The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform
Shibani S Mukerji - One of the best experts on this subject based on the ideXlab platform.
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fatal eastern equine encephalitis in a patient on maintenance rituximab a case report
Open Forum Infectious Diseases, 2017Co-Authors: Isaac H Solomon, Pedro D S C Ciarlini, Sandro Santagata, Asim A Ahmed, Umberto De Girolami, Sashank Prasad, Shibani S MukerjiAbstract:: A 63-year-old woman on rituximab maintenance for follicular lymphoma presented with headaches, vomiting, and fever, and was diagnosed with eastern equine Encephalomyelitis by cerebrospinal fluid polymerase chain reaction. Eastern equine Encephalomyelitis immunoglobulin (Ig)G/IgM remained negative due to rituximab treatment, and magnetic resonance imaging showed minimal abnormalities, making this a diagnostically challenging case. Despite therapy with intravenous Ig, the patient rapidly declined and died on hospital day 12. Autopsy revealed perivascular and parenchymal chronic inflammation, with an absence of B lymphocytes, and virally infected neurons throughout the central nervous system.
Ruth Gabizon - One of the best experts on this subject based on the ideXlab platform.
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Targeting of prion-infected lymphoid cells to the central nervous system accelerates prion infection
Journal of Neuroinflammation, 2012Co-Authors: Yael Friedman-levi, Tehila Mayer-sonnenfeld, Romana Hoftberger, Herbert Budka, Haim Ovadia, Oded Abramsky, Ruth GabizonAbstract:BackgroundPrions, composed of a misfolded protein designated PrPSc, are infectious agents causing fatal neurodegenerative diseases. We have shown previously that, following induction of experimental autoimmune Encephalomyelitis, prion-infected mice succumb to disease significantly earlier than controls, concomitant with the deposition of PrPSc aggregates in inflamed white matter areas. In the present work, we asked whether prion disease acceleration by experimental autoimmune Encephalomyelitis results from infiltration of viable prion-infected immune cells into the central nervous system.MethodsC57Bl/6 J mice underwent intraperitoneal inoculation with scrapie brain homogenates and were later induced with experimental autoimmune Encephalomyelitis by inoculation of MOG35-55 in complete Freund's adjuvant supplemented with pertussis toxin. Spleen and lymph node cells from the co-induced animals were reactivated and subsequently injected into naïve mice as viable cells or as cell homogenates. Control groups were infected with viable and homogenized scrapie immune cells only with complete Freund's adjuvant. Prion disease incubation times as well as levels and sites of PrPSc deposition were next evaluated.ResultsWe first show that acceleration of prion disease by experimental autoimmune Encephalomyelitis requires the presence of high levels of spleen PrPSc. Next, we present evidence that mice infected with activated prion-experimental autoimmune Encephalomyelitis viable cells succumb to prion disease considerably faster than do mice infected with equivalent cell extracts or other controls, concomitant with the deposition of PrPSc aggregates in white matter areas in brains and spinal cords.ConclusionsOur results indicate that inflammatory targeting of viable prion-infected immune cells to the central nervous system accelerates prion disease propagation. We also show that in the absence of such targeting it is the load of PrPSc in the inoculum that determines the infectivity titers for subsequent transmissions. Both of these conclusions have important clinical implications as related to the risk of prion disease contamination of blood products.
Anthony A. Marfin - One of the best experts on this subject based on the ideXlab platform.
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Post-infectious Encephalomyelitis associated with St. Louis encephalitis virus infection
Neurology, 2004Co-Authors: James J. Sejvar, Amy V. Bode, Michael Curiel, Anthony A. MarfinAbstract:Neurologic illness associated with acute St. Louis encephalitis, West Nile, and Japanese encephalitis virus infection includes acute aseptic meningitis, Encephalomyelitis, and a poliomyelitis-like syndrome. Few post-infectious immune-mediated neurologic events associated with flaviviral infection have been reported. The authors report on a woman with apparent post-infectious Encephalomyelitis associated with recent St. Louis encephalitis virus infection, suggesting that neurologic illness from flaviviruses may also be seen in the post-infectious period following mild clinical illness.
Isaac H Solomon - One of the best experts on this subject based on the ideXlab platform.
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fatal eastern equine encephalitis in a patient on maintenance rituximab a case report
Open Forum Infectious Diseases, 2017Co-Authors: Isaac H Solomon, Pedro D S C Ciarlini, Sandro Santagata, Asim A Ahmed, Umberto De Girolami, Sashank Prasad, Shibani S MukerjiAbstract:: A 63-year-old woman on rituximab maintenance for follicular lymphoma presented with headaches, vomiting, and fever, and was diagnosed with eastern equine Encephalomyelitis by cerebrospinal fluid polymerase chain reaction. Eastern equine Encephalomyelitis immunoglobulin (Ig)G/IgM remained negative due to rituximab treatment, and magnetic resonance imaging showed minimal abnormalities, making this a diagnostically challenging case. Despite therapy with intravenous Ig, the patient rapidly declined and died on hospital day 12. Autopsy revealed perivascular and parenchymal chronic inflammation, with an absence of B lymphocytes, and virally infected neurons throughout the central nervous system.
Yael Friedman-levi - One of the best experts on this subject based on the ideXlab platform.
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Targeting of prion-infected lymphoid cells to the central nervous system accelerates prion infection
Journal of Neuroinflammation, 2012Co-Authors: Yael Friedman-levi, Tehila Mayer-sonnenfeld, Romana Hoftberger, Herbert Budka, Haim Ovadia, Oded Abramsky, Ruth GabizonAbstract:BackgroundPrions, composed of a misfolded protein designated PrPSc, are infectious agents causing fatal neurodegenerative diseases. We have shown previously that, following induction of experimental autoimmune Encephalomyelitis, prion-infected mice succumb to disease significantly earlier than controls, concomitant with the deposition of PrPSc aggregates in inflamed white matter areas. In the present work, we asked whether prion disease acceleration by experimental autoimmune Encephalomyelitis results from infiltration of viable prion-infected immune cells into the central nervous system.MethodsC57Bl/6 J mice underwent intraperitoneal inoculation with scrapie brain homogenates and were later induced with experimental autoimmune Encephalomyelitis by inoculation of MOG35-55 in complete Freund's adjuvant supplemented with pertussis toxin. Spleen and lymph node cells from the co-induced animals were reactivated and subsequently injected into naïve mice as viable cells or as cell homogenates. Control groups were infected with viable and homogenized scrapie immune cells only with complete Freund's adjuvant. Prion disease incubation times as well as levels and sites of PrPSc deposition were next evaluated.ResultsWe first show that acceleration of prion disease by experimental autoimmune Encephalomyelitis requires the presence of high levels of spleen PrPSc. Next, we present evidence that mice infected with activated prion-experimental autoimmune Encephalomyelitis viable cells succumb to prion disease considerably faster than do mice infected with equivalent cell extracts or other controls, concomitant with the deposition of PrPSc aggregates in white matter areas in brains and spinal cords.ConclusionsOur results indicate that inflammatory targeting of viable prion-infected immune cells to the central nervous system accelerates prion disease propagation. We also show that in the absence of such targeting it is the load of PrPSc in the inoculum that determines the infectivity titers for subsequent transmissions. Both of these conclusions have important clinical implications as related to the risk of prion disease contamination of blood products.