How to Print Outlines
Sometimes when I copy and paste the outlines into the blog, the tabbing does not transfer. My suggestion to you is to copy the blog into Microsoft Word and then add the tabs yourself. Hopefully I can figure out how to overcome this glitch...but I don't have the time right now with exams coming up.
Tab 1x before every capital letter. Tab 2x before every numeral. Tab 3x before every lower case letter. Tab 4x before every lower case Roman numeral.
Thursday, April 17, 2008
Friday, April 11, 2008
Chpt 20 Antimicrobial Drugs
Antimicrobial Drugs
Chapter 20
I History of Chemotherapy
II Spectrum of Antimicrobial Activity
III Action of Antimicrobial Drugs
A. Bactericidal
B. Bacteriostatic
C. Inhibition of Cell wall synthesis
1. Peptidoglycan: alternating NAM and NAG subunit chains that are held together by peptide bridges.
a. When reproducing and growing, bacteria must synthesize more NAG/NAM units to add.
2. Antibiotic types ( Natural Beta – lactams): Prevent cross-linkage of NAM subunits
a. penicillin: narrow spectrum, kills only gram +
b. methicillin: works on some gram -
c. cephalosporin: works on some gram -
d. vancomycin: works on gram +
e. bacitracin: works on gram +
f. isoniazid: block mycolic acid addition to cell walls as well as peptidoglycan production
D. Inhibition of Protein synthesis
1. Ribosomes: The major structure of a cell that caries out protein synthesis
a. eukaryotic: 80s ribosomes
b. prokaryotic: 30s + 50s ribosomes = 70s
2. Antibiotic types
a. aminoglycosides:
i. streptomycin: change the shape of the 30s subunit
ii. gentomycin: change the shape of the 30s subunit
iii. tetracycline: prevent amino acids from entering the ribosome at the 30s subunit
b. chloramphenicol: blocks 50s ribosome, preventing peptide bond formation
c. macrolides:
i. bind to 50s ribosome
ii. prevent movement from one codon to the next, halting translation
iii. ex: erythromycin
E. Injury to the Plasma Membrane (Disruption of cytoplasmic membranes)
1. plasma membranes: phospholipids bi-layers that contain sterols (lipids)
a. polymyxin: disturbs phospholipids bi-layers
i. effective against gram – (Pseudomonas)
ii. toxic to kidneys and is usually used for external pathogens
2. Fungi contain a sterol called ergosterol, humans = cholesterol
3. Antifungal drugs:
a. polyenes: attach to ergosterol in the membrane
b. azoles: inhibit ergosterol synthesis
F. Inhibition of Nucleic Acid (DNA/RNA) Synthesis 21, 22, 23
G. Inhibiting the Synthesis of essential metabolites (anti-metabolic agents/inhibit metabolism) 17
1. Metabolism: all of the chemical reactions within a cell used to store or release energy
a. organisms often have unique metabolic pathways
b. most narrow antibiotic
2. Sulfonamides
a. Para-Aminobenzoic acid (PABA) 18, 19
H. Block attachment
I. Antifungal Drugs
J. Antiviral Drugs 20, 24
K. Antiprotozoan and Antihelminthic Drugs
IV Tests to Guide Chemotherapy
V Effectiveness of chemotherapeutic agents
VI Clinical considerations
Definitions:
Chemotherapy: the treatment of disease with chemicals (drugs) taken into the body.
Chemotherapeutic agents: drugs used for chemotherapy
Antimicrobial drugs: The class of chemotherapeutic agents used to treat infectious diseases.
Selective toxicity: killing the harmful organism without harming the host
1. The drug must be more toxic to a pathogen than a pathogen’s host.
2. possible due to difference in structure or metabolism between the pathogen and the host.
Synthetic drugs: synthesized in the laboratory
Antibiotics: produced by microorganisms, and in small amounts, inhibit another mo.
1. naturally occurring (Penicillin)
2. Semi-synthetic: slight alterations to naturally occurring agents
Chapter 20
I History of Chemotherapy
II Spectrum of Antimicrobial Activity
III Action of Antimicrobial Drugs
A. Bactericidal
B. Bacteriostatic
C. Inhibition of Cell wall synthesis
1. Peptidoglycan: alternating NAM and NAG subunit chains that are held together by peptide bridges.
a. When reproducing and growing, bacteria must synthesize more NAG/NAM units to add.
2. Antibiotic types ( Natural Beta – lactams): Prevent cross-linkage of NAM subunits
a. penicillin: narrow spectrum, kills only gram +
b. methicillin: works on some gram -
c. cephalosporin: works on some gram -
d. vancomycin: works on gram +
e. bacitracin: works on gram +
f. isoniazid: block mycolic acid addition to cell walls as well as peptidoglycan production
D. Inhibition of Protein synthesis
1. Ribosomes: The major structure of a cell that caries out protein synthesis
a. eukaryotic: 80s ribosomes
b. prokaryotic: 30s + 50s ribosomes = 70s
2. Antibiotic types
a. aminoglycosides:
i. streptomycin: change the shape of the 30s subunit
ii. gentomycin: change the shape of the 30s subunit
iii. tetracycline: prevent amino acids from entering the ribosome at the 30s subunit
b. chloramphenicol: blocks 50s ribosome, preventing peptide bond formation
c. macrolides:
i. bind to 50s ribosome
ii. prevent movement from one codon to the next, halting translation
iii. ex: erythromycin
E. Injury to the Plasma Membrane (Disruption of cytoplasmic membranes)
1. plasma membranes: phospholipids bi-layers that contain sterols (lipids)
a. polymyxin: disturbs phospholipids bi-layers
i. effective against gram – (Pseudomonas)
ii. toxic to kidneys and is usually used for external pathogens
2. Fungi contain a sterol called ergosterol, humans = cholesterol
3. Antifungal drugs:
a. polyenes: attach to ergosterol in the membrane
b. azoles: inhibit ergosterol synthesis
F. Inhibition of Nucleic Acid (DNA/RNA) Synthesis 21, 22, 23
G. Inhibiting the Synthesis of essential metabolites (anti-metabolic agents/inhibit metabolism) 17
1. Metabolism: all of the chemical reactions within a cell used to store or release energy
a. organisms often have unique metabolic pathways
b. most narrow antibiotic
2. Sulfonamides
a. Para-Aminobenzoic acid (PABA) 18, 19
H. Block attachment
I. Antifungal Drugs
J. Antiviral Drugs 20, 24
K. Antiprotozoan and Antihelminthic Drugs
IV Tests to Guide Chemotherapy
V Effectiveness of chemotherapeutic agents
VI Clinical considerations
Definitions:
Chemotherapy: the treatment of disease with chemicals (drugs) taken into the body.
Chemotherapeutic agents: drugs used for chemotherapy
Antimicrobial drugs: The class of chemotherapeutic agents used to treat infectious diseases.
Selective toxicity: killing the harmful organism without harming the host
1. The drug must be more toxic to a pathogen than a pathogen’s host.
2. possible due to difference in structure or metabolism between the pathogen and the host.
Synthetic drugs: synthesized in the laboratory
Antibiotics: produced by microorganisms, and in small amounts, inhibit another mo.
