03174nas a2200325   4500008004100000020001400041024001700055245017700072210006900249260030900318300001400627490000700641520185700648653002802505653002002533100001802553700002602571700001702597700002102614700002002635700001702655700002102672700001902693700001702712700001802729700001702747700002002764700001902784856004502803       2014                        eng d  a0041-1337  awej, 013214400aDonor-Derived West Nile Virus Infection in Solid Organ Transplant Recipients:  Report of Four Additional Cases and Review of Clinical, Diagnostic, and Therapeutic Features.0 aDonorDerived West Nile Virus Infection in Solid Organ Transplant  a(C) 2014 by Lippincott Williams & Wilkinsb(1) UCLA Medical Center, Los Angeles, CA.(2) Mayo Clinic, Phoenix, AZ.(3) U.S. Centers for Disease Control and Prevention, Fort Collins, CO.(4) Stanford University School of Medicine, Stanford, CA.(5) Mendez National Institute of Transplantation, Los Angec2014  a881 - 8890 v973 a: We describe four solid-organ transplant recipients with donor-derived West Nile virus (WNV) infection (encephalitis 3, asymptomatic 1) from a common donor residing in a region of increased WNV activity. All four transplant recipients had molecular evidence of WNV infection in their serum and/or cerebrospinal fluid (CSF) by reverse transcription polymerase chain reaction (RT-PCR) testing. Serum from the organ donor was positive for WNV IgM but negative for WNV RNA, whereas his lymph node and spleen tissues tested positive for WNV by RT-PCR. Combination therapy included intravenous immunoglobulin (4 cases), interferon (3 cases), fresh frozen plasma with WNV IgG (2 cases), and ribavirin (1 case). Two of the four transplant recipients survived., Review of the 20 published cases of organ-derived WNV infection found that this infection is associated with a high incidence of neuroinvasive disease (70%) and severe morbidity and mortality (30%). Median time to onset of symptomatic WNV infection was 13 days after transplantation (range 5-37 days). Initial unexplained fever unresponsive to antibiotic therapy followed by rapid onset of neurologic deficits was the most common clinical presentation. Confirmation of infection was made by testing serum and CSF for both WNV RNA by RT-PCR and WNV IgM by serological assays. Treatment usually included supportive care, reduction of immunosuppression, and frequent intravenous immunoglobulin. The often negative results for WNV by current RT-PCR and serological assays and the absence of clinical signs of acute infection in donors contribute to the sporadic occurrence of donor-derived WNV infection. Potential organ donors should be assessed for unexplained fever and neurological symptoms, particularly if they reside in areas of increased WNV activity., (C) 2014 by Lippincott Williams & Wilkins10aDonor-derived infection10aWest Nile virus1 aWINSTON, DREW1 aVikram, Holenarasipur1 aRabe, Ingrid1 aDhillon, Gundeep1 aMulligan, David1 aHong, Johnny1 aBusuttil, Ronald1 aNowicki, Marek1 aMone, Thomas1 aCiven, Rachel1 aTecle, Selam1 aTrivedi, Kavita1 aHocevar, Susan  uhttps://notifylibrary.org/reference/4210