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The neurologic effects of noxious marine creatures.

The concept of the sea as a source of noxious agents is perhaps not a familiar one to clinical neurologists, judging by the lack of reference to these agents in standard textbooks. Chemical, physiologic, and pharmacologic laboratories are increasingly investigating the properties of marine toxins, finding in them compounds with interesting and novel structures or unusual physiologic effects. Such substances are seen as possible agents for biologic and, more particularly, physiologic research, and as possible sources of new pharmaceuticals. These include hormone-like substances and antiviral or antitumor agents. Despite these specialized developments, which are in large measure a consequence of the technological advances of the present century, the clinician is at times directly concerned with the effects of marine toxic substances. For example, in Japan, puffer fish or tetrodotoxic poisoning is one of the major causes of deaths from food poisoning. Another marine toxin that has caused many explosive outbreaks of food poisoning. with many deaths in various parts of the world, comes from clams or mussels. This toxin, saxitoxin, is produced by species of marine protozoa including Gonyaulax, and is concentrated in filter-feeding molluscs. These two examples were of significant interest in medicine long before the technologic developments of the twentieth century. In the last few decades, entirely new problems of marine intoxication have arisen as a result of marine pollution from the disposal of industrial wastes in the sea. The most striking example of a man-made marine intoxication has been the outbreak of Minamata disease. In Minamata, Japan, the disposal of mercury-contaminated industrial wastes from a plastics factory into an enclosed bay, followed by human consumption of the contaminated fishes, crabs, or shellfish, led to many instances of acute cerebral degeneration. With the increasing exploration of the sea for both pleasure and economic exploitation, which is a feature of the second half of the twentieth century, it may be expected that the frequency and variety of human intoxications by marine creatures will be increased. This chapter reviews the neurologic effects of noxious substances of marine biologic origin. The subject is now developing so rapidly that overall surveys, such as this, of the general animal life of theocens will soon be beyond the scope of a single review. Nevertheless, it is hoped that the references given will enable the interested reader to pursue particular aspects further.

Adult↗

Pectenotoxin-2 seco acid, 7-epi-pectenotoxin-2 seco acid and pectenotoxin-2 in shellfish and plankton from Portugal.

Pectenotoxin-2 seco acid (PTX2sa) and 7-epi-pectenotoxin-2 seco acid (7-epi-PTX2sa) were found in Portuguese shellfish both by fluorescence detection after ADAM derivatisation and, liquid chromatography coupled with mass spectrometry detection. Two time-series both with blue mussel (Mytilus edulis) and common cockle (Cerastoderma edule) from Aveiro lagoon illustrate how PTX2sa has a strong association with Dinophysis acuta occurrence in the plankton, as well as Dinophysis fortii. Data so far excludes D. acuminata from contributing to contamination with pectenotoxins. It also shows that mussel may not be the best indicator of contamination with PTX2sa. At Aveiro lagoon also oyster, razor clam and clams were all less toxic than cockle. Pectenotoxin-2 seco acid was not involved in a previously reported incident of human poisoning that took place in February 1998 after consumption of Donax trunculus. In plankton extracts the most abundant pectenotoxin found was PTX2. Concentration of PTX2sa was around 10% of PTX2, and 7-epi-PTX2sa was not detected.

Animals↗

Vibrio parahaemolyticus-food poisoning: case report.

Symptoms of food poisoning occurred following the ingestion of raw shellfish purchased in the Auckland area. Vibrio parahaemolyticus was recoverer from the patient. The potential of this and closely related microorganisms to cause illness is reviewed.

Adult↗

An outbreak of Salmonella enteritidis phage type 19 infection associated with cockles.

An outbreak of infection with Salmonella enteritidis was detected because some of the cases lived near each other. Swift investigation identified cockles as the vehicle of infection. The cockles had been gathered and cooked by a member of the public. Phage typing of the S. enteritidis revealed phage type 19, which is rarely seen in the United Kingdom. The outbreak illustrates the need for care in handling and preparation of shellfish for human consumption. Catering establishments should be wary when offered foodstuffs from unfamiliar suppliers.