1. naturally occurring (Penicillin)
2. Semi-synthetic: slight alterations to naturally occurring agents
Chpt 19 Disorders Associated with the Immune System
Disorders Associated with the Immune System
Chapter 19
Hypersenstivity: sensitivity beyond what is considred normal. It occurs in people who have been previously sensitized by exposure to an antigen (allergen). Once sensitized, another exposure to the antigen triggers an immune response that damages host tissue. Based on mechanism and time, there are 4 types of hypersensitivity reactions:
I Type I (Anaphylaxis) Reactions
A. Mechanisms:
1. Involve IgE and the release of mediators such as histamine by mast cells and basophils (granulated cells)
2. involve allergens, sensitization and triggering
B. Time course: rapid, usually within 30 minutes
C. Clinical manifestations
1. Systemic anaphylaxis: System wide dramatic response to an allergen. Treated with epinephrine.
a. causes:
i. hormones: insulin, vasopressin
ii. antibiotics: penicillin, amphotericin B
iii. other: diazepam (valium), barbiturates
2. Localized anaphylaxis (atopic diseases): usually associated with antigens that are ingested or inhaled. Antihistamines to treat.
a. causes
i. peanuts
ii. tree nuts
iii. shellfish
iv. dairy
v. egg whites
vi. wasp or bee stings
vii. inhalants such as: pollen, fungal spores, animal dander, house dust mites
b. Allergic rhinitis symptoms
i. itchy, teary eyes
ii. congested nasal passages
iii. sneezing
3. Asthma
a. causes
i. allergens, irritants, exertion, stress
ii. triggers airway narrowing and mucus production
b. incidence
i. number of cases and deaths has increased significantly
c. symptoms
i. cough, wheezing, difficulty breathing
ii. reversible airway obstruction
d. treatment
i. smooth muscle relaxants
ii. corticosteroids
4. Hives (Urticaria)
a. cause: usually food or drugs
b. symptoms: swollen plaques on the skin
5. Food allergies
a. most common causes: wheat, eggs, milk, fish, peanuts, strawberries, tomatoes, crustaceans, nuts
b. symptoms: hives, itching, swollen lips, nausea, vomiting
c. treatment: antihistamines, avoiding contact of sensitizing agents
D. Prevention
1. desensitization: consists of a series of injections with a small dose of the antigen.
II Type 2 (Cytotoxic) Reactions
A. Mechanisms
1. involve antibodies (IgG, IgM) and causing cell damage
B. Time course: variable, usually 5 – 12 hours
1. ex: transfusion reactions
a. ABO
b. Rh
c. Target is donor RBCs
d. Hemolytic disease of the newborn (Rh disease)
i. Rh – mother
ii. Rh+ fetus, or ABO incompatible
III Type 3 (Immune Complex) Reactions
A. Mechanisms
1. involve antibodies (IgG or IgM) forming immune complexes and triggering local tissue damage
2. antigen: exogenous or endogenous
B. Time Course: variable, usually 3 – 8 hours
IV Type 4 (Delayed) Reactions (Delayed Cell-Mediated Reactions/Hypersensitivity)
A. Mechanisms
1. involve T cells and macrophages triggering inflammation
B. Time Course: slow, usually 24 – 48 hours
C. Clinical manifestations
1. Contact dermatitis
a. localized to the skin
b. maximum response 24 – 48 hours after exposure
c. symptoms: erythema, induration, sometimes blistering
d. triggered by certain materials: metals, clothing, rubber, leather, cosmetics, plants (poison ivy)
e. TB test: intentionally trigger a type 4 reaction for diagnosis
**** Only hypersensitivity is being covered in this chapter, not autoimmunity. That is why I did not outline the rest of the chapter.
Chapter 19
Hypersenstivity: sensitivity beyond what is considred normal. It occurs in people who have been previously sensitized by exposure to an antigen (allergen). Once sensitized, another exposure to the antigen triggers an immune response that damages host tissue. Based on mechanism and time, there are 4 types of hypersensitivity reactions:
I Type I (Anaphylaxis) Reactions
A. Mechanisms:
1. Involve IgE and the release of mediators such as histamine by mast cells and basophils (granulated cells)
2. involve allergens, sensitization and triggering
B. Time course: rapid, usually within 30 minutes
C. Clinical manifestations
1. Systemic anaphylaxis: System wide dramatic response to an allergen. Treated with epinephrine.
a. causes:
i. hormones: insulin, vasopressin
ii. antibiotics: penicillin, amphotericin B
iii. other: diazepam (valium), barbiturates
2. Localized anaphylaxis (atopic diseases): usually associated with antigens that are ingested or inhaled. Antihistamines to treat.
a. causes
i. peanuts
ii. tree nuts
iii. shellfish
iv. dairy
v. egg whites
vi. wasp or bee stings
vii. inhalants such as: pollen, fungal spores, animal dander, house dust mites
b. Allergic rhinitis symptoms
i. itchy, teary eyes
ii. congested nasal passages
iii. sneezing
3. Asthma
a. causes
i. allergens, irritants, exertion, stress
ii. triggers airway narrowing and mucus production
b. incidence
i. number of cases and deaths has increased significantly
c. symptoms
i. cough, wheezing, difficulty breathing
ii. reversible airway obstruction
d. treatment
i. smooth muscle relaxants
ii. corticosteroids
4. Hives (Urticaria)
a. cause: usually food or drugs
b. symptoms: swollen plaques on the skin
5. Food allergies
a. most common causes: wheat, eggs, milk, fish, peanuts, strawberries, tomatoes, crustaceans, nuts
b. symptoms: hives, itching, swollen lips, nausea, vomiting
c. treatment: antihistamines, avoiding contact of sensitizing agents
D. Prevention
1. desensitization: consists of a series of injections with a small dose of the antigen.
II Type 2 (Cytotoxic) Reactions
A. Mechanisms
1. involve antibodies (IgG, IgM) and causing cell damage
B. Time course: variable, usually 5 – 12 hours
1. ex: transfusion reactions
a. ABO
b. Rh
c. Target is donor RBCs
d. Hemolytic disease of the newborn (Rh disease)
i. Rh – mother
ii. Rh+ fetus, or ABO incompatible
III Type 3 (Immune Complex) Reactions
A. Mechanisms
1. involve antibodies (IgG or IgM) forming immune complexes and triggering local tissue damage
2. antigen: exogenous or endogenous
B. Time Course: variable, usually 3 – 8 hours
IV Type 4 (Delayed) Reactions (Delayed Cell-Mediated Reactions/Hypersensitivity)
A. Mechanisms
1. involve T cells and macrophages triggering inflammation
B. Time Course: slow, usually 24 – 48 hours
C. Clinical manifestations
1. Contact dermatitis
a. localized to the skin
b. maximum response 24 – 48 hours after exposure
c. symptoms: erythema, induration, sometimes blistering
d. triggered by certain materials: metals, clothing, rubber, leather, cosmetics, plants (poison ivy)
e. TB test: intentionally trigger a type 4 reaction for diagnosis
**** Only hypersensitivity is being covered in this chapter, not autoimmunity. That is why I did not outline the rest of the chapter.
Chpt 18 Practical Applications of Immunology
Practical Applications of Immunology
Chapter 18
I Vaccines (injection of antigens)
A. Principles and Effects of Vaccination
1. vaccine: a suspension of microorganisms, or some part or product of them, that will induce immunity when it is administered to the host.
