Content area
Full text
About the Authors:
Mary G. Krauland
* E-mail: [email protected]
Affiliation: Infectious Diseases Epidemiology Research Unit, School of Medicine and Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvanian, United States of America
Julie C. Dunning Hotopp
Affiliation: The Institute for Genome Sciences, University of Maryland School of Medicine, University of Maryland, Baltimore, Maryland, United States of America
David R. Riley
Affiliation: The Institute for Genome Sciences, University of Maryland School of Medicine, University of Maryland, Baltimore, Maryland, United States of America
Sean C. Daugherty
Affiliation: The Institute for Genome Sciences, University of Maryland School of Medicine, University of Maryland, Baltimore, Maryland, United States of America
Jane W. Marsh
Affiliation: Infectious Diseases Epidemiology Research Unit, School of Medicine and Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvanian, United States of America
Nancy E. Messonnier
Affiliation: Meningitis and Vaccine Preventable Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America
Leonard W. Mayer
Affiliation: Meningitis and Vaccine Preventable Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America
Hervé Tettelin
Affiliation: The Institute for Genome Sciences, University of Maryland School of Medicine, University of Maryland, Baltimore, Maryland, United States of America
Lee H. Harrison
Affiliation: Infectious Diseases Epidemiology Research Unit, School of Medicine and Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvanian, United States of America
Introduction
Neisseria meningitidis is a leading cause of bacterial meningitis world-wide [1]. The most common disease-causing serogroups are A, B, C, X, W-135, and Y. In the United States, serogroup Y N. meningitidis was responsible for an increasing proportion of all meningococcal disease during the 1990s and also for an increased incidence of disease. For example, during 1989–1991, ∼ 2% of invasive meningococcal strains in the U.S. were serogroup Y, whereas by the mid 1990s, over a third of cases were caused by this serogroup. The predominant genetic lineage of serogroup Y isolates from this time period was the ST-23 clonal complex [2], [3], [4].
In a previous study, we demonstrated that the emergence and maintenance of ST-23 complex serogroup Y meningococcal disease in Maryland was associated with antigenic shift in three key meningococcal outer membrane proteins (OMPs), PorA, FetA, and PorB. A change in the pulsed field...