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Grazing protozoa and the evolution of the Escherichia coli O157:H7 Shiga toxin-encoding prophage.

Steinberg KM, Levin BR - Proc. Biol. Sci. (2007)

Bottom Line: Why then does E. coli O157:H7 code for virulence determinants, like the Shiga toxins (Stxs), responsible for the morbidity and mortality of colonized humans?Here, we test the hypothesis that the carriage of the Stx-encoding prophage of E. coli O157:H7 increases the rate of survival of E. coli in the presence of grazing protozoa, Tetrahymena pyriformis.In the presence but not the absence of Tetrahymena, the carriage of the Stx-encoding prophage considerably augments the fitness of E. coli K-12 as well as clinical isolates of E. coli O157 by increasing the rate of survival of the bacteria in the food vacuoles of these ciliates.

View Article: PubMed Central - PubMed

Affiliation: Graduate Program in Population Biology, Ecology and Evolution, Emory University, Atlanta, GA 30322, USA. kmeltz@emory.edu

ABSTRACT
Humans play little role in the epidemiology of Escherichia coli O157:H7, a commensal bacterium of cattle. Why then does E. coli O157:H7 code for virulence determinants, like the Shiga toxins (Stxs), responsible for the morbidity and mortality of colonized humans? One possibility is that the virulence of these bacteria to humans is coincidental and these virulence factors evolved for and are maintained for other roles they play in the ecology of these bacteria. Here, we test the hypothesis that the carriage of the Stx-encoding prophage of E. coli O157:H7 increases the rate of survival of E. coli in the presence of grazing protozoa, Tetrahymena pyriformis. In the presence but not the absence of Tetrahymena, the carriage of the Stx-encoding prophage considerably augments the fitness of E. coli K-12 as well as clinical isolates of E. coli O157 by increasing the rate of survival of the bacteria in the food vacuoles of these ciliates. Grazing protozoa in the environment or natural host are likely to play a significant role in the ecology and maintenance of the Stx-encoding prophage of E. coli O157:H7 and may well contribute to the evolution of the virulence of these bacteria to colonize humans.

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Mixtures of clinical isolates of E. coli O157:H7 or E. coli O157:H− and C600 in the presence and absence of Tetrahymena. Ratio of O157 to C600 initially and after 3 days with and without Tetrahymena, means ±s.e. (a) Clinical isolates with Stx1- and Stx2-encoding prophage. (b) Clinical isolates with Stx1-encoding prophage. (c) Clinical isolates with no Stx-encoding prophage. For each experiment, there were two control and six experimental cultures (*p<0.05, **p<0.005 and ***p<0.0005). White bars, initial without Tetrahymena; black bars, after 3 days without Tetrahymena; light grey bars, initial with Tetrahymena; dark grey bars, after 3 days with Tetrahymena.
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fig2: Mixtures of clinical isolates of E. coli O157:H7 or E. coli O157:H− and C600 in the presence and absence of Tetrahymena. Ratio of O157 to C600 initially and after 3 days with and without Tetrahymena, means ±s.e. (a) Clinical isolates with Stx1- and Stx2-encoding prophage. (b) Clinical isolates with Stx1-encoding prophage. (c) Clinical isolates with no Stx-encoding prophage. For each experiment, there were two control and six experimental cultures (*p<0.05, **p<0.005 and ***p<0.0005). White bars, initial without Tetrahymena; black bars, after 3 days without Tetrahymena; light grey bars, initial with Tetrahymena; dark grey bars, after 3 days with Tetrahymena.

Mentions: To ascertain whether the advantage of E. coli lysogenic for the Stx-encoding prophage in the presence of Tetrahymena obtains for E. coli O157 lysogens as well as E. coli K-12 lysogens, we performed these pairwise mixed culture experiments with C600 and clinical isolates of E. coli O157:H7 and E. coli O157:H−. In figure 2, we plot the ratio of E. coli O157 and C600 at the start of these experiments and after 3 days in the presence and absence of Tetrahymena.