2. herd immunity: when most, but not all, of the population is immune
B. Types of Vaccines and their characteristics
1. Inactivated (killed) Organism Vaccines: injection of killed mo
a. killed by:
i. phenol
ii. formalin
b. examples:
i. influenza: inactivated influenza virus
ii. rabies: inactivated rabies virus
2. whole agent
3. attenuated (weakened) whole agent: mimic actual infection and usually provide better immunity.
a. injection of weakened strain of mo
b. disadvantage: organism can become virulent
c. examples:
i. measles (MMR) attenuated measles virus
ii. TB (BCG) Mycobacterium bovis
4. Subunit (Component)Vaccines: uses only those antigenic fragments of a mo that are best suited to stimulate an immune response.
a. injection of part of microorganism
b. advantages: safe
c. examples:
i. tetanus: toxoid of Clostridium tetani (toxoid: inactivated bacterial virus)
ii. HIB: polysaccharide of Haemophilus influenzae
iii. Hepatitis B: HBV surface antigen (HBsAg)
5. Carrier Vaccines: injection of harmless organism
a. containing/expressing gene from disease causing organism
6. DNA vaccines
a. injection of DNA from mo
b. new technology
7. Passive immunization
a. injection of antibodies
b. instant immunity
c. protection lasts 5-6 months
d. examples
i. antivenom (antivenin)
II Diagnostic Immunology
A. Essential diagnostic tests for determining immunity:
1. sensitivity: the probability that the test is reactive if the specimen is a true positive
2. specificity: the probability that a positive test will not be reactive if a specimen is a true negative
A. Monoclonal Antibodies and their uses
B. Precipitation Reactions: involve the reaction of soluble antigens with IgG or IgM antibodies to form large lattices.
1. Ag - IgM or IgG react to form a complex
2. Ag – Ab complex form lattices and precipitate from solution
3. Ag – Ab ratio is optimal
4. Antigens – soluble
5. Immunoprecipitation: antigens and antibodies precipitate in agarose
6. Remember these test from lab.
C. Agglutination Reactions: involve particulate antigens that can be linked together by antibodies.
1. Direct agglutination
a. cells to be identified are agglutinated by antibodies.
b. titer: concentration of antibody in a serum
2. Indirect (passive) agglutination
a. antibodies or antigens are attached to plastic beads
b. beads clump
c. easy to do
D. Neutralization Reactions
1. antitoxin
2. viral hemagglutination inhibition test
E. Complement-fixation reactions
F. Fluorescent-antibody techniques (immunofluorescence)
1. antibodies labeled with a fluorescent dye
2. can look for antigens or antibodies
3. dyes are combined with antibodies to make them fluoresce when exposed to ultraviolet light.
4. methods:
a. direct
b. indirect
G. Enzyme-Linked Immunosorbent Assay (ELISA)
1. antibodies are labeled with an enzyme in a micro titer plate
2. enzyme causes color change for positive result
3. flexible, sensitive
4. home tests: early pregnancy tests
5. methods:
a. direct: goal is to identify an unknown antigen such as a drug in a serum sample
b. indirect: object is to determine the presence of certain antibodies in the serum. (AIDS virus)
Chapter 18
I Vaccines (injection of antigens)
A. Principles and Effects of Vaccination
1. vaccine: a suspension of microorganisms, or some part or product of them, that will induce immunity when it is administered to the host.
2. herd immunity: when most, but not all, of the population is immune
B. Types of Vaccines and their characteristics
1. Inactivated (killed) Organism Vaccines: injection of killed mo
a. killed by:
i. phenol
ii. formalin
b. examples:
i. influenza: inactivated influenza virus
ii. rabies: inactivated rabies virus
2. whole agent
3. attenuated (weakened) whole agent: mimic actual infection and usually provide better immunity.
a. injection of weakened strain of mo
b. disadvantage: organism can become virulent
c. examples:
i. measles (MMR) attenuated measles virus
ii. TB (BCG) Mycobacterium bovis
4. Subunit (Component)Vaccines: uses only those antigenic fragments of a mo that are best suited to stimulate an immune response.
a. injection of part of microorganism
b. advantages: safe
c. examples:
i. tetanus: toxoid of Clostridium tetani (toxoid: inactivated bacterial virus)
ii. HIB: polysaccharide of Haemophilus influenzae
iii. Hepatitis B: HBV surface antigen (HBsAg)
5. Carrier Vaccines: injection of harmless organism
a. containing/expressing gene from disease causing organism
6. DNA vaccines
a. injection of DNA from mo
b. new technology
7. Passive immunization
a. injection of antibodies
b. instant immunity
c. protection lasts 5-6 months
d. examples
i. antivenom (antivenin)
II Diagnostic Immunology
A. Essential diagnostic tests for determining immunity:
1. sensitivity: the probability that the test is reactive if the specimen is a true positive
2. specificity: the probability that a positive test will not be reactive if a specimen is a true negative
A. Monoclonal Antibodies and their uses
B. Precipitation Reactions: involve the reaction of soluble antigens with IgG or IgM antibodies to form large lattices.
1. Ag - IgM or IgG react to form a complex
2. Ag – Ab complex form lattices and precipitate from solution
3. Ag – Ab ratio is optimal
4. Antigens – soluble
5. Immunoprecipitation: antigens and antibodies precipitate in agarose
6. Remember these test from lab.
C. Agglutination Reactions: involve particulate antigens that can be linked together by antibodies.
1. Direct agglutination
a. cells to be identified are agglutinated by antibodies.
b. titer: concentration of antibody in a serum
2. Indirect (passive) agglutination
a. antibodies or antigens are attached to plastic beads
b. beads clump
c. easy to do
D. Neutralization Reactions
1. antitoxin
2. viral hemagglutination inhibition test
E. Complement-fixation reactions
F. Fluorescent-antibody techniques (immunofluorescence)
1. antibodies labeled with a fluorescent dye
2. can look for antigens or antibodies
3. dyes are combined with antibodies to make them fluoresce when exposed to ultraviolet light.
4. methods:
a. direct
b. indirect
G. Enzyme-Linked Immunosorbent Assay (ELISA)
1. antibodies are labeled with an enzyme in a micro titer plate
2. enzyme causes color change for positive result
3. flexible, sensitive
4. home tests: early pregnancy tests
5. methods:
a. direct: goal is to identify an unknown antigen such as a drug in a serum sample
b. indirect: object is to determine the presence of certain antibodies in the serum. (AIDS virus)
Chpt 17 Specific Defenses of the Host: Adaptive Immunity
Specific Defenses of the Host: Adaptive Immunity
Chapter 17
Functional divisions of immunity:
Nonspecific immunity
Specific immunity
Specific immunity usually functions when organisms get past nonspecific defenses. Involves recognition and memory. It is slower to respond and uses antibodies and lymphocytes. (Immunity: specific antibody and lymphocyte response to an antigen)
I The adaptive immune system: so called because it adapts to conditions
II Dual nature of the adaptive immune system
A. Humoral immunity: brought about by antibodies (antibody mediated immunity)
1. antibodies (Ab) *antibodies = B cells
a. Proteins made in response to an antigen.
b. involves antibodies made by B cells (made in the bone marrow)
2. Defends primarily against bacteria, bacterial toxins, and freely circulating viruses.
B. Cellular immunity (cell mediated immunity) *Cellular imm = t cells
1. T cells: involves T lymphocytes that act directly against foreign organisms.
a. T cell receptors
2. Activates other immune cells like macrophages
3. Effective against bacteria/viruses within host cells, also against eukaryotic infections.
III Antigens and Antibodies
A. The nature of Antigens (immunogens) Ag: A substance that causes the body to produce specific antibodies or sensitized T cells. (The nature of an antigen is a protein or carbohydrate. A foreign substance to which our bodies produce antibodies.)
1. Antigenic Determinants (epitopes)
a. antibodies recognize and react with specific antigenic determinates.
