The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat.

Abstract

Although Escherichia coli strains possessing the Kl capsule are predominant among isolates from neonatal E. coli meningitis and most of these Kl isolates are associated with a limited number of 0 lipopolysaccharide (LPS) types, the basis of this association of Kl and certain 0 antigens with neonatal E. coli meningitis is not clear. The present study examined in experimental E. coli bacteremia and meningitis in newborn and adult rats whether or not the Kl capsule and/or 0-LPS antigen are critical determinants in the development of meningitis. Rats received subcutaneously a Kl E. coli strain (018+K1+) or mutants lacking either the Kl capsule (018+K1-) or 0 side-chain (018-K1+). 12-24 h later, blood and cerebrospinal fluid (CSF) specimens were obtained for quantitative cultures. The isolation of E. coli from CSF was observed in both newborn and adult rats infected with K1+ strains regardless of LPS phenotype (018+ or 18-) who also developed a high degree of bacteremia (e.g., > 104 CFU/ml of blood). In contrast, none of the newborn and adult rats infected with 018+K1-and developing bacteremia of > 10' were found to have positive CSF cultures.These findings indicate that the presence of the Kl capsule and a high degree ofbacteremia are key determinants in the development of E. coli meningitis, suggesting that there may be specific binding sites present in the brain which have an affinity for the Kl capsule and thus may be responsible for the entry of Kl-encapsulated E. coli into the meninges. (J. Clin. Invest. 1992. 90:897-905.)

Development of a novel ex vivo insect model for studying virulence determinants of Escherichia coli K1

“…The finding that the rough LPS mutant exhibited significantly reduced invasion of locust brain appears in contrast to previous findings in the rat model that this mutant produces E. coli K1 meningitis at levels similar to the wild-type strain (Kim et al, 1992). This may be due to difference between the models, i.e.…”

“…A rough LPS mutant, constructed using chemical mutagenesis, was also used. For simplicity, the rough LPS mutant is referred to as Dlps, although there were no genetic manipulations (Kim et al, 1992). E. coli K12 strain HB101, a noninvasive isolate was used as a negative control.…”

“…DneuDB) and the rough LPS mutant to invade locust brain. Several lines of evidence suggest that the capsule plays an important role in E. coli K1 invasion of the CNS in vivo by enhancing E. coli serum resistance and anti-phagocytic properties (Allen et al, 1987;Kim et al, 1992), as well as helping prevent intracellular degradative processes . Here, these studies have shown that the capsule is critical in E. coli K1 traversal of the blood-brain barrier.…”

“…Several lines of evidence suggest that the capsule plays an important role in E. coli K1 invasion of the CNS in vivo by enhancing E. coli serum resistance and anti-phagocytic properties (Allen et al, 1987;Kim et al, 1992), as well as helping prevent intracellular degradative processes . Here, these studies have shown that the capsule is critical in E. coli K1 traversal of the blood-brain barrier.The finding that the rough LPS mutant exhibited significantly reduced invasion of locust brain appears in contrast to previous findings in the rat model that this mutant produces E. coli K1 meningitis at levels similar to the wild-type strain (Kim et al, 1992). This may be due to difference between the models, i.e.…”

Transcriptome of Escherichia coli K1 bound to human brain microvascular endothelial cells

“…Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. meningitis in our laboratory [2][3][4][5]. These efforts indicate that a large number of bacterial virulence determinants are involved in the E. coli K1 traversal of the blood-brain barrier, such as K1 capsule, O-LPS, OmpA, Ibe proteins, AslA, TraJ, and CNF1 [1,6].…”