Limits...
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.

Show MeSH

Related in: MedlinePlus

Mixtures of stx2-positive strains and isogenic stx2-negative constructs in the presence and absence of Tetrahymena initially and after 3 days, means ±s.e. (a) Ratio of C600PT+ and C600PT−. (b) Ratio of P2T+ and P2T−. For each experiment, there were two control and six experimental cultures (*p<0.05 and ****p<0.00005). White bars, initial; grey bars, after 3 days.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2211389&req=5

fig4: Mixtures of stx2-positive strains and isogenic stx2-negative constructs in the presence and absence of Tetrahymena initially and after 3 days, means ±s.e. (a) Ratio of C600PT+ and C600PT−. (b) Ratio of P2T+ and P2T−. For each experiment, there were two control and six experimental cultures (*p<0.05 and ****p<0.00005). White bars, initial; grey bars, after 3 days.

Mentions: Four E. coli lysogens were used in these experiments: (i) C600PT+ which carry a prophage with a functional stx2, (ii) C600PT− which carry the same prophage as C600PT+, but in which the stx2 locus was replaced with a chloramphenicol resistance cassette (Schmidt et al. 1999), (iii) P2T+, an E. coli O157:H7 strain which carry a prophage with a functional stx2 locus, and (iv) P2T−, the above E. coli O157:H7 which carry the same prophage as P2T+, but in which the stx2 locus is deleted (Gunzer et al. 1998). These Stx+ and Stx− lysogens were mixed with C600 (figure 3). We also performed these pairwise mixed culture experiments with mixtures of otherwise isogenic Stx+ and Stx− lysogens (figure 4).


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 stx2-positive strains and isogenic stx2-negative constructs in the presence and absence of Tetrahymena initially and after 3 days, means ±s.e. (a) Ratio of C600PT+ and C600PT−. (b) Ratio of P2T+ and P2T−. For each experiment, there were two control and six experimental cultures (*p<0.05 and ****p<0.00005). White bars, initial; grey bars, after 3 days.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Mixtures of stx2-positive strains and isogenic stx2-negative constructs in the presence and absence of Tetrahymena initially and after 3 days, means ±s.e. (a) Ratio of C600PT+ and C600PT−. (b) Ratio of P2T+ and P2T−. For each experiment, there were two control and six experimental cultures (*p<0.05 and ****p<0.00005). White bars, initial; grey bars, after 3 days.
Mentions: Four E. coli lysogens were used in these experiments: (i) C600PT+ which carry a prophage with a functional stx2, (ii) C600PT− which carry the same prophage as C600PT+, but in which the stx2 locus was replaced with a chloramphenicol resistance cassette (Schmidt et al. 1999), (iii) P2T+, an E. coli O157:H7 strain which carry a prophage with a functional stx2 locus, and (iv) P2T−, the above E. coli O157:H7 which carry the same prophage as P2T+, but in which the stx2 locus is deleted (Gunzer et al. 1998). These Stx+ and Stx− lysogens were mixed with C600 (figure 3). We also performed these pairwise mixed culture experiments with mixtures of otherwise isogenic Stx+ and Stx− lysogens (figure 4).

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