2. Haptens: low –molecular weight antigens that are not antigenic unless first attached to a carrier molecule.
a. Can bind with a protein or a carb.
b. inflammation starts when phagocytes start to attack it because it sees it as a foreign substance.
c. penicillin
B. The nature of Antibodies (Immunoglobulins Ig): Antibodies are proteins made in response to an antigen.
1. Globulins: proteins of a certain solubility characteristic
2. Antigen bonding sites: each antibody has at least two antigen bonding sites.
a. Binding of antibody to antigen does not destroy the antigen. Instead, the antibody tags foreign cells and molecules for destruction by phagocytes and complement.
b. Valence: the number of antigen bonding sites on the antibody
4. Antibody structure
a. light (L) chains
b. heavy (H) chains
c. variable (V) regions: the end of the Y shaped antibody. V region joins to the epitope.
d. antigen-binding sites
C. Immunogloblulin classes:
1. IgG
a. most abundant
b. crosses placenta to give immunity to the fetus
c. protect against circulating bacteria and viruses
d. neutralize bacterial toxins
e. trigger the complement system
f. bind to antigens to enhance action of phagocytic cells.
g. long lived: its presence may indicate immunity against a past disease.
2. IgM
a. first to appear in response to an antigen, but their concentration declines rapidly.
b. predominant antibody in the ABO blood group antigen reactions.
3. IgA
a. main function is preventing attachment of viruses and certain bacteria to mucosal surfaces.
4. IgD: unknown
5. IgE
a. releases histamine
IV B Cells and Humoral Immunity
A. B cells: A special group of lymphocytes which develop from stem cell precursors. (made and matured in bone marrow)
B. B cells and T cells have specific antigen receptors.
1. A mature B cell recognizes antigen receptors using IgM and IgD antibodies.
2. The intensity of a humoral response is reflected by the antibody titer. (the amount of antibody in the serum)
C. Clonal selection of antibody-producing cells involve T-dependent antigens. (an antigen that requires a Th cell for antibody production)
1. Out of 5 B cells only 1 recognizes the antigen and creates antibodies.
2. It gets divided into:
a. plasma cells: get turned into antibodies
b. memory cells
2. T-independent antigen
D. Diversity of antibodies
V Antigen-antibody binding and its results
A. Antigen-antibody complex
1. affinity
2. specificity
B. Antibody function
1. agglutination
a. hinder pathogenic activity
b. increase chances of phagocytosis
2. neutralization
a. binding and neutralizing toxins
b. block adherence to host cell
3. opsonization
a. stimulate phagocytosis
4. antibody-dependent cell mediated toxicity
5. activation of the complement system
a. non-specific chemical defense against pathogens
b. uses a series of blood serum proteins to destroy invading microbes.
c. Effects of complement activation: See chapter 16 for cascade
i. opsonization or immune adherence: enhanced phagocytosis
ii. membrane attack complex: cytolysis
iii. attract phagocytes.
VI T cells and cellular immunity (Cell mediated Immunity)
A. Intracellular antigens stimulate cell-mediated immunity
B. Specialized lymphocytes, mostly T cells, respond to intracellular antigens
C. T cells differentiate into effector T cells when stimulated by an antigen
D. Some effector T cells become memory cells
E. Classes of T cells
1. Helper T Cells (TH): CD4 adhesion molecule
a. TH1: activate cells related to cell-mediated immunity
b. TH2: activated B cells to produce eosinophils, IgM, and IgE
2. Cytotoxic T cells (TC): CD8 adhesion molecule, attack any cell which is altered
3. Delayed Hypersensitivity T cells (TD)
4. Suppressor T cells
a. turn off immune response when Ag no longer present
VII Antigen-presenting cells (APCs): antigens should be processed to be recognized by T cells.
VIII Extracellular killing by the immune system (did not go over)
IX Antibody-dependent cell mediated cytotoxicity (did not go over)
X Cytokines
A. Chemical messengers
B. Produced mainly by T helper cells
C. Induces the migration of leukocytes on to area of infection: chemotaxis
XI Immunological memory (did not go over)
XII Types of adaptive immunity: Active and Passive Immunity
A. Acquired Immunity
1. Naturally acquired
a. active: antigens enter the body naturally; body produces antibodies and specialized lymphocytes.
b. passive: antibodies pass from mother to fetus via placenta or to infant in the mother’s milk.
2. Artificially acquired
a. active: antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes.
b. passive: preformed antibodies in immune serum introduced in body by injection. (snake venom….when we need it fast)
Various notes:
Sushma likes the term antigenic determinants instead of the term epitopes. Make sure you remember that they mean the same thing.
All enzymes are proteins. If a mo is making an enzyme, we will produce an antibody.
Look at charts in textbook
TC cell = killer cell
Need a lot of T cells to trigger others
I may go blind trying to read the last slide that summarized everything. If I can enlarge it I will.
Study pages: 504-516
Cytokines 518
Immunological memory 519
Types of adaptive immunity 520 – 521
The extra credit III questions are below:
1. Define epitopes and give two characteristics about ideal anitgen. (****she said it should be a protein or a carb with a molecular weight higher than 10, 000)
2. Describe 5 different kinds of immunoglobulins. (so name and characteristics)
3. Name at least three different kinds of anitgen-antibody complexes.
4. What are two major types of T cells and explain the differences among them.
5. List four major differences between Humoral and Cellular immunity. (KNOW THIS QUESTION AS IT ACCOUNTS FOR 15% OF NEXT EXAM QUESTIONS.)
Chapter 17
Functional divisions of immunity:
Nonspecific immunity
Specific immunity
Specific immunity usually functions when organisms get past nonspecific defenses. Involves recognition and memory. It is slower to respond and uses antibodies and lymphocytes. (Immunity: specific antibody and lymphocyte response to an antigen)
I The adaptive immune system: so called because it adapts to conditions
II Dual nature of the adaptive immune system
A. Humoral immunity: brought about by antibodies (antibody mediated immunity)
1. antibodies (Ab) *antibodies = B cells
a. Proteins made in response to an antigen.
b. involves antibodies made by B cells (made in the bone marrow)
2. Defends primarily against bacteria, bacterial toxins, and freely circulating viruses.
B. Cellular immunity (cell mediated immunity) *Cellular imm = t cells
1. T cells: involves T lymphocytes that act directly against foreign organisms.
a. T cell receptors
2. Activates other immune cells like macrophages
3. Effective against bacteria/viruses within host cells, also against eukaryotic infections.
III Antigens and Antibodies
A. The nature of Antigens (immunogens) Ag: A substance that causes the body to produce specific antibodies or sensitized T cells. (The nature of an antigen is a protein or carbohydrate. A foreign substance to which our bodies produce antibodies.)
1. Antigenic Determinants (epitopes)
a. antibodies recognize and react with specific antigenic determinates.
2. Haptens: low –molecular weight antigens that are not antigenic unless first attached to a carrier molecule.
a. Can bind with a protein or a carb.
b. inflammation starts when phagocytes start to attack it because it sees it as a foreign substance.
c. penicillin
B. The nature of Antibodies (Immunoglobulins Ig): Antibodies are proteins made in response to an antigen.
1. Globulins: proteins of a certain solubility characteristic
2. Antigen bonding sites: each antibody has at least two antigen bonding sites.
a. Binding of antibody to antigen does not destroy the antigen. Instead, the antibody tags foreign cells and molecules for destruction by phagocytes and complement.
b. Valence: the number of antigen bonding sites on the antibody
4. Antibody structure
a. light (L) chains
b. heavy (H) chains
c. variable (V) regions: the end of the Y shaped antibody. V region joins to the epitope.
d. antigen-binding sites
C. Immunogloblulin classes:
1. IgG
a. most abundant
b. crosses placenta to give immunity to the fetus
c. protect against circulating bacteria and viruses
d. neutralize bacterial toxins
e. trigger the complement system
f. bind to antigens to enhance action of phagocytic cells.
g. long lived: its presence may indicate immunity against a past disease.
