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1) The first abstract suggest that predator / prey relationship outcome of P.fiesteria and
rhodomonas is determined by presence and absence of specific bacterium that is a alpha-
proteobacterium which have sequence similarity with roseobactor species present in toxic
dianoflagellete species. In the presence of this bacterial isolate consumption of rhodomonas is
increase that ultimately leads to the growth of Pfiesteria. Molecular analysis of ameboied stages
of toxic culture of clonal P. fiesteria species by verious research group suggested that P. fiesteria
species differe in response to fresh fish mucus, algal prey and inorganic nutrient enrichment
depending on funtional type or toxicity status. There are three functional type of P. fiesteria
ToxA, ToxB, NonIND depending upon their toxicity in the presence of fish, zoospore production
and attraction to fish excreta and mucus. So, this study suggest that Non IND strain should not
used for research about environment control on toxic strain of P fiesteria species.
Right environment condition (overencrichment of nutrient (N&P) - P. fiesteria exposed to large
number of finfish- increase toxin production- distroy fish epidermis- once fish dead- reduce its
toxin production- feeds on the fish either as zoospores or other forms
Whenenvironment condition change- finfish few or low in number - P.fiesteria become nontoxic
or dormant
P. fiesteria also effect people learning and reading capacity and couse other symptoms who are
very close to the contaminated water such as fishermen.
P. fiesteria growth is controlled by temperature and water quality.
3) Production of toxin, toxic activity and attraction to fresh fish tissue and excreta are the
responsed that activated by signal in variably toxic strains of P.fiesteria.
4) inorganic nutrient enrichment, presence of fresh fish and algal prey cause the development of
three strains
5) development of toxicity in Pfiesteria is caused by presence of fresh fish tissue and excreta and
its couse death of live fish. ToxA cause maximum killing have strong attraction to live fish
whereas Tox B has intermediate effect, and Non IND has negligible effect becouse have low
attraction to fresh fish and maximum zoospore production capacity.
2) THE symbiotic relationship of bacteria with Pfiesteria control its growth and consumption of
rhodomonas so to increase consumption of itself P.fiesteria adopt a colonization with bacteria.
Solution
1) The first abstract suggest that predator / prey relationship outcome of P.fiesteria and
rhodomonas is determined by presence and absence of specific bacterium that is a alpha-
proteobacterium which have sequence similarity with roseobactor species present in toxic
dianoflagellete species. In the presence of this bacterial isolate consumption of rhodomonas is
increase that ultimately leads to the growth of Pfiesteria. Molecular analysis of ameboied stages
of toxic culture of clonal P. fiesteria species by verious research group suggested that P. fiesteria
species differe in response to fresh fish mucus, algal prey and inorganic nutrient enrichment
depending on funtional type or toxicity status. There are three functional type of P. fiesteria
ToxA, ToxB, NonIND depending upon their toxicity in the presence of fish, zoospore production
and attraction to fish excreta and mucus. So, this study suggest that Non IND strain should not
used for research about environment control on toxic strain of P fiesteria species.
Right environment condition (overencrichment of nutrient (N&P) - P. fiesteria exposed to large
number of finfish- increase toxin production- distroy fish epidermis- once fish dead- reduce its
toxin production- feeds on the fish either as zoospores or other forms
Whenenvironment condition change- finfish few or low in number - P.fiesteria become nontoxic
or dormant
P. fiesteria also effect people learning and reading capacity and couse other symptoms who are
very close to the contaminated water such as fishermen.
P. fiesteria growth is controlled by temperature and water quality.
3) Production of toxin, toxic activity and attraction to fresh fish tissue and excreta are the
responsed that activated by signal in variably toxic strains of P.fiesteria.
4) inorganic nutrient enrichment, presence of fresh fish and algal prey cause the development of
three strains
5) development of toxicity in Pfiesteria is caused by presence of fresh fish tissue and excreta and
its couse death of live fish. ToxA cause maximum killing have strong attraction to live fish
whereas Tox B has intermediate effect, and Non IND has negligible effect becouse have low
attraction to fresh fish and maximum zoospore production capacity.
2) THE symbiotic relationship of bacteria with Pfiesteria control its growth and consumption of
rhodomonas so to increase consumption of itself P.fiesteria adopt a colonization with bacteria.

