To assess the contributions of bacterial virulence factors and defects in host defense to Escherichia coli bacteremia, we examined isolates and available medical records from 169 episodes at two hospitals. Adhesins and hemolysin virulence factors were documented in 84% of bacteremia-associated isolates originating from the urinary and respiratory tracts and in 50% of such isolates originating from other extraurinary foci. Of the evaluable episodes of bacteremia involving 35 adhesin-negative isolates, 21 (60%) were in patients who had mucocutaneous defects at the primary site of infection, and another 13 (37%) were in patients who had comorbid systemic diseases (i.e., chronic renal failure or alcoholism) associated with impaired leukocyte function. In contrast, of 93 evaluable episodes with adhesin-positive isolates, 22 (24%) were in patients who had none of these host conditions (P = .008). Overall, of evaluable episodes of bacteremia involving 128 isolates, 71 (55%) had both bacterial virulence-associated and host-related risk factors. Mortality was related to the severity of comorbid illnesses and was not affected by the presence of the bacterial virulence factors assessed.

The clonal relationships among 187 bloodstream isolates of Escherichia coli from 179 patients at Boston, Mass., Long Beach, Calif., and Nairobi, Kenya, were determined by multilocus enzyme electrophoresis (MLEE), analysis of polymorphisms associated with the ribosomal operon (ribotyping), and serotyping. MLEE based on 20 enzymes resolved 101 electrophoretic types (ETs), forming five clusters; ribotyping resolved 56 distinct patterns concordant with the analysis by MLEE. The isolates at each study site formed a genetically diverse group and demonstrated similar clonal structures, with the same small subset of lineages accounting for the majority of isolates at each site. Moreover, two ribotypes accounted for ϳ30% of the isolates at each study site. One cluster contained the majority (65%) of isolates and, by direct comparison of the ETs and ribotypes of individual isolates, was genetically indistinguishable from the largest cluster for each of two other collections of E. coli causing pyelonephritis and neonatal meningitis (R. K.