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GMU Microbiology T.4
Chapters 14, 16, 17, 18
| Question | Answer |
|---|---|
| CH14 What is Etiology? | The cause of disease |
| CH14 What does pathology deal with? | Etiology (cause), Pathogenesis (qualities of etiology), Effects (on body) |
| CH14 What conditions define a disease? | Tissue damage |
| CH14 What is the difference between "normal flora" and "Transient flora"? | Normal - Permanent residents (always present). Generally do not cause disease Transient flora - Comes and Goes |
| CH14 What is microbial antagonism? | Competition between Microbiobes |
| CH14 Bacteriocins | Peptides with antimicrobial properties |
| CH14 How do Normal flora protect the host? | Producing acids, bacteriocins, competing with pathogen for space |
| CH14 Commensalism | One benefits, other unaffected |
| CH14 Name an example of commensalism | Staphylococcus epidermidis protecting skin |
| CH14 Mutualism | Both benefit |
| CH14 Name an example of mutualism | E. coli in intestines produce vitamin B/K |
| CH14 Parasitism | One benefits, other is hurt |
| CH14 Name an example of parasitism | ANY pathogen |
| CH14 What disease can S. aureus cause? | Toxic shock syndrome |
| CH14 What is a characteristic of opportunistic microorganisms? | Only pathogenic when it has a chance |
| CH14 What can change from commensal to parasitic? | Some Normal microbiota |
| CH14 Synergism | 2 is greater than one |
| CH14 Name an example of SYNERGISM [1] | Mycoplasma fermentans & HIV - if 1 cell is infected by both the cell will die much faster than when infected by either one alone |
| CH14 Name an example of SYNERGISM [2] | Pathogens that cause periodontal disease and gingivitis bind to streptococci on the teeth instead of binding directly to the teeth |
| CH14 What is a SYNDROME? | A group of symptoms that describes a disease |
| CH14 What is a sign? | Measurable changes in the body due to a disease |
| CH14 What is a symptom? | Changes Felt by the patient as the result of a disease |
| CH14 What is the difference between a sign and a symptom? | Sign is empirical while a symptom is subjective |
| CH14 Is tetanus a communicable disease? | NO |
| CH14 What describes incidence and prevalence of a disease? | Incidence is how many people with a disease per total. Prevalence is the largest reduced fraction of incidence. |
| CH14 Endemic Disease | constantly present in a population |
| CH14 Epidemic disease | acquired by many hosts in a given area in a short time. |
| CH14 Pandemic disease | Worldwide epidemic |
| CH14 Sporadic disease | Localized occurrences |
| CH14 Acute disease | Symptoms develop rapidly |
| CH14 Subclinical disease | No noticeable signs or symptoms. Carrier for a disease. |
| CH14 Latent disease | : Disease with a period of no symptoms when the causative agent is inactive |
| CH14 Local infection | Pathogens are limited to a small area of the body (ex: a boil) |
| CH14 Systemic infection | An infection throughout the body |
| CH14 Name an example of a systemic infection | Chicken pox |
| CH14 Focal infection | Multiple but defined areas of infection |
| CH14 Name an example of a focal infection | Tuberculosis |
| CH14 Sepsis | Inflammation due to spread of bacteria/toxins |
| CH14 Bacteremia | Bacteria transported through the blood stream but not multiplying |
| CH14 Septicemia | Bacteria multiplying in blood |
| CH14 Toxemia | Bacteria producing poisons in blood |
| CH14 Viremia | Viruses in blood |
| CH14 Primary infection | Acute infection that causes the initial illness |
| CH14 Secondary Infection | Infection after the first infection |
| CH14 What are the stages of disease development? | Incubation, Prodomal (mild), Invasive (full blown), decline, Convalescent(no symptoms), |
| CH14 What is a Reservoir | continual source of the disease causing organisms, it can be living or inanimate objects (viruses) |
| CH14 zoonoses | |
| CH14 Name one Indirect way of Spreading Disease | Formites, glasses, utensils, syringes, tools.... |