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1) The first abstract suggest that predator prey relationship outc.pdf

  • 1. 1) The first abstract suggest that predator / prey relationship outcome of P.fiesteria and rhodomonas is determined by presence and absence of specific bacterium that is a alpha- proteobacterium which have sequence similarity with roseobactor species present in toxic dianoflagellete species. In the presence of this bacterial isolate consumption of rhodomonas is increase that ultimately leads to the growth of Pfiesteria. Molecular analysis of ameboied stages of toxic culture of clonal P. fiesteria species by verious research group suggested that P. fiesteria species differe in response to fresh fish mucus, algal prey and inorganic nutrient enrichment depending on funtional type or toxicity status. There are three functional type of P. fiesteria ToxA, ToxB, NonIND depending upon their toxicity in the presence of fish, zoospore production and attraction to fish excreta and mucus. So, this study suggest that Non IND strain should not used for research about environment control on toxic strain of P fiesteria species. Right environment condition (overencrichment of nutrient (N&P) - P. fiesteria exposed to large number of finfish- increase toxin production- distroy fish epidermis- once fish dead- reduce its toxin production- feeds on the fish either as zoospores or other forms Whenenvironment condition change- finfish few or low in number - P.fiesteria become nontoxic or dormant P. fiesteria also effect people learning and reading capacity and couse other symptoms who are very close to the contaminated water such as fishermen. P. fiesteria growth is controlled by temperature and water quality. 3) Production of toxin, toxic activity and attraction to fresh fish tissue and excreta are the responsed that activated by signal in variably toxic strains of P.fiesteria. 4) inorganic nutrient enrichment, presence of fresh fish and algal prey cause the development of three strains 5) development of toxicity in Pfiesteria is caused by presence of fresh fish tissue and excreta and its couse death of live fish. ToxA cause maximum killing have strong attraction to live fish whereas Tox B has intermediate effect, and Non IND has negligible effect becouse have low attraction to fresh fish and maximum zoospore production capacity. 2) THE symbiotic relationship of bacteria with Pfiesteria control its growth and consumption of rhodomonas so to increase consumption of itself P.fiesteria adopt a colonization with bacteria. Solution 1) The first abstract suggest that predator / prey relationship outcome of P.fiesteria and rhodomonas is determined by presence and absence of specific bacterium that is a alpha- proteobacterium which have sequence similarity with roseobactor species present in toxic
  • 2. dianoflagellete species. In the presence of this bacterial isolate consumption of rhodomonas is increase that ultimately leads to the growth of Pfiesteria. Molecular analysis of ameboied stages of toxic culture of clonal P. fiesteria species by verious research group suggested that P. fiesteria species differe in response to fresh fish mucus, algal prey and inorganic nutrient enrichment depending on funtional type or toxicity status. There are three functional type of P. fiesteria ToxA, ToxB, NonIND depending upon their toxicity in the presence of fish, zoospore production and attraction to fish excreta and mucus. So, this study suggest that Non IND strain should not used for research about environment control on toxic strain of P fiesteria species. Right environment condition (overencrichment of nutrient (N&P) - P. fiesteria exposed to large number of finfish- increase toxin production- distroy fish epidermis- once fish dead- reduce its toxin production- feeds on the fish either as zoospores or other forms Whenenvironment condition change- finfish few or low in number - P.fiesteria become nontoxic or dormant P. fiesteria also effect people learning and reading capacity and couse other symptoms who are very close to the contaminated water such as fishermen. P. fiesteria growth is controlled by temperature and water quality. 3) Production of toxin, toxic activity and attraction to fresh fish tissue and excreta are the responsed that activated by signal in variably toxic strains of P.fiesteria. 4) inorganic nutrient enrichment, presence of fresh fish and algal prey cause the development of three strains 5) development of toxicity in Pfiesteria is caused by presence of fresh fish tissue and excreta and its couse death of live fish. ToxA cause maximum killing have strong attraction to live fish whereas Tox B has intermediate effect, and Non IND has negligible effect becouse have low attraction to fresh fish and maximum zoospore production capacity. 2) THE symbiotic relationship of bacteria with Pfiesteria control its growth and consumption of rhodomonas so to increase consumption of itself P.fiesteria adopt a colonization with bacteria.