Background: Viridans group streptococci (VGS) cause significant morbidity in children treated for acute myeloid leukemia (AML). Our goals were to determine the occurrence and impact of these infections in children treated for AML and to understand the factors that increase the risk of VGS infections and viridans streptococcal shock syndrome (VSSS) in this population.
Methods: We conducted a retrospective, population-based cohort study that included children ≤18 years of age with de novo AML treated at 15 Canadian centers. We evaluated factors related to VGS infection and VSSS.
Results: Among 341 children with AML, VGS occurred in 78 (22.9%) children over the entire course of therapy and 16 had recurrent episodes. VGS infection occurred in 97 of 1277 courses of chemotherapy (7.6%). VSSS occurred in 19.6% of these episodes and included 11 patients who required intensive care services with 2 VGS infections resulting in death. In multiple regression analysis, factors independently related to VGS included treatment on a Medical Research Council-based protocol (odds ratio (OR) 2.87, 95% confidence interval (CI) 1.53–5.39; P = 0.001), cytarabine dose per gram/m2 (OR 1.04, 95% CI 1.01–1.07; P = 0.002) and prolonged neutropenia (OR 1.58, 95% CI: 0.97–2.56; P = 0.06). None of the evaluated factors were predictive of VSSS.
Conclusions: VGS infections occur in 7.6% of chemotherapy courses and remain an important cause of morbidity and even mortality in children being treated for AML. Interventions to reduce VGS need to be identified.
From the *Hematology/Oncology/Transplant Program, Alberta Children’s Hospital, Calgary, Alberta; †Hematology/Oncology, Cancer Care Manitoba, Winnipeg, Manitoba; ‡Hematology/Oncology, Montreal Children’s Hospital, Montréal, Quebec; §Pediatric Hematology/Oncology, British Columbia Children’s Hospital, Vancouver, British Columbia; ¶Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Ontario; ‖Hematology/Oncology, Children’s Hospital of Eastern Ontario, Ottawa, Ontario; **Pediatric Hematology/Oncology, Centre Hospitalier Universitaire de Quebec, Quebec, Quebec, ††Stollery Children’s Hospital, University of Alberta Hospital, Edmonton, Alberta; ‡‡Hematology/Oncology, McMaster Children’s Hospital at Hamilton Health Sciences, Hamilton, Ontario; §§Hematology/Oncology, Cancer Centre of Southeastern Ontario at Kingston, Kingston, Ontario; ¶¶Hematology/Oncology, Centre Hospitalier Universitaire Sainte-Justine, Montreal, Quebec; ‖‖Pediatrics, IWK Health Centre, Halifax, Nova Scotia; ***Hematology/Oncology, Janeway Child Health Centre, St. John's, Newfoundland; †††Hematology/Oncology, London Health Sciences, London, Ontario; ‡‡‡Hematology/Oncology, Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec; ¶§§§Population Genomics Program, Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton; and ¶¶¶¶Division of Haematology/Oncology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Accepted for publication August 21, 2013.
This work was supported by the Canadian Cancer Society (Grant #019468) and the C17 Research Network. L.S. is supported by a New Investigator Award from the Canadian Institutes of Health Research. The authors have no other funding or conflicts of interest to disclose.
All authors contributed to data collection and manuscript writing. J.B. and L.S. contributed to data analysis and interpretation, and B.G., M.C.E. and L.S. also contributed to study conception and design. All authors have approved the final version of the manuscript.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com).
Address for correspondence: Lillian Sung, MD, Division of Haematology/Oncology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada, M5G 1X8. E-mail: email@example.com.