| CH14 What is disease transmission by Droplet? | Transmission by airborne liquids |
| CH14 What is a vehicle | Transmission by inanimate reservoir |
| CH14 Name some examples of vehicles | food, water, air |
| CH14 How do vectors transmit disease? | Through Insects |
| CH14 What is the difference between mechanical and biological transmission? | Mechanical uses a physical carrier like arthropods while biological is the reproduction of the pathogen itself being transmitted |
| CH14 What are Nosocomial infections? | Transmitted through a hospital |
| CH14 How are nosocomial infections transmitted? | staff to patient; patient to patient; formites; ventilation system |
| CH14 How can nosocomial infections be controlled? | Good technique, monitoring for drug resistence |
| CH14 What contributes to emerging infectious disease? | Recombination, new strains, improper antibiotic use |
| CH14 What disease is transported by modern transportation? | West Nile Virus |
| CH14 What disease is prevalent in settlement/war? | Coccidioidomycosis |
| CH14 What disease is prevalent in improper animal control? | Lyme Disease |
| CH14 What disease is prevalent in problems in public health control? | Diphtheria |
| CH14 What is Epidemiology? | Study of when, where, and how diseases are transmitted |
| CH14 What is Morbidity? | Incidence of a disease |
| CH14 What is mortality? | Deaths from a disese |
| CH14 What is morbidity rate? | Rate of people affected by disease |
| CH14 What is Mortality rate? | Rate of people died from the disease |
| CH14 What did John Snow do? | Mapped Cholera in London |
| CH14 What did Semmelweis do? | Discovered that handwashing lowered puerperal fever |
| CH14 What did Nightingale do? | She shows that sanitation diseased typhus |
| CH14 What is the difference between descriptive, analytical, experimental experiments | Descriptive: Data Collection/Analysis. Analytcal: Comparing disease/healthy groups, experimental: Controlled Experiments |
| CH16 Susceptibility | Lack of Resistance |
| CH16 Innate Immunity | Non-specific. Defense against any pathogen. |
| CH16 Adaptive Immunity | Acquired immunity to a specific pathogen |
| CH16 What line of defense is innate immunity | 1st (skin,mucus) and 2nd (macrophages,fever, inflamation, neutrophils,etc) |
| CH16 What line of defense is adaptive immunity | 3rd (T/B Cells, antibodies) |
| CH16 What is a protective protein of the epidermis? | Keratin |
| CH16 Cilary Escalator | Mucus transported away from lungs |
| CH16 Lacrimal Apparatus | Washes eye |
| CH16 Chemical Immunity Examples | Sebum (fungistatic fatty acids), skin low ph, stomach low ph, vag. low ph. Lysozyme. |
| CH16 What infects urinary tract | Enteric |
| CH16 Name some examples of enterics | E. Coli P. aeruginosa. S. Saprophyticus. |
| CH16 What causes kidney infections? | Leptospira interrogans (spirochete) |
| CH16 Blood | formed cellular elements suspended in a liquid matrix called plasma |
| CH16 Plasma | Electrolytes, solutes, proteins (including antibodies), clotting factors, etc |
| CH16 Serum | Plasma with no clotting factors |
| CH16 Lymph | Plasma, leukocytes (white blood cells), cellular waste products |
| CH16 Pus | lymph, increased leukocytes, bacteria and bacterial cell debris, host cell debris, etc |
| CH16 Red Blood Cells | Transport O2 and CO2 |
| CH16 White Blood Cells: Neutrophils Granulocyte | Phagocytosis |
| CH16 Basophiles (mast cells) Granulocyte | Histamine |
| CH16 Eosinophils Granulocyte | Kill parasites (helminths, protozoans) |
| CH16 Monocytes (macrophages) Granulocyte | Phagocytosis |
| CH16 Dendritic cells Non-circulating | Antigen-presentation Phagocytosis |
| CH16 Natural killer cells lymphocytes | Destroy target cells |
| CH16 T cells lymphocytes | Cell-mediated immunity |
| CH16 B cells lymphocytes | Produce antibodies |
| CH16 “Professional” phagocytes: | Neutrophils Macrophages Dendritic cells |