Animals↗

Minamata disease: methylmercury poisoning in Japan caused by environmental pollution.

Minamata disease (M. d.) is methylmercury (MeHg) poisoning that occurred in humans who ingested fish and shellfish contaminated by MeHg discharged in waste water from a chemical plant (Chisso Co. Ltd.). It was in May 1956, that M. d. was first officially "discovered" in Minamata City, south-west region of Japan's Kyushu Island. The marine products in Minamata Bay displayed high levels of Hg contamination (5.61 to 35.7 ppm). The Hg content in hair of patients, their family and inhabitants of the Shiranui Sea coastline were also detected at high levels of Hg (max. 705 ppm). Typical symptoms of M. d. are as follows: sensory disturbances (glove and stocking type), ataxia, dysarthria, constriction of the visual field, auditory disturbances and tremor were also seen. Further, the fetus was poisoned by MeHg when their mothers ingested contaminated marine life (named congenital M. d.). The symptom of patients were serious, and extensive lesions of the brain were observed. While the number of grave cases with acute M. d. in the initial stage was decreasing, the numbers of chronic M. d. patients who manifested symptoms gradually over an extended period of time was on the increase. For the past 36 years, of the 2252 patients who have been officially recognized as having M. d., 1043 have died. This paper also discusses the recent remaining problems.

Disease Outbreaks↗

A semi-quantitative seafood safety risk assessment.

As part of a semi-quantitative risk assessment of 10 seafood hazard/product combinations, a risk assessment tool was used to generate a Risk Ranking. The tool is in a spreadsheet software format and provides a risk estimate, which is scaled between 0 and 100, where 0 represents no risk and 100 represents all meals containing a lethal dose of the hazard. A full description of the tool is contained in Ross and Sumner (this issue). Based on their ranking, seafoods in Australia fell into three risk categories. Hazard/product pairs with ranking < 32 included mercury poisoning (Relative Risk = 24), Clostridium botulinum in canned fish (RR = 25), or in vacuum-packed cold-smoked fish (RR = 28), parasites in sushi/sashimi (RR = 31), viruses in shellfish from uncontaminated waters, (RR = 31), enteric bacteria in imported cooked shrimp (RR = 31) and algal biotoxins from controlled waters (RR = 31). It is noted that there have been no documented cases of food-borne illness from any of the above hazard/product pairings in Australia. Those with rankings 32-48 included Vibrio parahaemolyticus in cooked prawns (RR = 37), V. cholerae in cooked prawns (RR = 37), Listeria monocytogenes in cold-smoked seafoods (RR = 39), scombrotoxicosis (RR = 40), V. vulnificus in oysters (RR = 41), ciguatera in the general Australian population (RR = 45), L. monocytogenes in susceptible (RR = 45) and extremely susceptible populations (RR = 47) and enteric bacteria in imported cooked shrimp eaten by vulnerable consumers (RR = 48). Almost all the hazard/product pairs in this category have caused the outbreaks of food poisoning in Australasia. Those hazard/product pairs with rankings >48 included ciguatera from recreational fishing in susceptible areas (RR = 60), viruses in shellfish from contaminated waters (RR = 67) and algal biotoxins from uncontrolled waters in an algal event (RR = 72). There have been significant (>100 cases) food poisoning incidents involving viruses and biotoxins in shellfish, while ciguatera poisoning is prevalent among coastal communities in Australia's warmer waters.

Australia↗

Sequential involvement of distinct glutamate receptors in domoic acid-induced neurotoxicity in rat mixed cortical cultures: effect of multiple dose/duration paradigms, chronological age, and repeated exposure.

