revealed an opening pressure of 44, WBC 56, protein 56, glucose 22, and positive cryptococcal antigen (1:160 titer). He was restarted on induction therapy with Amphotericin B and flucytosine due to concern for cryptococcal meningitis recurrence, and serial lumbar punctures were performed with persistently elevated opening pressures. Blood cultures and multiple CSF cultures had no growth throughout the hospital admission. Due to persistent negative cultures, the patient was now thought to have immune reconstitution inflammatory syndrome (IRIS). He was started on prednisone, and serial lumbar
punctures were continued to reduce intracranial pressure. The last opening pressure was 20, and the patient was discharged on a prednisone taper. Discussion: This case illustrates the importance of considering IRIS in patients who have undergone treatment for disseminated cryptococcus or cryptococcal meningitis and initiation of antiretroviral therapy, even beyond the classic timeframe. Furthermore, if IRIS is on the differential, following the CSF cultures is crucial to help distinguish IRIS from recurrence of cryptococcal meningitis.
ONE VIRAL REACTIVATION AFTER THE NEXT: CASE STUDY IN HCV- POSITIVE RENAL ALLOGRAFT TRANSPLANTATION Shivani Jain, Mihran V Naljayan, Sean Barry, Erwin Antonio Aguilar; LSUHSC School of Medicine, New Orleans, LA.
Introduction: Direct-acting antiviral therapy (DAA) has enabled kidney transplantation (KT) with hepatitis-C virus (HCV)-positive allografts. However, factors associated with HCV reactivation in transplant recipients require further understanding. Case: A 48-year-old male with a history of ESRD secondary to FSGS was found to have hepatitis-C virus (HCV) reactivation after KT with an HCV-positive allograft. The patient was negative for HCV, HBV, HIV1/2, and BK polyoma before KT in July 2021. His induction therapy included thymoglobulin, and his maintenance immunosuppressive regimen included mycophenolate mofetil (MMF), tacrolimus, and prednisone. A week after KT, the patient tested positive for HCV genotype 1a and was started on sofosbuvir/velpatasvir. HCV viral load (VL) was undetectable 2 months later. As of January 2022, urinalysis and hepatic function tests remained unremarkable. However, the patient was positive for BK polyoma and COVID-19 at this time. By February, HCV VL was again positive with the same genotype as prior. This raised the possibility of HCV
reactivation from the allograft. Given recurrence of HCV VL, the patient underwent therapy with sofosbuvir/velpatasvir/voxilaprevir, achieving sustained viral response (SVR) as of October 2022. Recent guidelines for preventing HCV reactivation in allograft-positive KT recipients state that individuals should achieve SVR after 8-12 weeks of DAA. The patient completed DAA post-transplantation with a successful negative VL 2 months later. However, he did not achieve SVR because his VL was again positive 3 months after completion of therapy. Discussion: Reactivation of BKV, a DNA virus that establishes lifelong infection in renal tubular and uroepithelial cells, is common among KT recipients, but there is insufficient evidence to establish a causal association between BKV reactivation and HCV reactivation. This case highlights the importance of close follow-up monitoring for HCV and BKV among KT recipients and the need to explore the relationship between BKV reactivation, HCV reactivation, and immunosuppression regimen.
INTRAVENOUS IMMUNOGLOBULIN THERAPY IN A CASE OF SUSPECTED VIRAL MENINGOENCEPHALITIS Joseph Vaughan, Tiffany W. Ardoin; LSUHSC School of Medicine, New Orleans, LA.
Introduction: While intravenous immunoglobulin (IVIG) can be used in neuroimmunologic disorders such as autoimmune or paraneoplastic
Case: A 26-year-old male with no significant past medical history presented to the emergency department with new-onset urinary retention, constipation, gait difficulty, generalized tremor, and headache after a week-long history of unremitting fever, body aches, nausea, vomiting, and diarrhea. 47
encephalitis, mixed efficacy has been reported in viral meningoencephalitis.
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