| CH16 Toll-like receptors (TLRs) attach to | Pathogen-associated molecular patterns (PAMPs |
| CH16 Pathogen-associated molecular patterns (PAMPs) = | peptidoglycan, LPS, flagellin, viral DNA and RNA, etc |
| CH16 TLRs induce | adherence and recognition of phagocytes with foreign cel |
| CH16 Cytokines | = small cell signaling molecules (proteins) that regulate immune response |
| CH16 How do bacteria inhibit phagocytosis? | Inhibit adherence Kill (lyse) phagocytes Escape phagosome Prevent phagosome/lysosome fusion Survive within phagolysosome |
| CH16 Damage to host tissues and phagocytosis leads to production of | inflammatory cytokines like TNF-α |
| CH16 Acute-phase proteins | activated (complement, cytokines, and kinins) |
| CH16 Vasodilation | induced (release of histamine, kinins, prostaglandins, and leukotrienes) |
| CH16 Histamine | Vasodilation, increased permeability of blood vessels |
| CH16 Kinins | Vasodilation, increased permeability of blood vessels |
| CH16 Prostaglandins | Intensity histamine and kinin effect |
| CH16 Leukotrienes | Increased permeability of blood vessels, phagocytic attachment |
| CH16 Fever: PAMP causes | phagocytes to release interleukin–1 (IL–1) |
| CH16 Fever: Hypothalamus releases prostaglandins | reset the hypothalamus to a high temperature |
| CH16 Complement System Activated By | by the cleavage of C3 into C3a and C3b |
| CH16 C3b causes | opsonization (phagocyte adherence) |
| CH16 C3b cleaves | C5 into C5a and C5b |
| CH16 C3a + C5a induce | inflammation |
| CH16 C5a = | chemotactic response (attracts macrophages) |
| CH16 C5b + C6 + C7 + C8 + C9 | cause cell lysis The MAC attack complex |
| CH16 Effects of Complement Activation | inflammation (histamine release),phagocytes (chemotactic response, immune adherence: Enhanced phagocytosis, Membrane attack complex: Cytolysis |
| CH16 Classical Pathway of Complement Activation | KNOW THIS |
| CH16 Classical Pathway of Complement Activation | |
| CH16 Lectin Pathway of Complement Activation | |
| CH16 How do bacteria evade complement? | Capsule, Surface lipids prevent membrane attack complex, Enzymatic digestion of C5a |
| CH16 Interferons | Interfere” with the replication of viruses. |
| CH16 Describe Interferons | Small protein cytokines. |
| CH16 What are the 3 types of interferons? | Alpha, beta, gamma |
| CH16 What does alpha interferons do? | Produced by B lymphocytes and monocytes. Is antiviral. |
| CH16 What does beta interferons do? | Produced by fibroblasts and epithelial cells. Is antiviral |
| CH16 What does gamma interferons do? | Produced by T cells. Is an immunomodulator. Induces neutrophils and macrophages to kill bacteria by phagocytosis. |
| CH16 Are interferons specific to viruses? | IFNs are not virus specific. They will stop the replication of most viruses. |
| CH16 A interferons species specific? | IFNs are species specific, i.e., all human interferons are the same. |
| CH16 What uses do recombinant interferons have? | Used to treat zoster, the flu, some types of cancer, HCV, etc. |
| CH16 What are transferrins | Iron-binding proteins in blood, milk, saliva, and tears. Bind iron, reducing iron availability to pathogens |
| CH16 siderophores | Bacteria scavenge iron |
| CH16 Antimicrobial peptides | Small, anti-microbial peptides (12 amino acids long) |
| CH16 What are antimicrobial peptides produced by? | mucous-membrane cells and phagocytes |
| CH16 What do antimicrobial peptides bind to? | membranes of bacteria causing cell lysis |
| CH18 Variolation | The introduction of infected tissue into healthy individuals to prevent disease |
| CH18 vaccine | A preparation of microorganisms or parts of microorganisms used to induce immunity. |
| CH18 What type of immunity does a vacine provide? | A type of artificially acquired active immunity. |
| CH18 Who invented vaccines? | Edward jenner's cow pox (vacca = cow) |
| CH18 Pasteur made vaccines for what diseases? | Anthrax, rabies (failed), etc |
