Beyond Urinary Tract Infections (UTIs) and Delirium

Chae, Jung Hee; Miller, Brian J.

doi:10.1097/pra.0000000000000105

Cited by 41 publications

(16 citation statements)

References 38 publications

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“…Urinary tract infections have been described in the setting of various neuropsychiatric conditions including delirium, dementia, psychotic disorders, and mood disorders. A systematic review found that 88% of the articles reviewed in this area demonstrated a positive association between UTI and neuropsychiatric disorders [9]. In addition, 47% of these articles described UTI being involved in exacerbating or even precipitating these conditions [9].…”

Section: Discussionmentioning

confidence: 99%

Acute Psychosis Precipitated by Urinary Tract Infection in a Patient with Gliosis of the Basal Ganglia

Lee

Oleszak

Nihalani

et al. 2019

AJMCR

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Background: Urinary tract infections (UTI) have been found to be associated with a variety of neuropsychiatric disorders, and could play a role in the pathophysiology of relapse of affective and nonaffective psychosis. In addition, prior history of infarction in areas of the brain such as the cerebellum, basal ganglia, and mid-brain have been reported in patients with new onset psychotic symptoms. Case presentation: A 29-year-old woman was brought to the hospital with acute mental status changes and signs of sepsis. Infectious work-up was initiated including blood cultures, brain imaging, lumbar tap and urinalysis. Brain MRI revealed abnormalities in the basal ganglia and the urinalysis revealed signs of a urinary tract infection (UTI). Further history revealed episodes of mania and depression compatible with bipolar disorder with psychotic features that had acutely worsened. The patient's condition improved with intravenous antibiotics and the introduction of anti-psychotics. She was discharged in stable condition with outpatient psychiatric follow-up. Conclusion: Infectious diseases (UTIs in particular) are not only more prevalent among patients with acute relapse of psychiatric disorders, but have also been found to have triggered acute psychosis among stable psychiatric patients. Organic brain lesions must be thoroughly investigated among patients presenting with new psychiatric disorders in order to initiate appropriate therapy to control the symptoms.

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Section: Discussionmentioning

confidence: 99%

Acute Psychosis Precipitated by Urinary Tract Infection in a Patient with Gliosis of the Basal Ganglia

Lee

Oleszak

Nihalani

et al. 2019

AJMCR

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“…Where does blood endotoxin come from? Active bacterial infections may produce endotoxin, and for example, urinary tract infections are associated with dementia, delirium and other neuropsychiatric disorders [35]. However, in the absence of infection, endotoxin still crosses the mucosal membranes of gut, gums, nose or lungs, the main source being intestinal permeability [36, 37].…”

Section: Serum Endotoxinmentioning

confidence: 99%

The endotoxin hypothesis of neurodegeneration

Brown

2019

J Neuroinflammation

342

240

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The endotoxin hypothesis of neurodegeneration is the hypothesis that endotoxin causes or contributes to neurodegeneration. Endotoxin is a lipopolysaccharide (LPS), constituting much of the outer membrane of gram-negative bacteria, present at high concentrations in gut, gums and skin and in other tissue during bacterial infection. Blood plasma levels of endotoxin are normally low, but are elevated during infections, gut inflammation, gum disease and neurodegenerative disease. Adding endotoxin at such levels to blood of healthy humans induces systemic inflammation and brain microglial activation. Adding high levels of endotoxin to the blood or body of rodents induces microglial activation, priming and/or tolerance, memory deficits and loss of brain synapses and neurons. Endotoxin promotes amyloid β and tau aggregation and neuropathology, suggesting the possibility that endotoxin synergises with different aggregable proteins to give different neurodegenerative diseases. Blood and brain endotoxin levels are elevated in Alzheimer’s disease, which is accelerated by systemic infections, including gum disease. Endotoxin binds directly to APOE, and the APOE4 variant both sensitises to endotoxin and predisposes to Alzheimer’s disease. Intestinal permeability increases early in Parkinson’s disease, and injection of endotoxin into mice induces α-synuclein production and aggregation, as well as loss of dopaminergic neurons in the substantia nigra. The gut microbiome changes in Parkinson’s disease, and changing the endotoxin-producing bacterial species can affect the disease in patients and mouse models. Blood endotoxin is elevated in amyotrophic lateral sclerosis, and endotoxin promotes TDP-43 aggregation and neuropathology. Peripheral diseases that elevate blood endotoxin, such as sepsis, AIDS and liver failure, also result in neurodegeneration. Endotoxin directly and indirectly activates microglia that damage neurons via nitric oxide, oxidants and cytokines, and by phagocytosis of synapses and neurons. The endotoxin hypothesis is unproven, but if correct, then neurodegeneration may be reduced by decreasing endotoxin levels or endotoxin-induced neuroinflammation.

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“…It is appreciated that the aging brain may be more vulnerable to pathological changes in response to acute illness and infections. For example, urinary tract infections, which are not associated with cognitive symptoms in the young, can cause delirium and other neuropsychiatric conditions in the elderly [49]. Rodent models also suggest that aged mice have more severe neuroinflammatory responses and exacerbated behavioral outcomes following peripheral immune stimuli [50].…”

Section: Age-associated Changes In Neuroimmune Functionsmentioning

confidence: 99%

Age-Associated Changes in the Immune System and Blood–Brain Barrier Functions

Erickson

Banks

2019

IJMS

139

107

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Age is associated with altered immune functions that may affect the brain. Brain barriers, including the blood–brain barrier (BBB) and blood–CSF barrier (BCSFB), are important interfaces for neuroimmune communication, and are affected by aging. In this review, we explore novel mechanisms by which the aging immune system alters central nervous system functions and neuroimmune responses, with a focus on brain barriers. Specific emphasis will be on recent works that have identified novel mechanisms by which BBB/BCSFB functions change with age, interactions of the BBB with age-associated immune factors, and contributions of the BBB to age-associated neurological disorders. Understanding how age alters BBB functions and responses to pathological insults could provide important insight on the role of the BBB in the progression of cognitive decline and neurodegenerative disease.

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Beyond Urinary Tract Infections (UTIs) and Delirium

Cited by 41 publications

References 38 publications

Acute Psychosis Precipitated by Urinary Tract Infection in a Patient with Gliosis of the Basal Ganglia

Acute Psychosis Precipitated by Urinary Tract Infection in a Patient with Gliosis of the Basal Ganglia

The endotoxin hypothesis of neurodegeneration

Age-Associated Changes in the Immune System and Blood–Brain Barrier Functions

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