RARE CASE OF PARVOVIRUS INFECTION CAUSING PURE RED CELL APLASIA IN A KIDNEY-PANCREAS TRANSPLANT RECIPIENT
Dr Oscar Perry1, Dr Robert Ellis1,2, Dr Sanjana Dang1,2, Dr George John1,2, Dr Stephanie Hendry3, Dr Monica Suet Ying Ng1,2,4,5
1Kidney Health Service, Royal Brisbane and Women’s Hospital, Herston, Australia, 2Faculty of Medicine, University of Queensland, Herston, Australia, 3Microbiology, Pathology Queensland, Herston, Australia, 4Institute of Molecular Biosciences, University of Queensland, St Lucia, Australia, 5Conjoint Internal Medicine Laboratory, Chemical Pathology, Pathology Queensland, Herston, Australia
Background: Parvovirus B19 infection can rarely manifest with pure red cell aplasia in immunocompromised hosts. We report a case of parvovirus B19-associated pure red cell aplasia in a kidney-pancreas transplant recipient, and discuss the workflow completed to exclude iatrogenic infection and monitor treatment effect.
Case Report: A 48-year-old male, 11 years post kidney pancreas transplant was admitted with a thigh abscess and a chronic normocytic anaemia (haemoglobin 72g/L). The recipient had been admitted four months prior with a bleeding peptic ulcer, requiring eight units of packed red blood cells. In the following months, the recipient required eight further packed red blood cell units despite normal upper and lower gastrointestinal endoscopies. He had normal haematinics, with persistent reticulocytopenia (0.3%, 7×109 cells/L) despite 80mcg per week of darbepoetin alfa. Platelet and leukocyte counts were within normal limits. Parvovirus B19 PCR test result was “detected” with a low cycle threshold value of 13. Transfusion transmitted parvovirus was considered and retrospective testing demonstrated that parvovirus serology and PCR results were “not detected” pre-transfusion; and that the first “detected” PCR result occurred post packed red blood cell transfusion. Australian Red Cross Lifeblood was notified and Lookback investigations excluded the blood products as a route for parvovirus transmission, postulating that community acquisition was most likely. High dose intravenous immunoglobulin (IVIG 2g/kg over 5 days) and immunosuppression reduction led to haemoglobin stability to >80g/L over 14 days. Treatment response was further extrapolated by cycle threshold value increase to 25, 7 days after first IVIG dose.
Conclusions: Treatment response may be monitored by following cycle threshold values of PCR, although a quantitative PCR would be a gold standard test to monitor treatment response.
Biography:
Dr Monica Ng is a kidney specialist at Royal Brisbane and Women’s Hospital, senior lecturer at University of Queensland, editorial fellow at Kidney360 and early career clinician scientist. Dr Ng graduated from UQ in 2014 with MBBS with first class honours. She completed her PhD studies in 2019. Dr Ng’s has research interests in developing omics workflows for kidney biomarker discovery, registry analyses for describing kidney disease epidemiology and extracellular vesicles. She is a site PI on multiple clinical trials assessing novel therapies for kidney disease.