| CH18 What are the types of vaccines? | Major types 1. Attenuated, whole agent vaccines 2. Inactivated, whole agent vaccines 3. Toxoids 4. Subunit vaccines 5. Nucleic acid vaccines Vaccines of any type may be conjugated (administered together) |
| CH18 What types of vaccines can be combined? | Any kind |
| CH18 What defines can attenuated vaccine? | weakened and nonvirulent viruses/bacteria |
| CH18 Name some examples for attentuated vaccines | Salmonella typhi for typhoid fever Measles, mumps and rubella viruses (MMR) vaccine Sabin oral polio vaccine (OPV) |
| CH18 What defines an inactivated agent vaccine? | Killed bacterium or inactivated virus |
| CH18 Name some examples of an inactivated agent vaccine | Pertussis vaccine is an acellular vaccine (The aP of DTaP vaccine) Rabies vaccine Salk inactivated polio vaccine (IPV) |
| CH18 Toxoid | modified toxins. They're nontoxic but antigenic |
| CH18 Name some toxoid vaccines | diphtheria toxoid and the tetanus toxoid. (The D and T of the DTaP vaccine, respectively.) |
| CH18 What defines subunit vaccines? | Contain parts of a microorganism or virus |
| CH18 Name some examples of subunit viruses | a. Capsule. Example: Streptococcus pneumoniae and Hemophilus influenzae type b (the Hib vaccine) b. Peplomer of a virus. Example: HBV vaccine is a recombinant, subunit vaccine. Gene for peplomer was put into Saccharomyces cerevisiae |
| CH18 What are nucleic acid vaccines? | Inject the DNA that codes for the protein wanted as a antigen. Thus, the protein is synthesized in the person |
| CH18 What are conjugated vaccines? | Principle: combining a poorly immunogenic antigen with one that elicits a good immune response |
| CH18 What is an example of a conjugated virus? | Hemophilus influenzae b polysaccharide capsule is combined with diphtheria toxoid. |
| CH17 A “complete” immune system only found in | vertebrate animals |
| CH17 T and B cells develop from | stem cells in red bone marrow |
| CH17 Cellular immunity Due to | T cells |
| CH17 T cells mature in | thymus |
| CH17 Humoral immunity due to | B cells/Due to antibodies |
| CH17 B cells mature in the | bone marrow |
| CH17 Antibodies (Ab) interact with | epitopes or antigenic determinants |
| CH17 excellent antigens | Proteins |
| CH17 Hapten | Small or poor antigen is combined with carrier molecules and illicits antibody production |
| CH17 Example of Hapten | Penicillin |
| CH17 Where are epitopes located? | On Antigen |
| CH17 Immunoglobulins have what shape? | Globular |
| CH17 Immunoglobulins PRODUCED BY | B-cells |
| CH17 Basic structure of immunoglobulins | 2 heavy and 2 light polypeptides |
| CH17 Each B cell (or each clone of B cells) produces | one specific antibody |
| CH17 The light chain consists of | 3 parts: V, J and C |
| CH17 Germ line DNA has about 200 | 200 variable genes for antibodies designated V |
| CH17 The germ line DNA has 4 | joining genes designated J, e.g. J1, J2, etc. |
| CH17 The germ line has 1 | constant region (C) for each class of antibody |
| CH17 Any combinations that react to “self” before birth | are eliminated |
| CH17 By rearranging genes (and by mutations), | millions of antibody combinations are possible |
| CH17 Lymphocytes use only about 400 to 500 genes to | code for millions of abs |
| CH17 IgG Antibodies location | In blood, lymph, and intestine |
| CH17 IgG content pertentage | 80% of serum Abs |
| CH17 IgG Structure | Monomer |
| CH17 IgG Function | Enhance phagocytosis; neutralize toxins and viruses; protects fetus and newborn |
| CH17 IgG halflife | 23 days |
| CH17 IgM location | In blood, in lymph, and on B cells |
| CH17 IgM content pertentage | 5–10% of serum Abs |
| CH17 IgM Structure | Pentamer |
| CH17 IgM Function | Agglutinates microbes; first Ab produced in response to infection |
| CH17 IgM halflife | Half-life = 5 days |
| CH17 IgA location | In secretions |
| CH17 IgA content pertentage | 10–15% of serum Abs |
| CH17 IgA Structure | Dimer |
| CH17 IgA Function | Mucosal protection |
| CH17 IgA halflife | 6 days |
