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Haemorrhagic colitis is typically a self-limiting, acute, bloody diar-
rhoea lasting 4–10 days. Symptoms start with stomach cramps and
watery diarrhoea 1–2 (sometimes 3–8) days after eating the contaminated
food and, in most cases, progress over the next 1–2 days to a bloody
diarrhoea with severe abdominal pain. It can be distinguished from
inflammatory colitis by the usual lack of fever and absence of leukocytes
in the stools. It affects mainly adults, with a peak incidence in the
summer months, and can be life-threatening in the elderly.
Haemolytic uraemic syndrome is characterized by three features, acute
renal failure, haemolytic anaemia (reduction in the number of red blood
cells) and thrombocytopaenia (a drop in the number of blood platelets),
sometimes preceded by a bloody diarrhoea. It is most common in
children among whom it is the leading cause of acute renal failure in
western Europe and North America. Approximately 10% of children
under 10 with symptomaticE. coliO157 infection go on to develop HUS;
half will require kidney dialysis and the mortality rate is generally 3–5%.
In 70 cases seen in London between 1980 and 1986 the fatality rate was
6%, with 13% of cases showing some long-term kidney-damage. In one
outbreak in a North American nursing home, the fatality rate among the
55 affected residents was 31%.
Thrombotic thrombocytopaenic purpura is a less common complica-
tion which is largely confined to adults. It is related to HUS but causes
less kidney damage and includes fever and neurological symptoms
resulting from blood clots in the brain.
Attachment is an important factor in virulence and O157:H7 strains
possess the LEA pathogenicity island and adhere by a mechanism similar
to EPEC, characterised by intimate attachment of the bacteria to the
epithelial cells and effacement of the underlying microvilli.
EHEC strains produce the cytotoxin Verotoxin (so-called because of
its ability to kill Vero (African Green Monkey Kidney) cells). Studies
have revealed the presence of at least two toxins VTI and VTII which
because of their similarity to Shiga toxin (see Section 6.6) have also been
called Shiga-like toxins, SLTI and SLTII. It has been proposed that the
nomenclature for these toxins be rationalised as Shiga family toxins so
that the prototype toxin Shiga toxin is designated Stx, and SLTI and II
become Stx 1 and Stx 2 respectively. Stx 1 bears the closest resemblance
to Shiga toxin; it cross reacts with antisera to Shiga toxin, is also
composed of A (Mr32 kDa) and B (Mr7.7 kDa) subunits and the B
units are structurally identical. The B units bind specifically to the
glycolipid receptor, globotriaosylceramide (Gb 3 ), on the eukaryotic cell
surface and the susceptibility of the kidney in O157 infections may be due
to higher levels of these receptors in kidney glomeruli. Following bind-
ing, the toxin is internalized by endocytosis and the A subunit activated.
It then hydrolyses theN-glycosidic bond of a specific adenosine residue


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