151
At a very low temperature, such as in space, many of them would likely survive for well
over 10,000 years.12 The characteristics of this organism make E. coli an ideal laboratory
research tool.
Virulence
E. coli can be divided into two major groups: pathogenic and avirulent E.coli. The patho-
genic groups have evolved with the ability to cause disease in several body systems. Until
recently, the food industry focused E. coli prevention efforts on a single strain of the bacte-
ria, known as 0157:H7, which was responsible for scores of outbreaks and recalls.
Public health experts and the CDC have identified six rarer forms, often referred to
as the “Big Six.” They have increasingly been found to be the cause of illness related to
food.13 The six strains of non-0157:H7 identified by the CDC as responsible for the major-
ity of the non-0157 illnesses and deaths are 026, 0111, 0103, 045, 0121 and 0140.
These strains, like 0157, have the ability to manufacture Shiga-like verotoxins that
attack red blood cells, ultimately destroying the scaffolding of blood vessels and essen-
tially cutting off blood flow to vital organs. The acronym STEC, or Shiga toxin producing
E. coli, is frequently used to describe these strains. The life-threatening condition it pro-
duces is described as hemolytic uremic syndrome. Unlike other pathogens, it only takes a
very small number of E. coli bacteria to cause illness.14
Most infections caused by E. coli are initiated by the colonization of the host gastro-
intestinal, respiratory and urinary tracts. E. coli is particularly adept at colonizing these
mucosal surfaces because of its rapid multiplication and ability to attach to cells that line
the mucosa. A number of factors appear to enhance the virulence of E. coli, including the
serotype, serum resistance, hemolysin and aerobactin production and fimbriae.
E. coli strains are differentiated on the basis of lipopolysacchride O, flagellar H and
polysaccharide K antigens. Determination of the O:K:H serotype is a refined method
for typing E. coli, as there are more than 170 O-, about 56 H- and approximately 100
K-antigens. Together, they constitute the O:H system, which has played an important role
in studies on epidemiology and pathogenesis of E. coli infection.
Serum resistance for E. coli is the outcome of the combined effects of the organism’s
lipopolysaccharide, capsule and certain membrane proteins. Aerobactin and α-hemolysin
are secreted by pathogenic E. coli. Both have the ability to break down erythrocytes
and extract iron-containing compounds necessary for the organism to multiply. Type-1
Fimbriae (thin, hair-like projections) enhance the organism’s adherence to intestinal
mucosa or urinary tract and play a vital role in initiating an infection.
There are other virulence factors to consider as well, including different varieties of
Shiga toxin, intimin (a bacterial outer-membrane protein) or the arcanely described patho-
genicity islands (PAIs). Intimin is required for intimate attachment to the host cell. The
most common site of human infections is the gastrointestinal tract due to the ease of access
of E. coli ingested in food and drink.15
There are at least five major classes of enterovirulent E. coli that cause disease in humans.
• Enterotoxigenic E. coli (ETEC) produce a heat-vulnerable enterotoxin, a heat
stable enterotoxin or both. They also possess surface antigens that enable them to
attach to intestinal epithelial cells.
• Enteroinvasive E. coli (EIEC) invade and multiply in epithelial cells of the colon,
causing a dysentery-like illness.
• Enterohemorrhagic E. Coli (EHEC) may be the leading cause for epidemics of
severe infections. It has been estimated that more than 70,000 human cases of
EHEC infections occur in the US each year.16
• Virulence mechanisms of the two remaining classes—enteropathic E. coli (EPEC)
and enteroaggregative E. coli (EaggEC)—are less clear.17,18
Escherichia coli: Friend or Foe?
At a very low temperature, such as in space, many of them would likely survive for well
over 10,000 years.12 The characteristics of this organism make E. coli an ideal laboratory
research tool.
Virulence
E. coli can be divided into two major groups: pathogenic and avirulent E.coli. The patho-
genic groups have evolved with the ability to cause disease in several body systems. Until
recently, the food industry focused E. coli prevention efforts on a single strain of the bacte-
ria, known as 0157:H7, which was responsible for scores of outbreaks and recalls.
Public health experts and the CDC have identified six rarer forms, often referred to
as the “Big Six.” They have increasingly been found to be the cause of illness related to
food.13 The six strains of non-0157:H7 identified by the CDC as responsible for the major-
ity of the non-0157 illnesses and deaths are 026, 0111, 0103, 045, 0121 and 0140.
These strains, like 0157, have the ability to manufacture Shiga-like verotoxins that
attack red blood cells, ultimately destroying the scaffolding of blood vessels and essen-
tially cutting off blood flow to vital organs. The acronym STEC, or Shiga toxin producing
E. coli, is frequently used to describe these strains. The life-threatening condition it pro-
duces is described as hemolytic uremic syndrome. Unlike other pathogens, it only takes a
very small number of E. coli bacteria to cause illness.14
Most infections caused by E. coli are initiated by the colonization of the host gastro-
intestinal, respiratory and urinary tracts. E. coli is particularly adept at colonizing these
mucosal surfaces because of its rapid multiplication and ability to attach to cells that line
the mucosa. A number of factors appear to enhance the virulence of E. coli, including the
serotype, serum resistance, hemolysin and aerobactin production and fimbriae.
E. coli strains are differentiated on the basis of lipopolysacchride O, flagellar H and
polysaccharide K antigens. Determination of the O:K:H serotype is a refined method
for typing E. coli, as there are more than 170 O-, about 56 H- and approximately 100
K-antigens. Together, they constitute the O:H system, which has played an important role
in studies on epidemiology and pathogenesis of E. coli infection.
Serum resistance for E. coli is the outcome of the combined effects of the organism’s
lipopolysaccharide, capsule and certain membrane proteins. Aerobactin and α-hemolysin
are secreted by pathogenic E. coli. Both have the ability to break down erythrocytes
and extract iron-containing compounds necessary for the organism to multiply. Type-1
Fimbriae (thin, hair-like projections) enhance the organism’s adherence to intestinal
mucosa or urinary tract and play a vital role in initiating an infection.
There are other virulence factors to consider as well, including different varieties of
Shiga toxin, intimin (a bacterial outer-membrane protein) or the arcanely described patho-
genicity islands (PAIs). Intimin is required for intimate attachment to the host cell. The
most common site of human infections is the gastrointestinal tract due to the ease of access
of E. coli ingested in food and drink.15
There are at least five major classes of enterovirulent E. coli that cause disease in humans.
• Enterotoxigenic E. coli (ETEC) produce a heat-vulnerable enterotoxin, a heat
stable enterotoxin or both. They also possess surface antigens that enable them to
attach to intestinal epithelial cells.
• Enteroinvasive E. coli (EIEC) invade and multiply in epithelial cells of the colon,
causing a dysentery-like illness.
• Enterohemorrhagic E. Coli (EHEC) may be the leading cause for epidemics of
severe infections. It has been estimated that more than 70,000 human cases of
EHEC infections occur in the US each year.16
• Virulence mechanisms of the two remaining classes—enteropathic E. coli (EPEC)
and enteroaggregative E. coli (EaggEC)—are less clear.17,18
Escherichia coli: Friend or Foe?