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96 Cards in this Set
- Front
- Back
most important component of complement
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C3
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indiv w/ deficiencies in complement susceptible to what diseases:
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1. pyogenic bacteria
2. illness involving the production of Ab's/IC's |
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anaphylatoxins
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potent inducers of inflammation
-C5a, C3a -recruit inflammatory cells, activate effector mechanisms |
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C5a function/ effect
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activator of all cell types of the myeloid lineage (phagocytes)
-neutrophils respond chemotactically, degranulate, release free O2 rads -inc. surface expression of adhesion molecules -macs secret IL5+6 -basophils+ mast degran=histamine |
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specific immunodeficiency
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abnormalities of T + B cells (cells of adaptive immune system)
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non-specific immunodeficiency
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abnormalities in complement, phagocytes,
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primary immunodeficiency
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intrinsic defects in cells of immune system; genetic
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X-linked agammaglobulinaemia
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failure of Bcell maturation
-few or no Bcells in blood/lymphoid tissues -no IgA, IgM, IgD, IgE |
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In immunodeficiency with increased IgM (HIGM)isotype, _______does not occur
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isotype switching
-Bcells cannot make the switch from IgM to IgG and IgA (mutation of CD40 ligand) |
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common variable immunodeficiency (CVID)
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defects in Tcell signaling to Bcells
-Bcells not defective but fail to receive signaling -susceptible to pyogenic infec/ intestinal protozoa |
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transient hypogammaglobulinaemia of infancy
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in some infants IgG synthesis delayed up to 36 mo. (don't have mom's anymore)
-Bcells normal but lack CD4 TH stimulus -susceptible to pyogenic infx |
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Tcell deficiency
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no Tcells or poor function = opportunistic infections
-results in Bcell deficiency since require Tcell help |
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severe combined immunodeficiency (SCID)
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thymus never developed
-most profound -treatment = bone marrow transplant |
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causes of SCID
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1. defect on X chromosome (50%)- defective gene encodes the gamma chain of IL2 receptor- this also forms parts of IL-4,7,11,15 receps
2. other 50% due to recessive genes on other chromosomes= deficiency of ADA adenosine deaminase or PNP purine nucleoside phosphorylase - purines degredation enzymes = accum. of dATP and dGTP= toxic to lymphoid cells |
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MHC class II deficiency
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TH cell deficiency results
-develop. of CD4+TH cells depends on positive selection by MHCII molecules -auto recessive -children have recurrent gastrointestinal infx |
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DiGeorge anomaly
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defect in thymus embryogenesis
-Tcell deficiency variable depending upon effect on thymus -wide eyes, low ears, upper lip shortened, cardiac malform |
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hereditary ataxia-telangectasia (AT)
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-breaks in chromosome 7 and 14 at site of Tcell and Ig genes (auto recess)
-variable Tcell deficiency- some IgA def., others also IgG2 and IgG4 -infants develop ataxia @18 mo + sinus, lung infx |
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Wilscott-Aldrich syndrome (WAS)
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-Tcell defects and abnormal Ig levels -> small+abnormal platelets, abnormal Tcells
-eczema, pyogenic, opp infx -X-linked |
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increased susceptibility to pyogenic infections caused by deficiencies of C__ and Factor __or___
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C3, factor H or I
(C3 plays a big role in opsonization) -all inherited as auto recess |
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deficiencies in classical complement pathway results in development of ___
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immune complexes (ie lupus)
-complement normally dissolves immune complxes) |
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hereditary angineurotic edema (HAE)
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C1 inhibotor deficiency
*most important deficiency of complement -C1 inhib responsible for dissociation of activated C1 -> swelling occurs in various parts of body -auto dominant |
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chronic granulomatous disease (CGD)
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defect in ox/red pathway:
defective NADPH oxidase that catalyzes red of O2 to O2- phagocytes incapable of forming superoxide anions (O2-)so can't kill ingested microog- they stay alive->cell med response to persistant Ag = granuloma |
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Leukocyte adhesion deficiency (LAD)
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complement receptor 3 (CR3) is deficient(normally binds C3b on opsonized organisms)
-severe bacterial/gastro infx |
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secondary immunodeficiencies examples
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chemo-toxic to Tcells
protein malnutrition- results in Tcell deficiency diarrhea-lose Ig's burns-lose Ig's infections (AIDS) |
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proteins on HIV membrane
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gp120, gp41
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cells that carry CD4
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dendritic cells, langerhans cells, microglia of CNS
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HIV cycle
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binds gp120 to CD4
enters CD+ cell, loses coat, ssDNA copy of viral RNA made by HIV reverse transcriptase, comp strand made and integrates when Tcell activated, HIV particles made and released by budding |
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effect of steroids
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dec. circ lymphocytes
dec. circ monocytes inc. circ neutrophils *inhibit synth of cytokines overall= inhibition of TH cells and macrophages |
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cyclophosphamide
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-alkylates DNA- interferes with strand sep during repro
-B cells more affected than Tcells, dec. lymphocytes not PMN's *good to manage auntoAb and allograft rejection |
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azathioprine
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fraudulent base in DNA- affects synthesis
-active only on dividing (cytostatic) dec. T+B cells, suppress NK + K cell activity |
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methotrexate
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analog of folic acid (essential for DNA synth)
dec. in all Ig isotypes anti-inflam cause suppress PMN's no effect on Tcells |
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cyclosporin, tacrolimus (FK506), rapamycin
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-bind to class of cytoplas proteins
-inhib Tcells and Ag presentation |
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iron def.