The increasing occurrence of poisoning accidents in marine animals caused by the amnesic shellfish toxin, domoic acid (DOM), necessitates a better understanding of the factors contributing to DOM neurotoxicity. Here we evaluated the contribution and temporal involvement of NMDA, non-NMDA- and metabotropic-type glutamate receptors (GluRs) in DOM-induced neuronal death using rat primary mixed cortical cultures. Co-application of antagonists for AMPA/kainate- (NBQX) and NMDA-type GluRs (D-AP5) but not for metabotropic GluRs reduced DOM toxicity induced by either of three EC50 dose/duration exposure paradigms. Maximal protection offered by D-AP5 and NBQX either extended or not to the 30- to 60-min period after DOM exposure, respectively. Antagonists were ineffective if applied with a 2-h delay, indicating the presence of a critical time window for neuronal protection after DOM exposure. Early effects correlated with neuronal swelling was seen as early as 10 min post-DOM, which has been linked to non-NMDAR-mediated depolarization and release of endogenous glutamate. That DOM toxicity is dictated by iGluRs is supported by the finding that increased efficacy and potency of DOM with in vitro neuronal maturation are positively correlated with elevated protein levels of iGluR subunits, including NR1, GluR1, GluR2/3, GluR5, and GluR6/7. We determined the time course of DOM excitotoxicity. At >10 microM maximal neuronal death occurs within 2 h, while doses < or = 10 microM continue to produce death during the subsequent 22-h washout period, indicating a quicker progression of the neuronal death cascade with high DOM concentrations. Accordingly, NBQX applied 30 min post-DOM afforded better protection against low dose/prolonged duration (3 microM/24 h) than against high dose/brief duration exposure (50 microM/10 min). Interestingly, prior exposure to subthreshold DOM dose-dependently aggravated toxicity produced by a subsequent exposure to DOM. These findings provide greater insight into the complex properties underlying DOM toxicity, including the sequential involvement of multiple GluRs, greater potency with increasing neuronal maturation and protein levels of iGluRs, varying efficacy depending on dose, duration, and prior history of DOM exposure.

Animals↗

Characterization of a cloned pR72H probe for Vibrio parahaemolyticus detection and development of a nonisotopic colony hybridization assay.

Vibrio parahaemolyticus is a halophilic bacterium often found in shellfish and is an important causative agent of food poisoning in Taiwan. A rapid and efficient detection method is required to identify this foodborne pathogen. A 0.76-Kb HindIII DNA fragment was cloned from the chromosomal DNA of V. parahaemolyticus strain no. 93, designated as pR72H fragment, was used as a polynucleotide probe. It was labeled with digoxigenin-11-dUTP (DIG) by the random primer-labeling method. The sensitivity and specificity of the digoxigenin-labeled 0.76-Kb DNA probe was determined by colony hybridization assay. Under stringent hybridization conditions, 122 of 124 isolates of V. parahaemolyticus showed positive hybridization reaction with DIG-0.76-Kb DNA probe; the negative strains were attributed to slow growth. The DIG-0.76-Kb probe did not hybridize with 86 isolates of other vibrios and a number of other enterics as well as nonenteric microorganisms. The sensitivity and specificity of this DIG probe are 98% and 100%, respectively. This nonisotopic colony hybridization assay can be very useful for routine monitoring of V. parahaemolyticus in the food industry, environmental analysis and clinical laboratories.

Chromosomes, Bacterial↗

Occurrence of Vibrio parahaemolyticus in estuarine waters and oysters of New Hampshire.

Vibrio parahaemolyticus was isolated from water and oysters collected from seven different sampling stations in the Great Bay and Little Bay estuarine areas of New Hampshire. The morphological and biochemical characteristics of 50 isolates conformed in general to those described for this organism in the literature. All isolates produced hemolysis on blood-agar. To date, there have been no reports of V. parahaemolyticus food poisoning outbreaks due to the consumption of fish or shellfish harvested from this estuarine region.

Animals↗

[An ecological study for prediction of Vibrio parahaemolyticus food poisoning in Shizuoka prefecture].

