Week 11 Microbiology 101 Lecture Notes
Week 11 Microbiology 101 Lecture Notes 101.0
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This 9 page Class Notes was uploaded by Isabel Markowski on Sunday December 6, 2015. The Class Notes belongs to 101.0 at University of Wisconsin - Madison taught by a professor in Fall 2015. Since its upload, it has received 29 views. For similar materials see General Microbiology in Microbiology at University of Wisconsin - Madison.
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Date Created: 12/06/15
Microbiology Week 11 Lecture Notes Adaptive Immune System Innate Immune system triggers adaptive immune system Macrophages and dendritic cells consume pathogen or take up soluble antigens Travel to lymph nodes Present antigen to lymphocytes (initiate adaptive immune system) APC: Antigen Presenting Cell (macrophages/dendritic cells) Specific (looks for antigens) and response takes time/long-lasting (immunity) Divided into cell-mediated (CMI) and antibody-mediated (AMI, humoral) Main players: APC, lymphocytes (T and B cells) T Cells B Cells In lymph nodes, also circulate In lymph nodes, also circulate T-cell Receptor (TCR) on surface B cell Receptor (BCR) on surface Types: Usually = inactive o Helper T cells (TH orhT ) o Active by antigen & T cell CD4 receptor o Then differentiate to plasma cells Differentiate to TH1 or TH2 cells (produce antibodies) Activate other cells o Regulatory T cells, TH17 cells, etc. o Cytotoxic T cells (TC oc T ) CD8 receptor Kill infected host cells How do cells recognize pathogens? Antigen: any molecule – elicits specific immune response o Contain several antigenic determinants (epitopes) o Proteins (best/most common), lipids, polysaccharides, small molecules o Single protein antigen = have multiple epitopes BCR recognizes antigen o Antibodies = secreted versions, recognize same antigen TCR recognizes antigen (but only when antigen is presented via MHC proteins) Lymphocytes = each specific for different antigen, billions = recognized Basis of adaptive When antigen is present, only lymphocytes specific for that antigen are activated response Antigen Presentation 1. Dendritic cell takes up pathogen for degradation 2. Pathogen taken apart 3. Pathogen proteins = unfolded/cut into smaller pieces 4. Peptides bind to MHC molecules and go to cell surface 5. Antigen presentation 6. T-cell receptors bind 2 types of antigen presentation: MHCI (APC and B cells) & MHCII (almost all cells) Antibody-Mediated Immunity (AMI) Goal: Production of antigen-specific antibodies and generate memory cells Requires THcells, APC, and B cells Steps: o Dendritic cells present tH T celH (T cell differentiateH2into T cells) o B cell recognizes antigen with BCR o T cell stimulates B cell – become plasma (produce antibodies) H2 B-cell activation o Antigen specific = same as BCR o Some B cells become memory cells Can later differentiate into plasma cells Antibodies o Antibodies = proteins – recognize and bind to antigens o Immunoglobulins, Ig o 4 polypeptides (2 light chains, 2 heavy chains) o Several types, defined by different heavy chains (IgA, IgM, IgG, IgD, IgE) o 2 antigen binding sites per antibody o Parts F(ab) = attach to antigens, variable in amino acid sequence Fc= attach to Fcreceptors on phagocytes and to complement (antibodies/phagocytes), constant o Antigen-antibody interactions – very specific for one epitope Fab region = highly variable between antibodies Ex: can have many antibodies for individual parts of antigens o Functions Neutralize viruses/toxins (direct inactivation by binding) Opsonization (recognizes Fcportion of antibody Activation of complement system (in blood – can kill microbes) / pore formation Agglutination (can bridge 2 different cells, bring a lot together and hold in place while wait for immune cells) o Only B cells that recognize specific antigen are stimulated B cells differ in antigen specificity Clonal Selection Clone of memory cells Clone of plasma cells Cell-Mediated Immunity (CMI) Goal: activate certain immune cells TH1ells activate macrophages – better phagocytosis CD8 T cells = activated to become cytotoxic T cells o Dendritic cells present foreign antigen on MHCI to CD8 T cell o CD8 T cell = activated to become cytotoxic T cell Cytotoxic T cells: recognize infected host cells via MHCI presentation Kill cell (toxic peptides/secreted proteins: induce suicide) Differentiation: self vs. non-self o MHCI presents intracellular antigens (widespread – all types of cells) o Uninfected cells present cellular proteins (“self” – not