Microbiology Lecture Test 4 – Flashcards
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Unlock answers| - The study of disease |
| Pathology |
| - The study of the cause of a disease |
| Etiology |
| - The development of disease |
| Pathogenesis |
| - Colonization of the body by pathogens |
| Infection |
| - An abnormal state in which the body is not functioning normally |
| Disease |
| How long may Transient Microbiata be present for? |
| Days, weeks, or months |
| How long may Normal Microbiata be present for? |
| Normal microbiota permanently colonize the host. |
| - The relationship between normal microbiota and the host |
| Symbiosis |
| - Form of symbiosis when one organism is benefited and the other is unafected |
| Commensalism |
| - Form of symbiosis when both organisms benefit |
| Mutualism |
| - Form of symbiosis when one organism is benefited at the expense of the other |
| Parasitism |
| - Microorganism that does not ordinarily cause a disease but can become pathogenic under certain circumstances |
| Opportunistic Pathogen (ex. E. coli) |
| Location of normal microbiota on and in the human body: |
All surfaces colonized besides blood stream and tissue.
|
| - Competition between microbes |
| Microbial antagonism |
| Normal microbiata protect the host by: |
Occupying niches that pathogens might occupy Producing acids Producing bacterions (chemicals that kill of competition) |
| - Live microbes applied to or ingested into the body, intended to exert a beneficial effect |
| Probiotics |
| A common source of probiotics: |
| Yogurt |
| - They are used to prove the cause of an infectious disease |
| Koch's Postulates |
| Koch's Postulates (4): |
1. Suspect microbe always found in diseased individual never in healthy one (exceptions - carriers of yeast infections) 2. Be able to culture microbe on artificial medium in lab (not always possible) 3. Pure cultures of microbe must be able to cause the disease in test animals 3. Reisolate same microbe from experimentally infected animal |
- A disease that is spread from one host to another - Example? |
Communicable disease Ex. HIV |
- A disease that is easily spread from one host to another - Example? |
Contagious disease Ex. Flu |
- A disease that is not transmitted from one host to another - Example? |
Noncommunicable disease Ex. Skin cancer |
| - A type of occurence of disease which the disease is constantly present in a population |
| Endemic Disease |
| - A type of occurence of disease which the disease is acquired by many hosts in a given area in a short time |
| Epidemic disease |
| - A type of occurence of disease which the disease is a worldwide epidemic |
| Pandemic disease |
| - A type of occurence of disease which there is immunity in most of population |
| Herd immunity |
- A type of severity or duration of a disease in which the SYMPTOMS DEVELOP RAPIDLY (DISEASE ENDS SOON) -Example? |
Acute Disease Ex. Flu |
- A type of severity or duration of a disease in which the DISEASE DEVELOPS SLOWLY (DISEASE LAST A LONG TIME) -Example? |
Chornic disease Ex. Arthritis |
- A type of severity or duration of a disease in which the DISEASE HAS A PERIOD OF NO SYMPTOMS WHEN THE PATIENT IS INACTIVE - Example? |
Latent disease Ex. Herpes |
| - An extend of host involvement in which PATHOGENS ARE LIMITED TO A SMALL AREA OF THE BODY |
| Local infection |
| - An extent of host involvement in which AN INFECTION IS THROUGHT THE BODY |
| Systemic infection |
| - An extent of host involvement that was a SYSTEMIC INFECTION THAT BEGAIN AS A LOCAL INFECTION |
| Focal infection |
| - Bacteria in the blood |
| Bacteremia |
| - Growth of bacteria in the blood |
| Septicemia |
| - Toxins in the blood |
| Toxemia |
| - Viruses in the blood |
| Viremia |
| - Acute infection that causes the initial illness |
| Primary infection |
- Opportunisic infection after a primary (predisposing) infection -Example? |
Secondary infection Ex. Bacterial pnemonia |
- A disease with no noticeable signs or symptoms (inapparent infection, asymptomatic) - Example? |
Subclinical disease Ex. Typhloid Mary |
