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first line defense
- 1. mechanical factors
- 2. chemical factors
- 3. normal flora
- - skin- keratin
- - mucuous membrane- ciliary escalator
- - glands
- - hair
- - 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
relationship bewteen microbes and host
give them something to survive off of and they give us something in return
we dont benefit but bacteria isnt harmful either
one benefits at the other expense
second line defenses
- 1. WBC
- 2. phagocytosis
- 3. lymphatic system
toxic to parasites, allergic reactions, some phagocytosis
phagocytosis as mature macrophages
spleen, liver, lungs
cells recruited to infection
process of phagocytosis
- 1. chemotaxis
- 2. attachment
- 3. engulfment
- 4. phagosome lysosome fusion
- 5. destruction
- 6. exocytosis
heat, pain, swelling, redness
chemicals released by damaged cells
histamine, kinins, prostaglandins, leukotrienes
programmed cell death
what causes fever?
fever inducing cytokines
what is the complement system?
- - inactive proteins
- - strengthens adaptive immunity
- - casade of enzymatic reactions
name the pathways of the complement system
- 1. classical
- 2. alternative
- 3. lectin
- - quickest and most efficient
- - activation requires antibodies
- - membrane attack complex
- - easily initated
- - activation by C3b to cell surface
- activation requires mannon-binding lectins
alpha and beta interferons
cause cells to produce antiviral proteins that inhibit viral replication
causes neutrophils and macrophages to phagocytize bacteria
2 kinds of adaptive immunity
- 1. cell-mediated
- 2. humoral
primary lymphoid organs
- - bone marrow- B cells maturation
- - thymus- T cells maturation
secondary lymphoid organs
- - encounter antigens
- - nodes, spleen, tonsils
stimulates immune system
3 antigen characteristics
- 1. protein structure
- 2. can be carbohydrates
- 3. molecular wieght > 10 kilo Daltons
2 parts of anitbody
- 1. Fc region (constant)- determines class
- 2. Fab region (variable)- binding site
- - first to respond to infection
- - pentamer but found on B lymphocytes as a monomer
- - only one formed by the fetus
- - dominant in circulation
- - monomer
- - can cross placenta
- - memory
- - found in secretions, not circulating
- - monomer in serum but dimer in secretions
- - maturation of antibody response
- - monomer
- - barely detectable in circulation
- - monomer
- - allergic rxns
specific response of mature B cells to an antigens epitopes
repeated cycles of cell division generates population of copied antibodies
prevents toxin from interactin with cell
coating of bacteria with antibody to enhance phagocytosis
- - form of natural selection
- - occurs among proliferating B cells
- - 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
- - endogenous
- 2. 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?
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?
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
activates CD4, B, CD8, and NK cells
differentiation of CD4 cells
process of destroying B and T cells that react to self antigens
B cells undergo positive or negative selection?
T cells undergo positive or negative 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
live, weakened form of the pathogen
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
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?
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)
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. adherence
- 2. colonization- multiplying on a body surface
- 3. delivery of effector molecules that induce changes in the recipient cell
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
number of cases of illness divided by population at risk
population that dies from disease
number of new cases per specific time period
total number of existing cases
the extent and distribution of disease
name 3 reservoirs
humans, animals, environmental (nearly impossible to elimate)
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
comparing to healthy individuals that already had the disease
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
antimicrobial substance is synthesized and secreted by some true microorganism
antibiotic that is chemically altered after purification to impart new characteristics
antimicrobial substance synthesized in a lab
a high therapeutic index is more or less toxic to a patient?
- - inhibit bacterial growth
- - relies on host immunity to eliminate pathogen
- - 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 index
- 2. protein synthesis- targets ribosomes
- 3. nucleic acid synthesis- targets enzymes necessary for DNA replication
- 4. metabolic pathways- folic acid
this drug binds to gram (-) that alters the permeability which leads to leakage of cell components and cell death
2 drugs working together