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Infectious disease-associated encephalopathy (IDAE) is a form of encephalopathy (brain dysfunction) caused by infectious disease. It can be caused by infectious diseases including bacterial, viral, and protozoal infections. In IDAE, systemic inflammation in response to such infections, such as production of pro-inflammatory cytokines, results in neuroinflammation and consequent neurological and cognitive deficits. This can occur even though the pathogen does not necessarily directly infect the central nervous system.

Many different pathogens have been implicated in causing IDAE. These include bacterial infections like Klebsiella pneumoniae, protozoal infections like Plasmodium falciparum (malaria), and viral infections like influenza and SARS-CoV-2 (COVID-19). Post-COVID-19 syndrome (long COVID) may be a post-acute form of IDAE.

The hippocampus and associated processes like memory may be especially vulnerable in IDAE. Neurological and cognitive deficits associated with IDAE can persist for many years after the initial infection has been cleared or may be irreversible. IDAE may be associated with increased risk of neurodegenerative diseases.

Sepsis-associated encephalopathy

Sepsis-associated encephalopathy (SAE), also known as sepsis-associated brain dysfunction or septic encephalopathy, is a subtype of IDAE. It is an umbrella term referring to neurological complications following sepsis. The condition is common but poorly understood. Approximately 70% of people with sepsis experience SAE. The diagnosis of SAE is difficult, with no well-established biomarkers, and it is currently a diagnosis of exclusion based on clinical symptoms. However, electroencephalogram (EEG) may be helpful in aiding diagnosis.

Acute symptoms of SAE can include sickness behavior, lethargy, delirium, cognitive, memory, and attention impairment, depression, anxiety, agitation, motor problems, seizures, and, in severe cases, coma. Post-acute symptoms of SAE can include cognitive and memory deficits and neuromyopathy, among others.

There are currently no well-accepted treatments for the prevention or treatment of SAE symptoms, and treatment is largely symptom-based. In the acute phase, certain medications may aggravate symptoms and may be avoided, such as anticholinergics, antihistamines, sedatives, benzodiazepines, antipsychotics, and anticonvulsants (in those without seizures). Certain medications such as statins, the antidepressant fluoxetine, and resveratrol may reduce neuroinflammation and the acute and long-term symptoms of SAE. However, these findings are based on animal studies, and more research is needed in this area.

Causes

The following pathogens, among others, have specifically been implicated in causing IDAE:

• Bacteria
  • Klebsiella pneumoniae
  • Chlamydia pneumoniae
  • Chlamydia psittaci
  • Leptospira spp.
  • Listeria monocytogenes
  • Mycobacterium tuberculosis
  • Mycoplasma pneumoniae
  • Streptococcus pyogenes
  • Other Streptococcus spp.
• Protozoa/parasites
  • Toxoplasma gondii
  • Trypanosoma cruzi
  • Cryptococcus neoformans
  • Cryptococcus gattii
  • Plasmodium falciparum
  • Plasmodium vivax
• Viruses
  • Herpes simplex virus
  • Human herpesvirus
  • Influenza A virus
  • Influenza B virus
  • Human immunodeficiency virus
  • Human T-cell lymphotropic virus
  • Chikungunya virus
  • Cytomegalovirus
  • Dengue virus
  • Rift valley fever virus
  • Varicella zoster virus
  • SARS-CoV-2

History

The term "infectious disease-associated encephalopathy" was first coined in 2021 and this was also when the first literature review of the overarching concept was published. The term "sepsis-associated encephalopathy" was first used by 1990 and this was when the first comprehensive study of this condition was published.

See also

• HIV-associated neurocognitive disorder
• Myalgic encephalomyelitis/chronic fatigue syndrome
• Lyme disease
• Traumatic brain injury
• Cerebral hypoxia

References

1. ^ Barbosa-Silva MC, Lima MN, Battaglini D, Robba C, Pelosi P, Rocco PR, Maron-Gutierrez T (July 2021). "Infectious disease-associated encephalopathies". Crit Care. 25 (1): 236. doi:10.1186/s13054-021-03659-6. PMC 8259088. PMID 34229735.
2. ^ Ali Awan H, Najmuddin Diwan M, Aamir A, Ali M, Di Giannantonio M, Ullah I, Shoib S, De Berardis D (August 2021). "SARS-CoV-2 and the Brain: What Do We Know about the Causality of 'Cognitive COVID?". J Clin Med. 10 (15): 3441. doi:10.3390/jcm10153441. PMC 8347421. PMID 34362224. Apart from major respiratory symptoms, there are reports of acute and post-recovery cognitive deficits occurring in COVID-19 patients . Some authors have also coined a more generic term 'infectious disease-associated encephalopathy' to encompass neurological manifestations of both the classical and novel infections. While it is assumed to have a separate pathophysiology than encephalopathy of a non-infectious origin , and although evidence of central nervous system (CNS) involvement exists for the 1918 H1N1 Influenza Virus and 2002 SARS-CoV , there is a lack of academic evidence necessary to evaluate the causality of cognitive impairments accurately. Nevertheless, several mechanisms have been presented to explain SARS-CoV-2's acute and 'sequelae' effects on the brain. These include viral neurotropism, widespread systemic inflammation, and psychological burden of the pandemic across the world.
3. Bayat AH, Azimi H, Hassani Moghaddam M, Ebrahimi V, Fathi M, Vakili K, Mahmoudiasl GR, Forouzesh M, Boroujeni ME, Nariman Z, Abbaszadeh HA, Aryan A, Aliaghaei A, Abdollahifar MA (December 2022). "COVID-19 causes neuronal degeneration and reduces neurogenesis in human hippocampus". Apoptosis. 27 (11–12): 852–868. doi:10.1007/s10495-022-01754-9. PMC 9310365. PMID 35876935. Infectious disease-associated encephalopathy is an umbrella term used to describe neurological manifestations in infections—in this instance, SARS-CoV-2—which are assumed to have different pathophysiological mechanisms than encephalopathy of a non-infectious origin . Several hypotheses have now been proposed to explain the mechanism of acute and long-term SARS-CoV-2-associated cognitive impairment; including extensive systemic inflammation (e.g. microglia activation and cytokine signaling ), viral neurotropism, and psychological burden of the pandemic. Unfortunately, it has been shown that CNS dysfunction can lead to poorer prognosis in COVID-19 patients .
4. ^ Wilson JX, Young GB (May 2003). "Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts". Can J Neurol Sci. 30 (2): 98–105. doi:10.1017/s031716710005335x. PMID 12774948.
5. ^ Pan S, Lv Z, Wang R, Shu H, Yuan S, Yu Y, Shang Y (2022). "Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment". Oxid Med Cell Longev. 2022: 1328729. doi:10.1155/2022/1328729. PMC 9433216. PMID 36062193.
6. ^ Chaudhry N, Duggal AK (2014). "Sepsis Associated Encephalopathy". Adv Med. 2014: 762320. doi:10.1155/2014/762320. PMC 4590973. PMID 26556425.
7. Young GB, Bolton CF, Austin TW, Archibald YM, Gonder J, Wells GA (December 1990). "The encephalopathy associated with septic illness". Clin Invest Med. 13 (6): 297–304. PMID 2078909.

• Brain disorders
• Infectious diseases
• Inflammatory diseases of the central nervous system
• Sepsis