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Micro Final 2011
| Question | Answer |
|---|---|
| PAMP | Pathogen-Associated Molecular Patterns |
| Func. of Macrophages | Engulf and kill, induce inflammation, secrete cytockines to attract other immune cells (neutrophils and monocytes) |
| Func. of Dendritic Cells | phagocytic, moacrpinocytotic (always ingest extracellular fluid) MAIN FUNC.= professional APC |
| Class I MHC's | Major Histocompatibility Complex located on every cell in the body act as marker to prevent attack by persons own immune system |
| Class II MHC's | -only on professional antigen presenting cells -activate on acquired immune response when combined with specific antigens |
| Professional APC's | Macrophages, Dendritic cells, and ? |
| Neutrophils: Lifespan, primary function | phagocytic but not APC, short lived (3 days), migrate to tissue during infection |
| NK's | kill infected abnormal (cancer) cells or foreign cells that lack MHC I's secrete perforins that create pores, release granzymes that induce apoptosis |
| Inflammation | dilated blood vessels, increase perm. Of plasma to the infected tissue, neutrophils and monocytes enter tissue by diapedisis |
| 5 Cardinal signs of inflammation | -redness -warmth -swelling -pain -loss of function |
| Diapedisis | entrance of cells (WBCs) into tissue |
| Edema | swelling due to fluid in bodys tissue |
| AMP | Antimicrobial Peptides: Defensins= amphipathic molecules, insert into microbial membrane, congregate, form pores |
| Antimicrobial Enzymes | Lysosomes= present tears, saliva, mucus, milk Destroys bacterial cell wall |
| Interferons | release by cells w/ virus, bind to receptors of nearby cells, induce synthesis of antiviral proteins inside nearby cell, AVP temporarily inhibits protein synthesis |
| Complement system | ~30 proteins in serum and tissue -Enhance phagocytosis (opsonization) -Stimulate inflammation and attract phagocytes -Kills microbes directly (Membrane Attack Complex) |
| Humoral immunity | acts against extracellular pathogens (exogenous Ag) |
| Epitopes | binding sites |
| Antibodies | Immunoglobulins Host proteins made in response to foreign substances Variable Domain [Fab differs between antibody] and Constant Domain [differs between classes] |
| IgG | most abundant, main Ab of lymph and blood [gamma globulins] |
| IgM | first Ab to appear following antigenic stimulation |
| IgA | found in body secretions, protect mucosa membranes |
| IgE | causes mast cells + eosinophils to release histamine |
| IgD | low serum concentration, unknown func. |
| Func. of Antibodies | Enhance phagocytosis, prefent virus/toxin binding, cross link microbes, precipitate soluble Ag, activate complement |
| Naïve lymphocyte (B) | not yet encountered any Ag |
| Activated B cell generate two things: | Plasma (effector) cells- short lived, secrete specific Ab Memory Cells- long lived, enable rapid secondary response |
| Cell-mediated immunity | acts against intracellular pathogens [virus, some bacteria, some cancer] endogenous Ag |
| Two types of T cells | cytotoxic t lymphocytes, helper t cells |
| Co Receptors of T cells | CTL’s--CD8 binds with MHC I’s Helper--CD4 binds with MHC II’s |
| Func. of CTL's (???) | Directly kill infected/abnormal cells TCR’s bind to Ag, CD8 binds with MHC I, CTL releases perforins and granzymes to destroy |
| Func. of T Helper Cells | Secrete cytokines that ‘help’ other immune cells TCR recognizes Ag, CD4 binds with MHC II, depending on cytokine release, differentiate: TH1 cells- stimulate CTL response TH2 cells- stimulate humoral (extracellular) response |
| Products of T Cell clonal expansion: | Effector T cells: CTLs kill infected cells, TH cells coordinate immune response Memory T cells: enable rapid response to subsequent infection |
| Lymph nodes. What do they do and what's there? | High concentration of B cells, T cells (CTLs and helpers) Lymph carries APC and Ag to lymph nodes, activate B and T cells, go to site of infection |
| Active Immunity [Natural/Artificial] | Active- exposure to foreign Ag produces Ab, slow acting but induces memory Natural- exposure to Ag, Illness Arificial- exposure to dead/weakened Ag, VACCINATION |
| Passive Immunity [Natural/Artificial] | Passive- Abs received from donor, fast acting, temporary protection Natural- Abs from mother to fetus (IgG) or via breast milk Artificial- isolated Abs injected (ex. Tetanus, Rabbies, antivenum, antiserum) |
| Vaccination | inoculation of person w/ weakened, dead, or fractionated microbes to generate immunity |
| What type of pathogen is vaccination most effective against and why? | Viral vaccines more effective/longer lasting- capsid and spike proteins more antigenic |
| Herd immunity | immunity in most of population limits outbreaks to a few cases |
| What are the 5 types of vaccines? | Attenuated (live), Inactivated, Toxoid, Conjugate, Subunit |
