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Web Review of Todar's Online Textbook of Bacteriology. "The Good, the Bad, and the Deadly".

Tag words: Escherichia coli, E. coli, E. coli O157:H7, enteropathogenic E. coli, EPEC, enterotoxigenic E. coli, ETEC, LT toxin, ST toxin, vero toxin, shiga toxin, food poisoning, gastroenteritis, hemolytic uremic syndrome, HUS, neonatal meningitis, urinary tract infection, UTI.

Escherichia coli

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Escherichia
Species: E. coli








Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

Bacillus cereus bacteria.Print this Page

Pathogenic E. coli (page 2)

(This chapter has 4 pages)

© Kenneth Todar, PhD

Escherichia coli in the Gastrointestinal Tract

The commensal E. coli strains that inhabit the large intestine of all humans and warm-blooded animals comprise no more than 1% of the total  bacterial biomass.

The E. coli flora is apparently in constant flux. One study on the distribution of different E. coli strains colonizing the large intestine of women during a one year period (in a hospital setting) showed that 52.1% yielded one serotype, 34.9% yielded two, 4.4% yielded three, and 0.6% yielded four.  The most likely source of new serotypes of E. coli is acquisition by the oral route.

To study oral acquisition, the carriage rate of E. coli carrying antibiotic-resistance plasmids (R factors) was examined among vegetarians, babies, and nonvegetarians. It was assumed that nonvegetarians might carry more E. coli with R factors due to their presumed high incidence in animals treated with growth-promoting antimicrobial agents. However, omnivores had no higher an incidence of R-factor-containing E. coli than vegetarians, and babies had more resistant E. coli in their feces than nonvegetarians. No suitable explanation could be offered for these findings. Besides, investigation of the microbial flora of the uninhabited Krakatoa archipelago has shown the presence of antibiotic-resistant E. coli associated with plants.

The bottom line seems to be that most of us have more than one strain of E. coli in our gut, and intestinal strains tend to displace one another about three or four times a year.


Pathogenesis of E. coli

Over 700 antigenic types (serotypes) of E. coli are recognized based on O, H, and K antigens. At one time serotyping was important in distinguishing the small number of strains that actually cause disease. Thus, the serotype O157:H7 (O refers to somatic antigen; H refers to flagellar antigen) is uniquely responsible for  causing HUS (hemolytic uremic syndrome). Nowadays, particularly for diarrheagenic strains (those that cause diarrhea) pathogenic E. coli are classified based on their unique virulence factors and can only be identified by these traits. Hence, analysis for pathogenic E. coli usually requires that the isolates first be identified as E. coli before testing for virulence markers.

Pathogenic strains of E. coli are responsible for three types of infections in humans: urinary tract infections (UTI), neonatal meningitis, and intestinal diseases (gastroenteritis). The diseases caused (or not caused) by a particular strain of E. coli depend on distribution and expression of an array of virulence determinants, including adhesins, invasins, toxins, and abilities to withstand host defenses. These are summarized in Table 1 and applied to the discussion of pathogenic strains E. coli below.


Table 1. Summary of the Virulence Determinants of Pathogenic E. coli

Adhesins
CFAI/CFAII
Type 1 fimbriae
P fimbriae
S fimbriae
Intimin (non-fimbrial adhesin)
EPEC adherence factor

Invasins

hemolysin
Shigella-like "invasins" for intracellular invasion and spread

Motility/chemotaxis

flagella

Toxins
LT toxin
ST toxin
Shiga toxin
cytotoxins
endotoxin (LPS)

Antiphagocytic surface properties

capsules
K antigens
LPS

Defense against serum bactericidal reactions

LPS
K antigens

Defense against immune responses

capsules
K antigens
LPS
antigenic variation

Genetic attributes

genetic exchange by transduction and conjugation
transmissible plasmids
R factors and drug resistance plasmids
toxin and other virulence plasmids
siderophores and siderophore uptake systems
pathogenicity islands





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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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