The mean MPN viable cell counts in 15 samples of sea water in which clams were held at the time of the onset of mass outbreaks of food poisoning, the number of food poisoning outbreaks, and prevalence of Kanagawa phenomenon-positive strains, and effectiveness of measures to control food poisoning were investigated over 6 years from 1990 to 1995. The results obtained were as follows: 1. Of 6 materials, including sea water and shellfish, which were examined to determine the best marker material for prediction of Vibrio parahaemolyticus food poisoning, sea water in which clams were held was found to be the most appropriate. 2. Except for the outbreaks in 1994, all Vibrio parahaemolyticus food poisoning occurred after the mean MPN viable cell count in 15 samples of sea water in which clams are kept reached 10(5) cells/100 ml. 3. The number of outbreaks of Vibrio parahaemolyticus food poisoning could be predicted based on the time at which the mean MPN viable cell count reached 10(5) cells/100 ml. 4. In 1995, sea water in which clams were held was cultured and examined for thermostable direct hemolysin gene by PCR method. Thermostable direct hemolysin gene was detected in 3 of 82 samples. Thirty-nine Kanagawa phenomenon-positive strains were isolated from 2 of these 3 samples. 5. Kanagawa phenomenon-positive strains were detected after the mean MPN viable cell count in 15 samples of sea water in which clams were kept reached 10(5) cells/100 ml. 6. Four serotypes of Kanagawa phenomenon-positive strains were detected, and they were involved in 5 (45%) of the 11 cases of Vibrio parahaemolyticus food poisoning that occurred in the same year. These serotypes were observed also in 28 (38%) of the 74 strains isolated from food poisoning patients. 7. No conclusion could be made concerning the effectiveness of measures to control food poisoning.

Ecology↗

Seafood-associated disease outbreaks in New York, 1980-1994.

BACKGROUND: Seafood-associated disease outbreaks in New York were examined to describe their epidemiology and to identify areas for prevention and control efforts. METHODS: We reviewed reports submitted to the New York State Department of Health (NYSDOH) of seafood-associated outbreaks occurring from January 1, 1980, through December 31, 1994. RESULTS: During 1980-1994, 339 seafood-associated outbreaks were reported, resulting in 3959 illnesses, 76 hospitalizations, and 4 deaths. During this period, seafood-associated outbreaks accounted for 19% of all reported foodborne outbreaks and 10% of foodborne illnesses. Shellfish, the most frequently implicated seafood item, accounted for 64% of seafood outbreaks, followed by finfish (31% of outbreaks). Of the 148 seafood-associated outbreaks with a confirmed etiologic agent, Norwalk virus and scombrotoxin were the most frequently identified agents: Norwalk virus accounted for 42% of outbreaks and 42% of illnesses, and scombrotoxin accounted for 44% of outbreaks and 19% of illnesses. Three of the 4 seafood-associated deaths were caused by Clostridium botulinum; the remaining death was caused by Vibrio vulnificus. CONCLUSIONS: Reducing the number of seafood outbreaks will require continued and coordinated efforts by many different agencies, including those involved with water quality; disease surveillance; consumer education; and seafood harvesting, processing, and marketing. New York's foodborne disease surveillance data highlight potential areas on which to focus prevention efforts, including: (1) commodities and associated pathogens causing the largest number of seafood-associated outbreaks and illnesses, namely shellfish-associated viral gastroenteritis and finfish-associated scombroid fish poisoning, and (2) venues at which seafood were most frequently consumed in reported outbreaks, such as commercial food establishments and catered events.

Disease Outbreaks↗

[Arsenic poisoning].

BACKGROUND: Arsenic poisoning has been discussed frequently in Norway during the past year on the background of a suspected crime case. There seem to be several uncertainties regarding this issue, also in the medical profession. MATERIAL AND METHODS: We have searched the literature and made a review based upon the present knowledge about arsenic and arsenic poisoning. RESULTS: Arsenic can be found in numerous chemical compounds with different properties. Inorganic arsenic compounds, like arsenic trioxide, are reactive and can cause damage to the body. Organic arsenic compounds, which are found in high concentrations in fish and shellfish, are not considered toxic. Ingestion of inorganic arsenic affects cellular energy production; lethal poisonings can occur. Common clinical features after acute intoxication with arsenic are dysphagia, nausea, vomiting, abdominal pain, diarrhoea, intense thirst, and muscle cramps. Clinical features of chronic poisoning are hyperkeratosis in the palms and foot soles, pigmentation and conjunctivitis. INTERPRETATION: Arsenic poisoning is a rare condition; its clinical features are uncharacteristic and the diagnosis must be confirmed by analysis of blood, urine and hair.

Arsenates↗