| - Continual sources of infection |
| Reservoirs of infection |
| What are human reservoirs of infection for: |
| AIDS, gonorhea |
| What are animals reservoirs of infection for: |
| Rabies, Lyme disease |
| What are nonliving substances resevoirs of infection for: |
| Botulism, tetanus |
| When humans are resevoirs of infection, the carriers may have __________________. |
| Inapparent infections or latent diseases |
| When animals are reservoirs of infection, some zoonoses may be ________________. |
| Transmitted to humans |
| What is an example of a nonliving reservoir of infection? |
| Soil - spores cause it |
| - A type of transmission of disease through contact that requires close association between infected and susceptible host |
| Direct contact |
| - A type of transmission of disease through contact that spreads by fomites (inanimate objects (doorknobs, telephones, keyboards)) |
| Indirect contact |
| - A type of transmission of disease through contact that transmission is via airborne droplets (sneezing, coughing, breathing) |
| Droplet contact |
| - A type of transmission of disease occurs by an inanimate reservoir (food, water) |
| Vehicle |
| - A type of transmission of disease that occurs by arthropods, especially fleas, ticks, and mosquitoes |
| Vectors |
| - A type of transmission of disease that occurs when arthropod carried pathogen on feet |
| Mechanical |
- A type of transmission of disease that occurs when pathogen reproduces in vector (When someone who is sick flies acrossed America and spreads the disease) |
| Biological |
| - Hospital-acquired infections |
| Nosocomial infections |
| What percent of all hospital patients acquire nosocomial infections? |
| 5-15% |
| Percent of Nosocomial Infections that are Gram (+) cocci: |
| 51% |
| Percent of Nosocomial Infections that are Gram (-) rods: |
| 30% |
| Percent of Nosocomial Infections that are Clostridium difficile: |
| 13% |
| Percent of Nosocomial Infections that are Fungi: |
| 6% |
| Percentage of Gram (+) cocci Nosocomial Infections that are Resistant to Antibiotics: |
| 29-89% |
| Percentage of Gram (-) rod Nosocomial Infections that are Resistant to Antibiotics: |
| 3-32% |
| - The ability to cause disease |
| Pathogenicity |
| - The extent of pathogenicity |
| Virulence |
| - Ability to overcome host resistance |
| Infectivity |
| High infectivity + High toxicity = |
| A very dangerous pathogen |
| 3 Portals of Entry: |
Mucous membranes Skin Parenteral route |
| 4 Examples of the Portal of Entry - Mucous Membrane: |
Respiratory tract GI tract Genitourinary tract Conjunctiva |
| 3 Examples of the Portal of Entry - Skin: |
Most often thru broken skin Sometimes hair follicles Sweat ducts |
| 5 Examples of the Portal of Entry - Parenteral Route: |
Injections Bites Surgery Cuts Dry skin splitting |
| - A type of portal of entry that gets infected thru skin to underlying tissues |
| Parenteral Route |
| 2 Virulence Factors: |
Adherence Enzymes |
| __________ bind to receptors on host cells. |
| Adhesins/ligands |
| - Attempted colonization |
| Favor establishment |
| 2 types of Adhesins/Ligands: |
Glycocalyx: Streptococcus mutans
|
| What do enzymes do to influence virulence: |
| Promote pathogen survival, spreading, host injury |
| 7 Examples of Enzymes that influence Virulence: |
Coagulase: Coagulate blood Kinases: Digest fibrin clots Hyaluronidase: Hydrolyses hyaluronic acid Collagenase: Hydrolyzes collagen IgA proteases: Destry IgA antibodies Siderophores: Take iron from host iron-binding proteins Antigenic variation: Alter surface proteins |
| - Substances that contribute to pathogenicity |
| Toxin |
| - Ability to produce a toxin |
| Toxigenicity |
| - Presence of toxin in the host's blood |
| Toxemia |
- Inactivated toxin used in a vaccine Ex. Tetanus vaccine |
| Toxoid |
| - Antibodies against a specific toxin |
| Antitoxin |
Is this a ENDOTOXINS or EXOTOXINS: Source: Gram (-) Relation to microbe: Present in LPS of outer membrane Chemistry: Lipid Fever?: Yes Neutralized by antitoxin?: No LD50: Relatively large |
