A new study (see cite at the end of this post) looked at 52 adult victims of the 2011 E. coli O104:H4 outbreak in Europe. Of the 52 victims, 48 had hemolytic uremic syndrome (HUS), and all but one of the 48 had neurological symptoms, some mild, some severe. Some HUS neurological problems, including stroke, are caused by the tiny blood clots resulting from HUS. This study suggests that other problems may be caused by a “toxic-metabolic pathology”, meaning toxins created by the HUS-induced kidney failure (renal failure) disrupt normal metabolism, the process of converting food to energy on a cellular level. We hope this leads to a better understanding of HUS and new treatments.
Objective: To describe the neurologic and neuroradiologic complications of Shiga toxin producing Escherichia coli infection (STEC)–associated hemolytic-uremic syndrome (HUS) in adults.
Methods: All 52 adult patients with STEC O104:H4 infection cared for at Hannover Medical School during the outbreak in Germany through May–July 2011 are considered in this observational study. Forty-three of the 52 patients underwent a standard neurologic diagnostic procedure including clinical examination, Mini-Mental State Examination, and Glasgow Coma Scale Score. Thirty-six patients underwent EEG, and 26 had cerebral MRI, 9 of them repeatedly. Case records of 9 patients who had not been seen by a neurologist were analyzed retrospectively.
Results: Forty-eight of the 52 patients had HUS. All but 1 of these showed neurologic symptoms. Focal neurologic signs like double vision, difficulties in finding words, or hyperreflexia were present in 23, additional deficits in orientation, attention, memory, or constructive abilities in 9, and marked impairment of consciousness in 15. MRI showed brainstem, midbrain, thalamus, corpus callosum, and white matter lesions in half of the patients, predominantly in diffusion-weighted images. The extent of MRI lesions did not correlate with clinical symptoms. General slowing but no focal alteration was found in half of the patients examined by EEG.
Conclusion: Our findings suggest a toxic-metabolic pathology behind the neurologic impairment instead of multiple infarction due to microthrombosis. Future studies should aim to clarify if early antibiotic therapy or bowel cleansing might help to decrease the rate of neurologic complications in STEC-HUS.
The above is an abstract of an article published in Neurology, a medical journal. We did not contact the authors regarding this post, but we would like to thank them for their work. If any of the authors have any concerns, we would like to hear from them.