Rapid Test for Detection of the Focus of Infection in Post Neurosurgical Patients.

Hepatocyte growth factor (HGF) is local acute phase protein with regenerative properties that become biologic inactive during chronic inflammation and loses the binding affinity to glycosaminoglycan in the extracellular ma-trix. HGF is excreted into the gastrointestinal tract and is not detected in normal urine. Nosocomial meningitis can occur when brain surgical procedures are complicated by infection. Due to underlying CNS disease processes and CNS devices in situ, the principal agents of nosocomial bacterial meningitis differ from the agents of community-acquired meningitis. For example, in nosocomial infections, slow growing, opportunistic microorganisms predominate. The CSF leukocyte profile is affected by intracerebral haemorrhage, and CSF lactate might be elevated, due to ischemia. Moreover, altered consciousness can make it difficult to establish a diagnosis in patients on ventilators that develop fever after neurosurgical operations. In other words, it is often difficult to determine whether the injured brain has been invaded by environmental bacterial flora.

Due to the challenges in establishing a diagnosis, and the lack of gold standards, physicians are motivated to treat suspected infections in serious dis-eases with broad-spectrum antibiotics. The emerging problems of multiple-resistance bacteria, high costs, and complications related to new antibiotics have called for diagnostic tests that can minimize antibiotic consumption.

Currently, the diagnosis of bacterial meningitis remains based on standard methods of direct microscopy, differential analyses of white blood cells, lactate, and protein, and cultures of blood and CSF . However, post-neurosurgical infections are difficult to distinguish from the effects of neurosurgical procedures. Moreover, due to prophylaxis treatments, the cultures are negative in a large group of patients, and the presence of skin flora, like Coagulase negative Staphylococcus or Propionbacterium acnes, may indicate either infection or contamination. Survival from this life-threatening condition depends on a rapid diagnosis and prompt empirical antibiotic therapy designed to cover the likely pathogens.

Where is the focus of infection? Is it a bacterial (septic) meningitis? Is the broad-spectrum antibiotic administration indicated? The background of the project: 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 inflammatory response is caused by the release of various pro-inflammatory cytokines from meningeal cells into the subarachnoid space. As a result, neutrophils move into the subarachnoid space and cause pleocytosis in the CSF. The consequences include the breakdown of the blood-brain barrier, cerebral oedema, reduced cerebral blood flow, focal areas of hypo perfusion, 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.

Other causes of febrile meningitis include acute viral meningitis and non-pyogenic meningitis, where the clinical picture is typically sub-acute or chronic. The diagnostic procedures consist of a lumbar puncture to analyse the CSF for cells and bacteria, microbiological cultures of blood and CSF, serological tests involving PCR and antigen-detection, and radiographic techniques [2]. In community-acquired meningitis, a combination of discriminating values from the CSF analysis can differentiate acute bacterial meningitis from other, non-ambulatory causes with quite high sensitivity [3].