and related dinoflagellates, the authors noted design flaws in some of the Maryland studies, including non-blinding of examiners, case detection depending on neuropsychological tests alone, and no proper control group. The authors suggested that at least 1 other dinoflagellate, Cryptoperidiniopsis, may have played a role in patient symptoms (Smith & Music, 1998).
    6) In a review of the events surrounding the outbreak of symptoms in Maryland in the summer of 1997, Greenberg et al (1998) concluded that the symptoms were not consistent with that of a mass psychogenic illness.
    7) CASE SERIES - Glasgow et al (1995) presented 3 cases in which scientists working with cultures of Pfiesteria or handling fish exposed to Pfiesteria developed neuropsychological symptoms. Symptoms included difficulty concentrating, disorientation, poor memory, depersonalization, irritability, loss of judgment, and personality changes (Glasgow et al, 1995).
    8) Based upon case reports of neurologic deficits from fishermen in Maryland, 3 case reports of scientists exposed to Pfiesteria, and preliminary results of PET scans of a group of symptomatic Maryland cases, Bever et al (1998) suggested that the symptoms were consistent with a limited encephalopathy, possibly involving the inferior frontal and temporal cerebral regions.
    9) In a review of symptomatic persons calling the Maryland Pfiesteria Hotline, low Rey Auditory Verbal Learning Test (RAVLT) scores were correlated with Pfiesteria associated illness. This test is a standardized word list learning task (Golub et al, 1998).
    10) DURATION - In a review of Pfiesteria-associated illness, Grattan (1998) stated that memory and cognitive disturbances seemed to improve gradually over 3 to 6 months (Grattan, 1998).
    B) HEADACHE
    1) In a retrospective study of 24 people who had contact with the Pocomoke river and other waters of the Chesapeake Bay during periods with high numbers of fish killed with Pfiesteria-like lesions, people with high exposure were significantly more likely to have headache compared to controls (Grattan, 1998).
    C) SECONDARY PERIPHERAL NEUROPATHY
    1) CASE REPORT - A laboratory worker experienced acute onset of numbness and tingling of the hands and feet and difficulty walking after working with dilute cultures of Pfiesteria piscicida. The symptoms resolved over a 1 to 2 year period (Glasgow et al, 1995).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MENTAL STATUS CHANGES
    a) In a rat model of learned tasks (e.g., radial-arm maze), rats injected with Pfiesteria piscicida showed a significant learning deficit compared to controls. The effects persisted up to 10 weeks. For rats that had already learned a task, injection of Pfiesteria had no effect on recall of the task (Levin et al, 1997).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea, vomiting, and abdominal cramps have been reported following exposure to Pfiesteria (Samet et al, 2001; CDC, 1997; Matuszak et al, 1998; Glasgow et al, 1995).
    2) CASE REPORTS - A 23-year-old man and a 30-year old woman who were in the water 500 yards downstream of a Pfiesteria fish kill experienced abrupt onset headache and nausea. The woman also had diarrhea and cramping abdominal pain (Shoemaker, 1997).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea has been reported following exposure to Pfiesteria (Samet et al, 2001).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Skin rashes or skin lesions have been observed with Pfiesteria contact (Samet et al, 2001; CDC, 1997; Shoemaker, 1997; Morris, 1999).
    B) DERMATITIS
    1) Skin complaints are relatively common following exposure and may include itching, red bumps or sores, and scaling flat regions (Grattan et al, 2001; Samet et al, 2001).
