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Volume 20, Number 10—October 2014

Research

Clinical Isolates of Shiga Toxin 1a–Producing Shigella flexneri with an Epidemiological Link to Recent Travel to Hispañiola

Miranda D. Gray, Keith A. Lampel, Nancy A. Strockbine, Reinaldo E. Fernandez, Angela R. Melton-Celsa, and Anthony T. MaurelliComments to Author 
Author affiliations: Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA (M.D. Gray, R.E. Fernandez, A.R. Melton-Celsa, A.T. Maurelli); US Food and Drug Administration, College Park, Maryland, USA (K.A. Lampel); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (N.A. Strockbine)

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Figure 2

Mitomycin C induces production of Shiga toxin 1a (Stx1a) in a recA-dependent manner. Exponentially growing cultures of the indicated parental strains or recA mutants were grown with or without 0.5 μg/mL mitomycin C (mito C) for 3 hours. Supernatants (A) or whole cell lysates (B) were prepared for determination of cytotoxicity for Vero cells. CD50/mL values were determined as described in Figure 1. Data are averages of 3 biological replicates. Error bars indicate standard error. Δ indicates sampl

Figure 2. Mitomycin C induces production of Shiga toxin 1a (Stx1a) in a recA-dependent manner. Exponentially growing cultures of the indicated parental strains or recA mutants were grown with or without 0.5 μg/mL mitomycin C (mito C) for 3 hours. Supernatants (A) or whole cell lysates (B) were prepared for determination of cytotoxicity for Vero cells. CD50/mL values were determined as described in Figure 1. Data are averages of 3 biological replicates. Error bars indicate standard error. Δ indicates samples that are recA mutants.

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Page created: September 12, 2014
Page updated: September 12, 2014
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