2. IgM
a. first to appear in response to an antigen, but their concentration declines rapidly.
b. predominant antibody in the ABO blood group antigen reactions.
3. IgA
a. main function is preventing attachment of viruses and certain bacteria to mucosal surfaces.
4. IgD: unknown
5. IgE
a. releases histamine
IV B Cells and Humoral Immunity
A. B cells: A special group of lymphocytes which develop from stem cell precursors. (made and matured in bone marrow)
B. B cells and T cells have specific antigen receptors.
1. A mature B cell recognizes antigen receptors using IgM and IgD antibodies.
2. The intensity of a humoral response is reflected by the antibody titer. (the amount of antibody in the serum)
C. Clonal selection of antibody-producing cells involve T-dependent antigens. (an antigen that requires a Th cell for antibody production)
1. Out of 5 B cells only 1 recognizes the antigen and creates antibodies.
2. It gets divided into:
a. plasma cells: get turned into antibodies
b. memory cells
2. T-independent antigen
D. Diversity of antibodies
V Antigen-antibody binding and its results
A. Antigen-antibody complex
1. affinity
2. specificity
B. Antibody function
1. agglutination
a. hinder pathogenic activity
b. increase chances of phagocytosis
2. neutralization
a. binding and neutralizing toxins
b. block adherence to host cell
3. opsonization
a. stimulate phagocytosis
4. antibody-dependent cell mediated toxicity
5. activation of the complement system
a. non-specific chemical defense against pathogens
b. uses a series of blood serum proteins to destroy invading microbes.
c. Effects of complement activation: See chapter 16 for cascade
i. opsonization or immune adherence: enhanced phagocytosis
ii. membrane attack complex: cytolysis
iii. attract phagocytes.
VI T cells and cellular immunity (Cell mediated Immunity)
A. Intracellular antigens stimulate cell-mediated immunity
B. Specialized lymphocytes, mostly T cells, respond to intracellular antigens
C. T cells differentiate into effector T cells when stimulated by an antigen
D. Some effector T cells become memory cells
E. Classes of T cells
1. Helper T Cells (TH): CD4 adhesion molecule
a. TH1: activate cells related to cell-mediated immunity
b. TH2: activated B cells to produce eosinophils, IgM, and IgE
2. Cytotoxic T cells (TC): CD8 adhesion molecule, attack any cell which is altered
3. Delayed Hypersensitivity T cells (TD)
4. Suppressor T cells
a. turn off immune response when Ag no longer present
VII Antigen-presenting cells (APCs): antigens should be processed to be recognized by T cells.
VIII Extracellular killing by the immune system (did not go over)
IX Antibody-dependent cell mediated cytotoxicity (did not go over)
X Cytokines
A. Chemical messengers
B. Produced mainly by T helper cells
C. Induces the migration of leukocytes on to area of infection: chemotaxis
XI Immunological memory (did not go over)
XII Types of adaptive immunity: Active and Passive Immunity
A. Acquired Immunity
1. Naturally acquired
a. active: antigens enter the body naturally; body produces antibodies and specialized lymphocytes.
b. passive: antibodies pass from mother to fetus via placenta or to infant in the mother’s milk.
2. Artificially acquired
a. active: antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes.
b. passive: preformed antibodies in immune serum introduced in body by injection. (snake venom….when we need it fast)
Various notes:
Sushma likes the term antigenic determinants instead of the term epitopes. Make sure you remember that they mean the same thing.
All enzymes are proteins. If a mo is making an enzyme, we will produce an antibody.
Look at charts in textbook
TC cell = killer cell
Need a lot of T cells to trigger others
I may go blind trying to read the last slide that summarized everything. If I can enlarge it I will.
Study pages: 504-516
Cytokines 518
Immunological memory 519
Types of adaptive immunity 520 – 521
The extra credit III questions are below:
1. Define epitopes and give two characteristics about ideal anitgen. (****she said it should be a protein or a carb with a molecular weight higher than 10, 000)
2. Describe 5 different kinds of immunoglobulins. (so name and characteristics)
3. Name at least three different kinds of anitgen-antibody complexes.
4. What are two major types of T cells and explain the differences among them.
5. List four major differences between Humoral and Cellular immunity. (KNOW THIS QUESTION AS IT ACCOUNTS FOR 15% OF NEXT EXAM QUESTIONS.)
Chpt 15 Innate Immunity, etc
Innate Immunity: Nonspecific Defenses of the Host
Nonspecific Immunity
Chapter 16
Functional divisions of immunity:
Nonspecific immunity
Specific immunity
Nonspecific immunity is our first line of defense. It stops most potential pathogens and prevents them from entering the body. It involves various barriers and mechanisms.
I Skin and Mucous Membranes
A. Mechanical factors
1. Skin
a. effective barrier
b. dry, low pH. (stops bacteria, but fungi like low pH)
c. has antimicrobial secretions
d. hard for bacteria to penetrate
e. skin layers
i. dermis
ii. epidermis: contains keratin
2. Mucous membranes: line the body cavities
a. barrier, protects underlying cells
b. traps organisms in mucous. (mucous also keeps the cavities from drying out)
c. offers less protection than skin
d. Eyes
i. lacrimal apparatus: manufactures and drains away tears.
e. Oral cavity:
i. saliva: produced by salivary glands washes microorganisms from the surfaces of the teeth and mucous membranes of the mouth. Prevents colonization.
f. Respiratory tract:
i. Cilia in the respiratory tract move trapped mo’s out
ii. epiglottis cover the larynx during swallowing
iii. Ciliary (mucociliary) elevator: move and propel mo’s trapped in mucous out of the respiratory system
iv. alveolar macrophages
v. coughing and sneezing
h. Digestive tract
1. defecation and vomiting
2. mucous lining
i. urination
1. urinary pH
2. production of urine
3. normal flora
B. Chemical factors
1. sebum: sebaceous oil glands in the skin which form a protective film over the skin surface
2. sweat glands: produce perspiration which flushes mo’s from the skin surface Sweat contains lysozyme which breaks down cell walls of gram + bacteria.
3. Eye: tears contain lysozyme
4. Oral Cavity:
a. saliva: contains lysozyme and salivary enzymes
5. Digestive tract:
a. stomach acid: (gastric juice) Low pH destroys most organisms.
i. Helicobacter can grow in the low pH of the stomach
b. enzymes
c. bile
d. normal flora
C. Normal microbiota (flora) and nonspecific resistance
1. Compete with disease causing organisms (competitive exclusion)
2. inhibit disease causing organisms
3.
II Phagocytosis: the ingestion of solids by eukaryotic cells
A. Formed elements in blood: cells and cell fragments.
1. Plasma: blood fluid
2. Leukocytes: white blood cells.
a. leukocytosis: an increase of white blood cells during infection
b. leucopenia: decreased white blood cells
3. Types of leukocytes:
a. neutrophils (nonspecific): a phagocyte
b. eosinophiles (nonspecific)
c. basophiles (nonspecific)
d. monocytes (become macrophages which are phagocytes)
e. lyphocytes (specific)
i. T cell
ii. B cell
iii. NK cell
B. Actions of phagocytic cells. (did not go over)
C. Mechanism of phagocytosis
1. Chemotaxis: the attraction of mo’s to chemicals
2. Adherence: (attachment) between the cell membrane of the phagocyte and the organism. Facilitated by chemotaxis.
3. Ingestion: the process of a phagocyte folding inward and forming a sac around a mo.
4. Digestion
D. Microbial evasion of phagocytosis (did not go over)
III Inflammation: a host response to tissue damage, characterized by redness, pain, heat, swelling, and perhaps loss of function. A major protective mechanism in response to injury or infection. Activated in multiple ways:
A. Vasodilation: The first stage of inflammation; involving an increase in blood vessel diameter thereby causing more blood flow to the injured area.
