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Set 04.docx

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Department
Biology
Course
BIOL 444
Professor
Christine Dupont
Semester
Fall

Description
BIOL444 – Microorganisms & Diseases Fall 2012 Set 04 – Nervous System Infections - Nervous system: Sterile, immune-privileged site that’s protected from the circulatory system by the blood- brain barrier (endothelium lining w/ tight cell junctions) o Only small molecules (e.g. glucose) can get in, prevents entrance of immune cells from the rest of the body to prevent destructive inflammation o Contains own immune cells called microglia cells  Non-inflammatory immune response - CNS: Brain + Spinal cord, bathed by cerebrospinal fluid, surrounded by meninges (3 layers), encased in bone - PNS: Motor + Sensory nerves, connected to CNS - Encephalitis: Inflammation restricted to the brain (viral origin, or severe bacterial infection) - Meningitis: Inflammation of the meninges o Aseptic meningitis: Viral infection (Most common cause) o Bacterial meningitis: Bacterial infection - Invasions of the Central Nervous System o Foci close to CNS via venous pathways, via sheaths of cranial/spinal nerves o Directly via anatomical, surgical, congenital defects, or shuts & tubes placed post neurosurgery o Classification of CNS infections via Clinical Features  Purulent meningitis “pus”  Bacterial infection, acute onset & progression “bad very quick”  Shock & death  Chronic meningitis  Mycobacteria or fungi infection, slower & insidious onset & progression  Aseptic meningitis  Viral infection - Diagnostic procedures o Lumbar puncture/Spinal tap: Sample the cerebral spinal fluid  Monitors CSF pressure: ↑ in pressure if immune cells moves in & bacteria grows in CNS  Analysis for leukocytes: CNS is an immune privileged site, presence = abnormal  Drop in glucose: Bacteria utilizes glucose for metabolism  Increase in protein: Due to cellular damage & bacterial growth o Bacterial culturing & gram stain of CSF Bacterial Meningitis (3 main causal agents) - Streptococcus pneumoniae (Most common today) - Neisseria meningitidis (Next most common today) - Haemophilus influenzae serotype B (Hib/Childhood meningitis that targets kids <5) (Was most common until development of Hib B vaccine) Neonatal meningitis (Meningitis for new born babies) - Due to bacteria colonizing the birth canal o Gram-negative rods (certain E. coli strain, fetal contamination) o Group B streptococci (Streptococcus agalactiae)  Colonizes vagina in up to 70% of pregnant women - Before labour screening & appropriate medication o High doses of penicillin for the mother, not to stop the colonization but to get penicillin through to the babies’ circulation st Haemophilus influenzae - 1 organism to have its entire chromosome sequenced, was once thought to cause influenza - Strictly human reservoir, diseases are transferred from adults to kids, high mortality before vaccine - Gram-negative coccobacilli, may be encapsulated (capsule is the main virulence factor) o Non-encapsulated: Common URT inhabitants, carrier rates up to 80% for children & 20-50% for adults, responsible for pink-eye, sinus & inner ear infections (not meningitis) o Encapsulated (causes meningitis): Highly contagious, carried by 3-7% of healthy adults in URT. Infects weaned children <5 (IgA & IgG from mother’s breast milk still protects breast feeding kids) - Growth requires hematin & NAD (metabolic by-products of RBC), adheres to respiratory epithelium via pili BIOL444 – Microorganisms & Diseases Fall 2012 - Pathway: Upper Respiratory Tract (URT) infections  Bacteremia (Bacteria in blood stream)  Meningitis o Inflammatory response in CNS  Purulent “pus formation”  Brain swelling  CSF flow obstructed  Tissue necrosis/death - Virulence Factor o Type B capsule (Carbohydrate polyribitol phosphate PRP)  Poor binding with C3b (Complement), no complement activation or opsonization  T-independent antigen, composed of highly repetitive units of polyribitol (carbohydrates) instead of peptide, these particles can be bound by B-cell Receptors but cannot be presented to THcells (MHC II molecules)  Cannot stimulate T cells or B memory cells  Prevents opsonization & immune response, avoids detection by early immune system & replicated very quickly into large amounts to overwhelm the immune system  > 5: B-cells respond to T-independent antigens, can trigger response without presentation to T cells. Generally have memory response to PRP that’s been acquired over time from similar cell envelope components of other bacteria o The cross-linking of many BCRs on a B cell stimulates the B cells to undergo clonal expansion & differentiation into plasma cells, and produces low affinity IgM antibodies without the formation of B memory cells. o IgM coats the pathogen for phagocytosis during the period in which the bacteria would rapidly expand, keeps the window of response happening until the primary response (T-dependent response) kicks in (~14 days)  Production of B memory cells & IgG  Prevents infection  < 5: Do not have all the sub-populations of B cells, do not respond to T-independent antigens, no IgM production, little protection until ~5 y
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