Privacy Statement   Terms & Conditions   Sitemap  
  Diseases   Research   About us  
TBE Meningococcal Disease Influenza Smallpox
 


  Pathogenesis

The picture of manifest TBE depends on the virulence of the virus, and the individual resistance of the patient. After the bite of an infected tick, the virus usually replicates in the dermal cells at the site of the tick bite. This replication in Langerhans cells, as well as in neutrophilic granulocytes, is unhindered, due to an immunodeficiency inducted by the tick's saliva. Furthermore, the TBE virus does not only use Langerhans cells and granulocytes for replication, but also as vehicles to reach regional lymph nodes via lymph capillaries. Thus the virus spreads via the lymphatic system and, a few days later, reaches the bloodstream (viremia). Then it invades other susceptible organs or tissues especially the reticuloendothelial system (thymus, spleen, liver). Massive virus replication takes place there, and only after this stage it is possible for the virus to reach the central nervous system. High production of the virus in the primarily affected organs is a prerequisite for the virus to cross the blood-brain barrier since the capillary endothelium is not easily infected. Once it has invaded these endothelial cells from the lumen, the virus replicates and enters the central nervous system by seeding through the capillary endothelium into the brain tissue. TBE virus may also spread along nerve fibers. This route may be relevant, especially in laboratory infections by aerosols. After infecting the neuroepithelial cells of the nasal mucous membrane, the virus directly enters the brain via the fila olfactoria. Considering the short incubation period and the often extremely severe course of such infections, this route of entry seems likely. However, in arthropod-borne infections neural spread of the virus is of little importance.
Histopathological studies from lethal human cases revealed neuronal and glial destruction, spongiform focal necrosis, inflammation and perivascular infiltration, cellular nodule formation and edema. Residual pathological lesions are characterized by neuronal loss and microglial scarring. Detection of viral RNA during the encephalitic stage of disease in cerebrospinal fluid (CSF) is difficult, which indicates that the main pathogenic mechanism may be due to inflammatory mediators, even if TBEV may be concealed in the neurons without leaking into the CSF.


 » Printversion

 
 
  » find


 

Baxter Announces Final Phase I/II Data and Initiation of Phase III Clinical Trial for Candidate Pandemic H5N1 Influenza Vaccine
» read more

Baxter receives preparedness contract from Austrian Ministry of Health for Pandemic Influenza Vaccine
» read more

Baxter Announces Safety and Immunogenicity Results from Phase I/II Clinical Trial of Cell-Based Candidate H5N1 Pandemic Vaccine
» read more

 
Baxter Vaccines Industriestrasse 67, A-1221 Wien, Tel: +43-1-20100,