Grazing protozoa and the evolution of the Escherichia coli O157:H7 Shiga toxin-encoding prophage.

Steinberg KM, Levin BR - Proc. Biol. Sci. (2007)

Mixtures of clinical isolates of E. coli O157:H7 or E. coli O157:H− and C600 in the presence and absence of Tetrahymena. Ratio of O157 to C600 initially and after 3 days with and without Tetrahymena, means ±s.e. (a) Clinical isolates with Stx1- and Stx2-encoding prophage. (b) Clinical isolates with Stx1-encoding prophage. (c) Clinical isolates with no Stx-encoding prophage. For each experiment, there were two control and six experimental cultures (*p<0.05, **p<0.005 and ***p<0.0005). White bars, initial without Tetrahymena; black bars, after 3 days without Tetrahymena; light grey bars, initial with Tetrahymena; dark grey bars, after 3 days with Tetrahymena.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2211389&req=5

fig2: Mixtures of clinical isolates of E. coli O157:H7 or E. coli O157:H− and C600 in the presence and absence of Tetrahymena. Ratio of O157 to C600 initially and after 3 days with and without Tetrahymena, means ±s.e. (a) Clinical isolates with Stx1- and Stx2-encoding prophage. (b) Clinical isolates with Stx1-encoding prophage. (c) Clinical isolates with no Stx-encoding prophage. For each experiment, there were two control and six experimental cultures (*p<0.05, **p<0.005 and ***p<0.0005). White bars, initial without Tetrahymena; black bars, after 3 days without Tetrahymena; light grey bars, initial with Tetrahymena; dark grey bars, after 3 days with Tetrahymena.
Mentions: To ascertain whether the advantage of E. coli lysogenic for the Stx-encoding prophage in the presence of Tetrahymena obtains for E. coli O157 lysogens as well as E. coli K-12 lysogens, we performed these pairwise mixed culture experiments with C600 and clinical isolates of E. coli O157:H7 and E. coli O157:H−. In figure 2, we plot the ratio of E. coli O157 and C600 at the start of these experiments and after 3 days in the presence and absence of Tetrahymena.

Bottom Line: Why then does E. coli O157:H7 code for virulence determinants, like the Shiga toxins (Stxs), responsible for the morbidity and mortality of colonized humans?Here, we test the hypothesis that the carriage of the Stx-encoding prophage of E. coli O157:H7 increases the rate of survival of E. coli in the presence of grazing protozoa, Tetrahymena pyriformis.In the presence but not the absence of Tetrahymena, the carriage of the Stx-encoding prophage considerably augments the fitness of E. coli K-12 as well as clinical isolates of E. coli O157 by increasing the rate of survival of the bacteria in the food vacuoles of these ciliates.

View Article: PubMed Central - PubMed

Affiliation: Graduate Program in Population Biology, Ecology and Evolution, Emory University, Atlanta, GA 30322, USA. kmeltz@emory.edu

ABSTRACT
Humans play little role in the epidemiology of Escherichia coli O157:H7, a commensal bacterium of cattle. Why then does E. coli O157:H7 code for virulence determinants, like the Shiga toxins (Stxs), responsible for the morbidity and mortality of colonized humans? One possibility is that the virulence of these bacteria to humans is coincidental and these virulence factors evolved for and are maintained for other roles they play in the ecology of these bacteria. Here, we test the hypothesis that the carriage of the Stx-encoding prophage of E. coli O157:H7 increases the rate of survival of E. coli in the presence of grazing protozoa, Tetrahymena pyriformis. In the presence but not the absence of Tetrahymena, the carriage of the Stx-encoding prophage considerably augments the fitness of E. coli K-12 as well as clinical isolates of E. coli O157 by increasing the rate of survival of the bacteria in the food vacuoles of these ciliates. Grazing protozoa in the environment or natural host are likely to play a significant role in the ecology and maintenance of the Stx-encoding prophage of E. coli O157:H7 and may well contribute to the evolution of the virulence of these bacteria to colonize humans.

Show MeSH
Related in: MedlinePlus