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Contribution and Interaction of Shiga Toxin Genes to Escherichia coli O157:H7 Virulence.
Toxins (Basel). 2019 10 18; 11(10)T

Abstract

Escherichia coli O157:H7 is the predominant cause of diarrhea-associated hemolytic uremic syndrome (HUS) worldwide. Its cardinal virulence traits are Shiga toxins, which are encoded by stx genes, the most common of which are stx1a, stx2a, and stx2c. The toxins these genes encode differ in their in vitro and experimental phenotypes, but the human population-level impact of these differences is poorly understood. Using Shiga toxin-encoding bacteriophage insertion typing and real-time polymerase chain reaction, we genotyped isolates from 936 E. coli O157:H7 cases and verified HUS status via chart review. We compared the HUS risk between isolates with stx2a and those with stx2a and another gene and estimated additive interaction of the stx genes. Adjusted for age and symptoms, the HUS incidence of E. coli O157:H7 containing stx2a alone was 4.4% greater (95% confidence interval (CI) -0.3%, 9.1%) than when it occurred with stx1a. When stx1a and stx2a occur together, the risk of HUS was 27.1% lower (95% CI -87.8%, -2.3%) than would be expected if interaction were not present. At the population level, temporal or geographic shifts toward these genotypes should be monitored, and stx genotype may be an important consideration in clinically predicting HUS among E. coli O157:H7 cases.

Authors+Show Affiliations

Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, AB T3B 6A8, Canada. gtarr@umn.edu.Department of Laboratory Medicine and Pathology, University of Alberta and Alberta Public Labs, Edmonton, AB T6G 2J2, Canada. tstokows@ualberta.ca.Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA 99163, USA. smriti_shringi@wsu.edu.Division of Gastroenterology, Hepatology, and Nutrition, Washington University School of Medicine, St. Louis, MO 63110, USA. tarr@wustl.edu.Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, AB T3B 6A8, Canada. stephen.freedman@ahs.ca.Washington State Department of Health, Shoreline, WA 98155, USA. hanna.oltean@doh.wa.gov.Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195, USA. peterr7@uw.edu.Department of Laboratory Medicine and Pathology, University of Alberta and Alberta Public Labs, Edmonton, AB T6G 2J2, Canada. linda.chui@albertapubliclabs.ca.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

31635282

Citation

Tarr, Gillian A M., et al. "Contribution and Interaction of Shiga Toxin Genes to Escherichia Coli O157:H7 Virulence." Toxins, vol. 11, no. 10, 2019.
Tarr GAM, Stokowski T, Shringi S, et al. Contribution and Interaction of Shiga Toxin Genes to Escherichia coli O157:H7 Virulence. Toxins (Basel). 2019;11(10).
Tarr, G. A. M., Stokowski, T., Shringi, S., Tarr, P. I., Freedman, S. B., Oltean, H. N., Rabinowitz, P. M., & Chui, L. (2019). Contribution and Interaction of Shiga Toxin Genes to Escherichia coli O157:H7 Virulence. Toxins, 11(10). https://doi.org/10.3390/toxins11100607
Tarr GAM, et al. Contribution and Interaction of Shiga Toxin Genes to Escherichia Coli O157:H7 Virulence. Toxins (Basel). 2019 10 18;11(10) PubMed PMID: 31635282.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Contribution and Interaction of Shiga Toxin Genes to Escherichia coli O157:H7 Virulence. AU - Tarr,Gillian A M, AU - Stokowski,Taryn, AU - Shringi,Smriti, AU - Tarr,Phillip I, AU - Freedman,Stephen B, AU - Oltean,Hanna N, AU - Rabinowitz,Peter M, AU - Chui,Linda, Y1 - 2019/10/18/ PY - 2019/09/24/received PY - 2019/10/14/revised PY - 2019/10/16/accepted PY - 2019/10/23/entrez PY - 2019/10/23/pubmed PY - 2019/10/23/medline KW - Escherichia coli O157:H7 KW - Shiga toxin-producing Escherichia coli KW - hemolytic uremic syndrome KW - stx genes JF - Toxins JO - Toxins (Basel) VL - 11 IS - 10 N2 - Escherichia coli O157:H7 is the predominant cause of diarrhea-associated hemolytic uremic syndrome (HUS) worldwide. Its cardinal virulence traits are Shiga toxins, which are encoded by stx genes, the most common of which are stx1a, stx2a, and stx2c. The toxins these genes encode differ in their in vitro and experimental phenotypes, but the human population-level impact of these differences is poorly understood. Using Shiga toxin-encoding bacteriophage insertion typing and real-time polymerase chain reaction, we genotyped isolates from 936 E. coli O157:H7 cases and verified HUS status via chart review. We compared the HUS risk between isolates with stx2a and those with stx2a and another gene and estimated additive interaction of the stx genes. Adjusted for age and symptoms, the HUS incidence of E. coli O157:H7 containing stx2a alone was 4.4% greater (95% confidence interval (CI) -0.3%, 9.1%) than when it occurred with stx1a. When stx1a and stx2a occur together, the risk of HUS was 27.1% lower (95% CI -87.8%, -2.3%) than would be expected if interaction were not present. At the population level, temporal or geographic shifts toward these genotypes should be monitored, and stx genotype may be an important consideration in clinically predicting HUS among E. coli O157:H7 cases. SN - 2072-6651 UR - https://www.unboundmedicine.com/medline/citation/31635282/Contribution_and_Interaction_of_Shiga_Toxin_Genes_to_Escherichia_coli_O157:H7_Virulence_ L2 - https://www.mdpi.com/resolver?pii=toxins11100607 DB - PRIME DP - Unbound Medicine ER -