| Endotoxin |
Is this ENDOTOXINS or EXOTOXIN: Source: Mostly Gram (+) Relation to microbe: By-products of growing cell Chemistry: Protein Fever?: No Neutralized by antitoxin?: Yes LD50: Small |
| Exotoxin |
| - Membrane-disrupting toxin |
| Exotoxin |
| 2 Ways Exotoxins Lyse Host's cells: |
Making protein channels in the plasma membrane Disrupting phospholipid bilayer |
| - Exotoxins that act on GI tract |
| Enterotoxins |
| What is the purpose of diarrhea? |
| The pathogen wants to spread. |
| - These cause an intesne immune response due to release of cytokines from host cells |
| Superantigens |
| 6 Examples of Superantigens' immune response: |
Fever Nausea Vomiting Diarrhea Shock Death |
| 2 Examples of Superantigens: |
S. aureus Steptococcus pyogenes |
| 5 Portals of Exit: |
Respiratory tract Gastrointestinal tract Genitourinary tract Skin - lesions Blood |
| 2 Examples of the Portal of Exit - Respiratory Tract: |
Coughing Sneezing |
| 2 Examples of the Portal of Exit -Gastrointestinal tract: |
Feces Saliva |
| 2 Examples of the Portal of Exit - Genitourinary tract: |
Urine Vaginal secretions |
| 1 Examples of the Portal of Exit -Skin: |
| Lesions |
| 3 Examples of the Portal of Exit - Blood: |
Biting arthropods Needles Syringes |
| - Lack of resistance to disease |
| Susceptibility |
| - Ability to ward off disease |
| Immunity |
| - Defense against only pathogens |
| Innate immunity |
| - Immunity, resistance to a specific pathogen |
| Adaptive (acquired) immunity |
| 3 First line of defense for Innate (Nonspecific) Immunity: |
Intact skin Mucous membrane and their secretions Normal microbiota |
| 4 Second line of defense for Innate (Nonspecific) Immunity: |
Natural killer cells and phagocytic white blood cells Inflammation Fever Antimicrobial substances |
| 7 Physical Factors in the First line defense: |
Skin - keratin is a protective protein Mucous membranes Ciliary escalatory: microbes trapped in mucus are transported away from the lungs Lacrimal apparatus: Washes eye Saliva: Washes microbes off Urine: Flows out Vaginal secretions: Flows out |
| 6 Chemical Factors on the First Line Defense: |
Fungistatic fatty acid in sebum Low pH (3-5) of skin Lysozyme in perspiration, tears, saliva, and tissue fluids Low pH (1.2-3.0) of gastric juice Transferrins in blood find iron NO (Nitric oxide) inhibits ATP production |
| - Normal microbiota complete with pathogens |
| Microbial antagonism/competitive exclusion |
| 6 White Blood Cells on Second Line Defense: |
Neutrophils: Phagocytic Basophils: Produce histamine Eosinophils: Toxic to parasites and some phagocytic Dendritic cells: Initiate adaptive immune response Monocytes: Phagocytic as mature macrophages Lymphocytes: Involved in specific immunity |
| - From Greek, meaning eat |
| Phago |
| - From Greek, meaning cell |
| Cyte |
| - Ingestion of microbes or particles by a cell, performed by phagocytes |
| Phagocytosis |
| 8 Components of Inflammation in the Second Line Defense: |
Redness (erythema) Pain Heat Swelling (edema) Acute-phase proteins activated (complement, cytokine, and kinins) Vasodilation (histamine, kinins, prostaglandins, and leukotrienes) Margination and emigration of WBCs Tissue repair |
| 4 Chemicals Released by Damaged Cells: |
Histamine Kinins Prostaglandins Leukotrienes |
| 5 Components of Fever (Abnormally High Body Temperature) Second Line Defense: |
Hypothalamus normally set at 37 degrees Celsius. Gram (-) endotoxin cause phagocytes to release interleukin-1 (IL-1). Hypothalamus releases prostaglandins that reset the hypothalaus to a high temperature Body increases rate of metabolism and shivering which raise temperature When IL-1 is eliminated, body temperature falls (crisis) |
| What happens in the Complement System? |
| Serum proteins activate in a cascade. |
| What is the function of The Complement System? |
| To poke holes through cell membrane |
| Three pathways to activate complements: |
Classical Alternative Lectin |
| 2 things involved in Innate Immunity: |
Transferrins Antimicrobial peptides |