    2) A scientist developed skin lesions on the hands and arms, with pustular blisters, after handling dilute concentrations of Pfiesteria (Glasgow et al, 1995).
    3) In a retrospective study of 24 people who had contact with the Pocomoke river and other waters of the Chesapeake Bay during periods with high numbers of fish killed with Pfiesteria-like lesions, people with high exposure reported significantly more skin lesions and a burning sensation on the skin compared to controls (Grattan, 1998).
    4) In 13 patients exposed to Pfiesteria on the Pocomoke river during 1997, 9 reported an intense cutaneous burning sensation on contact with the water, with 7 patients developing skin lesions. The authors suggested that many of the skin findings were unrelated to Pfiesteria. However, unexplained skin reactions possibly related to Pfiesteria included edematous, erythematous, or skin-colored papules on the trunk or extremities. Histopathologic examination indicated an inflammatory, toxic, or allergic process. The skin reactions improved within 2 to 4 weeks (Grattan, 1998).
    5) In a review of Pfiesteria, the authors suggested that many of the reported skin lesions may have been attributable to bacteria and other organisms known to cause human skin problems. Further studies were suggested to validate claims of human cell necrosis due to Pfiesteria (Smith & Music, 1998).
    6) In a North Carolina study, 252 crabbers working in waterways affected by Pfiesteria or related organisms were compared to 114 crabbers working in a non-affected area and 125 controls (non-fishermen in the community). The 3 groups were similar except for an increased incidence of skin disorders among crabbers in both Pfiesteria-affected and non-affected waterways, indicating a possible occupational hazard of crab fishing rather than Pfiesteria exposure (Rullan & Jenkins, 1998).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Muscle and leg cramping have been observed following exposure to Pfiesteria (Samet et al, 2001; CDC, 1997; Matuszak et al, 1998)
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) Joint pain has been reported following Pfiesteria exposure (Samet et al, 2001).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    C) Monitor mental status in symptomatic patients. Neuropsychological tests may be indicated in symptomatic individuals exposed to Pfiesteria toxin.
    4.1.2) SERUM/BLOOD
    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) NEUROPSYCHOLOGICAL ASSESSMENT
    a) Neuropsychological testing may be useful in patients with persistent neurocognitive complaints after exposure to Pfiesteria toxin. Ongoing surveillance is also indicated. Further research in this area is suggested to standardize the protocol(s) to be used for neurological assessment following Pfiesteria exposure (Samet et al, 2001).
    2) VISUAL CONTRAST SENSITIVITY TESTS
    a) Visual contrast sensitivity tests have been used as a basis for diagnosing Pfiesteria exposure. Several tests (ie, Lanthony D-15 or Farnsworth-Munsell 100 Hue) have been used to assess color vision. The value of these screening tests, however, may be limited due to underlying eye disorders, which can include corneal and lens disorders that effect contrast sensitivity. In addition, individuals typically exposed to Pfiesteria toxin are more likely to spend significant amounts of time exposed to ultraviolet light which can lead to eye disease (ie, lenticular opacity, age-related macular degeneration). Further study is suggested to determine the usefulness of these studies and the sensitivity of a positive screening finding (Morris, 2001; Samet et al, 2001).

