<i>Escherichia coli</i>K1 Capsular Polysaccharide Associated with Neonatal Meningitis

Robbins, John B.; McCracken, George H.; Gotschlich, Emil C.; Ørskov, Frits; Ørskov, Ida; Hanson, Lars Å.

doi:10.1056/nejm197405302902202

Cited by 465 publications

(282 citation statements)

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“…Similar high frequencies of K 1-carrying strains have been found in Europe Mulder, van Alphen & Zanen, 1984). K1 strains are found frequently but with lower frequencies in faeces of infants and adults (Robbins et al 1974a;Sarff et al 1975;0rskov & Orskov, 1975). The most frequent 0 groups associated with K 1 among American strains were 07, 018, 01 and 06 (Robbins et al 1974a;McCracken et al 1974), and the same 0 groups are found in European strains from neonatal meningitis.…”

Section: Role Of Adhesion For Experimental Infectionsupporting

confidence: 62%

“…108 bacteria were installed, was that the binding capacity for cell-surface receptor molecules present in the mice epithelial cells was nullified by the Tamm Horsfall protein, and this effect could be overcome when larger doses were given. NEONATAL MENINGITIS: 0 AND K ANTIGEN E. coli is a major cause of neonatal meningitis, and E. coli meningitis has a high mortality rate and frequency of sequelae (Robbins et al 1974a;. Robbins et al (1974a), McCracken et al (1974) and Sarff et al (1975) showed that 840% of E. coli isolated all over the U.S.A. from patients with this disease carried the K 1 antigen.…”

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

“…NEONATAL MENINGITIS: 0 AND K ANTIGEN E. coli is a major cause of neonatal meningitis, and E. coli meningitis has a high mortality rate and frequency of sequelae (Robbins et al 1974a;. Robbins et al (1974a), McCracken et al (1974) and Sarff et al (1975) showed that 840% of E. coli isolated all over the U.S.A. from patients with this disease carried the K 1 antigen. Similar high frequencies of K 1-carrying strains have been found in Europe Mulder, van Alphen & Zanen, 1984).…”

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

“…K1 strains are found frequently but with lower frequencies in faeces of infants and adults (Robbins et al 1974a;Sarff et al 1975;0rskov & Orskov, 1975). The most frequent 0 groups associated with K 1 among American strains were 07, 018, 01 and 06 (Robbins et al 1974a;McCracken et al 1974), and the same 0 groups are found in European strains from neonatal meningitis. However, at least one 0 group, 083, which is highly prevalent in continental Europe (Handriuck et al 1982;Mulder, van Alphen & Zanen, 1984), has only rarely been found in the U.S.A. Based on these results, it was natural to call the K 1 antigen a virulence factor.…”

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

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Escherichia coliin extra-intestinal infections

Ørskov

1985

J. Hyg.

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220

161

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When Theodor Escherich (1885a, b) first describedEscherichia colihe looked on it as a saprophytic organism. Soon several investigators found that colibacteria could be isolated from intestinal infections and from many infections outside the intestine, like urinary tract infections (UTI), cholecystitis, wound infections, meningitis, septicaemia, pulmonary infections, and many more. Uhlenhuth (1897) showed that coli strains from pathological processes were more pathogenic in animal experiments than strains isolated from the normal intestine. Smith (1927), who examined strains from white scours in calves, showed that spontaneous acapsular mutants could be obtained from certain colibacteria, and that such mutants were less virulent when injected intra-peritoneally into guinea-pigs.

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Section: Role Of Adhesion For Experimental Infectionsupporting

confidence: 62%

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

Section: Role Of Adhesion For Experimental Infectionmentioning

confidence: 99%

See 2 more Smart Citations

Escherichia coliin extra-intestinal infections

Ørskov

1985

J. Hyg.

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220

161

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“…Escherichia coli K1 is a leading cause of neonatal meningitis, septicaemia and urinary tract infections in children (Kasper et al, 1973;Robbins et al, 1974;Kaijser et al, 1977;Ørskov et al, 1979). One of the primary virulence factors in these diseases, the K1 antigen, is a homopolymeric glycan (polysialic acid) consisting of 100 or more ␣2→8-linked sialyl units (for reviews, see Silver and Vimr, 1990;Troy, 1992).…”

Section: Introductionmentioning

confidence: 99%

Reduced polysialic acid capsule expression in Escherichia coli K1 mutants with chromosomal defects in kpsF

Cieslewicz

Vimr

1997

Molecular Microbiology

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SummaryNeuroinvasive Escherichia coli K1 synthesizes and assembles a polysialic acid capsule virulence factor on the external leaflet of the outer membrane. This capsule functions in pathogenesis by blocking nonimmune host defence mechanisms and acting as a relatively non-immunogenic molecular mimic of the polysialic acid chains found in high concentrations on neural cell adhesion molecules of the human embryo and neonate. The synthetic, regulatory and export components for capsule expression are encoded in three functionally distinct gene blocks or regions of the 20 kb kps 'pathogenicity island'. These regions are organized as two convergently transcribed operons inserted into the monocistronic tRNA gene, pheV. The six genes of the so-called region 1 operon are transcribed in the same direction as pheV, and at least four of these genes are required for polysialic acid export. Expression of this operon is thermoregulated by transcriptional control of its first gene, kpsF. To investigate the function of region 1 further, two independent chromosomal disruptions were engineered by inserting promoterless, terminatorless kanamycin or chloramphenicol resistance cassettes into the HindIII site of the kpsF coding sequence. The chromosomal insertions were regulated by temperature in the same way as the wild-type operon, demonstrating that this control mechanism remained intact in these mutants. Chemical, immunological and ultrastructural microscopical methods demonstrated that full-length polysialic acid chains were synthesized but not exported by the kpsF mutants. This phenotype was correlated with decreased plaque diameter when the mutants were infected with the capsule-specific bacteriophage K1F. The export defect could not be complemented in trans with kpsF þ containing its cis-regulatory region because of titration of an apparent positive regulator of region 1 expression, whereas complementation was observed with a plasmid expressing kpsF from a physiologically irrelevant promoter. An N-terminal polyhistidine peptide was attached to KpsF and used to purify the overproduced polypeptide. Antibodies raised against KpsF identified at least one of its paralogues in E. coli, GutQ, suggesting that KpsF and its homologues are membrane associated. The results indicate the requirement for a precise balance between region 1 components of the capsule export machinery, and that KpsF plays a positive role in the assembly, operation or regulation of this apparatus.

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Bacterial Meningitis in Older Neonates

Baumgartner¹

1983

Arch Pediatr Adolesc Med

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Escherichia coliK1 Capsular Polysaccharide Associated with Neonatal Meningitis

Cited by 465 publications

References 23 publications

Escherichia coliin extra-intestinal infections

Escherichia coliin extra-intestinal infections

Reduced polysialic acid capsule expression in Escherichia coli K1 mutants with chromosomal defects in kpsF

Bacterial Meningitis in Older Neonates

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