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The incidence of CMV after ASCT is much lower (1 - 9%) than after allogeneic transplantation. However, with recent use of R, there has been increasing concern about opportunistic infections. The objective of our study was to determine the disease burden and characteristics of CMV infection/ reactivation after ASCT in recent years.
Methods:
Records were searched in Karmanos Cancer Center database for the occurrence of CMV infection/ disease during the post-transplantation period in patients undergoing ASCT between December 2007 and December 2013. Charts were reviewed retrospectively to identify characteristics of CMV infection/ reactivation/ disease, demographic features and outcomes of the affected patients.
Results:
Seven of 978 ASCT recipients {multiple myeloma (MM): 601 patients (pts), non-Hodgkins lymphoma (NHL): 252 pts, Hodgkins lymphoma (HD): 99 pts} were found to be viremic by CMV PCR within the first 3 months after transplant, during work up for antibiotic resistant fever. The median time for development of CMV PCR positive status was 33 days post-transplantation (range, 18 – 78 days). CMV viremia developed in 3 of the 236 patients who received R with induction or preparative regimens as compared to 4 of 742 who did not receive R (p= 0.2). In all 7 patients, viremia developed after neutrophil engraftment.
Of the 7 patients, 3 developed bacterial and/ or fungal infection within 60 days from onset of viremia. Median level of CMV viremia was 16,912 copies/ ml (range, 724 – 33,100) in these 3 patients. All 3 patients received anti-viral and other appropriate anti-microbial therapy. The viremia resolved in a median of 17.5 days (range, 9 – 26 days). One of these patients died at 28 days from onset of CMV viremia due to invasive candidiasis and septic shock.
The remaining 4 patients, who did not develop bacterial or fungal infection within 60 days from viremia, had median CMV copies/ ml of 700 (range, 250 – 1707). Only one of these 4 patients received anti-CMV therapy but he died shortly, thereafter (at 19 days from onset of viremia), due to progression of primary malignancy.
None of the 7 patients had documented evidence of tissue invasive CMV disease.
Conclusion:
Despite the use of R prior to ASCT, frequency of CMV infection/ disease remains low in this population. Low level of CMV viremia does not appear to warrant therapy. Higher levels of viremia were associated with development of subsequent bacterial/ fungal infections.