1. responsible for the redness, heat, edema and pain of inflammation
B. Permeability: (swelling/edema) allows defense substances in the blood to pass through the walls of the blood vessels.
1. histamine can increase permeability
C. Phagocyte migration and phagocytosis (did not call it that… called it) Leukocyte accumulation/chemotaxis
D. Tissue repair: the final stage of inflammation (connective tissue)
E. Fever
1. Temp can be altered by the ingestion of gram – bacteria by phagocytes.
2. protective mechanism
3. inhibits growth of bacteria and viruses
4. enhances immune response
F. Pus: The last step of inflammation. (according to Sushma) Sign that inflammation has ended.
IV Antimicrobial Substances
A. The complement system
1. Complement: consist of a group of over 20 different proteins found in blood serum. (30 proteins produced by the liver)
a. blood serum: the liquid portion of blood that remains after it is drawn and clotting proteins for a clot with the formed elements.
2. Complements participate in:
a. lysis of foreign cells
b. inflammation
c. phagocytosis
3. Can be activatied by:
a. classical pathway: initiated when antibody molecules bind to the antigen (ex: bacterial cell)
b. alternative pathway: (Does not involve antibodies) Complement proteins, and proteins called factors B, D and P, combine with certain microbial polysaccharides. Especially affected are the lopopolysaccharade cell wall portions (endotoxins) of gram – enteric bacteria.
c. lectin pathway: macrophage stimulate the liver to release lectins which enhance opsonization by binding to cell carbohydrates.
4. Complement proteins act in an ordered sequence, or cascade. (one protein activates another)
a. Designated by “C” numbered 1 through 9
b. Inactive state is denoted by “C”
c. Upon activation they split into Ca; Cb; etc
d. C3 plays a central role in both the classical and alternative pathways.
B. The Result of Complement Activation:
1. Cytolysis: complement protein then binds to 2 adjacent antibodies and initiates a sequence known as the membrane attack complex.
2. transmembrane channels (membrane pores): circular lesions that cause the eventual lysis of the cell to which the antibodies are attached.
3. Inflammation
4. opsonization (immune adherence) promotes attachment of a phagocyte to the microbe.
5. Attract pahgocytes
C. Interferons (IFNs): proteins produced in response to viruses.
1. inhibit viral replication inside cells
2. activates NK cells and macrophages
*********************************************************
Extra Stuff
Definitions:
Immunity: (resistance) Our ability to ward off disease through our defenses.
Susceptibility: Our vulnerability or lack of resistance to disease
Innate (nonspecific) immunity: defenses that tend to protect us from any kind of pathogen.
Adaptive (specific) immunity: is based on antibody production and is a defense against a particular organism.
Immunology: the study of a host’s defense to a pathogen.
Phagocytes: blood cells or derivatives of blood cells that ingest mo’s or a particulate matter.
Immunology is complicated because there are many different enemies out to get you.
3 steps of defense (what I wrote down from lecture, but isn’t inflammation and fever the same thing?)
1. inflammation
2. phagocytosis
3. fever
Ok, the lines of defense: (according to the study guide)
First: skin and mucous membranes
Second: phagocytosis
Signs of inflammation: Pa, He Reads Swell
Pain
Heat
Redness
Swelling
There is a slide from the second handout that discusses ways of preventing phagocytosis. It is not in my study guide:
Inhibit adherence capsules K. ?
Kill phagocytes S. aureus
Escape phagosome Shigella
Prevent phagosome-lysozome fusion HIV and ?
C3 and C5 are major in the complement system
Study pages:
474-484
486-488
Fever 489
Complement system 490-494
Nonspecific Immunity
Chapter 16
Functional divisions of immunity:
Nonspecific immunity
Specific immunity
Nonspecific immunity is our first line of defense. It stops most potential pathogens and prevents them from entering the body. It involves various barriers and mechanisms.
I Skin and Mucous Membranes
A. Mechanical factors
1. Skin
a. effective barrier
b. dry, low pH. (stops bacteria, but fungi like low pH)
c. has antimicrobial secretions
d. hard for bacteria to penetrate
e. skin layers
i. dermis
ii. epidermis: contains keratin
2. Mucous membranes: line the body cavities
a. barrier, protects underlying cells
b. traps organisms in mucous. (mucous also keeps the cavities from drying out)
c. offers less protection than skin
d. Eyes
i. lacrimal apparatus: manufactures and drains away tears.
e. Oral cavity:
i. saliva: produced by salivary glands washes microorganisms from the surfaces of the teeth and mucous membranes of the mouth. Prevents colonization.
f. Respiratory tract:
i. Cilia in the respiratory tract move trapped mo’s out
ii. epiglottis cover the larynx during swallowing
iii. Ciliary (mucociliary) elevator: move and propel mo’s trapped in mucous out of the respiratory system
iv. alveolar macrophages
v. coughing and sneezing
h. Digestive tract
1. defecation and vomiting
2. mucous lining
i. urination
1. urinary pH
2. production of urine
3. normal flora
B. Chemical factors
1. sebum: sebaceous oil glands in the skin which form a protective film over the skin surface
2. sweat glands: produce perspiration which flushes mo’s from the skin surface Sweat contains lysozyme which breaks down cell walls of gram + bacteria.
3. Eye: tears contain lysozyme
4. Oral Cavity:
a. saliva: contains lysozyme and salivary enzymes
5. Digestive tract:
a. stomach acid: (gastric juice) Low pH destroys most organisms.
i. Helicobacter can grow in the low pH of the stomach
b. enzymes
c. bile
d. normal flora
C. Normal microbiota (flora) and nonspecific resistance
1. Compete with disease causing organisms (competitive exclusion)
2. inhibit disease causing organisms
3.
II Phagocytosis: the ingestion of solids by eukaryotic cells
A. Formed elements in blood: cells and cell fragments.
1. Plasma: blood fluid
2. Leukocytes: white blood cells.
a. leukocytosis: an increase of white blood cells during infection
b. leucopenia: decreased white blood cells
3. Types of leukocytes:
a. neutrophils (nonspecific): a phagocyte
b. eosinophiles (nonspecific)
c. basophiles (nonspecific)
d. monocytes (become macrophages which are phagocytes)
e. lyphocytes (specific)
i. T cell
ii. B cell
iii. NK cell
B. Actions of phagocytic cells. (did not go over)
C. Mechanism of phagocytosis
1. Chemotaxis: the attraction of mo’s to chemicals
2. Adherence: (attachment) between the cell membrane of the phagocyte and the organism. Facilitated by chemotaxis.
3. Ingestion: the process of a phagocyte folding inward and forming a sac around a mo.
4. Digestion
D. Microbial evasion of phagocytosis (did not go over)
III Inflammation: a host response to tissue damage, characterized by redness, pain, heat, swelling, and perhaps loss of function. A major protective mechanism in response to injury or infection. Activated in multiple ways:
A. Vasodilation: The first stage of inflammation; involving an increase in blood vessel diameter thereby causing more blood flow to the injured area.
