Abstract
BackgroundDue to anatomical restrictions, the inflammatory response to intracerebral bacterial infections exposes swollen brain tissues to pressure and ischemia, resulting in life-threatening damage. Rapid diagnosis and immediate empirical antibiotic therapy is highly important. However, diagnosing meningitis in patients after neurosurgery is complicated, due to brain tissue damage and changes in cerebrospinal fluid (CSF) caused by surgery. Hepatocyte growth factor (HGF) is a local, acute-phase protein with healing properties. Previous studies on community-acquired septic meningitis reported high levels of intrathecally produced HGF. The present study focused on nosocomial meningitis in assessing the levels of HGF in the CSF.MethodsHGF concentrations (ELISA) and HGF binding to receptors; c-Met receptor and heparan sulfate proteoglycan were determined in CSF samples (surface plasmon resonance). CSF samples from patients with community-acquired or nosocomial meningitis (217 samples from 135 patients) were compared to those from controls without signs of cerebral nervous system involvement (N = 36) and patients with Alzheimer’s disease (N = 20).ResultsCompared to samples from patients that had undergone neurosurgery and had other infectious diseases, CSF samples from patients with nosocomial meningitis had significantly higher HGF concentrations (p < 0.001) and binding affinity to c-Met (p < 0.001) and HSPG (p = 0.043) receptors. The sensitivity and specificity to identify nosocomial septic meningitis were 69.7 and 93.4 %, respectively. The HGF concentration and binding affinity to HGF receptors were significantly higher in CSF from patients with community-acquired septic meningitis compared to patients with aseptic (viral and subacute) meningitis as well as controls (p < 0.001). The sensitivity and specificity to identify community-acquired septic meningitis were 95.4 and 95.7 %, respectively.DiscussionIn febrile nosocomial infections that occurred post neurosurgery, HGF assessment could substantially improve the differentiation of meningitis from other infections and therefore might be a tool for rapid diagnosis, limiting injuries and guiding antibiotic therapy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12987-015-0020-z) contains supplementary material, which is available to authorized users.
Highlights
Due to anatomical restrictions, the inflammatory response to intracerebral bacterial infections exposes swollen brain tissues to pressure and ischemia, resulting in life-threatening damage
cerebrospinal fluid (CSF) samples from patients with septic meningitis was significantly higher in Hepatocyte growth factor (HGF) concentrations (p = 0.0014), HGF binding to heparan sulfate proteoglycan (HSPG) (p < 0.0001), and HGF binding to c-Met (p < 0.0001) compared to samples from patients with aseptic meningitis
CSF samples from patients with septic meningitis was higher from samples from the control group and from patients with Alzheimer’s disease in HGF concentration (p < 0.0001, p = 0.0010, respectively), HGF binding to HSPG (p < 0.0001 and p = 0.9, respectively), and HGF binding to c-Met
Summary
The inflammatory response to intracerebral bacterial infections exposes swollen brain tissues to pressure and ischemia, resulting in life-threatening damage. An invasion of bacteria into the central nervous system (CNS) is followed by a rapidly evolving inflammatory process that affects the arachnoid space, the pia mater, and the cerebrospinal fluid (CSF) This condition leads to clinical symptoms of headache, fever, and meningism. The consequences include the breakdown of the blood–brain barrier, cerebral edema, reduced cerebral blood flow, focal areas of hypoperfusion, vascular thrombosis, ischemia, enhanced glucose metabolism via the anaerobic glycolytic pathway, and enhanced lactate accumulation in the brain and CSF [1]. Survival from this life-threatening condition depends on a rapid diagnosis and prompt empirical antibiotic therapy designed to cover the likely pathogens
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