Two groups have identified new strategies to treat or prevent hemolytic uremic syndrome, a potentially lethal complication of Escherichia coli infection. A team at the University of Toronto has suggested that the marketed CXC chemokine receptor 4 antagonist Mozobil plerixafor could be repurposed for the indication, whereas Carnegie Mellon University researchers have found that the natural metal ion manganese could neutralize the toxin that causes the condition.1,2
Hemolytic uremic syndrome (HUS) is caused by the release of Shiga toxins from pathogenic bacteria such as the O157:H7 strain of E. coli and triggers symptoms such as anemia, thrombocytopenia and acute renal injury.
There are no available tests to determine whether a patient with gastrointestinal
E. coli infection will develop HUS, and there are no therapeutics that actually neutralize the toxin. Current treatments are palliative and include dialysis, blood transfusions and corticosteroids. The mortality rate is 5%-7%, and many patients who do recover have long-term