| CH17 IgD location | In blood, in lymph, and on naive B cells |
| CH17 IgD content pertentage | 0.2% of serum Abs |
| CH17 IgD Structure | Monomer |
| CH17 IgD Function | On B cells, initiate immune response |
| CH17 IgD halflife | 3 days |
| CH17 IgE location | On mast cells, on basophils, and in blood |
| CH17 IgE content pertentage | 0.002% of serum Abs |
| CH17 IgE Structure | Monomer |
| CH17 IgE Function | Allergic reactions; lysis (?) of parasitic worms |
| CH17 IgE halflife | 2 days |
| CH17 Activation of B Cells | MHC,T-dependent antigens, T-independent antigens |
| CH17 T-dependent antigens | Ag presented with (self) MHC to TH cell TH cell produces cytokines that activate the B cell |
| CH17 T-independent antigens | Stimulate the B cell to make Abs |
| CH17 What is an example of a T-Independent antigen | Polysaccharides (pattern molecule) bind to B cell receptors IgD |
| CH17 Examples of cytokines | interleukin-1 (IL-1), IL-2, IL-12, and more interferons tumor necrosis factor (TNF) colony-stimulating factor Chemokines/chemotaxins |
| CH17 Cells of the immune system communicate with each other by | cytokines |
| CH17 Lymphokine | lymphocyte |
| CH17 Interleukin | A cytokine that communicates only between leukocytes |
| CH17 During clonal selection, B cells differentiate into | Antibody-producing plasma cells First IgM Seroconvert to IgG |
| CH17 Clonal deletion eliminates | harmful B cells. Mainly occurs during fetal development |
| CH17 T cells respond to Ag by | T-cell receptors (TCRs) |
| CH17 T cells require | antigen-presenting cells (APCs) |
| CH17 APC’s are concentrated in | lymphatic tissues but also in peripheral tissues as well |
| CH17 pathogens entering the gastrointestinal or respiratory tracts pass through | M (microfold) cells over Peyer’s patches, which contain APCs |
| CH17 Helper T is distinguished by what characteristic? | CD4+ |
| CH17 TCRs recognize Ags and MHC II on | APC |
| CH17 Toll-like receptor (TLR) can be a costimulatory signal on | APC and TH |
| CH17 TH cells proceed through | clonal expansion |
| CH17 TH cells produce cytokines and differentiate into | TH1 TH2 Memory cells |
| CH17 TH1 produces IFN-gamma which | activates cells related to cell-mediated immunity, macrophages, and Abs |
| CH17 TH2 | activate eosinophils and B cells to produce IgE |
| CH17 T Cytotoxic Cells are distinguised by | CD8+ |
| CH17 T Cytotoxic Cells Target | host cells that are expressing antigens |
| CH17 T Cytotoxic Cells Activated into | cytotoxic T lymphocytes (CTLs) |
| CH17 Function of CTL | CTLs recognize Ag + MHC I Induce apoptosis in target cell |
| CH17 CTL releases | perforin and granzymes |
| CH17 perforin and granzymes effective against | intracellular pathogens (viruses). |
| CH17 T Regulatory Cells (Treg cells ) aka ___ distinguished by: | (aka inhibitory T-cells) CD4 and CD25 on surface |
| CH17 Treg cells Secrete | anti-inflammatory cytokines Down-regulate immune response over time Suppress immune response to “self” antigens |
| CH17 Natural Killer (NK) Cells | Granular lymphocytes that destroy cells that don’t express MHC I (foreign cells) |
| CH17 Natural Killer (NK) Cells kill___ | virus-infected and tumor cells Attack parasites MHC class I on almost all cells MHC class II on immune cells |
| CH17 ADCC | Attacks large parasites |
| CH17 Antibody titer | is the amount of Ab in serum |
| CH17 Types of Adaptive immunity | Naturally acquired active immunity Resulting from infection Naturally acquired passive immunity Transplacental or via colostrum Artificially acquired active immunity Injection of Ag (vaccination) Artificially acquired passive immunity Injection of |
| CH17 Serology | The study of reactions between antibodies and antigens |
| CH17 Antiserum: | The generic term for serum because it contains Ab |
| CH17 Globulins | Serum proteins |
| CH17 Gamma globulin | Serum fraction containing Ab |
Created by:
NathanielZhu
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