The rise and fall of Escherichia coli O 15 in a London Teaching Hospital

Abstract

A marked increase in the prevalence of bacteraemia due to Escherichia coli of serogroup O15 was noted during November and December 1986 at Charing Cross Hospital. This multiresistant strain had been reported by several hospitals in south London. All isolates of E. coli from patients with bacteraemia between October 1986 and the end of September 1988 were assessed for the presence of the O15 antigen and for the unusual pattern of resistance to six antimicrobial agents. As a guide to faecal carriage, isolates from urine were similarly assessed during seven 4-week periods between January 1987 and June 1988. Of the 123 E. coli isolates from blood, 25 (20%) were serogroup O15 and 20 of these expressed the same pattern of multiresistance; 17 of these multiresistant isolates occurred in the 4-month period 1 Nov. 1986-28 Feb. 1987. During the remaining 19 months of the study only eight isolates were serogroup O15 of which only three were multiresistant. In the first 4-week period that urine isolates were studied 21 Jan. 1987-17 Feb. 1987, 26 (13.2%) of the 195 isolates were serogroup O15 of which 20 were multiresistant. The proportion of serogroup O15 isolates fell gradually until, in June 1988, the last period studied, only 8 (4.2%) of the 189 isolates were serogroup O15, of which only one was multiresistant. In a preliminary study of plasmids in six serogroup O15 isolates from blood, three multiresistant isolates and one that was sensitive to chloramphenicol appeared to carry a similar plasmid of c. 100 Mda.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid and Specific Detection of the O15:K52:H1 Clonal Group of Escherichia coli by Gene-Specific PCR

“…The O15:K52:H1 clonal group of Escherichia coli is a globally distributed extraintestinal pathogen, often associated with multi-antimicrobial drug resistance (7,13,15,17,18,20,21). It first gained notoriety during a community-wide outbreak of drug-resistant urinary tract infections in London, England, in 1986England, in -1987.…”

Global Molecular Epidemiology of the O15:K52:H1 Extraintestinal Pathogenic Escherichia coli Clonal Group: Evidence of Distribution beyond Europe

“…Our findings provide the first genetic evidence of the presence of the O15:K52:H1 clonal group outside of Europe (32,33,36,38; Dalmau et al, letter; Eykyn and Phillips, letter; Reeves et al, letter; Waghorn et al, letter; Wright and Perinpanayagam, letter). The validity of the PCR-based phylotyping is supported by the placement within the same cluster of all five Spanish O15:K52:H1 control strains, which were previously shown to be clonally related according to ribotyping and biotyping (38), and by the placement within this cluster also of the two urosepsis isolates from Seattle which were already known to be of serotype O15:K52:H1 (21,23).…”

“…coli serotype O15:K52:H1 does not represent one of the traditionally recognized "virulent clones" of extraintestinal pathogenic E. coli (34,35). Members of this serotype first came to attention as significant extraintestinal pathogens when they caused a large-scale epidemic of UTI, septicemia, and diverse other extraintestinal infections in South London, England, in the winter of 1986 to 1987, in association with a distinctive multiple antimicrobial resistance profile (32,36 Recently, in a prospective study from Barcelona, Spain, E. coli O15:K52:H1 was shown to be a significant cause of community-acquired and nosocomial UTI (38). Compared with E. coli urine isolates of other serotypes, those of serotype O15:K52:H1 were more likely to cause clinical pyelonephritis and to infect young adults, evidence of enhanced virulence.…”

Antibiotic Resistance in Urinary Tract Infections: Current Issues and Future Solutions

“…A year-long outbreak of O15:K52:H1 E. coli occurred in London in 1986-7, causing up to 13% of UTIs in this area during this time period. Most of these isolates were resistant to SXT, ampicillin, chloramphenicol, streptomycin and tetracycline (Phillips et al, 1988, O'Neill et al, 1990. Analysis of 100 different O15:K2:H1 clones, isolated over a span of 30 years, revealed that SXT resistance first emerged in this lineage in 1986 and fluoroquinolone resistance in 1995 (Olesen et al, 2009).…”