Related Experiment Video

Updated: Apr 28, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

10.5K

Infection-induced inflammation and cerebral injury in preterm infants

Tobias Strunk1, Terrie Inder2, Xiaoyang Wang3

  • 1Centre for Neonatal Research and Education, School of Paediatrics and Child Health, The University of Western Australia, Perth, WA, Australia; Neonatal Clinical Care Unit, King Edward Memorial Hospital, Perth, WA, Australia.

The Lancet. Infectious Diseases
|June 1, 2014
PubMed

Insights

Bacteraemia and inflammation in preterm infants can cause serious health issues, including brain injury, even without direct central nervous system infection. This review highlights the link between bloodstream infections and adverse neurological outcomes in premature babies.

Area of Science:

  • Neonatal Medicine
  • Infectious Diseases
  • Neuroscience

Background:

  • Preterm birth and infections are leading causes of neonatal mortality globally.
  • Rising preterm birth rates (11% of births) increase infant infection risk.
  • Neonatal bacteraemia/inflammation in preterm infants is linked to death, lung disease, and neurodevelopmental issues.

Purpose of the Study:

  • To review evidence linking bacteraemia, inflammation, and cerebral injury in preterm infants.
  • To explore the biological mechanisms, clinical aspects, and potential treatments for this association.
  • To emphasize the significant impact of neonatal infections on long-term infant health.

Main Methods:

  • Systematic review of existing scientific literature.
  • Analysis of studies on neonatal bacteraemia and inflammation.
  • Examination of research on cerebral injury in preterm infants.

Main Results:

  • Evidence strongly associates bacteraemia and inflammation with cerebral injury in preterm neonates.
  • Cerebral injury may occur due to bacteraemia even without direct central nervous system bacterial invasion.
  • Inflammatory processes triggered by bacteraemia are implicated in brain damage.

Conclusions:

  • Bacteraemia and associated inflammation represent a critical pathway to cerebral injury in preterm infants.
  • Understanding these mechanisms is crucial for developing targeted interventions.
  • Translational research is needed to mitigate long-term neurodevelopmental impairments in this vulnerable population.

More Related Videos

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury07:36

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

Published on: November 19, 2019

6.8K
A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development08:50

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

Published on: June 24, 2020

3.1K

Related Concept Videos

Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
16
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
12
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
20
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
11
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
14
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial...
16