Micro Chp 15-21


innate


nonspecific


acquired


specific


first line defense


1. mechanical factors2. chemical factors3. normal flora


mechanical factors


- skin- keratin- mucuous membrane- ciliary escalator- glands- hair


chemical factors


- skin secrete sebum- pH 3-5- gastric juice- pH 1-3- lysozomes and peroxidase- transfeerins in blood compete for iron binding- nitric oxide- inhibits ATP production


normal flora


relationship bewteen microbes and host


synergism


give them something to survive off of and they give us something in return


commensalism


we dont benefit but bacteria isnt harmful either


antagonism


one benefits at the other expense


second line defenses


1. WBC2. phagocytosis3. lymphatic system


neutrophils


phagocytic


basophils


produce histamine


eosinophils


toxic to parasites, allergic reactions, some phagocytosis


monocytes


phagocytosis as mature macrophages


fixed macrophages


spleen, liver, lungs


wondering macrophages


roam tissues


chemotaxis


cells recruited to infection


process of phagocytosis


1. chemotaxis2. attachment3. engulfment4. phagosome lysosome fusion5. destruction6. exocytosis


cardinal signs


heat, pain, swelling, redness


chemicals released by damaged cells


histamine, kinins, prostaglandins, leukotrienes


apoptosis


programmed cell death


what causes fever?


pyrogens


endogenous


fever inducing cytokines


exogenous


bacterial endotoxins


what is the complement system?


- inactive proteins- strengthens adaptive immunity- casade of enzymatic reactions


name the pathways of the complement system


1. classical 2. alternative3. lectin


classical pathway


- quickest and most efficient- activation requires antibodies- membrane attack complex


alternative pathway


- easily initated- activation by C3b to cell surface


lectin pathway


- activation requires mannon-binding lectins


alpha and beta interferons


cause cells to produce antiviral proteins that inhibit viral replication


gamma interferon


causes neutrophils and macrophages to phagocytize bacteria


2 kinds of adaptive immunity


1. cell-mediated2. humoral


primary lymphoid organs


- bone marrow- B cells maturation- thymus- T cells maturation


secondary lymphoid organs


- encounter antigens- nodes, spleen, tonsils


epitopes


stimulates immune system


3 antigen characteristics


1. protein structure2. can be carbohydrates3. molecular wieght > 10 kilo Daltons


2 parts of anitbody


1. Fc region (constant)- determines class2. Fab region (variable)- binding site


IgM


- first to respond to infection- pentamer but found on B lymphocytes as a monomer- only one formed by the fetus


IgG


- dominant in circulation- monomer- can cross placenta- memory


IgA


- found in secretions, not circulating- monomer in serum but dimer in secretions


IgD


- maturation of antibody response- monomer


IgE


- barely detectable in circulation- monomer- allergic rxns


clonal selection


specific response of mature B cells to an antigens epitopes


clonal expansion


repeated cycles of cell division generates population of copied antibodies


neutralization


prevents toxin from interactin with cell


opsonization


coating of bacteria with antibody to enhance phagocytosis


affinity maturation


- form of natural selection- occurs among proliferating B cells


cell-mediated immunity


- T cells never prducec antibodies- antigens must be present by antigen presenting cell to T cell receptor


2 components of MHC


1. class 1- expressed on every nucleated cell - binds to CD8 cells - endogenous2. class 2- expressed only on APC like macrophages - binds to CD4 - exogenous


2 parts of helper T cells


- Th1- related to cell mediated immunity, sends out cytokines- Th2- activate B cells to produce eosinophils, IgM, IgE


what does CD8 kill the cell with?


perforin


delayed hypersensitivity T cells


allergic rxns, TB test


suppressor T cells


turns off immune system when no antigen in present to avoid autoimmune effect


what do natural killer cells lack?


antigen specidicity


how do natural killer cells recognize antigens?


the Fc portion of the IgG antibodies


natural killer cells recognize destroyed host cells with...


no MHC class 1 surface molecule- important for viral infections


interleukin 1


stimulates CD4


interleukin 2


activates CD4, B, CD8, and NK cells


interleukin 12


differentiation of CD4 cells


clonal deletion


process of destroying B and T cells that react to self antigens


B cells undergo positive or negative selection?


negative


T cells undergo positive or negative selection?


both


positive selection


differentiation of T cells will only occur if the cell recognizes MHC molecule


naturally acquried active immunity


antibodies resulting from infection


naturally acquired passive immunity


Ab through placenta


artifically acquired active immunity


injection of antigens (vaccines)


artifically acquired passive immunity


injection of Ab


attenuated vaccines


live, weakened form of the pathogen


inactivated vaccines


contains killed organisms or inactivated virus


what are the advantages of attenuated vaccines?


