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Pampee P Young - One of the best experts on this subject based on the ideXlab platform.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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Brown Recluse Spider bite mediated hemolysis: clinical features, a possible role for complement inhibitor therapy, and reduced RBC surface glycophorin A as a potential biomarker of venom exposure.
Public Library of Science (PLoS), 1Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom.We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naïve cells.Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro.Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation
Richard S. Vetter - One of the best experts on this subject based on the ideXlab platform.
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brown Recluse Spider loxosceles reclusa envenomation in small animals
Journal of Veterinary Emergency and Critical Care, 2009Co-Authors: Lonny B Pace, Richard S. VetterAbstract:Objective – To provide a comprehensive review of relevant literature regarding the brown Recluse Spider (BRS) and to define those criteria that must be satisfied before making a diagnosis of brown Recluse envenomation. Etiology – The complex venom of the BRS contains sphingomyelinase D, which is capable of producing all the clinical signs in the human and some animal models. Diagnosis – There is no current commercially available test. In humans there are many proposed guidelines to achieve a definitive diagnosis; however, there are no established guidelines for veterinary patients. Therapy – Currently, no consensus exists for treatment of BRS envenomation other than supportive care, which includes rest, thorough cleaning of the site, ice, compression, and elevation. Prognosis – Prognosis varies based on severity of clinical signs and response to supportive care.
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Distribution of the brown Recluse Spider (Araneae: Sicariidae) in Georgia with comparison to poison center reports of envenomations.
Journal of medical entomology, 2009Co-Authors: Richard S. Vetter, Nancy C. Hinkle, Lisa M. AmesAbstract:Georgia is on the southeastern margin of the native range of the brown Recluse Spider, Loxosceles reclusa Gertsch and Mulaik. The brown Recluse is not a common Georgia Spider and has limited distribution in the state. Using recent submissions, previously published records, and examination of museum specimens, we document the Spider's presence in 31 (19.5%) of Georgia's 159 counties, with almost all being found in the northern portion. The Spider was collected almost exclusively north of the Fall Line (a transition zone separating the Piedmont and the Coastal Plain geological provinces). Only two locations in the southern Coastal Plain province produced L. reclusa specimens; these southern finds are considered Spiders that were transported outside their range. There were six finds of the non-native world tramp species, L. rufescens (Dufour), three south of the Fall Line. In conspicuous contrast, over a 5-yr period, a Georgia poison center database recorded 963 reports of brown Recluse Spider bites from 103 counties. These figures greatly outnumber the historic verifications of brown Recluses in the state for both specimen quantity and county occurrence, indicating improbable Spider involvement and the overdiagnosis of bites. In the southern half of the state, medical diagnoses of brown Recluse Spider bites have virtually zero probability of being correct. Bite diagnoses should be made with caution in north Georgia given the Spider's spotty distribution with low frequency of occurrence.
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Reports of Presumptive Brown Recluse Spider Bites Reinforce Improbable Diagnosis in Regions of North America Where the Spider Is Not Endemic
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Envenomations by the brown Recluse Spider have been reported throughout North America, despite the fact that the Spider's range is limited to the South and central Midwest of the United States. Several of these medical reports have originated from regions of nonendemicity where the Spider has never or rarely been documented and brown Recluse Spider populations are unknown. In most of these reports, no Spider is positively identified in association with the dermonecrotic wound, and diagnosis has been based on clinical examination findings. Considering the extreme rarity of brown Recluse Spiders in areas of nonendemicity, the diagnosis of a presumptive bite is a misdiagnosis that reinforces the assumption that brown Recluse Spiders are common local etiologic agents of necrosis. There are many medical conditions of diverse origin that have been misdiagnosed as brown Recluse Spider bites, some of which can be fatal or debilitating. Physicians' awareness of these conditions will increase diagnostic accuracy in areas of North America where bites from brown Recluse Spiders are improbable.
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the diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology
Annals of Emergency Medicine, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Abstract [Vetter RS, Bush SP. The diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology. Ann Emerg Med. May 2002;39:544-546.]
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the diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology
Annals of Emergency Medicine, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Abstract [Vetter RS, Bush SP. The diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology. Ann Emerg Med. May 2002;39:544-546.]
Eric A Gehrie - One of the best experts on this subject based on the ideXlab platform.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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Brown Recluse Spider bite mediated hemolysis: clinical features, a possible role for complement inhibitor therapy, and reduced RBC surface glycophorin A as a potential biomarker of venom exposure.
Public Library of Science (PLoS), 1Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom.We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naïve cells.Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro.Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation
Sean P. Bush - One of the best experts on this subject based on the ideXlab platform.
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Reports of Presumptive Brown Recluse Spider Bites Reinforce Improbable Diagnosis in Regions of North America Where the Spider Is Not Endemic
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Envenomations by the brown Recluse Spider have been reported throughout North America, despite the fact that the Spider's range is limited to the South and central Midwest of the United States. Several of these medical reports have originated from regions of nonendemicity where the Spider has never or rarely been documented and brown Recluse Spider populations are unknown. In most of these reports, no Spider is positively identified in association with the dermonecrotic wound, and diagnosis has been based on clinical examination findings. Considering the extreme rarity of brown Recluse Spiders in areas of nonendemicity, the diagnosis of a presumptive bite is a misdiagnosis that reinforces the assumption that brown Recluse Spiders are common local etiologic agents of necrosis. There are many medical conditions of diverse origin that have been misdiagnosed as brown Recluse Spider bites, some of which can be fatal or debilitating. Physicians' awareness of these conditions will increase diagnostic accuracy in areas of North America where bites from brown Recluse Spiders are improbable.
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the diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology
Annals of Emergency Medicine, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Abstract [Vetter RS, Bush SP. The diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology. Ann Emerg Med. May 2002;39:544-546.]
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the diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology
Annals of Emergency Medicine, 2002Co-Authors: Richard S. Vetter, Sean P. BushAbstract:Abstract [Vetter RS, Bush SP. The diagnosis of brown Recluse Spider bite is overused for dermonecrotic wounds of uncertain etiology. Ann Emerg Med. May 2002;39:544-546.]
Hui Nian - One of the best experts on this subject based on the ideXlab platform.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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brown Recluse Spider bite mediated hemolysis clinical features a possible role for complement inhibitor therapy and reduced rbc surface glycophorin a as a potential biomarker of venom exposure
PLOS ONE, 2013Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:Background The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. Study Design and Methods We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naive cells. Results Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Conclusion Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
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Brown Recluse Spider bite mediated hemolysis: clinical features, a possible role for complement inhibitor therapy, and reduced RBC surface glycophorin A as a potential biomarker of venom exposure.
Public Library of Science (PLoS), 1Co-Authors: Eric A Gehrie, Hui Nian, Pampee P YoungAbstract:The venom of Loxosceles reclusa (Brown Recluse Spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom.We performed a 10-year chart review of cases of Brown Recluse Spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naïve cells.Most victims of severe Brown Recluse Spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse Spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro.Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation