Lecture 10 - Meningicoccal Disease

Lecture 10 - Meningicoccal Disease - MENINGOCOCCAL DISEASE...

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EVO MENINGOCOCCAL DISEASE Edwin Oaks, Ph.D. George Mason University Fall 2008
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EVO MENINGOCOCCAL DISEASE Causative agent: Neisseria meningitidis Gram negative, diplococcus Related to N. gonorrhoeae Proteins in outer membrane involved in interactions with host cells Outer membrane surrounded by polysaccharide capsule Prevents phagocytosis Prevents complement-mediated lysis OM proteins and capsule are the major surface antigens Many serotypes of N. meningitidis Typing is based on capsular polysaccharide 13 different types Types A, B, C, Y and W-135 are most virulent and associated with disease Other antigens include outer membrane proteins (OMPs) called Porin B and Por A. Organism must attach (colonize) and invade to cause disease Antibodies can prevent systemic spread
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QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. (a) Electron micrograph showing paired bacteria (arrow) within a splenic macrophage. (b) Schematic representation showing the major adhesins. Pathogenic N. meningitidis possesses several surface-expressed adhesins. The type IV pilus mediates initial interactions with host cells. The opacity proteins Opa and Opc are phase-variable outer membrane proteins believed to play a role in later stages of adhesion and invasion, and enable adhesion in the absence of pili. The lipopolysaccharide (LPS) molecules display variation in side chains; the unsialylated forms of LPS might contribute to adhesion by binding to asialoglycoprotein receptors. The polysaccharide capsule is believed to inhibit adhesion to cells, possibly due to negatively charged molecules such as sialic acid that repel host cells or by masking the exposure of other surface adhesins. Meningococci
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This note was uploaded on 04/29/2009 for the course BIOL 420 taught by Professor Edwardsoaks during the Fall '08 term at George Mason.

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Lecture 10 - Meningicoccal Disease - MENINGOCOCCAL DISEASE...

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