- usually a single dose- has added potential for being spread to un-immunized individuals


what are the disadvantages of attenuated vaccines?


- could cause disease in immunocompromised individuals


what is the advantage of inactivated vaccines?


- can not cause disease- immunogenic- process of gaining immunity


what are the disadvantages of inactivated vaccines?


- magnitude of response is limited- no amplification of the dose in vivo (booster shots)


examples of whole agents that are inactivated vaccines


cholera, plague, flu, salk polio


examples of fragment agents that are inactivated vaccines


DTP and hep B


what is type 1 hypersensitivitiy called?


immediate IgE mediated


immediate IgE mediated


- inherited- charaterized by immediate reaction of the sensitized individual


sensitization


occurs when antigen induces plasma cells to secrete IgE antibodies


Fc region of IgE binds to receptors on what cells?


mast and basophils


what is type 2 hypersensitivity called?


cytotoxic


type 2 hypersensitivity involves what antibodies?


IgG or IgM or ADCC that all cause cell death


examples of type 2 hypersensitivity


tranfusion rxns and hemolytic disease of the newborn


what is type 3 called?


immune complex mediated


immune complex mediated


IgG and antigens form complexes (usually adhere to the Fc receptors are destroyed and removed)


immune complex mediated initates what?


blood clotting mechanism and inflammation


immune complex mediated complexes are deposited where?


skin, kidneys, joints


type 4 hypersensitivity is called?


delayed cell mediated


what is delayed hypersensitivites due to?


cytotoxic T cells that release cytokines that initiate inflammation that attracts marcophages (nothing to due with Ab binding to Ag)


septicemia


acute life threatening illness causes by infectious agent or its products circulating in blood


what are the steps for a pathogen to take in order to establish a diesase?


1. adherence2. colonization- multiplying on a body surface3. delivery of effector molecules that induce changes in the recipient cell


communicable disease


disease transmitted from one host to another


what are the 2 things for a pathogen in a communicable disease?


- must have a suitable environment (reservoir)- must leave the reservoir to be transmitted


morbidity rate


number of cases of illness divided by population at risk


mortality rate


population that dies from disease


incidence


number of new cases per specific time period


prevalence


total number of existing cases


reservoirs affect....


the extent and distribution of disease


name 3 reservoirs


humans, animals, environmental (nearly impossible to elimate)


horizontal transmission


pathogen passed to next reservoir via contact with food, water or living agent


epidemiologists investigate disease outbreak to determine...


- causative agent- reservoir- route of transmission


cross- sectional study


survey of range of people to determine prevalence of number of characteristics


retrospective study


comparing to healthy individuals that already had the disease


prospective study


looking ahead to see if risk factor from retrospective study predict tendency to develop disease


nosocomial infections are known as


hospital acquired infections


what factors determines which organisms and agents are responsible for nosocomial infections?


- length of time of exposure- manner of exposure- virulence and number of organisms- state of host defenses


antibiotics


antimicrobial substance is synthesized and secreted by some true microorganism


semisynthetics


antibiotic that is chemically altered after purification to impart new characteristics


synthetics


antimicrobial substance synthesized in a lab


a high therapeutic index is more or less toxic to a patient?


less


bacteriostatic drugs


- inhibit bacterial growth- relies on host immunity to eliminate pathogen


bacteriocidal drugs


- kills bateria- useful when host defenses can not be relied upon to control pathogen


if gram (+) then antimicrobial drugs cause...


inhibition of cell wall synthesis


antimicrobial drugs can cause inhibition to...


1. cell wall synthesis- high therapeutic index2. protein synthesis- targets ribosomes3. nucleic acid synthesis- targets enzymes necessary for DNA replication4. metabolic pathways- folic acid


this drug binds to gram (-) that alters the permeability which leads to leakage of cell components and cell death


polymyxin B


synergistic drugs


2 drugs working together