Toxin Genotypes and Plasmid Profiles as Determinants of Systemic Sequelae in Escherichia coli O157:H7 Infections

SM Ostroff, PI Tarr, MA Neill, JH Lewis… - Journal of Infectious …, 1989 - academic.oup.com
SM Ostroff, PI Tarr, MA Neill, JH Lewis, N Hargrett-Bean, JM Kobayashi
Journal of Infectious Diseases, 1989academic.oup.com
Abstract In 1987, 93 Escherichia coli O157: H7 isolates were collected during routine
surveillance for this pathogen in the state of Washington. Toxin genotypes and plasmid
profiles were correlated with the clinical sequelae of illness in 88 of the 93 patients from
whom these strains were isolated. Thirteen plasmid patterns were observed among the 88
tested isolates; four patterns accounted for 82% of the isolates. Genetic probing for Shiga-
like toxins (SLT) I and II demonstrated the presence of both genes in 67 (76%), SLT I alone …
Abstract
In 1987, 93 Escherichia coli O157:H7 isolates were collected during routine surveillance for this pathogen in the state of Washington. Toxin genotypes and plasmid profiles were correlated with the clinical sequelae of illness in 88 of the 93 patients from whom these strains were isolated. Thirteen plasmid patterns were observed among the 88 tested isolates; four patterns accounted for 82% of the isolates. Genetic probing for Shiga-like toxins (SLT) I and II demonstrated the presence of both genes in 67 (76%), SLT I alone in three (3%), and SLT II alone in 18 (20%). The hemolytic uremic syndrome or thrombotic thrombocytopenic purpura developed in seven (39%) of 18 patients infected with isolates having only the SLT II gene, while these complications occurred in only four (6%) of 70 patients infected with isolates having the other two genotypes (relative risk, 6.8; 95% confidence interval, 1.9, 26.4). This study shows that E. coli O157:H7 isolates systematically collected from a single geographic region over a defined time period exhibit considerable diversity in plasmid content and toxin genotype and that the toxin genotype of the infecting strain may influence the risk of developing microangiopathic sequelae.
Oxford University Press