| Attenuated (live) vaccines: | Live Ag but low virulence, ‘weakened’, could revert and cause illness, long lasting MMR Cowpox oral Polio |
| Inactivated vaccines: | Whole agents, antigenically weakened, no cell replication, requires boosters, adjuvants Injected Polio |
| toxoid vaccines: | Inactivated toxins, weak few epitopes, requires boosters Tetanus |
| Conjugate vaccines: | Combine bacteria capsule polysacc w/ protein Makes capsular components more immunogenic Hib vaccine, protects vs meningitis from Hemophillus influenza b |
| Subunit | Administer antigenic determinants only, effective, safe, inexpensive Hep B, HPV |
| Adjuvants | Chemicals added to increase effective angtigenicity, stimulate inflammation, slows processing AND degradation of Ag Ex. Aluminum salts |
| Ideal Vaccine | Not injected, lifelong immunity/single dose, stable w/o refrigeration, affordable, no interference w/ other vaccines so multiple can be given at once |
| Issues related to vaccine safety: | Mild toxicity common [somewhat desireable] Risk of anaphylactic shock—Allergic Reaction against egg, adjuvant, or preservative Residual virulence from attenuated viruses No connection to autism allegations |
| Commensalism and Synergistic | -only microbe benefits from host -both microbe and host benefit |
| Benefits for host of microbiota | -compete w/ pathogens for attachment and nutrients -Prime immune system -produce vitamins/other beneficial substances -aid in digestion of food -produce bacteriocins (toxins that kill closely related species) |
| Pathogenicity | ability to gain entry and bring change |
| Virulence | degree of pathogenicity |
| Virulence Factor | microbe produces factors enabling invasion |
| Pathogenicity Islands | clusters of genes encoding virulence factors |
| Avirulent strains lack what? | pathogenicity islands |
| Common steps of infectious disease | Exposure Entry Evasion of Host Defenses Cause Damage Exit + Infect Others |
| Endogenous, Exogenous, and Reservoir of Infection | -caused by something on own body -caused by agents outside of the body -where microbe usually lives, Ex. Skin, soil, animals Communicable, Symptomatic, Asymptomatic Zoonotic/Zoonoses Environment |
| Horizontal infection- | human to human/animal: body contact, body fluids, inhalation of resp droplets |
| fomites | contaminated inanimate objects |
| Vehicle transmission- | contaminated food, water, aerosol |
| Vector | living intermediate carrer infectious agent reservoir to new host Mechanical- passive Biological- replicates in vector ex. Malaria |
| infectious dose | number of invading microbes |
| Infectivity | ability to attach and multiply |
| Adhesins | microbial protein that binds to receptor on host, enabling attachment (usually pili) |
| ways of evading INNATE immune system: | -capsule not recognized by PRR (pattern recognition receptors) -inhibit recruitment of phagocytes -kill phagocytes -avoid engulfment via capsule -survive within phagocyte -shelter/hide within cells of normal biota, go unrecognized |
| C5a peptidase | kills C5a to prevent attraction of phagocytes |
| Leukocidins | secreted proteins that kill phagocytes |
| Invasin | bacterial protein that induces uptake by non phagocytic cell |
| ways of evading ACQUIRED immune system: | -antigenic variation: periodically change surface Ag to limit effectiveness of Ab -destroy/deactivate Ab Ig pretease- cleaves Ab molecule FC receptor- binds to Fc portioin of Ab (wrong end) -Block Class I MHC signaling pathway |
| Non-invasive vs. Invasive | Non-invasive: on surface of tissue Invasive: penetrates cells of tissues |
| Dissemination | localized: limited to small areas systemic: spreads to other parts of body |
| toxemia and septicemia | Toxemia- toxin in blood stream Septicemia-microbe in blood (bacteremia, viremia) |
| signs and symptoms | Sign- measureable/observable Symptom- sensation patient experiences as told by patient |
| Acute and Chronic | Acute-short incubation, short duration Chronic- long incubation, much longer duration |
| Recurrent and Latent | Recurrent- becomes active again after period of inactivity Latent- infilous agent persists in a non-replicating form |
| Chemotherapy | use of drugs to treat active case of disease |
| Antibiotics | substance produced by microbe that kills/inhibits growth of other microbes |
| Modes of Action of antibacterial drugs | -inhibit cell wall synthesis -inhibit protein synthesis -inhibit DNA replication/trans -inhibit other metabolic reactions -disrupt bacterial membrane |
| Spectrum of Activity | Narrow: affects one or few types of microbes Broad: affects many Extended: affects more types than previous generations of drug |
| Innate drug resistance: | -microbe lacks target enzyme/cell structure -drug cannot enter cell |
| Acquired resistance: | -acquired by mutation/gene transfer -natural selection increases prevalence: -inactivate/destroy the drug -modify target of drug -avoid uptake of drug |
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