| Innate Immunity is a _____ line defense. |
| 2nd |
| Why are Transferrins not effective against Borrelia (Lyme's disease)? |
| Because Borrellia uses mangenese instead of iron |
| Transferrins binds _________. |
| Seramions |
| Antimicrobial peptides lyse ___________. |
| Bacterial cells |
| - Specific antibody and lymphocyte response to antigen |
| Adaptive (acquired) immunity |
| - A substance that causes the body to produce specific antibodies or sensitized T cells |
| Antigen (An) |
| - Proteins made in response to an An; can combine with that An. |
| Antibody (Ab) |
| - Serum proteins that bind to Ab in an An-Ab reaction; cause cell lysis |
| Complement |
| What is meant by Adaptive Immunity being acquired? |
| It develops during an individual's lifetime. |
| Adaptive immunity offers which type of protection? |
| Long term |
| Adaptive immunity is mediated by complex interaction of which 3 things? |
Antibodies Lymphocytes Macrophages |
| 4 Advantages of Abnormally High Body Temperature: |
Increase transferrins Increase IL-1 activity Overall enhancement of immune function Inhibits some pathogens |
| 3 Disadvantages of Abnormally High Body Temperature: |
Tachycardia (Rapid heart beat) Acidosis Dehydration |
| - Defense against only pathogens |
| Innate immunity |
| _________ immunity involves antibodies produced by B cells. |
| Humoral |
| How do B cells recognize antigens? |
| By antibodies on their surfaces |
| What does Cell-mediated immunity involve? |
| T cells |
| How do T cells recognize antigens? |
| By TCRs (T-cell antigen receptor) on their surfaces |
| - The study of reactions etween antibodies and antigens |
| Serology |
| - The generic term for serum because it contains Ab |
| Antiserum |
| - Serum proteins |
| Globulins |
| - Antibodies |
| Immunoglobulins |
| - Serum fraction containing Ab |
| Gamma globulin |
| - Foreign substance that elicits immune response |
| Antigen (An) |
____________ and __________ are most antigenic. __________ and __________ are less antigenic |
Proteins and polysacchrides Lips and nucleic acid |
| What is the molecular weight of antigens required for immungenicity (antigenicity)? |
| 1,000 |
| - Specficity on antigen (antigenic determinants) |
| Epitopes |
| - A small compound not antigenic by itself but when coupled to larger molecule becomes antigenic |
| Hapten |
| 2 Example of Antigens Combinations: |
Penicillin + Serum proteins = Antigen Poison Ivy - Urusiol oil = Hapten; + Tissue proteins = Antigen |
| -Antibodies that are secreted by different B cell lineages within the body |
| Polyclona |
IgG- Structure: Location: Complement Fixation (Y/N): Placental Transfer (Y/N):
|
Structure: Monomer Location: Majority of serum antibodies Complement Fixation: Yes, Fix complement Placental Transfer: Yes, cross placenta |
IgM - Structure: Complement Fixation (Y/N): Known Function: |
Structure: Pentamer Complement Fixation: Yes, Fix complement Known Functions: Aggultinates microbes; first Ab produced in response to infection |
IgA- Structure: Location: Known Function: |
Structure: Dimers Location: In secretions Known Function: Mucosal protection |
IgD- Structure: Location: Known Function: |
Structure: Monomer Location: In blood, lymph, and on B cells Known Function: On B cells, initiate immune response |
IgE- Structure: Locations (3): Known Functions (2): |
Structure: Monomer Location: On mast cells, basophils, and in blood Known Functions: Allergic reactions; lysis of parasitic worms |
| - Antibodies bind to toxins before they exert toxic effect; bind to viruses preventing attachment |
| Neutralization |
| - Antibodies (Abs) specific toxins |
| Antitoxin |
| - Specific to snake venom, spider venom, etc. - can use only once |
| Antivenin (Antivenom) |
| Why can we use antivenin only once? |
| The injection is from another animal, which is foreign to humans. Next time you are injected with that antivenon, your body will have made antibodies to reject the foreign substance. |
| - Bacteria and other foreign particles clumped together for more efficient phagocytosis; clumping of bacteria retards their spread |
