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Brit Heidenreich - One of the best experts on this subject based on the ideXlab platform.
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Paralytic shellfish toxins seem absent in extracts of diarrhetic shellfish toxins
Environmental Toxicology and Chemistry, 1991Co-Authors: Ole B. Stabell, Magne Yndestad, Brit HeidenreichAbstract:It has been assumed that the water-soluble Paralytic shellfish toxins are extracted and concentrated by the organic-solvent extraction method used for diarrhetic shellfish toxins. As diarrhetic toxin extracts of mussels with high levels of Paralytic toxins are found nontoxic, it appears that Paralytic toxins are not present in those extracts.
Shanop Shuangshoti - One of the best experts on this subject based on the ideXlab platform.
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Dogs that develop rabies post-vaccination usually manifest the Paralytic subtype.
Preventive veterinary medicine, 2016Co-Authors: Veera Tepsumethanon, Wanlop Likitsuntonwong, Paul S. Thorner, Shanop ShuangshotiAbstract:Abstract Rabies infection can manifest as either encephalitic (furious) or Paralytic (dumb) types, with a ratio of approximately 2:1 in dogs. The clinical type of rabies that develops post-vaccination has only been reported in studies from one country, all with similar findings. We report a study of 36 rabid dogs with obtainable vaccination history, presenting to The Queen Saovabha Memorial Institute, Bangkok, Thailand during 2002–2008. Dogs were classified into encephalitic or Paralytic types. Of 22 non-vaccinated dogs, 16 (73%) had the encephalitic type. In contrast, of the 14 vaccinated dogs, 10 (71%) had the Paralytic type, a difference that was significant ( p = 0.016). Recent studies on canine brains have shown that lymphocyte response is more pronounced in Paralytic rabies at the brainstem level, whereas viral burden is greater in the encephalitic form. We postulate partial immune response in the vaccinated dogs might influence rabies to manifest as the Paralytic type. These results can serve as a natural experiment that can help explain the basis for the differences between the Paralytic and encephalitic forms of canine rabies.
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Reduced viral burden in Paralytic compared to furious canine rabies is associated with prominent inflammation at the brainstem level
BMC Veterinary Research, 2013Co-Authors: Shanop Shuangshoti, Supaporn Wacharapluesadee, Veera Tepsumethanon, Nischol Thepa, Pornchai Phukpattaranont, Akanitt Jittmittraphap, Nirun Intarut, Paul Scott Thorner, Thiravat HemachudhaAbstract:Background The mechanisms that differentiate rabies infections into furious and Paralytic forms remain undetermined. There are no neuropathological features in human brains that distinguish furious and Paralytic rabies. This could be due to methodology and/or examination of specimens late in the disease course. In this study, postmortem examination of brain (5 furious and 5 Paralytic) and spinal cord (3 furious and 3 Paralytic) specimens was performed in 10 rabies-infected dogs, sacrificed shortly after developing the illness. Rabies virus (RABV) antigen (percentage of positive neurons, average antigen area in positive neurons and average antigen area per neuron) and RNA were quantified at 15 different central nervous system (CNS) regions. The distribution and degree of inflammation were also studied. Results More RABV antigen was detected in furious rabies than Paralytic in many of the CNS regions studied. Caudal-rostral polarity of viral antigen distribution was found in both clinical forms in order from greatest to least: spinal cord, brainstem, cerebellum, midline structures (caudate, thalamus), hippocampus, and cerebrum. In contrast, RABV RNA was most abundant in the cerebral midline structures. Viral RNA was found at significantly higher levels in the cerebral cortex, thalamus, midbrain and medulla of dogs with the furious subtype. The RNA levels in the spinal cord were comparable in both clinical forms. A striking inflammatory response was found in Paralytic rabies in the brainstem. Conclusions These observations provide preliminary evidence that RABV antigen and RNA levels are higher in the cerebrum in furious rabies compared to the Paralytic form. In addition, brainstem inflammation, more pronounced in Paralytic rabies, may impede viral propagation towards the cerebral hemispheres.
