Haemolytic-uraemic syndrome (HUS) is primarily a disease of infancy and early childhood and is classically characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure.
Haemolytic uraemic syndrome is part of a disease category known as thrombotic microangiopathies.
Haemolytic uraemic syndrome is characterized by the involvement of widespread occlusive microvascular thromboses resulting in thrombocytopenia, microangiopathic hemolytic anemia, and variable signs and symptoms of end-organ ischemia.
After entering the circulation via the gastrointestinal mucosa, the toxin preferentially localizes to the kidneys, inhibiting protein synthesis and eventually leading to cell necrosis or apoptosis. Endothelial cell damage subsequently potentiates renal microvascular thrombosis by promoting activation of the blood coagulation cascade. Platelet aggregation results in a consumptive thrombocytopenia. Microangiopathic hemolytic anemia results from mechanical damage to red blood cells circulating through partially occluded microcirculation.
E coli serotype O157:H7 has been associated with more than 80% of infections leading to hemolytic uremic syndrome.
The new E. coli variant of the rare strain O104 out of Germany is the cause of a new European outbreak.
E. coli O104’s present strain variant posesses a gene which produces a toxin and another which helps the bacterium colonise the gut more efficiently, which effectively means even more toxin is produced.