| Agglutination |
| - Small soluble proteins ppt, more easily phagocytized |
| Precipitation |
| - Coating of antigen with Abs enchances phagocytosis |
| Opsonization |
| - Binding of IgG, IgM to foreign cell activates complement cascade |
| Complement fixation |
| - Complex series of reactions causing soluble serum proteins to sequentially bind to antigen-antibody complexes on target cells |
| Complement cascade |
| Complement proteins form hollow tubes in target cell membranes by _________. |
| Cell lysis |
| Why are antibodies moer effective against gram (-) and less effective against gram (+)? |
| Because it pokes through the membrane and gram (+) have a thick cell wall making it harder to get in. |
| 7 Mechanisms of Ab Action: |
Neutralization Antitoxin ; Antivenin Agglutination Precipitation Opsonization Complement fixation Complement cascade |
| For every potential antigen there exists a _______ that can prouce an ______ specific to it. |
| B cell, Antibody |
| During embryonic development, regions of ___ genes combine with __ genes to produce ;1015 different antibodies. |
| V, C |
- Exposure to antigen stimulates B cell proliferation and differentiation into plasma cells + memory cells - Plasma cells produce ABs in quantity - Memory cells produce Abs next time antigen present |
| Clonal Selection |
| - A form of activation of B cells when antigen alone stimulates B cell proliferation |
| T-independent antigen |
| - A form of activation of B cells when most of the time anitgen presenting cell (APC) is required |
| T-dependent antigen |
| 3 Antigen fragments on Antigen-Presenting Cells with Major Histo Compacitibility Complex: |
B cells (specific) Dendritic cells (general) Macrophages (general) |
| - Macrophages stimulated by ingesting Antigens or by cytokines (interleukins) |
| Activated macrophages |
How long does it take humoral immunity to work: 1° (primary) respsone 2° (secondary) response |
1° (primary) respsone - typically 7-10 days, IgMs first then IgG 2° (secondary) response - typically 1-3 days, mostly IgG from memory cells
|
| What is meant by self-tolerance when talking about antibodies? |
| The body doesn't make antibodies against self. |
| - The process of destroying B and T cells that react to self antigens |
| Colonal deletion |
| - Strength of the bond between Ab and An |
| Affinity |
| - Ab recognizes a specific epitope |
| Specficity |
| What does the Helper T Cells TH1 do: |
| Activate cells related to cell-mediated immunity |
| What do the Helper T Cells TH2 cells do: |
| Activate B cells to produce eosinophils, IgM, and IgE |
| Where to Cyotoxic T Cells (CD8, Tc) activate? |
| In cytotoic T lymphocytes |
| Cytotoxic T Cells induce ______________. |
| Induce Apoptosis in target cell |
Regulatory T Cells (TR): Supress __________________ Shuts down _______________ Maintain __________________ |
Supress other T cells Shuts down T-cell mediated immune response Maintain immunological tolerance--supres autoreactive T-cells |
| What does the extracellular Natural killer kill? |
Cells which don't express MHC 1. Ex. Fluke |
| -Antibody production after exposure to antigen |
| Active Immunity |
| Is active immunity short or long term protection? |
| Long term protection |
| 2 Examples of Active immunity: |
Natural- Infection Artificial- Vaccine/Toxoid |
| - Form of immunity when it receives foreign antibodies |
| Passive Immunity |
| Is passive immunity long or short term protection? |
| Short term protection |
| 2 Example of Passive Immunity: |
Natural - mother to fetus across placenta; colostrum Artificial - antibodies produced in another animals (ex. horse), purified |
| - Blood serum containing specific antibodies |
| Antiserum |
- Over-reaction of immune system resulting in host tissue damage or death Examples (3)? |
Hypersensitivity Ex. Allergies, Transplant rejection, Autoimmunity |
| How many types of Hypersensitivity reactions are there? |
| 4 (or 5) types |
