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Recurring hyperammonemic encephalopathy induced by bacteria usually not producing urease
Christian Cordano, Elisabetta Traverso, Valentina Calabrò
1Institute of Neurology, Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Largo Daneo 3, 16132 Genova, Italy. lucio.marinelli@unige.it.
BMC Research Notes
|June 3, 2014
Summary
Recurrent hyperammonemic encephalopathy (HE) occurred in a patient with a neurogenic bladder due to urinary tract infections. This case highlights the potential for urease-negative bacteria like E. coli and E. faecalis to cause HE.
Area of Science:
- Nephrology
- Neurology
- Infectious Diseases
Background:
- Hyperammonemic encephalopathy (HE) can arise from urease-positive bacteria in the urinary tract producing ammonia.
- Neurogenic bladder is a predisposing factor for urinary tract infections (UTIs) and urine stagnation, increasing HE risk.
Observation:
- A 66-year-old woman with a neurogenic bladder experienced two episodes of HE following UTIs.
- During the second UTI, Escherichia coli and Enterococcus faecalis were identified in the urine.
- Neurological findings included psychomotor slowing, impaired reflexes, nystagmus, and asterixis; EEG showed triphasic waves.
Findings:
- Escherichia coli and Enterococcus faecalis, typically urease-negative, were implicated in causing HE.
- This is the first reported instance of recurrent HE secondary to UTIs caused by these specific bacteria.
Implications:
- This case expands the understanding of potential pathogens causing HE, including commonly urease-negative bacteria.
- Highlights the importance of considering HE in patients with neurogenic bladder and recurrent UTIs, even with atypical bacterial culprits.
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