Brevetoxin
Brevetoxins are neurotoxins that bind to voltage-gated sodium channels in nerve cells, leading to disruption of normal neurological processes and causing the illness clinically described as neurotoxic shellfish poisoning (NSP).
Previous studies of the citric acid pathway revealed three and four carbon units that can potentially explain the atypical condensation and oxidation pattern seen in BTX-B.
For instance, pulmonary receptors associated with ligand-gated epithelial Na+ channels and cathepsin inhibition in macrophages have been reported to be affected by brevetoxin exposure.
[10] In humans, the characteristic symptoms of NSP include Paresthesia (tingling), reversal of hot-cold temperature sensation, myalgia (muscle pain), vertigo, ataxia (loss of coordination), abdominal pain, nausea, diarrhea, headache, bradycardia (slow heart rate), dilated pupils and, as previously mentioned, respiratory distress.
Brevetoxins in nature namely results in massive fish kills and the poisoning of marine mammals and other aquatic invertebrates, which in turn are a source of human health problems.
In marine mammals, a clear vector is difficult to identify due to confounding variables such as inability to confirm exposure and complicated pathological testing measures.
In this study, scientists also examine by what category they were exposed, by aerosols or ingestion, which is analyzed by measuring the levels of brevetoxin in the lungs versus in the stomach contents.
These organs include the liver, kidneys, brain, lungs, and stomach contents of all of these animals, and compared them to see where in the food web they were exposed, and to what extent.
Dolphins in this study did not show much tissue damage compared to the other two, indicating that brevetoxin has a more profound lethal impact at lower concentrations.
[12] The range and degree of human health effects seems to vary annually and temporally in coastal regions, depending on the red tide density as well as variation in toxicity differences among dinoflagellate strains and their subsequent consumers.
[8] The Gulf of Mexico, and in particular the west coast of Florida, is the most heavily impacted by the adverse health and environmental effects of nearly annual K. brevis blooms.
This region has suffered significant economic losses in local communities that rely on tourism and recreational fishing along with bad publicity over the years.
It has been shown that the main toxin produced by K. brevis, PbTx-2, is rapidly metabolized, resulting in the production of metabolites that endure in the animal's system for a significantly longer period of time.
Scallops are not monitored, although scallop-related NSP does not normally occur because in most cases, the muscle which does not accumulate brevetoxin to dangerous levels is consumed.
However, smaller bivalves such as chione clams and coquinas can accumulate extremely high levels of brevetoxins and are not monitored, which could potentially impact both human and wildlife health in negative ways.
It is conjectured that chronic low-level exposure to brevetoxin metabolites can occur through shellfish and fish, although the effects of this have not been studied in detail and remain largely unknown.
[17] Along the west coast of Florida, the early phase of K. brevis blooms are initiated by northerly winds, resulting in upwelling events that cause nutrients to rise towards the surface of the water and transport multiple Karenia cell species towards the shore.
The most likely proposition is some combination of the upwelling of subsurface nutrients, land runoff (agricultural and sugar plantations, cattle ranches, golf courses, theme parks, septic systems, etc.)
Hardison concluded that this data suggest that the exposure of marine ecosystems to significantly different toxin levels depends on the nutrient status of the K. brevis cells.
One major concern of this is that management of shellfish bed closures operating under the assumption that brevetoxin concentrations per cell do not vary may compromise public safety if a bloom became nutrient limited.