| A type of hypersensitivity reaction that is immediate and results from IgE binding to mast cells and basophils, mast cells especially contain granules of histamines |
| Type 1 (Anaphylactic) Reactions |
| When histamines are released what happens (4)? |
Itching Edema (increased capillary permeability) Vascular dilation (erythema) Smooth muscle contraction (Ex. bronchial constriction -- not asthma) |
| What is asthma mediated by? |
| By leukotrienes and prostaglandins (synthesized by activated mast cells) |
| What does location of symptoms in Type 1 (Anaphylatic) Reactions? |
| Location of symptoms depends on location of mast cells. |
| In a Type 1 (Anaphylactic) Reaction, if the mast cells are located in the respiratory tract you will have what allergy? |
| Hay fever (Itchy and watery eyes, noses, increased mucous secretion) |
| In a Type 1 (Anaphylactic) Reaction, if the mast cells are located in the intestinal tract you will have what allergy? |
| Food allergy symptoms often not manifest in GI tract (ex. hives, systemic anaphylaxis) |
| In a Type 1 (Anaphylactic) Reaction, if the mast cells are located in the skin you will have what allergy? |
| Local inflammation (ex. dermatitis) |
| What happens in Type 1 Reactions after exposure to antigen? |
Exposure to Anitgen Triggering peripheral blood vessel dilation throughout entire body Lower blood pressure Shock |
| What happens in Type I Reactions when massive histamine and other mediator (leukotrienes, prostoglandins) release? |
Edema Respiratory constriction Death |
| What is required for treatment of Type I Reactions? |
| Immediate treatment with adrenalin (apinephrine) |
| What happens during the 1st and 2nd exposure to allergen? |
1st exposure to allergen = SENSITIZING DOSE, NO ALLERGINIC RESPONSE 2nd exposure = SHOCKING DOSE, SIGNIFICANT MASSIVE ALLERGIC RESPONSE |
| - Process of exposing allergic host to controlled doses of allergen(s) |
| Desensitization |
| What is the process of Allergy Desensitization? (4) |
Induce formation of IgG's to allergen IgG's do not induce mast cell degranulation IgG's compete with IgE's for binding antigen = blocking If allergens bound to IgG's, they can't bind to IgE mast cells |
| What three things can be involved in Type II (Cytotoxic) Reactions? |
IgG or IgM antibodies Complement |
| What does complement activation in Type II (Cytotoxic) Reaction cause? |
| Causes cell lysis or damage by macrophages |
| In Type II (Cytotoxic) Reactions, target cell lysis is mediated by? |
Target cell lysis is mediated by Ab's (IgG, IgM) Complement Kiler cells |
| Type II (Cytotoxic) Reactions are associated with: (2) |
Incompatible blood transfusions Hemolytic disease of newborns |
| What happens during Type III (Immune Complex) Reactions? (3) |
An-Ab complexes get deposited on membranes in various tissues (ex. kidney, joints, lungs) Inflammation and complement activation Local destruction of host tissue (Ex. Glomerulonephritis) |
Respone in a Type IV (Cell-mediated) Reaction? 24-48 hours: 1st exposure: 2nd exposure: |
24-48 hours after contact with antigen most common = Contact dermatitis 1st Exposure = Sensitizing dose 2nd Exposure = Immune response |
| Urushiol oils (poison ivy), cosmetics, soaps, drugs (ex. penicillin), metal (ex. nickel), and iodine are all things that can cause reactions in what type of reaction? |
| Type IV (Cell-mediated) Reactions |
| Which hypersensitivities are humoral? |
Type I Type II Type III |
| _______ _______ during fetal development ensures self-tolerance. |
| Clonal Deletion |
| - Loss of self-tolerance |
| Autoimmunity |
| Type I - V of the Autoimmue Diseases: |
Type I - Anitbodies against pathogens Type II - Antibodies react with cell-surface antigens Type III (Immune Complex) - IgM, IgG, complement immune complexes deposit in tissues Type IV - Mediated by T cells Type V (Stimulatory) - Similar to Type II, but antibodies bind specifically to cell surface receptors |
| Example and Target Tissue of Type II (Cytotoxic) and Type V (Stimulatory) Autoimmune Diseases: |
Example: Grave's Disease Target Tissue: Thyroid->Stimulation |
| Example and Target Tissue (3) of Type III (Immune Complex) Autoimmune Diseases: |