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reduced viral burden in Paralytic compared to furious canine rabies is associated with prominent inflammation at the brainstem level
BMC Veterinary Research, 2013Co-Authors: Shanop Shuangshoti, Supaporn Wacharapluesadee, Veera Tepsumethanon, Paul S. Thorner, Nischol Thepa, Pornchai Phukpattaranont, Akanitt Jittmittraphap, Nirun Intarut, Thiravat HemachudhaAbstract:Background The mechanisms that differentiate rabies infections into furious and Paralytic forms remain undetermined. There are no neuropathological features in human brains that distinguish furious and Paralytic rabies. This could be due to methodology and/or examination of specimens late in the disease course. In this study, postmortem examination of brain (5 furious and 5 Paralytic) and spinal cord (3 furious and 3 Paralytic) specimens was performed in 10 rabies-infected dogs, sacrificed shortly after developing the illness. Rabies virus (RABV) antigen (percentage of positive neurons, average antigen area in positive neurons and average antigen area per neuron) and RNA were quantified at 15 different central nervous system (CNS) regions. The distribution and degree of inflammation were also studied.
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Furious and Paralytic rabies of canine origin: Neuroimaging with virological and cytokine studies
Journal of NeuroVirology, 2008Co-Authors: Jiraporn Laothamatas, Supaporn Wacharapluesadee, Boonlert Lumlertdacha, Sumate Ampawong, Vera Tepsumethanon, Shanop Shuangshoti, Patta Phumesin, Sawwanee Asavaphatiboon, Ladawan Worapruekjaru, Yingyos AvihingsanonAbstract:Furious and Paralytic rabies differ in clinical manifestations and survival periods. The authors studied magnetic resonance imaging (MRI) and cytokine and virus distribution in rabies-infected dogs of both clinical types. MRI examination of the brain and upper spinal cord was performed in two furious and two Paralytic dogs during the early clinical stage. Rabies viral nucleoprotein RNA and 18 cytokine mRNAs at 12 different brain regions were studied. Rabies viral RNA was examined in four furious and four Paralytic dogs during the early stage, and in one each during the late stage. Cytokine mRNAs were examined in two furious and two Paralytic dogs during the early stage and in one each during the late stage. Larger quantities of rabies viral RNA were found in the brains of furious than in Paralytic dogs. Interleukin-1β and interferon-γ mRNAs were found exclusively in the brains of Paralytic dogs during the early stage. Abnormal hypersignal T2 changes were found at hippocampus, hypothalamus, brainstem, and spinal cord of Paralytic dogs. More widespread changes of less intensity were seen in furious dog brains. During the late stage of infection, brains from furious and Paralytic rabid dogs were similarly infected and there were less detectable cytokine mRNAs. These results suggest that the early stage of furious dog rabies is characterized by a moderate inflammation (as indicated by MRI lesions and brain cytokine detection) and a severe virus neuroinvasiveness. Paralytic rabies is characterized by delayed viral neuroinvasion and a more intense inflammation than furious rabies. Dogs may be a good model for study of the host inflammatory responses that may modulate rabies virus neuroinvasiveness.
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Difference in neuropathogenetic mechanisms in human furious and Paralytic rabies.
Journal of the neurological sciences, 2005Co-Authors: Erawady Mitrabhakdi, Jiraporn Laothamatas, Shanop Shuangshoti, Pongsak Wannakrairot, Richard A Lewis, Keiichiro Susuki, Thiravat HemachudhaAbstract:Whereas paralysis is the hallmark for Paralytic rabies, the precise pathological basis of paralysis is not known. It is unclear whether weakness results from involvement of anterior horn cells or of motor nerve fibers. There is also no conclusive data on the cause of the neuropathic pain which occurs at the bitten region, although it has been presumed to be related to sensory ganglionopathy. In this study, six laboratory-proven rabies patients (three Paralytic and three furious) were assessed clinically and electrophysiologically. Our data suggests that peripheral nerve dysfunction, most likely demyelination, contributes to the weakness in Paralytic rabies. In furious rabies, progressive focal denervation, starting at the bitten segment, was evident even in the absence of demonstrable weakness and the electrophysiologic study suggested anterior horn cell dysfunction. In two Paralytic and one furious rabies patients who had severe paresthesias as a prodrome, electrophysiologic studies suggested dorsal root ganglionopathy. Postmortem studies in two Paralytic and one furious rabies patients, who had local neuropathic pain, showed severe dorsal root ganglionitis. Intense inflammation of the spinal nerve roots was observed more in Paralytic rabies patients. Inflammation was mainly noted in the spinal cord segment corresponding to the bite in all cases; however, central chromatolysis of the anterior horn cells could be demonstrated only in furious rabies patient. We conclude that differential sites of neural involvement and possibly different neuropathogenetic mechanisms may explain the clinical diversity in human rabies.
