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Non-O157 Shiga Toxin-Producing Escherichia coli Infections in the United States, 1983-2002
John T. Brooks, Evangeline G. Sowers, Joy G. Wells, Katherine D. Greene, Patricia M. Griffin, Robert M. Hoekstra and Nancy A. Strockbine
The Journal of Infectious Diseases
Vol. 192, No. 8 (Oct. 15, 2005), pp. 1422-1429
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30087559
Page Count: 8
You can always find the topics here!Topics: Escherichia coli O157, Escherichia coli, Hemolytic uremic syndrome, Diseases, Diarrhea, Infections, Shiga toxins, Preventive medicine, Epidemiology, Public health
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Background. Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a well-recognized cause of bloody diarrhea and hemolytic-uremic syndrome (HUS). Non-O157 STEC contribute to this burden of illness but have been underrecognized as a result of diagnostic limitations and inadequate surveillance. Methods. Between 1983 and 2002, 43 state public health laboratories submitted 940 human non-O157 STEC isolates from persons with sporadic illnesses to the Centers for Diseases Control and Prevention reference laboratory for confirmation and serotyping. Results. The most common serogroups were 026 (22%), O111 (16%), 0103 (12%), O121 (8%), O45 (7%), and O145 (5%). Non-0157 STEC infections were most frequent during the summer and among young persons (median age, 12 years; interquartile range, 3-37 years). Virulence gene profiles were as follows: 61% stx₁ but not stx₂; 22% stx₂ but not stx₁; 17% both stx₁ and stx₂; 84% intimin (eae); and 86% enterohemolysin (E-hly). stx₂ was strongly associated with an increased risk of HUS, and eae was strongly associated with an increased risk of bloody diarrhea. STEC O111 accounted for most cases of HUS and was also the cause of 3 of 7 non-O157 STEC outbreaks reported in the United States. Conclusions. Non-O157 STEC can cause severe illness that is comparable to the illness caused by STEC O157. Strains that produce Shiga toxin 2 are much more likely to cause HUS than are those that produce Shiga toxin 1 alone. Improving surveillance will more fully elucidate the incidence and pathological spectrum of these emerging agents. These efforts require increased clinical suspicion, improved clinical laboratory isolation, and continued serotyping of isolates in public health laboratories.
The Journal of Infectious Diseases © 2005 Oxford University Press