Author information Copyright and License information Disclaimer. Copyright notice. This article has been cited by other articles in PMC. Abstract An association between human illness and exposure to Pfiesteria was first observed among laboratory personnel working with the microorganism.
New 'phantom' dinoflagellate is the causative agent of major estuarine fish kills. Differential diagnosis of ulcerative lesions in fish. Insidious effects of a toxic estuarine dinoflagellate on fish survival and human health.
J Toxicol Environ Health. Potential human health effects associated with laboratory exposures to Pfiesteria piscicida. Learning and memory difficulties after environmental exposure to waterways containing toxin-producing Pfiesteria or Pfiesteria-like dinoflagellates. Inhibition of calcium-stimulated ATPase in the hen brain P2 synaptosomal fraction by organophosphorus esters: relevance to delayed neuropathy. J Toxicol Environ Health A. Pfiesteria and the skin: a practical update for the clinician.
Md Med J. A critical review of the Pfiesteria hysteria hypothesis. Similar disturbances in new learning were found in laboratory rats. Rats with an intraperitoneal injection of cells and water from active toxin-producing Pfiesteria cultures had significantly greater learning difficulties in an eight-arm radial maze task compared with control rats Levin et al. In a follow-up study Levin et al. The eight-arm radial maze learning deficit in Pfiesteria -exposed rats was replicated when rats were tested in the standard room, but it was was not observed when the rats were tested in a sound-attenuated chamber Levin et al.
Hence, the convergence of human and animal data suggests that an increased susceptibility to distraction may be associated with Pfiesteria -induced learning and memory deficits. The potential impact of environmental exposure, however, cannot be completely explained by disturbances in divided attention or new learning.
Published group data analyses did not reflect the symptom variability among exposed participants in the Pocomoke, Maryland, study. Analysis of individual cases suggested considerable diversity in the cognitive sequelae of exposure, particularly in persons with high levels of exposure. Three participants in the high-exposure group were functionally amnestic with severe levels of impairment on measures of anterograde memory new learning, free recall, and recognition memory , concentration, and psychomotor speed and dexterity.
Regardless of exposure level, language, visual spatial, and constructional abilities remained unaffected in the Maryland study. The aforementioned cognitive findings could not be explained by alterations in mood, anxiety, factitious memory disturbance, malingering, or mass hysteria Grattan et al. However, in persons with repeated high levels of exposure, the possibility of alterations in mood, affect, or personality after exposure cannot be precluded.
Glasgow and colleagues reported that a premorbidly mild-mannered individual had the new onset of irritability and even some rate attacks after repeated, intense laboratory exposures.
Such personality findings are not inconsistent with the potential effects of neurotoxic or neurologic insult and therefore need to be considered as potential sequelae of exposure.
Extent data Glasgow et al. In the case of environmental exposure, the rate of recovery is proportionate to the initial degree of exposure and neuropsychological insult see Figure 1. Most exposed persons were performing within the normal range, compared with national norms and their own controls, by 3 months postexposure.
Persons in the highly exposed group, with the most severe acute memory problems, returned to the normal range of performance 6 months postexposure. In the absence of baseline cognitive data and comprehensive neuropsychological assessment, we cannot definitively conclude that recovery was complete; however, rudimentary cognitive functions were significantly improved 6 months postexposure.
An additional and important concern is the possible effect of reexposure. It is well established that individuals who have an episode of ciguatara poisoning may have symptom recurrence for months or years Morris et al.
After an initial toxic exposure by ingesting affected fish, these symptoms may be triggered by eating fish with nontoxic levels of the ciguatoxin or consuming alcoholic beverages. One individual Glasgow et al. Recovery was reported after each exposure. However, with each episode, the intensity and number of symptoms increased and involved more neural and bodily symptoms see Table 1. Unfortunately, it was not until that individual was hospitalized for serious symptoms that he learned the Pfiesteria -associated toxin in his laboratory was the probable case of his episodic illnesses.
Fortunately, he was cautioned about this putative neurotoxin before an even more severe medical illness evolved. Preliminary data in our laboratory, albeit tentative, also raise the possibility that repeated environmental exposures at low levels may produce symptoms in some people. Data from clinical case studies to date suggest that exposure to a low-level fish kill event produces alterations in divided attention and memory only in persons with histories of previous high-level exposure.
In cases with a single, low-level exposure, cognitive functions have been consistently assessed as normal. With this potentiality in mind, further studies need to be conducted to examine the conditions under which persons may be at risk for symptom recurrence. Diverse medical, neurologic, and cognitive symptoms have been reported after presumed exposure to a Pfiesteria -related toxin in the laboratory and environmental setting. Acute medical, neurologic, dermatologic, and neuropsychological symptoms usually occur within hours of exposure cessation, and there appears to be a general dose—response relationship between exposure, severity of neuropsychological disturbance, and recovery time.