Example: Lupus Target Tissue: Systemic, Abs against cell components, kidneys |
| Example and Target Tissue of Type IV (Cell-mediated) Autoimmune Diseases: |
Example: Insulin-Dependent Diabetes Target Tissue: Insulin secreting cell of pancreas |
| What can transplants be attacked by? (3) |
T cells Macrophages Complement-fixing antibodies |
| - Concerning reactions to transplants, this is a region not exposed to immune surveillance |
| Priviledged site |
| Examples of Priviledged Site: (3) |
Brain Region of Cornea Testes
|
| - Concerning reactions to transplantations, this does not stimulate immune system |
| Privileged Tissue |
| Exampls of Privileged Tissue: (3) |
Heart Valves Achilles Tendon [After freezing] Fetus |
| - A type of graft that USES ONE'S OWN TISSUE |
| Autograft |
- A type of graft that USES AN IDENTICAL TWIN'S TISSUE Ex. Kidney |
| Isograft |
| - A type of graft that USES TISSUE FROM ANOTHER PERSON |
| Allograft |
- A type of graft that USES NON-HUMAN TISSUE Ex. Pig health valves |
| Xenograft |
| What results from transplanted bone marrow that contains immunocompetent cells? |
| Graft-versus-Host Disease |
| In order to prevent transplant rejection, the immune response _____________. |
| Must be partially suppressed. |
| What is an example of Immunosuppression Drug: |
| Cyclosporin |
| What is the most probable origin of AIDS? |
| Originated in animal, then crossed over to humans (probably from monkeys). |
| 3 types of Enzymes HIV Possesses and what they do: |
Reverse transcriptase - (aDNA polymerease) copies RNA -> DNA Integrase - (an andonuclease) inserts HIV DNA into host chromosomes Protease - cleaves viral core protein |
| How many receptors are needed for attachment of the Protein Binding Spikes to fusion-membrane fusion: |
| 2 Receptors Needed |
| - Nucleus, circularizes, and integrates into host hormones |
| Provirus |
| In HIV, the release does what to cell membrane? |
| Budding, takes part of cell membrane --> Cell death |
| How many genes are in HIV? |
| Only 9 or 10 genes |
| - Immune system suppressoin/deficiency |
| T4 Cell Depletion |
| What happens to the T4 helper cell when host vulnerable to opportunistic infections, cancers? |
| T4 helper cell can no longer stimulate macrophages, cytoxic T cells, or B cells |
| What is the causative organism of TB? |
| Mycobacterium tuberculosis |
| What are some characteristics of TB(7)? |
LRT infection Rod Obligate aerobe Slow grower Doesn't gram stain, but is acid fast Resists drying and most antimicrbials Immunity is cell mediated- macrophages and T-cells |
| 9 Steps in the Mode of Infection (simplified): |
1. Tubercle bacilli inhaled 2. Tb travels to alveoli, usually phagocytized by macrophages 3. Sometimes Tb survives inside macrophages --> dormant 4. Dormancy = Latent infection, can remain dormant > 80 years 5. Accumulation of macrophages and other cells around infected macrophage-> formation of tubercle 6. Host induced inflammation damages lung tissue 7. Over tie tubercle may heal becoming calcified (seen in X-rays) 8. If does not heal, lesion enlarges, Tbs multiply-> active infection -> highly contagious 9. Dormant Tb can be reactiated |
| Why is using only one or two anti-TB drugs usually not effective? |
There is resistance due to Random Chance Mutation. In any population of bacteria there is the probability of finding at least one organism that is already resistant. |
| What is the typical ratio of infected people who develop active TB? |
-10 % of people infected with TB, develop active TB -90% of people infected with TB, TB is dormant |
| What is the relationship between HIV infection and TB infection? What role does HIV play in TB infection? |
As the rate of HIV increases, TB increases. Dormant TB becomes reactivated in a person when s/he becomes infected with HIV and develop AIDS. |
| Why is it important to manage, treat, or even care about diseases in the third world when they are not problems in developed countries? |
Immigration Lack of isolation We are a global community |