1. responsible for the redness, heat, edema and pain of inflammation
B. Permeability: (swelling/edema) allows defense substances in the blood to pass through the walls of the blood vessels.
1. histamine can increase permeability
C. Phagocyte migration and phagocytosis (did not call it that… called it) Leukocyte accumulation/chemotaxis
D. Tissue repair: the final stage of inflammation (connective tissue)
E. Fever
1. Temp can be altered by the ingestion of gram – bacteria by phagocytes.
2. protective mechanism
3. inhibits growth of bacteria and viruses
4. enhances immune response
F. Pus: The last step of inflammation. (according to Sushma) Sign that inflammation has ended.
IV Antimicrobial Substances
A. The complement system
1. Complement: consist of a group of over 20 different proteins found in blood serum. (30 proteins produced by the liver)
a. blood serum: the liquid portion of blood that remains after it is drawn and clotting proteins for a clot with the formed elements.
2. Complements participate in:
a. lysis of foreign cells
b. inflammation
c. phagocytosis
3. Can be activatied by:
a. classical pathway: initiated when antibody molecules bind to the antigen (ex: bacterial cell)
b. alternative pathway: (Does not involve antibodies) Complement proteins, and proteins called factors B, D and P, combine with certain microbial polysaccharides. Especially affected are the lopopolysaccharade cell wall portions (endotoxins) of gram – enteric bacteria.
c. lectin pathway: macrophage stimulate the liver to release lectins which enhance opsonization by binding to cell carbohydrates.
4. Complement proteins act in an ordered sequence, or cascade. (one protein activates another)
a. Designated by “C” numbered 1 through 9
b. Inactive state is denoted by “C”
c. Upon activation they split into Ca; Cb; etc
d. C3 plays a central role in both the classical and alternative pathways.
B. The Result of Complement Activation:
1. Cytolysis: complement protein then binds to 2 adjacent antibodies and initiates a sequence known as the membrane attack complex.
2. transmembrane channels (membrane pores): circular lesions that cause the eventual lysis of the cell to which the antibodies are attached.
3. Inflammation
4. opsonization (immune adherence) promotes attachment of a phagocyte to the microbe.
5. Attract pahgocytes
C. Interferons (IFNs): proteins produced in response to viruses.
1. inhibit viral replication inside cells
2. activates NK cells and macrophages
*********************************************************
Extra Stuff
Definitions:
Immunity: (resistance) Our ability to ward off disease through our defenses.
Susceptibility: Our vulnerability or lack of resistance to disease
Innate (nonspecific) immunity: defenses that tend to protect us from any kind of pathogen.
Adaptive (specific) immunity: is based on antibody production and is a defense against a particular organism.
Immunology: the study of a host’s defense to a pathogen.
Phagocytes: blood cells or derivatives of blood cells that ingest mo’s or a particulate matter.
Immunology is complicated because there are many different enemies out to get you.
3 steps of defense (what I wrote down from lecture, but isn’t inflammation and fever the same thing?)
1. inflammation
2. phagocytosis
3. fever
Ok, the lines of defense: (according to the study guide)
First: skin and mucous membranes
Second: phagocytosis
Signs of inflammation: Pa, He Reads Swell
Pain
Heat
Redness
Swelling
There is a slide from the second handout that discusses ways of preventing phagocytosis. It is not in my study guide:
Inhibit adherence capsules K. ?
Kill phagocytes S. aureus
Escape phagosome Shigella
Prevent phagosome-lysozome fusion HIV and ?
C3 and C5 are major in the complement system
Study pages:
474-484
486-488
Fever 489
Complement system 490-494
Chpt 15 Microbial Mechanisms of Pathogenicity
Microbial Mechanisms of Pathogenicity
Chapter 15
Pathogenicity: the ability to cause disease in a host.
Virulence: the degree of pathogenicity. A measure of pathogenicity.
I. Portal of entry: the avenue by which a microbe gains access to the body. (There is also a portal of exit, which like portal of entry is often a characteristic of a disease.)
A. Mucous membranes: unlike skin, mucous membranes are warm, moist, thin living cells.
1. respiratory tract: the easiest, most frequently used route of entry for infectious microorganisms. (Sushma said best portal is broken skin)
a. common cold
b. pneumonia
c. TB
d. influenza
e. measles
f. small pox
2. gastrointestinal tract: microorganisms enter by contact with food, water, or fingers
a. poliomyelitis
b. hepatitis A
c. typhoid fever
d. amoebic dysentery
e. shigellosis
f. cholera
3. genitourinary tract
a. HIV/AIDS
b. Chlamydia
c. syphilis
d. gonorrhea
4. conjunctiva (eyes)
B. Skin
1. sweat glands
2. cuts (broken skin is the best portal of entry * according to Sushma)
C. Parenteral route: microorganisms entering through skin or mucous membranes that are punctured or injured (traumatized).
D. Preferred portal of entry (did not go over)
E. Numbers of invading microbes (did not go over)
F. Adherence: attachment between pathogen and host by the use of surface adhesions.
1. Suckers and hooks (helminthes)
2. Ligands: proteins on surface of bacteria and viruses found on fimbraie, flagella and glycocalyces.
a. adhesions: proteins on surface of bacteria
b. attachment proteins: proteins on surfaces of viruses.
3. Surface receptors: complementary receptors on host cells to which ligands attach.
II How bacterial pathogens penetrate host defenses.
A. Capsules: resist phagocytosis
1. Streptococcus pneumoniae
2. Haemophilus influenzae
B. Cell wall components: waxes in cell walls resist digestion by macrophages.
1. Mycobacterium tuberculosis
C. Enzymes
1. Extracellular enzymes: dissolve structural components/chemicals
a. Hyaluronidase and collagenase allow bacteria to invade deeper tissues
b. Coagulase: coagulates blood clot proteins, “hiding” the bacteria protecting it from phagocytosis. (produced by S. aureus)
c. Kinase: dissolves clots, releases bacteria from clots. A modified version can be used to dissolve blood clots.
i. Streptokinase
ii. Staphylokinase
D. Antigenic variation (did not go over)
E. Penetration into host cell cytoskeleton
1. Adhesins: microbes attach to host cells by adhesions.
III How bacterial pathogens damage host cells
A. Siderophores (did not go over)
B. Toxins: poisonous substance produced by certain microorganisms. Chemicals that harm tissue or elicit host immune response, damaging tissue.
1. Definitions:
a. Toxigenicity: the capacity to produce toxins.
b. Toxemia: the presence of toxins in the blood and lymph. Toxins enter the bloodstream and are carried to other parts of the body.
2. Types:
a. Exotoxins: proteins secreted by the bacterium, mostly gram +, into the surrounding medium or released following lysis. Destroy host cells or interfere with host cell metabolism by secreting toxin from cell.
i. highly specific
ii. among the most lethal substances known
iii. antitoxins: antibodies (produced by the body) that provide immunity to exotoxins.
iv. both gram + and gram – but mostly gram +
v. types of exotoxins
a. cytotoxins: attack any type of cell
b. neurotoxins: attack nerves. Cause paralysis, stiff muscles. (Clostridium gram +)
c. enterotoxins:attack the stomach (E coli gram -)
vi. hemolysins: toxins that target red blood cells. Streptococci
vii. representative extoxins (did not go over): named for the tissues they affect, such as neurotoxins, cardiotoxins, etc.
b. Endotoxins: not secreted by bacteria, but are part of the outer portion of the cell wall of gram – bacteria.
i. gram – cell wall
ii. have lipopolysaccharide layer on outer membrane (LPS)
iii. lipid A: the lipid part of LPS
a. released upon bacterial cell death often causing fever and inflammation. Also can be released during bacterial multiplication.
iv. at high levels can cause hemorrhaging and septic shock
v. released only after bacteria have died. (therefore to give antibiotics is wrong in this case because the dead bacteria would release all of the endotoxins. Hydrate patient.)