Radiographic Studies

    A) MAGNETIC RESONANCE IMAGING
    1) In several patients with severe alteration in mental status following environmental Pfiesteria exposure, MRI studies were obtained and the results were normal in all cases (Grattan et al, 2001). The utility of MRI has not been determined.
    B) FLUORODEOXYGLUCOSE COMBINED WITH POSITRON EMISSION TOMOGRAPHY (FDG-PET)
    1) In a small study of 8 environmentally exposed individuals, FDG-PET was performed to assess neuropsychological activity. The findings ranged from normal (in the mildly exposed group) to abnormal, but no specific pattern was observed to assess functional abnormality. Based on the complexity of performing and interpreting the results, further case-control studies are recommended to determine the utility of this test (Grattan et al, 2001).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities. A patient with comorbidities that put them at risk for decompensation from the symptoms of PEAS may benefit from admission for IV hydration and further support.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most patients with mild symptoms can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with severe gastrointestinal symptoms may need to be monitored for several hours to assess electrolyte and fluid balance. There is no evidence to suggest that asymptomatic patients are likely to develop symptoms and would benefit from observation.

Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    C) Monitor mental status in symptomatic patients. Neuropsychological tests may be indicated in symptomatic individuals exposed to Pfiesteria toxin.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) The portal of entry of Pfiesteria piscicida or related dinoflagellates is unknown. Prehospital gastrointestinal decontamination is generally not recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) The portal of entry of Pfiesteria piscicida or related dinoflagellates is unknown. Consider activated charcoal if the exposure is recent, the patient is not vomiting, and is able to maintain airway. However, the utility of gastric decontamination after ingestion of contaminated material is unknown.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. In an uncontrolled case series, cholestyramine plus sorbitol appeared to have beneficial effects in patients exposed to Pfiesteria toxin. The proposed mechanism of action was binding of the toxin in the small intestine with subsequent excretion. Neuropsychological tests may be indicated in symptomatic individuals.
    B) MONITORING OF PATIENT
    1) No specific laboratory tests are necessary unless otherwise clinically indicated.
    2) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    3) Monitor mental status in symptomatic patients. Neuropsychological tests may be indicated in symptomatic individuals exposed to Pfiesteria toxin.
    4) Exposure criteria and clinical criteria for evaluating adverse events associated with Pfiesteria piscicida and related organisms have been defined by a multistate CDC sponsored workshop (CDC, 1997; Matuszak et al, 1998).
    5) Exposure criteria are defined as exposure to estuarine water characterized by any of the following:
    a) fish with lesions consistent with Pfiesteria piscicida or morphologically related organism (MRO) toxicity (20% of a sample of at least 50 fish having lesions)
    b) a fish kill involving fish with lesions consistent with Pfiesteria piscicida or MRO toxicity
    c) a fish kill involving fish without lesions, if Pfiesteria piscicida or MROs are present and there is no alternative reason for the fish kill
    d) a documented event with fish displaying aberrant behavior consistent with Pfiesteria piscicida
    6) The clinical criteria defining Estuary Associated Syndrome include any of the following (CDC, 1997):
    a) memory loss
    b) confusion
    c) three or more of the following symptoms:
    1) headache
    2) skin rash
    3) eye irritation
    4) gastrointestinal complaints (nausea, vomiting, diarrhea, and/or abdominal cramps)
    5) acute burning sensation of skin on contact with estuarine water
    6) upper respiratory irritation
    7) muscle cramps
    C) EXPERIMENTAL THERAPY
    1) In an uncontrolled case series, cholestyramine plus sorbitol appeared to have beneficial effects in patients exposed to Pfiesteria toxin. The proposed mechanism of action was binding of the toxin in the small intestine with subsequent excretion (Shoemaker, 1998). Further studies are necessary to determine the role of cholestyramine in treatment of Pfiesteria-related illness.

Enhanced Elimination

    A) SUMMARY
    1) It is unknown if hemodialysis would be effective.

Summary

    A) TOXICITY: No specific data exist regarding the concentration or amount of Pfiesteria or related dinoflagellate necessary to cause human symptoms. No deaths have been associated with Pfiesteria exposure in humans.
    B) High concentrations of dinoflagellates may occur during "fish kills", when large numbers of dead fish are found on the surface or underwater due to dinoflagellate toxicity.

Minimum Lethal Exposure

    A) No deaths have been associated with Pfiesteria exposure in humans (Collier & Burke, 2002).

Toxicologic Mechanism

    A) The morphology and life cycle of Pfiesteria piscicida and other dinoflagellates is very diverse. At least 19 forms of Pfiesteria piscicida exist, including a nearly invisible cyst form that may live in the sediment of a waterway. Pfiesteria piscicida is the only dinoflagellate known to produce high quantities of exotoxins and show a targeted chemosensory killing response in the presence of fish or shellfish.
    B) When Pfiesteria piscicida detects a threshold concentration of fish feces or other secretions in the water, excystment occurs and a flagellated, photosynthesizing, free-swimming form develops. This form can then release multiple aqueous or lipid soluble toxins that can stun fish or attack the surface of the fish itself.
    C) The fish may develop narcosis, lethargy, exhibit a poor fright response, and swim erratically. The dinoflagellate can then form a pseudopodium, which becomes extended and allows attachment to fish tissue while digestion occurs. After the fish kill, the organism may then reenter the cyst phase and return to the sediment at the bottom of the waterway. The cysts can remain dormant for 2 years (Lutz & Burnett, 1998; Glasgow et al, 1995).
    D) Pfiesteria toxin has not been chemically identified, but reports have suggested a lipid soluble form as well as a water soluble form. The toxin may be unstable and degrade rapidly; it may disappear within 21 hours from the site of a fish kill (Smith & Music, 1998) Oldach et al, 1998; (Rullan & Jenkins, 1998; Glasgow et al, 1995).
    E) The portal of entry into humans is unknown, but may occur via aerosolization and entry through mucous membranes or through unbroken or abraded skin (Lutz & Burnett, 1998).
    F) Person-to-person, fish-to-fish, or fish-to-person transmission does not appear to occur. No reports of food borne illness have been described (Rullan & Jenkins, 1998; Matuszak et al, 1997).

