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Week 11 Microbiology 101 Lecture Notes

by: Isabel Markowski

Week 11 Microbiology 101 Lecture Notes 101.0

Marketplace > University of Wisconsin - Madison > Microbiology > 101.0 > Week 11 Microbiology 101 Lecture Notes
Isabel Markowski
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Here are the first week of notes of the material for Exam 4! Topics include the Adaptive Immune System, Types of Immunity, Microbes of the Skin, and Microbes of the Oral Tract.
General Microbiology
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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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