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reduced ability of neutrophils to kill bac. + fungus, impaired NK cell activ
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selenium + copper def.
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mutations in viruses= altered virulence
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vitamin A def.
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alters epith struc= increased bac binding
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vit B6 and folate def.
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reduced cell mediated immunity
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malnutrition
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decreased #s of CD4 cells, dec in opsonization
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TH2 cells...
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secrete cytokines IL13 and IL14 --> induce Bcell prolif, favor IgE production
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Type I hypersensitivity
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mast cells bind IgE via their Fc receptors, IgE induces degranulation of mast cell, releasing mediators (typical allergic rxn)
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when allergen encounters sensitized mast cell bound w/ IgE...
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cross-links surfacebound IgE-->inc. influx Ca, triggers release of PREFORMED histamine and proteases(tryptase,chymase) and NEWLY SYNTH mediators leucotrienes and prostaglandins
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2 types of mast cells
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MMC- mucosal mast cell
CTMC- connective tissue mast cell |
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the skin prick test produces...
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a wheel and flare reaction
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corticosteroids
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-suppress increase in mast cell #'s
-inhibit cytokine production incl. IL13 & IL4 |
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sodium cromoglycate
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prevents histamine release by inhibiting calcium influx into cell
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cyclosporin A
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inhibits expression of Il2 receptors = Bcells can't proliferate
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antihistamines
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block histamine after release
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hyposensitization therapy
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-increasing doses of allergen
-increase in allergen specific IgG and suppressor Tcell (suppress IgE response) |
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Hyp Type II
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-Ab against own cells
-cytotoxic action by K cells or complement-mediated lysis -ex. blood transfusions |
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Hyp Type III
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-immune complexes deposited in tissues
-complement activated -PMN's attracted to deposition site -tissue damage, inflam ex. lupus |
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Hyp Type IV
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-delayed-type
-Ag-sensitized Tcells release lymphokines when encounter the Ag a 2nd time -Tcells activating macrophages -granulomas |
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difference b/t Type II and Type III?
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II is restricted to specific cells or tissues bearing the Ag, III is against soluble Ag's in the serum
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major cause of HDN
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Rhesus system
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Goodpasture's syndrome
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nephritis from Ab's to glycoprotein on glomerular basement membrane- severe necrosis of glomerulus
(type II) |
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Pemphigus
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blistering of skin and mucous membranes
-Ab's to a desmosome protein that forms junctions b/t epidermal cells -breakdown of the epidermis |
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Myasthenia gravis
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Ab's to Ach receptors on surface of muscle membranes
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immune complexes of type III due to 3 possible causes:
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1. persistent infection/weak Ab response
2. autoimmune disease (phagocytes that remove complexes become overloaded, start to deposit) 3. inhalation of Ag material (actinomyces fungi in hay, pigeon poop - IgG produced rather than IgE) |
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vasoactive amines released by platelets, basophils, and mast cells cause...
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endothelial retraction = increased permeability allowing IC's to deposit on blood vessel wall
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large immune complexes removed faster or slower?