General Bibliography

    1) Anon: New source of fish fears. Env Health Perspect 1998; 106:A425-A426.
    2) CDC: Results of the public health response to Pfiesteria workshop - Atlanta, Georgia, September 29-30, 1997. CDC: MMWR 1997; 46:951-952.
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    4) Collier DN & Burke WA: Pfiesteria complex organisms and human illness. South Med J 2002; 95(7):720-726.
    5) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    6) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    7) Glasgow HB, Schmechel DE, & Tester PA: Insidious effects of a toxic estuarine dinoflagellate on fish survival and human health. J Toxicol Env Health 1995; 46:501-522.
    8) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    9) Golub JE, Haselow DT, & Hageman JC: Pfiesteria in Maryland: preliminary epidemiologic findings. Maryland Med J 1998; 47:137-143.
    10) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    11) Grattan LM, Oldach D, & Morris JG: Human helath risks of exposure to pfiesteria piscicida. Bioscience 2001; 51(10):853-857.
    12) Grattan LM, Oldach D, & Tracy JK: Neurobehavioral complaints of symptomatic persons exposed to Pfiesteria piscicida or morphologically related organisms. Maryland Med J 1998a; 127-129.
    13) Grattan LM: Current status and future directions for the investigation and management of the human health effects of exposure to Pfiesteria piscicida or Pfiesteria-like dinoflagellates. Maryland Med J 1998; 47:148-150.
    14) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    15) Kane AS, Oldach D, & Reimschuessel R: Fish lesions in the Chesapeake Bay: Pfiesteria-like dinoflagellates and other etiologies. Md Med J 1998; 47(3):106-112.
    16) Levin ED, Schmechel DE, & Burkholder JM: Persisting learning deficits in rats after exposure to Pfiesteria piscicida. Env Health Perspect 1997; 105:1320-1325.
    17) Lutz LL & Burnett JW: Pfiesteria piscicida. Cutis 1998; 61:122.
    18) Matuszak DL, Sanders M, & Taylor JL: Toxic Pfiesteria and human health. Maryland Med J 1997; 46:515-520.
    19) Matuszak DL, Taylor JL, & Dickson C: Toxic Pfiesteria - surveillance for human disease in Maryland. Maryland Med J 1998; 47:144-147.
    20) Morris JG: Human health effects and Pfiesteria exposure: a synthesis of available clinical data. Environ Health Perspect 2001; 109(Suppl 5):787-790.
    21) Morris JG: Pfiesteria, "the cell from hell", and other toxic algal nightmares. Clin Infect Dis 1999; 28:1191-1198.
    22) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    23) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    24) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    25) Rullan JV & Jenkins SR: The public health implications of Pfiesteria in Virginia. Virginia Med Quarterly 1998; 125:78-80.
    26) Samet J, Bignami GS, Feldman R, et al: Pfiesteria: review of the science and identification of research gaps. Report for the National Center for Environmental Health, Centers for Disease Control and Prevention. Environ Health Perspect 2001; 109(Suppl 5):639-659.
    27) Shoemaker R: Treatment of persistent Pfiesteria-human illness syndrome. Maryland Med J 1998; 47:64-66.
    28) Shoemaker RC: Diagnosis of Pfiesteria-human illness syndrome. Maryland Med J 1997; 521-523.
    29) Smith CG & Music SI: Pfiesteria in North Carolina. The medical inquiry continues. NC Med J 1998; 59:216-220.