Affiliation:
1. Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Park 256, Baltimore, MD 21287
Abstract
Escherichia coli
is the most common Gram-negative organism causing neonatal meningitis. Neonatal
E. coli
meningitis continues to be an important cause of mortality and morbidity throughout the world. Our incomplete knowledge of its pathogenesis and pathophysiology contributes to such mortality and morbidity. Recent reports of neonatal meningitis caused by
E. coli
strains producing CTX-M-type or TEM-type extended-spectrum β-lactamases create a challenge.
E. coli
penetration into the brain, the essential step in the development of
E. coli
meningitis, requires a high-degree of bacteremia and penetration of the blood-brain barrier as live bacteria, but the underlying mechanisms remain incompletely understood. Recent functional genomic approaches of meningitis-causing
E. coli
in both in vitro and in vivo models of the blood-brain barrier (e.g., human brain microvascular endothelial cells and animal models of experimental hematogenous
E. coli
meningitis, respectively) have identified several
E. coli
factors contributing to a high-degree of bacteremia, as well as specific microbial factors contributing to
E. coli
invasion of the blood-brain barrier. In addition,
E. coli
penetration of the blood-brain barrier involves specific host factors as well as microbe- and host-specific signaling molecules. Blockade of such microbial and host factors and host cell signaling molecules is efficient in preventing
E. coli
penetration into the brain. Continued investigation of the microbial and host factors contributing to
E. coli
bacteremia andinvasion of the blood-brain barrier is likely to identify new targets for prevention and therapy of
E. coli
meningitis, thereby limiting the exposure to emerging antimicrobial-resistant
E. coli.
Publisher
American Society for Microbiology
Cited by
2 articles.
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