Neisseria meningitides referred to as meningococcus, appears as a gram-negative diplococcus and test po sitive for cytochrome c oxidase exists as normal flora in the nasopharynx of up to 5-15% of adults, infects the host cell by sticking to it using Trimeric Autotransporter Adhesins Meningococci only infect humans, and is the only form of bacterial meningitis kn own to occur epidemically N. meningitidis exploits host cell signaling pathways to promote its uptake by h ost cells, induced by the type Iv pili, which are the main means of meningococcal 1 adhesion onto host cells. Formation of microvilli-like structures at the site of the bacterial-cell interaction then occurs, which trigger the internalization n of the bacteria into host cells A ma jor consequence of these signaling events is a reorganization of the actin c ytoskeleton, which leads to the formation of membrane protrusions, engulfing bac terial pathogens into intracellular vacuoles. Efficient internalization of N. me ningitidis also requires the activation of an alternative signaling pathway coup led with the activation of thetyrosine kinase receptor erbB2. Beside Type Iv pil 1, other outer membrane proteins may be involved in other mechanism of bacteria internalization into cell Initially produces general symptoms like fatigue, it can rapidly progress from f ever, headache and neck stiffness to coma and death ong with a notable non-b1 aching purpuric rashNeisseria meningitides referred to as meningococcus appears as a Gram-negative diplococcus and test po sitive for cytochrome c oxidase exists as normal flora in the nasopharynx of up to 5-15% of adults, infects the host cell by sticking to it using Trimeric Autotransporter Adhesins Meningococci only infect humans, and is the only form of bacterial meningitis kn own to occur epidemically exploits host cell signaling pathways to promote its uptake by h ost cells, induced by the type IV pili, which are the main means of meningococca l adhesion onto host cells. Formation of microvilli-like structures at the site of the bacterial-cell interaction then occurs, which trigger the internalizatio n of the bacteria into host cells. A major consequence of these signaling events is a reorganization of the actin c ytoskeleton, which leads to the formation of membrane protrusions, engulfing bac terial pathogens into intracellular vacuoles. Efficient internalization of also requires the activation of an alternative signaling pathway coup led with the activation of thetyrosine kinase receptor ErbB2. Beside Type IV pil i, other outer membrane proteins may be involved in other mechanism of bacteria internalization into cells Initially produces general symptoms like fatigue, it can rapidly progress from f ever, headache and neck stiffness to coma and death, along with a notable non-bl anching purpuric rash • • • • • • , N. meningitidis N. me ningitidis