Role of Bacterial Virulence Factors and Host Factors in the Outcome of Escherichia coli Bacteraemia

2000 ◽  
Vol 19 (4) ◽  
pp. 312-316 ◽  
Author(s):  
T. A. M. Hekker ◽  
A. B. J. Groeneveld ◽  
A. M. Simoons-Smit ◽  
P. de Man ◽  
H. Connell ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Bacterial Virulence ◽  
Host Factors

Role of host and bacterial virulence factors in Escherichia coli spontaneous bacterial peritonitis

2008 ◽  
Vol 20 (9) ◽  
pp. 924-929 ◽  
Author(s):  
Ferran Cereto ◽  
Xavier Herranz ◽  
Eva Moreno ◽  
Antònia Andreu ◽  
Mertxe Vergara ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Spontaneous Bacterial Peritonitis ◽  
Bacterial Virulence ◽  
Bacterial Peritonitis

scholarly journals Two Enteropathogenic Escherichia coli Type III Secreted Proteins, EspA and EspB, Are Virulence Factors

1998 ◽  
Vol 188 (10) ◽  
pp. 1907-1916 ◽  
Author(s):  
Akio Abe ◽  
Ursula Heczko ◽  
Richard G. Hegele ◽  
B. Brett Finlay
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Enterohemorrhagic Escherichia Coli ◽  
Laser Scanning Microscopy ◽  
Secreted Proteins ◽  
Confocal Laser ◽  
Infection Model ◽  
Enteropathogenic Escherichia Coli ◽  
Type Iii

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.

scholarly journals Role of Virulence Factors in Resistance of Avian Pathogenic Escherichia coli to Serum and in Pathogenicity

2003 ◽  
Vol 71 (1) ◽  
pp. 536-540 ◽  
Author(s):  
Melha Mellata ◽  
Maryvonne Dho-Moulin ◽  
Charles M. Dozois ◽  
Roy Curtiss ◽  
Peter K. Brown ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Bacterial Resistance ◽  
Serum Resistance ◽  
Temperature Sensitive ◽  
E Coli ◽  
Pathogenic Escherichia Coli ◽  
K1 Capsule

ABSTRACT In chickens, colibacillosis is caused by avian pathogenic Escherichia coli (APEC) via respiratory tract infection. Many virulence factors, including type 1 (F1A) and P (F11) fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) and plasmid DNA regions have been associated with APEC. A strong correlation between serum resistance and virulence has been demonstrated, but roles of virulence factors in serum resistance have not been well elucidated. By using mutants of APEC strains TK3, MT78, and χ7122, which belong to serogroups O1, O2, and O78, respectively, we investigated the role of virulence factors in resistance to serum and pathogenicity in chickens. Our results showed that serum resistance is one of the pathogenicity mechanisms of APEC strains. Virulence factors that increased bacterial resistance to serum and colonization of internal organs of infected chickens were O78 lipopolysaccharide of E. coli χ7122 and the K1 capsule of E. coli MT78. In contrast, curli, type 1, and P fimbriae did not appear to contribute to serum resistance. We also showed that the iss gene, which was previously demonstrated to increase resistance to serum in certain E. coli strains, is located on plasmid pAPEC-1 of E. coli χ7122 but does not play a major role in resistance to serum for strain χ7122.

scholarly journals Characterization of the Roles of Hemolysin and Other Toxins in Enteropathy Caused by Alpha-Hemolytic Escherichia coli Linked to Human Diarrhea

1998 ◽  
Vol 66 (5) ◽  
pp. 2040-2051 ◽  
Author(s):  
Simon J. Elliott ◽  
S. Srinivas ◽  
M. John Albert ◽  
Khorshed Alam ◽  
Roy M. Robins-Browne ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Virulence Factor ◽  
Adult Rabbit ◽  
Cell Hyperplasia ◽  
E Coli ◽  
Alpha Hemolysin ◽  
A Cell ◽  
Cytotoxic Necrotizing Factor 1

ABSTRACT Escherichia coli strains producing alpha-hemolysin have been associated with diarrhea in several studies, but it has not been clearly demonstrated that these strains are enteropathogens or that alpha-hemolysin is an enteric virulence factor. Such strains are generally regarded as avirulent commensals. We examined a collection of diarrhea-associated hemolytic E. coli (DHEC) strains for virulence factors. No strain produced classic enterotoxins, but they all produced an alpha-hemolysin that was indistinguishable from that of uropathogenic E. coli strains. DHEC strains also produced other toxins including cytotoxic necrotizing factor 1 (CNF1) and novel toxins, including a cell-detaching cytotoxin and a toxin that causes HeLa cell elongation. DHEC strains were enteropathogenic in the RITARD (reversible intestinal tie adult rabbit diarrhea) model of diarrhea, causing characteristic enteropathies, including inflammation, necrosis, and colonic cell hyperplasia in both small and large intestines. Alpha-hemolysin appeared to be a major virulence factor in this model since it conferred virulence to nonpathogenic E. colistrains. Other virulence factors also appear to be contributing to virulence. These findings support the epidemiologic link to diarrhea and suggest that further research into the role of DHEC and alpha-hemolysin in enteric disease is warranted.

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