Regulation of Virulence Factors of Enterohemorrhagic Escherichia coli O157:H7 by Self-Produced Extracellular Factors

2000 ◽  
Vol 64 (11) ◽  
pp. 2508-2511 ◽  
Author(s):  
Kyoko KANAMARU ◽  
Kengo KANAMARU ◽  
Ichiro TATSUNO ◽  
Toru TOBE ◽  
Chihiro SASAKAWA
2007 ◽  
Vol 190 (1) ◽  
pp. 438-441 ◽  
Author(s):  
Kenan C. Murphy ◽  
Jennifer M. Ritchie ◽  
Matthew K. Waldor ◽  
Anders Løbner-Olesen ◽  
M. G. Marinus

ABSTRACT Shiga toxin 2 (Stx2), one of the principal virulence factors of enterohemorrhagic Escherichia coli, is encoded by 933W, a lambda-like prophage. 933W prophage induction contributes to Stx2 production, and here, we provide evidence that Dam methyltransferase is essential for maintenance of 933W lysogeny. Our findings are consistent with the idea that the 933W prophage has a relatively low threshold for induction, which may promote Stx2 production during infection.


2004 ◽  
Vol 67 (3) ◽  
pp. 486-492 ◽  
Author(s):  
GERRY P. SCHAMBERGER ◽  
FRANCISCO DIEZ-GONZALEZ

A previously identified set of anti– Escherichia coli O157:H7 colicinogenic E. coli were characterized to assess the suitability of these isolates as a preharvest food safety intervention in cattle. This collection of 23 E. coli strains were screened for virulence factors, antibiotic resistance, type of colicin(s) present, and their ability to inhibit other pathogenic E. coli. With the use of PCR, pathogen genes were detected in six of the 23 colicinogenic E. coli. When the nonpathogenic strains were assessed for antibiotic resistance, four strains showed resistance to at least one antibiotic. The remaining set of 14 strains were evaluated for the presence of previously identified colicins. Seven colicins (B, E1, E2/E7, E7, Ia/Ib, K, and M) were detected. One half of the strains possessed multiple types of colicins. The most commonly detected colicins were B, E2/E7, and M, which were found in six strains each. DNA sequencing was also performed in order to classify the E2/E7 colicins separately from E7 colicins. The 14 colicinogenic E. coli also were evaluated for their ability to inhibit 10 different non-O157 pathogenic E. coli. Six of the colicinogenic E. coli were capable of inhibiting all 10 pathogens, and the remaining eight strains could each inhibit between six to eight of the pathogenic E. coli. This strain collection has great potential for inhibiting E. coli O157:H7 in cattle.


PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208520 ◽  
Author(s):  
Wanderson Marques Da Silva ◽  
Jinlong Bei ◽  
Natalia Amigo ◽  
María Pía Valacco ◽  
Ariel Amadio ◽  
...  

1998 ◽  
Vol 188 (10) ◽  
pp. 1907-1916 ◽  
Author(s):  
Akio Abe ◽  
Ursula Heczko ◽  
Richard G. Hegele ◽  
B. Brett Finlay

Enteropathogenic Escherichia coli (EPEC) belongs to a family of related bacterial pathogens, including enterohemorrhagic Escherichia coli (EHEC) O157:H7 and other human and animal diarrheagenic pathogens that form attaching and effacing (A/E) lesions on host epithelial surfaces. Bacterial secreted Esp proteins and a type III secretion system are conserved among these pathogens and trigger host cell signal transduction pathways and cytoskeletal rearrangements, and mediate intimate bacterial adherence to epithelial cell surfaces in vitro. However, their role in pathogenesis is still unclear. To investigate the role of Esp proteins in disease, mutations in espA and espB were constructed in rabbit EPEC serotype O103 and infection characteristics were compared to that of the wild-type strain using histology, scanning and transmission electron microscopy, and confocal laser scanning microscopy in a weaned rabbit infection model. The virulence of EspA and EspB mutant strains was severely attenuated. Additionally, neither mutant strain formed A/E lesions, nor did either one cause cytoskeletal actin rearrangements beneath the attached bacteria in the rabbit intestine. Collectively, this study shows for the first time that the type III secreted proteins EspA and EspB are needed to form A/E lesions in vivo and are indeed virulence factors. It also confirms the role of A/E lesions in disease processes.


1998 ◽  
Vol 72 (2) ◽  
pp. 89-96
Author(s):  
Sou-ichi MAKINO ◽  
Hiroshi ASAKURA ◽  
Toshikazu SHIRAHATA ◽  
Tetsuya IKEDA ◽  
Koichi TAKESHI ◽  
...  

2012 ◽  
Vol 423 (4) ◽  
pp. 789-792 ◽  
Author(s):  
Jong Chul Kim ◽  
Jang W. Yoon ◽  
Cheorl-Ho Kim ◽  
Mi-Sun Park ◽  
Seung-Hak Cho

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