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faster because more effective at fixing complement
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IC deposition occurs where BP is ____
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high
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3 variants of Type IV:
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1. contact hypersensitivity (poison ivy)
2. tuberculin-type (72 hrs) 3. granulomatous (21-28 days) |
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Leprosy
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granumolatous rxn at peripheral nerves (likes cooler areas)
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Tuberculosis
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lung- fibrosis and lesions
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Schistosomiasis
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host becomes sensitized to ova of trematode worms = granulomas
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Sarcoidosis
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tissues, lung, lymphs
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Crohn's disease
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ileum and colon
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live vaccines produce ____ and _______ immunity
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humoral, cell-mediated
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attenuation achieved by...
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mutations (large # mutations diminished virulence)
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killed vaccines produce primarily ______ immunity
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humoral
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chemicals used to inactivate pathogen
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formaldhyde = alkylating agents
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most sucessful bacterial vaccines
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inactivated toxins and toxoids
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limitation of polysaccharide vaccines
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inability to activate Th cells - activate B cells in a Tcell independent manner (not presenting Ag) = more IgM, low IgG , have to get every 4 to 5 years to boost Bcells
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recombinant antigen vaccines
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introduce gene encoding antigen of pathogen into attentuated virus or bacteria- organism serves as vector- replicates within host, expresses gene product of pathogen (also clone into yeast, ie. Hep B vx)
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DNA vaccine
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plasmid DNA encoding viral antigen injected into muscle of recipient, taken up by muscles cells and encoded protein is expressed
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anti-idiotype vaccine
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1.immunize mouse with Ag, Ab (idiotype) generated against Ag
2. immunize mouse with Ab, then anti-idiotype generated (this looks like original Ag) 3. anti-idiotype used as vaccine -testing for HIV vaccine |
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living vaccine advantage
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1. Ag challenge lasts for days or weeks
2. induces it at the right site 3. contains greatest # microbial Ag's |
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killed vaccine disadvantage
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do not replicate in host
repeated boosters needed |
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adjuvants
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enhance Ab production
-aluminum salts, added to Ag 1.concentrates Ag where lymphocytes exposed to it 2. induce cytokines |
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commensals
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benefits from host- host does not benefit but is not harmed
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pseudomembrane colitis
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antibiotics kill normal flora of bowel
-excessive toxin released by clostridium which is normally just a minor resident --> diarrhea |
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characteristics of normal flora
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1. adherence to host cells (proteins, polysacch's, pili) even thru desquamation
2.production of antimicrobial substance- inhibit other competing microbes |
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characteristics of skin that inhibit microorganisms
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1. dryness
2. low pH (b/t 3 and 4 due to organic acids such as lactic acid) 3. inhibitory substances (sweat glands secrete lysozyme, sebaceous secrete complex lipids that are degraded into inhibitory acids) |
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tears contain _____ which _____
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lyzozyme, cleaves peptidoglycan
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major cause of dental caries
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streptococcus mutans
-produces glucan that acts like cement to stick bacterial cells together |
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residents of adult vagina
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lactobacilli
-break down glycogen to form lactic acid |
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carriers
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aquried sufficient immunity but unable to eliminate pathogen from body
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adhesins
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fimbriae, pili, cell-surface structure that bind to receptors on surface of host's cells
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antiphagocytic mechanisms
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-capsules (slippery)
-fimbriae (prevent close contact) -siderophores- compete for iron = growth factor |
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hyaluronidase
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breaks down hyaluronic acid= connective tissue glue = spread
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streptokinase
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activates plasmin, causes disolution of blood clots = spread
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coagulase
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coag of plasma = fibrin layer around cell= Ab doesn't recognize
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hemolysins
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breakdown RBC = iron
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enterotoxins 2 types:
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1. stim cAMP causing electrolyte imbalance= H2O flows in
2.inhibit protein synth = kills epith cells |
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neurotoxins
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tetanus
-spastic paralysis - block inhibitory nerve impulses so fire all the time (botulism prevents Ach release) |
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pyrogenic toxins
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= superantigens --> induce secretions of TNF alpha and IL-1 = inflam, shock, death
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endotoxins
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Lipid A portion of Gram - cells
lipid A binds to macs, causing synth of TNF alpha and IL-1 |
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what prevents microbes from going deep into body (ie rhinovirus)
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temperature- higher temp inhibits growth inside
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