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Volume 3, Number 4—December 1997


Non-O157 Shiga Toxin-Producing Escherichia coli Infections in Europe

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EID Caprioli A, Tozzi AE, Rizzoni G, Karch H. Non-O157 Shiga Toxin-Producing Escherichia coli Infections in Europe. Emerg Infect Dis. 1997;3(4):578-579.
AMA Caprioli A, Tozzi AE, Rizzoni G, et al. Non-O157 Shiga Toxin-Producing Escherichia coli Infections in Europe. Emerging Infectious Diseases. 1997;3(4):578-579. doi:10.3201/eid0304.970425.
APA Caprioli, A., Tozzi, A. E., Rizzoni, G., & Karch, H. (1997). Non-O157 Shiga Toxin-Producing Escherichia coli Infections in Europe. Emerging Infectious Diseases, 3(4), 578-579.

To the Editor: Shiga toxin—producing Escherichia coli (STEC) infections are an important cause of severe human disease. Although most infections are caused by strains of serogroup O157, STEC pathogenic to humans may belong to other serogroups usually referred to as non-O157 STEC.

Recently, Tarr et al. (1) and Acheson et al. (2) described infections attributable to STEC O103 and expressed concern that non-O157 STEC may pose an underestimated threat to public health in the United States. In fact, non-O157 STEC is often overlooked in clinical microbiology laboratories because the toxigenic phenotype is not exploited to identify such pathogens. Rather, most laboratories use sorbitol MacConkey agar and serotyping (which cannot detect most non-O157 STEC) to identify E. coli O157:H7.

Since the end of the 1980s, non-O157 STEC infections have caused as many as 10% to 30% of sporadic cases of hemolytic uremic syndrome (HUS) in Germany (3), Italy (4), and the United Kingdom (5). Moreover, HUS outbreaks have been associated with STEC O111:H- in Italy (6) and France (7).

During 1996, we observed a sudden increase in infections attributable to STEC O103 and O26 in Germany and Italy. In our laboratory in Germany, E. coli O103:H2 was not identified among 345 non-O157 STEC isolated between 1985 and 1995 but represented 12 (18.2%) of 66 of the non-O157 STEC isolated during 1996. HUS developed in two infected patients.

Among cases reported to Italy's nationwide HUS surveillance system from 1988 to 1995, evidence of infection with STEC O103 or O26 was found in two (1.5%) and nine (6.6%) of 135 cases, respectively. Since 1996, infection with STEC O103 and O26 has been diagnosed in three (11%) and nine (33%) of 27 HUS cases, respectively.

These observations indicate that identification of non-O157 STEC should be considered by clinical laboratories. Immunoenzymatic tests (based on either toxin antibodies or receptors) that detect Shiga toxins produced by fecal bacterial isolates or present in stool specimens are now available (8,9). Use of these tests should be considered in analyzing the stools of patients with HUS, bloody diarrhea, or painful nonbloody diarrhea, if classic microbiologic analysis fails to yield E. coli O157:H7 or another standard enteric pathogen, such as Campylobacter, Salmonella, or Shigella.

The sudden appearance or increase of rare non-O157 STEC in our populations is worrisome. Most non-O157 STEC, as well as the sorbitol fermenting O157:H- strains (10) associated with HUS in several European countries, would be missed by laboratories using standard microbiologic detection methods, such as sorbitol MacConkey agar screening. Because of the considerable clinical and epidemiologic urgency, clinical microbiologists and physicians should seek out these such pathogens in appropriate clinical situations.

Alfredo Caprioli*, Alberto E. Tozzi*, Gianfranco Rizzoni†, and Helge Karch

Author affiliations: *Istituto Superiore di Sanità, Rome, Italy; †Ospedale Pediatrico Bambino Gesù, Rome, Italy; ‡Universitat Wuerzburg, Germany


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DOI: 10.3201/eid0304.970425

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Table of Contents – Volume 3, Number 4—December 1997