recognized by immune system) o If infected cell, pathogen antigens will be presented (non-self – recognized by immune system) Summary of Immune System Branches AMI CMI Control of extracellular pathogens, secreted Intracellular Pathogens toxins, and viral particles Interstitial spaces, Epithelial Surfaces Cytoplasmic Vesicular blood, lymph Complete each other (cover all bases) Summary of Adaptive Immune Response Specificity (triggered by specific antigens for specific pathogens vs. innate immunity – broad) Generate Memory Cells (ready for future infection) o Stronger and faster response o B Cells o T Cells Tolerance: recognize self and not respond o Ex: autoimmune diseases (attack self): don’t have tolerance Types of Immunity Passive Active Immune response given to you You make immune response Natural (from mother to fetus/infant) Natural (exposure to pathogens) Artificial (preformed antibodies used as Artificial (immunization – vaccines) antitoxins) Immunization Exposure: provides antigens – stimulate immune response Develop AMI or CMI from vaccine – already ready for future first infection Types of vaccines (whole cell) o Live Attenuated: microbe = reduced virulence, but still able to replicate Immunocompromised people may have reaction (ex: FluMist) o Inactivated: dead microbes or chemically inactivated virus Inactivation may denature antigens May be less effective, require more doses (safer) Ex: regular flu vaccine Types of vaccines (cell part) o Subunit Vaccine: individual antigens or combo Ex: pneumonia vaccine for streptococcus pneumoniae (capsule) o Toxoid Vaccine: inactivated toxins Ex: diphtheria vaccine = inactivated diphtheria toxin Effect of vaccines, sanitation, and antibiotics = increase life expectancy Herd Immunity: significant amount of population = immune and breaks pathogen infection cycle if get vaccinations (protects vulnerable individuals) Microbes of the Skin Structures/Defenses Physical: multiple layers, shedding Chemical: antimicrobial peptides, low pH, salts, fatty acids, lysozyme Immunological Microbial: commensals Microbiota of skin Bacteria, viruses, archaea, fungi, and mites o About 110 species of normally occurring microbes Diverse: skin = always covered Glands and hair follicles = colonized Variation o 10 volunteers sampled at multiple places (oily-sebaceous, moist, dry) o Results: variation b/n individuals, sites, and environmental conditions Roles of Microbiota on skin Colonization resistance Promote immune function Production of antimicrobials Some = commensal pathogens (Staphylococcus aureus, Staphyl. Epidermis, Strepto. Pyo., Propionibacterium Acnes) Staphylococcus Epidermidis Gram+ firmicute: present – everyone and all over body Beneficial o Produces bacteriocins: active vs. Staphyl. Aureus (toxins active vs. related microbe) o Inhibits S. aureus biofilm formation o Induces production of antimicrobial peptides by skin o Inhibits excessive inflammation after injury Also causes disease o Nosocomial infections on indwelling medical devices Biofilm formation on devices Rarely life-threatening, but frequent/difficult to treat Skin as Site of Disease Few pathogens can pass intact skin Damage makes it vulnerable (wounds, cuts, implants, injections, cosmetic procedures, burns, insect bites, etc.) Often diseases initiated at other sites have skin symptoms (ex: smallpox, measles, etc.) Microbial Pathogens of Skin Clostridium Tetani Basic Biology o Firmicute, endospores o Obligate anaerobe o Proteolytic o Ferments amino acids Reservoir: soil Transmission: soil containing spores introduced during deep wound (damaged tissue = anaerobic environment) Virulence: tetanus toxin (secreted protein – can go anywhere) Disease: tetanus Target: neurons (nervous system) o Normal: Glycine (G) release from inhibitory interneurons to stop acetylcholine release = muscle relaxation o Tetanus: Toxin binds to inhibitory neurons, prevent G release = muscles always contracted Vaccines: DTaP, Tdap, DT, Td (T = tetanus toxoid) Staphylococcus Aureus Gram+ Firmicute Catalase+, salt and desiccation tolerant Anaerobic/aerobic respiration/fermentation (metabolically flexible) Many = polysaccharide capsules Thick layer of peptidoglycan S. Aureus Also has carotenoid pigments, coagulase (clotting enzyme) Reservoir: humans (30% are long-term nasal carriers, others = non-carriers or transient carriers) Transmission o Transfer of bacteria one site other on carrier o Transfer from carrier susceptible individual Direct contact with skin Respiratory secretions Fomites (common) Nasal colonization (predominant