The haemolytic uraemic syndrome, first described in 1955 by Gasser, is
the number one cause of acute renal failure in infants. There are thr
ee types of the haemolytic uraemic syndrome: the seasonal epidemic for
m with prodromic diarrhoea and generally favourable outcome which usua
lly occurs in infants, a less typical form without signs of digestive
tract involvement and no seasonal prevalence which occurs more readily
in older children and sometimes in families has a less favourable pro
gnosis, and finally drug- or disease-related forms. Currently, overall
mortality due to haemolytic uraemic syndrome has been reduced to abou
t 4%, usually as a result of damage to the central nervous system. Sev
eral microorganism, including Shigella dysenteriae, Salmonella typhi,
Campylobacter jejuni, Streptococcus pneumoniae, Rickittsiae and certai
n viruses (Coksackiae, Influenzae, Epstein-Barr) have been identified
as causative agents. In 1983, digestive tract infection due to an Esch
erichia coli strain producing verotoxin was identified as capable of p
roducing haemolytic uraemic:syndrome and more rarely thrombopenic thro
mbotic purpura. The germ produces two exotoxins (whose effect is accen
tuated by the E. coli lipopolysaccharide endotoxin) which lead to the
glomerular microangiopathy causing haemolytic uraemic syndrome. Diagno
sis is based on identification (monoclonal antibodies, ELISA, PCR) of
the verotoxins themselves or the two encoding genes in stool samples.
Symptomatic treatment is essential but the effectiveness of antibiotic
s is still debated. Theoretically, antibiotics could worsen the syndro
me by increasing endotoxin release from lysed bacteria, but inversely
they could also prevent the syndrome if given early enough. Further re
search is required to acquire precise epidemiological data and identif
y animal reservoirs of verotoxin producing E. coli.