Laboratory Practices and Incidence of Non-O157 Shiga Toxin-producing Escherichia coli Infections

Kathleen A. Stigi; J. Kathryn MacDonald; Anthony A. Tellez-Marfin; Kathryn H. Lofy

Disclosures

Emerging Infectious Diseases. 2012;18(3):477-479. 

In This Article

Abstract and Introduction

Abstract

We surveyed laboratories in Washington State, USA, and found that increased use of Shiga toxin assays correlated with increased reported incidence of non-O157 Shiga toxin–producing Escherichia coli (STEC) infections during 2005–2010. Despite increased assay use, only half of processed stool specimens underwent Shiga toxin testing during 2010, suggesting substantial underdetection of non-O157 STEC infections.

Introduction

Strains of Shiga toxin (Stx)–producing Escherichia coli (STEC) are differentiated by the O antigen on their outer membrane and are broadly classified as O157 or non-O157 STEC.[1–3] The ability to produce Stx is a key virulence trait of STEC.[1,3,4] STEC infections in humans often cause a self-limited diarrheal illness but can be complicated by hemorrhagic colitis or hemolytic uremic syndrome.[1]

Unlike other E. coli strains, serogroup O157 isolates do not ferment sorbitol and are readily identified by culture, appearing colorless on sorbitol MacConkey agar.[1,2,4] Both O157 and non-O157 STEC can be identified by detecting Stx with nonculture assays that became commercially available in the United States in 1995.[2] The Centers for Disease Control and Prevention (CDC) published formal STEC testing recommendations for clinical laboratories in 2009, advocating that all stool specimens submitted for routine bacterial pathogen testing be simultaneously cultured for O157 STEC and tested with a nonculture assay to detect Stx. Use of this testing protocol ensures timely identification of all STEC infections.[2] Exclusive testing for Stx delays specific identification of O157 STEC and may impede prompt detection of common-source outbreaks.[2–4]

Non-O157 STEC infection has been a nationally notifiable condition since 2000.[5] Although studies have documented the increased incidence of reported non-O157 STEC infections over the past decade, few have determined the proportion of laboratories that routinely test all submitted stool specimens for Stx and, to our knowledge, no study has quantified STEC testing practices by proportion of stool specimens processed for bacterial culture. Our objectives, therefore, were to quantify statewide STEC testing practice by proportion of stool specimens processed for bacterial culture and to determine the contribution of enhanced STEC testing practice to increased reported incidence of non-O157 STEC infections.

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