A rat model for embolic encephalitis

Research output: Contribution to conferenceConference abstract for conferenceCommunication

Sepsis is the combined condition of infection and a systemic inflammatory response. Sepsis causes 10% of all deaths in the western world. The Gram positive bacterium Staphylococcus aureus is one of the leading causes of sepsis and the incidence of Gram positive sepsis is rising. Autopsy studies have recently shown that sepsis is a common cause of microabscesses in the brain, and that S. aureus is one of the most common organisms isolated from these abscesses. This raises the question whether the blood-brain barrier truly makes the brain an immune-privileged organ or not.
This makes the brain a most interesting organ in sepsis patients. However, symptoms of brain infection may be confused with systemic responses and gross neuropathologic lesions may be absent. Brain infection in sepsis patients is therefore prone to misclassification or diagnostic delay, and when the diagnosis is made it is difficult to obtain tissue for further examination. This puts a hard demand on animal models of brain lesions in sepsis.
We hereby present a novel animal model of embolic encephalitis. Our model introduces bacteria by an embolus to an area of brain necrosis and damage to the blood-brain-barrier. This provides our model with several advantages: minimized surgical intervention, bacteria gain access to the brain by the circulation and, no foreign materials are implated in the brain. We thereby mirror the human scenario in several ways: 1: Cerebral infarction by thrombosis or disseminated intravascular coagulation is a key mechanism involved in neurologic complications to human bacteriaemia. 2: Human brain abscesses are primarily located in the same anatomical area that we target in our model. Our model therefore offers a tool for several scientific areas within research of brain infection and inflammation.
Translated title of the contributionEn rottemodel for embolisk encephalitis
Original languageEnglish
Publication date17 Jun 2011
Number of pages1
Publication statusPublished - 17 Jun 2011

ID: 33626152