The actual medical and neurologic effects of exposure appear to subside within a few days to a week and the neuropsychological sequelae appear reversible within 1 to 6 months, depending on the severity of exposure. There is evidence that several hours of intense exposure may produce more severe symptoms than a lower-level exposure of longer duration. The possibility has also been raised that symptoms may reoccur with repeated, low-level exposures in persons with a history of intense exposure.
One of the greatest barriers to the current investigation of human health effects of exposure to P. Thus, while the convergence of data suggests that a Pfiesteria -related toxin causes human illness, it could be argued that another toxin-producing organism e.
The ongoing development of new assays for marine toxin identification is critical to advancing the link between exposure and human illness. Once the specific toxin is characterized, however, it is likely that a wide range of neurologic and neuropsychologic effects will be found to be associated with estuary-induced neurotoxicity.
As in reactions to other neurotoxins, human reactions to exposure are mitigated by numerous additional factors, including intensive of exposure; duration of exposure chronic low level versus intermittent high level ; route of exposure dermal versus inhalation ; confounding environmental factors; confounding behavioral factors; baseline cognitive status; developmental, neurologic, psychiatric, or substance abuse history; and genetics.
We anticipate that the relationship between exposure, medical symptoms, and human neurologic and neuropsychological sequelae will ultimately be very complex. Burkholder J. Noga E. Hobbs C. Glasgow H. Jr Smith S. New phantom dinoflagellate is the causative agent of major estuarine fish kills. Nature : — Erratum published in Nature. Google Scholar. Civelek A. Villergagne V. Dannals R. Grattan L. Morris J. Charache P. El-Nabawi A. Quesenberry M. Saito K. Silbergeld E.
Vasta G. Eldefrawi A. The N-methyl-p-aspartate neurotransmitter receptor is a mammalian brain target for the dinoflagellete Pfiesteria piscicida toxin. Toxicology and Applied Pharmacology : 84 — Jr Burkholder J. Schmechel D. Tester P. Rublee P. Insidious effects of a toxic estuarine dinoflagellate on fish survival and human health.
Journal of Toxicology and Environmental Health 46 : — Golub J. Haselow D. Hageman J. Lopex A. Oldach D. Peri T. Pfiesteria in Maryland: Preliminary epidemiologic findings. Maryland Medical Journal 47 : — Current status and future directions of the investigation and management of the human health effects of exposure to Pfiesteria piscicida or Pfiesteria -like dinoflagellates.
Learning and memory difficulties after environmental exposure to waterways containing toxin-producing Pfiesteria or Pfiesteria -like dinoflagellates. Lancet : — Greenberg D. Tracy J. A critical review of the Pfiesteria hysteria hypothesis. Excess nutrients are common pollutants in coastal waters. Chief sources of nutrient pollution in coastal areas are sewage treatment plants, septic tanks, polluted runoff from suburban landscapes and agricultural operations, and air pollutants that settle on the land and water.
State and federal agencies are working closely with local governments and academic institutions to address the problems posed by Pfiesteria. Federal agencies involved in the effort include the U. Geological Survey, and the U. Department of Agriculture. A few fish with lesions or even a few dead fish are not cause for alarm.
If you experience health problems after being exposed to fish, water, or air at the site of a fish kill or suspected toxic Pfiesteria outbreak, contact your physician and your state or local public health agency at once. Several states have set up Pfiesteria hotlines, listed on the following page. Swimming, boating, and other recreational activities in coastal waters are generally safe.
Do not go into or near the water in areas that are closed by the state. Most species of algae are not harmful. Algae are the energy producers at the base of the ocean's food web, upon which all other marine organisms depend. Scientists call such events "harmful algal blooms. Some harmful algal blooms, like toxic Pfiesteria outbreaks, can cause detrimental effects when the microbes are at low concentrations in the water and cannot be visibly detected.
In other cases, like certain red and brown tides, harmful effects occur when the algae reach high concentrations that discolor the water. Some kinds of algal blooms are harmful because the algae produce one or more toxins that poison fish or shellfish, and can pose human health risks when people come in contact with affected waters.
These toxic algal blooms may also kill seabirds and other animals indirectly as the toxins are passed up the food chain. Certain kinds of these toxic algal blooms can cause human health problems via contaminated seafood, like Ciguatera Fish Poisoning, Amnesic Shellfish Poisoning, and Paralytic Shellfish Poisoning. However, there is no evidence that Pfiesteria-Telated illnesses are associated with eating fish or shellfish.
Most algal blooms are not toxic, but they are still considered harmful if they reduce the amount of light or oxygen in the water, consequently killing sea grasses, fish or other marine life.
Pfiesteria is not a virus, fungus, or bacterium. It is not contagious or infectious, and cannot be "caught" like a cold or flu. Any human health problems associated with the microbe stem from its release of toxins into river and estuarine waters. Preliminary evidence suggests that exposure to Pfiesteria toxins in the air, water, or fish at the site of an outbreak can cause skin irritation as well as short-term memory loss, confusion, and other cognitive impairments in people.
0コメント