Jennifer S. Knaack - One of the best experts on this subject based on the ideXlab platform.
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Rapid and Sensitive ELISA Screening Assay for Several Paralytic Shellfish Toxins in Human Urine
Journal of analytical toxicology, 2017Co-Authors: Padmanabhan Eangoor, Amruta S. Indapurkar, M Vakkalanka, Jihee Stephanie Yeh, Jennifer S. KnaackAbstract:Paralytic shellfish poisoning is caused by a group of Paralytic shellfish toxins that are produced by dinoflagellates. Toxins in this group include saxitoxin, neosaxitoxin and gonyautoxins. A rapid diagnostic test to identify poisoning by these toxins can be helpful in guiding the appropriate treatment of victims. Additionally, quick receipt of diagnostic results can provide timely proof that shellfish harvesting should be stopped in a given area, thereby preventing additional exposures. We have developed and validated a rapid urinary enzyme-linked immunosorbent assay-based screening test to diagnose exposure to several major Paralytic shellfish toxins. The lower limit of detection (LLOD) for multiple Paralytic shellfish toxins was characterized as 0.02, 0.10, 0.10, 1.0, 1.0 and 15 ng/mL for saxitoxin, gonyautoxin 2,3, decarbamoyl gonyautoxin 2,3, decarbamoyl saxitoxin, neosaxitoxin and gonyautoxin 1,4, respectively. No interferences were identified in unspiked pooled urine or in specimens collected from unexposed individuals indicating that this method is specific for the Paralytic shellfish toxins tested. The accuracy of this test was demonstrated in 10 individual urine specimens with osmolalities ranging from 217 to 1,063 mOsmol/kg and pHs ranging between 5.06 and 7.45. These specimens were spiked with toxins at their LLODs and the presence of toxins at these concentrations was accurately identified in all cases. These results indicate that this diagnostic test can be used to rapidly and accurately screen urine for Paralytic shellfish toxins.
Ole B. Stabell - One of the best experts on this subject based on the ideXlab platform.
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Paralytic shellfish toxins seem absent in extracts of diarrhetic shellfish toxins
Environmental Toxicology and Chemistry, 1991Co-Authors: Ole B. Stabell, Magne Yndestad, Brit HeidenreichAbstract:It has been assumed that the water-soluble Paralytic shellfish toxins are extracted and concentrated by the organic-solvent extraction method used for diarrhetic shellfish toxins. As diarrhetic toxin extracts of mussels with high levels of Paralytic toxins are found nontoxic, it appears that Paralytic toxins are not present in those extracts.
Padmanabhan Eangoor - One of the best experts on this subject based on the ideXlab platform.
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Rapid and Sensitive ELISA Screening Assay for Several Paralytic Shellfish Toxins in Human Urine
Journal of analytical toxicology, 2017Co-Authors: Padmanabhan Eangoor, Amruta S. Indapurkar, M Vakkalanka, Jihee Stephanie Yeh, Jennifer S. KnaackAbstract:Paralytic shellfish poisoning is caused by a group of Paralytic shellfish toxins that are produced by dinoflagellates. Toxins in this group include saxitoxin, neosaxitoxin and gonyautoxins. A rapid diagnostic test to identify poisoning by these toxins can be helpful in guiding the appropriate treatment of victims. Additionally, quick receipt of diagnostic results can provide timely proof that shellfish harvesting should be stopped in a given area, thereby preventing additional exposures. We have developed and validated a rapid urinary enzyme-linked immunosorbent assay-based screening test to diagnose exposure to several major Paralytic shellfish toxins. The lower limit of detection (LLOD) for multiple Paralytic shellfish toxins was characterized as 0.02, 0.10, 0.10, 1.0, 1.0 and 15 ng/mL for saxitoxin, gonyautoxin 2,3, decarbamoyl gonyautoxin 2,3, decarbamoyl saxitoxin, neosaxitoxin and gonyautoxin 1,4, respectively. No interferences were identified in unspiked pooled urine or in specimens collected from unexposed individuals indicating that this method is specific for the Paralytic shellfish toxins tested. The accuracy of this test was demonstrated in 10 individual urine specimens with osmolalities ranging from 217 to 1,063 mOsmol/kg and pHs ranging between 5.06 and 7.45. These specimens were spiked with toxins at their LLODs and the presence of toxins at these concentrations was accurately identified in all cases. These results indicate that this diagnostic test can be used to rapidly and accurately screen urine for Paralytic shellfish toxins.
