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Todar's Online Textbook of Bacteriology |
Theodor Escherich first described E. coli in 1885, as Bacterium
coli commune, which he isolated from the feces of newborns. It was
later renamed Escherichia coli, and for many years the
bacterium was simply considered to be a commensal organism of the large
intestine. It was not until 1935 that a strain of E. coli was
shown to be the cause of an outbreak of diarrhea among infants.
E. coli is the head of the large bacterial family, Enterobacteriaceae, the enteric bacteria, which are facultatively anaerobic Gram-negative rods that live in the intestinal tracts of animals in health and disease. The Enterobacteriaceae are among the most important bacteria medically. A number of genera within the family are human intestinal pathogens (e.g. Salmonella, Shigella, Yersinia). Several others are normal colonists of the human gastrointestinal tract (e.g. Escherichia, Enterobacter, Klebsiella), but these bacteria, as well, may occasionally be associated with diseases of humans.
Physiologically, E. coli is versatile and well-adapted to its characteristic habitats. It can grow in media with glucose as the sole organic constituent. Wild-type E. coli has no growth factor requirements, and metabolically it can transform glucose into all of the macromolecular components that make up the cell. The bacterium can grow in the presence or absence of O2. Under anaerobic conditions it will grow by means of fermentation, producing characteristic "mixed acids and gas" as end products. However, it can also grow by means of anaerobic respiration, since it is able to utilize NO3, NO2 or fumarate as final electron acceptors for respiratory electron transport processes. In part, this adapts E. coli to its intestinal (anaerobic) and its extraintestinal (aerobic or anaerobic) habitats.
E. coli can respond to environmental signals such as chemicals, pH, temperature, osmolarity, etc., in a number of very remarkable ways considering it is a unicellular organism. For example, it can sense the presence or absence of chemicals and gases in its environment and swim towards or away from them. Or it can stop swimming and grow fimbriae that will specifically attach it to a cell or surface receptor. In response to change in temperature and osmolarity, it can vary the pore diameter of its outer membrane porins to accommodate larger molecules (nutrients) or to exclude inhibitory substances. With its complex mechanisms for regulation of metabolism the bacterium can survey the chemical contents in its environment in advance of synthesizing any enzymes that metabolize these compounds. It does not wastefully produce enzymes for degradation of carbon sources unless they are available, and it does not produce enzymes for synthesis of metabolites if they are available as nutrients in the environment.
E. coli is a consistent inhabitant of the human intestinal tract, and it is the predominant facultative organism in the human GI tract; however, it makes up a very small proportion of the total bacterial content. The anaerobic Bacteroides species in the bowel outnumber E. coli by at least 20:1. however, the regular presence of E. coli in the human intestine and feces has led to tracking the bacterium in nature as an indicator of fecal pollution and water contamination. As such, it is taken to mean that, wherever E. coli is found, there may be fecal contamination by intestinal parasites of humans.
Unstained cells of E. coli
viewed by phase microscopy. about 1000X magnification. CDC.
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.
The adhesin that has been most closely associated with uropathogenic E. coli is the P fimbria (or pyelonephritis-associated pili [PAP]). The letter designation is derived from the ability of P fimbriae to bind specifically to the P blood group antigen which contains a D-galactose-D-galactose residue. The fimbriae bind not only to red cells but to a specific galactose dissaccharide that is found on the surfaces uroepithelial cells in approximately 99% of the population.
The frequency of the distribution of this host cell receptor plays a role in susceptibility and explains why certain individuals have repeated UTI caused by E. coli. Uncomplicated E. coli UTI virtually never occurs in individuals lacking the receptors.
Uropathogenic strains of E. coli possess other determinants of virulence in addition to P fimbriae. E. coli with P fimbriae also possess the gene for Type 1 fimbriae, and there is evidence that P fimbriae are derived from Type 1 fimbriae by insertion of a new fimbrial tip protein to replace the mannose-binding domain of Type 1 fimbriae. In any case, Type 1 fimbriae could provide a supplementary mechanism of adherence or play a role in aggregating the bacteria to a specific manosyl-glycoprotein that occurs in urine.
Uropathogenic strains of E. coli usually produce siderophores that probably play an essential role in iron acquisition for the bacteria during or after colonization. They also produce hemolysins which are cytotoxic due to formation of transmembranous pores in host cell membranes. One strategy for obtaining iron and other nutrients for bacterial growth may involve the lysis of host cells to release these substances. The activity of hemolysins is not limited to red cells since the alpha-hemolysins of E. coli also lyse lymphocytes, and the beta-hemolysins inhibit phagocytosis and chemotaxis of neutrophils.