C. Anti-phagocytic factors: (whenever you see this term you should remember macrophages)
1. macrophages: white blood cells that engulf and remove invading pathogens.
a. capsules
i. made up of chemicals normally found in a host
ii. slippery glycocalyx blocks phagocytosis
b. antiphgocytic chemicals: chemicals that prevent the fusionof lysosomes with phagocytic vesicles.
i. M protein: protein produced on its cell wall by Streptococcus pyogenes
ii. Leudocidins: kill white blood cells
iii. Mycolic acid: lysozomes cannot enter. Mycobacterium
IV Plasmids, Lysogeny, and Pathogenicity (did not go over)
V Pathogenic properties of nonbacterial microorganisms (did not go over)
A. Viruses
1. Cytopathic effects of viruses:
B. Fungi
C. Protozoa
D. Helminths
E. Algae
Extra
This outline follows the book format which is different from Sushma’s format. All of the information that Sushma discussed is included on this outline, just in a way that is easier for me to understand. I hope it helps. :0)
Virulence: a measure of pathogenicity (the ability of an organism to cause disease)
Viurlence factors: (besides adhesions these can be classified into three categories)
I Adhesins
II Extracellular enzymes
II IToxins
IV Anti-phagocytic factors
Possible questions:
Which produces an endotoxin? Gram – (neg)
Need to know which bacteria are gram – for above question.
See table 15.3 page 464
Denatured proteins can renature when cooled causing food poisoning.
Protein in endotoxins are lipids
Damage to host cells occur in the Log phase.
Chapter 15
Pathogenicity: the ability to cause disease in a host.
Virulence: the degree of pathogenicity. A measure of pathogenicity.
I. Portal of entry: the avenue by which a microbe gains access to the body. (There is also a portal of exit, which like portal of entry is often a characteristic of a disease.)
A. Mucous membranes: unlike skin, mucous membranes are warm, moist, thin living cells.
1. respiratory tract: the easiest, most frequently used route of entry for infectious microorganisms. (Sushma said best portal is broken skin)
a. common cold
b. pneumonia
c. TB
d. influenza
e. measles
f. small pox
2. gastrointestinal tract: microorganisms enter by contact with food, water, or fingers
a. poliomyelitis
b. hepatitis A
c. typhoid fever
d. amoebic dysentery
e. shigellosis
f. cholera
3. genitourinary tract
a. HIV/AIDS
b. Chlamydia
c. syphilis
d. gonorrhea
4. conjunctiva (eyes)
B. Skin
1. sweat glands
2. cuts (broken skin is the best portal of entry * according to Sushma)
C. Parenteral route: microorganisms entering through skin or mucous membranes that are punctured or injured (traumatized).
D. Preferred portal of entry (did not go over)
E. Numbers of invading microbes (did not go over)
F. Adherence: attachment between pathogen and host by the use of surface adhesions.
1. Suckers and hooks (helminthes)
2. Ligands: proteins on surface of bacteria and viruses found on fimbraie, flagella and glycocalyces.
a. adhesions: proteins on surface of bacteria
b. attachment proteins: proteins on surfaces of viruses.
3. Surface receptors: complementary receptors on host cells to which ligands attach.
II How bacterial pathogens penetrate host defenses.
A. Capsules: resist phagocytosis
1. Streptococcus pneumoniae
2. Haemophilus influenzae
B. Cell wall components: waxes in cell walls resist digestion by macrophages.
1. Mycobacterium tuberculosis
C. Enzymes
1. Extracellular enzymes: dissolve structural components/chemicals
a. Hyaluronidase and collagenase allow bacteria to invade deeper tissues
b. Coagulase: coagulates blood clot proteins, “hiding” the bacteria protecting it from phagocytosis. (produced by S. aureus)
c. Kinase: dissolves clots, releases bacteria from clots. A modified version can be used to dissolve blood clots.
i. Streptokinase
ii. Staphylokinase
D. Antigenic variation (did not go over)
E. Penetration into host cell cytoskeleton
1. Adhesins: microbes attach to host cells by adhesions.
III How bacterial pathogens damage host cells
A. Siderophores (did not go over)
B. Toxins: poisonous substance produced by certain microorganisms. Chemicals that harm tissue or elicit host immune response, damaging tissue.
1. Definitions:
a. Toxigenicity: the capacity to produce toxins.
b. Toxemia: the presence of toxins in the blood and lymph. Toxins enter the bloodstream and are carried to other parts of the body.
2. Types:
a. Exotoxins: proteins secreted by the bacterium, mostly gram +, into the surrounding medium or released following lysis. Destroy host cells or interfere with host cell metabolism by secreting toxin from cell.
i. highly specific
ii. among the most lethal substances known
iii. antitoxins: antibodies (produced by the body) that provide immunity to exotoxins.
iv. both gram + and gram – but mostly gram +
v. types of exotoxins
a. cytotoxins: attack any type of cell
b. neurotoxins: attack nerves. Cause paralysis, stiff muscles. (Clostridium gram +)
c. enterotoxins:attack the stomach (E coli gram -)
vi. hemolysins: toxins that target red blood cells. Streptococci
vii. representative extoxins (did not go over): named for the tissues they affect, such as neurotoxins, cardiotoxins, etc.
b. Endotoxins: not secreted by bacteria, but are part of the outer portion of the cell wall of gram – bacteria.
i. gram – cell wall
ii. have lipopolysaccharide layer on outer membrane (LPS)
iii. lipid A: the lipid part of LPS
a. released upon bacterial cell death often causing fever and inflammation. Also can be released during bacterial multiplication.
iv. at high levels can cause hemorrhaging and septic shock
v. released only after bacteria have died. (therefore to give antibiotics is wrong in this case because the dead bacteria would release all of the endotoxins. Hydrate patient.)
C. Anti-phagocytic factors: (whenever you see this term you should remember macrophages)
1. macrophages: white blood cells that engulf and remove invading pathogens.
a. capsules
i. made up of chemicals normally found in a host
ii. slippery glycocalyx blocks phagocytosis
b. antiphgocytic chemicals: chemicals that prevent the fusionof lysosomes with phagocytic vesicles.
i. M protein: protein produced on its cell wall by Streptococcus pyogenes
ii. Leudocidins: kill white blood cells
iii. Mycolic acid: lysozomes cannot enter. Mycobacterium
IV Plasmids, Lysogeny, and Pathogenicity (did not go over)
V Pathogenic properties of nonbacterial microorganisms (did not go over)
A. Viruses
1. Cytopathic effects of viruses:
B. Fungi
C. Protozoa
D. Helminths
E. Algae
Extra
This outline follows the book format which is different from Sushma’s format. All of the information that Sushma discussed is included on this outline, just in a way that is easier for me to understand. I hope it helps. :0)
Virulence: a measure of pathogenicity (the ability of an organism to cause disease)
Viurlence factors: (besides adhesions these can be classified into three categories)
I Adhesins
II Extracellular enzymes
II IToxins
IV Anti-phagocytic factors
Possible questions:
Which produces an endotoxin? Gram – (neg)
Need to know which bacteria are gram – for above question.
See table 15.3 page 464
Denatured proteins can renature when cooled causing food poisoning.
Protein in endotoxins are lipids
Damage to host cells occur in the Log phase.
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