Antimicrobial Resistance of Escherichia coli O26, O103, O111, O128, and O145 From Animals and Humans

Carl M. Schroeder, Jianghong Meng, Shaohua Zhao, Chitrita DebRoy, Jocelyn Torcolini, Cuiwei Zhao, Patrick F. McDermott, David D. Wagner, Robert D. Walker, David G. White

Disclosures

Emerging Infectious Diseases. 2002;8(12) 

In This Article

Abstract and Introduction

Susceptibilities to fourteen antimicrobial agents important in clinical medicine and agriculture were determined for 752 Escherichia coli isolates of serotypes O26, O103, O111, O128, and O145. Strains of these serotypes may cause urinary tract and enteric infections in humans and have been implicated in infections with Shiga toxin-producing E. coli (STEC). Approximately 50% of the 137 isolates from humans were resistant to ampicillin, sulfamethoxazole, cephalothin, tetracycline, or streptomycin, and approximately 25% were resistant to chloramphenicol, trimethoprim-sulfamethoxazole, or amoxicillin-clavulanic acid. Approximately 50% of the 534 isolates from food animals were resistant to sulfamethoxazole, tetracycline, or streptomycin. Of 195 isolates with STEC-related virulence genes, approximately 40% were resistant to sulfamethoxazole, tetracycline, or streptomycin. Findings from this study suggest antimicrobial resistance is widespread among E. coli O26, O103, O111, O128, and O145 inhabiting humans and food animals.

The emergence and dissemination of antimicrobial resistance in bacteria has been well documented as a serious problem worldwide[1]. Selective pressure favoring antimicrobial-resistant phenotypes is applied whenever antimicrobials are used, including treating disease in clinical medicine and preventing disease and promoting growth in animal husbandry. As a consequence, antimicrobial-resistant bacteria are selected for, thereby posing a critical public health threat in that antimicrobial treatment efficacy may be reduced.

Escherichia coli are facultative anaerobes in the normal intestinal flora of humans and animals[2,3]; however, pathogenic strains of these bacteria are an important cause of bacterial infections. In humans, these strains are the foremost cause of urinary tract infections[4], as well as a major cause of neonatal meningitis[5], nosocomial septicemia, and surgical site infections[6]. Infection with Shiga toxin-producing E. coli (STEC) may also result in complications including thrombocytopenic purpura, severe hemorrhagic colitis, and hemolytic uremic syndrome[7]. While therapeutic options vary depending on the type of infection, antimicrobials including trimethoprim-sulfamethoxazole, fluoroquinolones, and third-generation cephalosporins are generally recommended for treating infections caused by E. coli other than STEC[6]. In contrast, because these antimicrobials may increase levels of free Shiga toxin in vivo, thus facilitating disease progression, the usefulness of antimicrobials in treating STEC infection remains less clear[6,8].

Recent reports have suggested the use of tetracyclines, sulfa drugs, cephalosporins, and penicillins to be a major factor in the emergence and dissemination of antimicrobial-resistant E. coli [9,10,11,12,13,14]. However, a relative paucity of information exists regarding antimicrobial resistance in E. coli from nonhospital sources, especially those from animal sources. In this study, antimicrobial susceptibility profiles were determined for E. coli isolates of serotypes O26, O103, O111, O128, and O145. Strains of these serotypes may cause urinary tract and enteric infections in humans and have been implicated in infections with STEC[15,16,17,18,19]. The isolates were originally gathered from diverse sources, including food animals, companion animals (i.e. dogs, cats, and rabbits), and humans. Our primary objective was to characterize the extent of antimicrobial resistance in these E. coli serotypes from agricultural and clinical settings.

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