Another factor thought to be involved in the pathogenicity of the
uropathogenic
strains of E. coli is their resistance to the
complement-dependent
bactericidal effect of serum. The presence of K antigens is associated
with upper urinary tract infections, and antibody to the K antigen
has been shown to afford some degree of protection in experimental
infections.
The K antigens of E. coli are "capsular" antigens that may be
composed
of proteinaceous organelles associated with colonization (e.g., CFA
antigens),
or made of polysaccharides. Regardless of their chemistry, these
capsules
may be able to promote bacterial virulence by decreasing the ability of
antibodies and/or complement to bind to the bacterial surface, and the
ability of phagocytes to recognize and engulf the bacterial cells. The
best studied K antigen, K-1, is composed of a polymer of N-acetyl
neuraminic
acid (sialic acid), which besides being antiphagocytic, has the
additional
property of being an antigenic disguise.
E. coli strains invade the blood stream of infants from the nasopharynx or GI tract and are carried to the meninges.
The K-1 antigen is considered the major determinant of virulence among strains of E. coli that cause neonatal meningitis. K-1 is a homopolymer of sialic acid. It inhibits phagocytosis, complement, and responses from the host's immunological mechanisms. K-1 may not be the only determinant of virulence, however, as siderophore production and endotoxin are also likely to be involved.
Epidemiologic studies have shown that pregnancy is associated with increased rates of colonization by K-1 strains and that these strains become involved in the subsequent cases of meningitis in the newborn. Probably, the infant GI tract is the portal of entry into the bloodstream. Fortunately, although colonization is fairly common, invasion and the catastrophic sequelae are rare.
Neonatal meningitis requires antibiotic therapy that usually
includes
ampicillin and a third-generation cephalosporin.
Lysis of a dividing pair of E.
coli
cells in the presence of a beta-lactam antibiotic. Some beta lactam
antibiotics, such as ampicillin and cephalosporin, are effective
in the treatment of meningitis caused by strains of E. coli
(above). The beta lactam antibiotics prevent cell wall synthesis and
assembly in the bacterium. When the bacterium grows in the presence of
the antibiotic, the cell wall becomes progressively weaker and weaker,
so the the organism eventually ruptures or "lyses", pouring out its
cytoplasmic contents as shown here.
ETEC adhesins are fimbriae which are species-specific. For example, the K-88 fimbrial Ag is found on strains from piglets; K-99 Ag is found on strains from calves and lambs; CFA I, and CFA II, are found on strains from humans. These fimbrial adhesins adhere to specific receptors on enterocytes of the proximal small intestine.
Symptoms ETEC infections include diarrhea without fever. The bacteria colonize the GI tract by means of a fimbrial adhesin, e.g. CFA I and CFA II, and are noninvasive, but produce either the LT or ST toxin. <>Adherence of EPEC strains to the intestinal mucosa is a very
complicated
process and produces dramatic effects in the ultrastructure of the
cells
resulting in rearrangements of actin in the vicinity of adherent
bacteria.
The phenomenon is sometimes called "attachment and effacing" of
cells.
EPEC strains are said to be "moderately-invasive", meaning they
are
not as invasive as Shigella,
and unlike ETEC or EAEC, they
cause
an inflammatory response. The diarrhea and other symptoms of EPEC
infections
probably are caused by bacterial invasion of host cells and
interference
with normal cellular signal transduction, rather than by production of
toxins.
Through volunteer
feeding studies the infectious dose of EPEC in healthy adults has been
estimated to be
106 organisms.
Some types of EPEC are referred to as diffusely
adherent E. coli
(DAEC), based on specific patterns of adherence. They are an
important
cause of traveler's diarrhea in Mexico and in North Africa.
EHEC are considered to be "moderately invasive". Nothing is known about the colonization antigens of EHEC but fimbriae are presumed to be involved. The bacteria do not invade mucosal cells as readily as Shigella, but EHEC strains produce a toxin that is virtually identical to the Shiga toxin. The toxin plays a role in the intense inflammatory response produced by EHEC strains and may explain the ability of EHEC strains to cause HUS. The toxin is phage encoded and its production is enhanced by iron deficiency.
E. coli O157:H7
Transmission EM. American Society for Microbiology
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Written and edited by Kenneth Todar University of Wisconsin-Madison Department of Bacteriology All rights reserved