location) Diseases: half million people acquire S. Aureus infection annually o Skin/soft tissue infections (SSTI), invasive infections, food intoxication SSTI Infections (pimples, boils, carbuncles, wound/surgical infections) Invasive species (can cause disease almost any tissue/organ in body b/c so versatile and produce so many virulence factors: o Adhesions for attachment & immune evasion At least 28 proteins to bind Significant functional overlap: binding fibrinogen (hide itself with human cells) o Degradative enzymes prod. nutrients for growth Staphylokinase: activates plasminogen to plasmin (dissolves blood clots) Hyaluronidase: destroys hyaluronic acid Lipases, nucleases, proteases o Toxins Pore-forming (lytic/toxic) Exfoliative (cause scalded skin syndrome) Superantigen (toxic shock syndrome Toxin-1) o Anti-immune Response (many) 6 proteins interfere with complement cascade Destroy immune chemotaxis signals Surface proteinA binds Ig F region (binds to antibodies – inhibits opsonization) c Staphylokinase aids in cleavage of IgG Control of S. Aureus disease (at…) o Reservoir: screening and decolonization therapy o Transmission: hygiene, skin care, disinfection of fomites o Infected individuals: single-patient rooms Antibiotic resistance = BIG problem (MRSA) (VRSA – vancomycin resistant) o No vaccine Microbes of the Oral Tract Wide range of habits o Tooth surfaces (low oxygen) o Tongue (variable oxygen) o Fissures (teeth) (high oxygen) o Gingival crevices (low oxygen o Mucosal surfaces (high oxygen) Antimicrobial Defenses Mechanical Hydrodynamic (salivary flow – 1 L per day) Mucus layer (shedding of epithelial cells) Antimicrobial activity (especially in saliva) o Lysozyme, iron-binding proteins, antimicrobial peptides, IgA, phagocytes – about 30,00 per minute transit through periodontal tissue) Normal Microbiota of Oral Tract 700 species of bacteria (each person = 100-200 species) Specific microbe- Late o Streptococci = common microbe colonizers Fungi, protists, archaea Anaerobes = common interactions Early Community interactions = important colonizers o Oxygen utilization, metabolic interactions, biofilm, coaggregation: Tooth Teeth = Unique Site Non-shedding Extensively colonized Microbe-microbe interactions = critical (coaggregation) Biofilm o Dental plaque o Microbes, microbial polymers, and host macromolecules Pathogens of Oral Tract Example: oral streptococci – dental caries (cavities) Periodontitis – systemic diseases Streptococcus Periodontitis Gram+ Firmicute Bacterially-induced Obligate fermenters (produce lactic acid from sugars) inflammatory disease (of Aerotolerant (don’t produce catalase) periodontium) Many non-pathogenic species (ex: used in cheese production) Dysbiosis (upsetting Dental caries microbial balance) o Most common infectious disease in humans Altered microbes leads to o Oral streptococcus (ex: strep. Mutans) inflammation, tissue o Dietary sugars acid production damage to enamel damage, bone loss Bacterium inhabit tissue Naming Streptococcus: species name: beneath tooth = cause Hemolysis (lysis of RBC) irritation and bone α β γ resorption Lancefield group Bacterial Endocarditis A, B, C,…W Oral bacteria make way to Streptococcus Pyogenes heart and grow (bloodstream o Β-hemolytic Group A (Group A Strep: GAS) infection, form o Some strains in oral/respiratory tract (others = skin) o Reservoir: only humans (asymptomatic carriers) plaques/”vegetation”) Bacteria o Transmission: respiratory secretions and saliva o Streptococcus > 50% o Skin infections o Staphylococcus 25% Impetigo, Erysipelas, Cellulitis o Enterococcus 15% Invasive infections (Necrotizing fasciitis “flesh-eating”) o Throat infections o HACEK (5 genera of slow growing gram-) Strep throat Inflammations of lining of Complications: Scarlet Fever, Rheumatic Fever, heart chambers/valves Rheumatic Heart Disease Complications o Other Systemic infections o Destruction of valves/other parts Post-infection complications (kidney damage) Toxic Shock Syndrome o Vegetation can break off and cause strokes Pneumonia Puerperal Sepsis (childbirth fever) Systemic Impacts of Oral Microbiota Virulence o Adhesion Inflammation liver Capsule (hyaluronic acid) Swallowing Gut Adhesions (17 known) Bacterial Dissemination o Anti-immune Heart M protein – antiphagocytic Inflammation-induced Streptococcal inhibitor of complement (SIC) o Invasion pregnancy complications Streptokinase: dissolves blood clots o Toxins Superantigen toxins (some strains) Streptolysin O and Streptolysin S (hemolysis)
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