The cause of historically higher rates of invasive pneumococcal disease among blacks than whites has remained unknown. We tested the hypothesis that sickle cell trait or hemoglobin C trait is an independent risk factor for invasive pneumococcal disease.
Eligible children were born in Tennessee (1996-2003), had a newborn screen, enrolled in TennCare aged <1 year, and resided in a Tennessee county with laboratory-confirmed, pneumococcal surveillance. Race/ethnicity was ascertained from birth certificates. Children were followed through 2005 until loss of enrollment, pneumococcal disease episode, fifth birthday, or death. We calculated incidence rates by race/ethnicity and hemoglobin type before and after pneumococcal conjugate vaccine (PCV7) introduction. Poisson regression analyses compared invasive pneumococcal disease rates among blacks with sickle cell trait or hemoglobin C trait with whites and blacks with normal hemoglobin, controlling for age, gender, time (pre-PCV7, transition year, or post-PCV7) and high-risk conditions (eg, heart disease).
Over 10 years, 415 invasive pneumococcal disease episodes occurred during 451,594 observed child-years. Before PCV7 introduction, disease rates/100,000 child-years were 2941 for blacks with sickle cell disease, 258 for blacks with sickle cell trait or hemoglobin C trait and 188, 172, and 125 for blacks, whites, and Hispanics with normal hemoglobin. Post-PCV7, rates declined for all groups. Blacks with sickle cell trait or hemoglobin C trait had 77% (95% CI = 22-155) and 42% (95% CI = 1-100) higher rates than whites and blacks with normal hemoglobin.
Black children with sickle cell trait or hemoglobin C trait have an increased risk of invasive pneumococcal disease.
From the Departments of aPediatrics, bEpidemiology and Prevention, and cBiostatistical Sciences, Wake Forest University Health Sciences, Winston-Salem, NC; and dDepartment of Preventive Medicine, Vanderbilt University Medical Center, Nashville, TN; eTennessee Department of Health, Nashville, TN; and fDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN.
Submitted 2 September 2009; accepted 19 November 2009; posted 9 March 2010.
Supported in part by March of Dimes Birth Defects Foundation research grant number 6-FY07-284 and Emerging Infections Cooperative Program Agreement grant U50/CCU416123 through the Centers for Disease Control and Prevention, Robert Wood Johnson Foundation Generalist Physician Faculty Scholars Program, National Institutes of Health grant K23 AI065805, and Wachovia Research Fund (to K.A.P.). M.R.G. received research funding from Wyeth and Medimmune. N.B.H. received research funding from Medimmune and Sanofi-Pasteur and served as a consultant for Novaris.
A.S.C. is currently affiliated with Centers for Disease Control and Prevention, National Center for Zoonotic, Vecterborne and Enteric Diseases, Division of Parasitic Diseases, Malaria Branch, Lusaka, Zambia; and M.R. is currently affiliated with Nationwide Children's Hospital, Columbus, OH.
W.S. was a consultant for Wyeth and served on a Data Safety Monitoring Board for experimental vaccines for Merck.
Editors' note: A commentary on this article appears on page 340.
Correspondence: Katherine A. Poehling, Department of Pediatrics, Wake Forest University Health Sciences, Winston-Salem, NC 27157. E-mail: firstname.lastname@example.org.