Antimicrobial drug-resistant Escherichia coli from humans and poultry products, Minnesota and Wisconsin, 2002-2004

Abstract

The food supply, including poultry products, may transmit antimicrobial drug-resistant Escherichia coli to humans. To assess this hypothesis, 931 geographically and temporally matched E. coli isolates from human volunteers (hospital inpatients and healthy vegetarians) and commercial poultry products (conventionally raised or raised without antimicrobial drugs) were tested by PCR for phylogenetic group (A, B1, B2, D) and 60 virulence genes associated with extraintestinal pathogenic E. coli. Isolates resistant to trimethoprim-sulfamethoxazole, quinolones, and extended spectrum cephalosporins (n = 331) were compared with drug-susceptible isolates (n = 600) stratified by source. Phylogenetic and virulence markers of drug-susceptible human isolates differed considerably from those of human and poultry isolates. In contrast, drug-resistant human isolates were similar to poultry isolates, and drug-susceptible and drug-resistant poultry isolates were largely indistinguishable. Many drug-resistant human fecal E. coli isolates may originate from poultry, whereas drug-resistant poultry source E. coli isolates likely originate from susceptible poultry-source precursors.

Figure 1

Principal coordinates analysis of distribution of 243 extraintestinal pathogenic Escherichia coli isolates from human feces and poultry products, Minnesota and Wisconsin, 2002–2004, on the axis 1–axis 2 plane. Data include extended virulence genotypes (60 traits) and phylogenetic group (A, B1, B2, D). The axes have no units; they reflect the total score for each isolate derived by summing the isolate's partial score for each variable, which is the product of the loading score assigned to the particular variable for a given axis and the isolate's status for that variable. Axis 1 (positive values to right, negative values to left of central vertical line) accounted for 37% of total variance and showed significant differences between susceptible human isolates versus each of the other groups. Axis 2 (positive values above, negative values below central horizontal line) accounted for 20% of total variance and did not show any significant between-group differences. Resistant, resistant to trimethoprim-sulfamethoxazole, nalidixic acid (quinolones), and ceftriaxone or ceftazidime (extended-spectrum cephalosporins). Susceptible, susceptible to all these agents (regardless of other possible drug resistance).

Figure 2

Distribution of virulence factor scores by source and resistance status among 243 extraintestinal pathogenic Escherichia coli isolates from human feces and poultry products, Minnesota and Wisconsin, 2002–2004. Resistant, resistant to trimethoprim-sulfamethoxazole, nalidixic acid (quinolones), and ceftriaxone or ceftazidime (extended-spectrum cephalosporins). Susceptible, susceptible to all these agents (regardless of other possible resistances). The virulence scores of the susceptible human isolates are an average of ≈4 points greater than those of the resistant human isolates or poultry isolates.

Figure 3

Dendrogram based on extended virulence profiles of 243 extraintestinal pathogenic Escherichia coli isolates from human feces and poultry products, Minnesota and Wisconsin, 2002–2004. The dendrogram (shown here in simplified form) was constructed by using the unweighted pair group method with arithmetic averages based on pairwise similarity relationships according to the aggregate presence or absence of 60 individual virulence genes plus phylogenetic group (A, B1, B2, D). Triangles indicate arborizing subclusters. Major clusters 1, 2, and 3, and subclusters 1a, 1b, 2a, 2b, 3a, and 3b are indicated. Colored boxes to right of dendrogram show the distribution (by source group) of constituent members of each subcluster. Resistant, resistant to trimethoprim-sulfamethoxazole, nalidixic acid (quinolones), and ceftriaxone or ceftazidime (extended-spectrum cephalosporins). Susceptible, susceptible to all these agents.