Identification of a genetic mutation of Neisseria meningitidis, the bacteria most likely to cause the re-emerging pathogen epidemic bacterial meningitis, may shed new light on why this deadly bacteria so easily and virulently colonizes the mucosal surfaces that line nasal passages, according to researchers from the medical school at the May meeting of the American Society of Microbiology.
"A better understanding of how pathogenic bacteria interact with human mucosal surfaces is leading to new strategies for design of vaccines that will protect against important bacterial infections," said David Stephens, senior author of an abstract presented at the meeting. Stephens is professor and director of the Division of Infectious Diseases in the Department of Medicine, and is an associate professor of microbiology and immunology.
"Many bacterial pathogens colonize human mucosal surfaces as an initial step in infection," he said. "As a model for this pathogenic event, current studies of our laboratory are directed at understanding in molecular terms, how N. meningitidis colonizes human upper respiratory mucosal surfaces."
The Emory group is particularly interested in N. meningitidis serogroup B strain, a major cause of epidemic bacterial meningitis for which no vaccine is available.
Emory graduate student and first author Giles C. Shih describes in the abstract the activity of lipooligosaccharide (LOS), a long chain of sugars located on the surface of N. meningitidis that interacts with mucosal cells. While investigating the theory that altering LOS might keep it from interacting with human cells (thus eliminating the first step in the infection process), Shih indeed found that when LOS is in mutant form 469, it dramatically changes the outer structure of the bacteria.
"We hope mutant 469 can be used in the design of vaccines against group B meningococcal meningitis," Shih said.
-- Lorri Preston