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150 Cards in this Set
- Front
- Back
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what kind of antigen does hummoral response respond to? |
exogenous |
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(hummoral response) during first exposure what happens right after the body recognizes and exogenous antigen? |
colonial selection of B-cell with the right BCR |
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( HR) after the right b-cell is selected what happens? |
B-cell is activated by the TH2 cell |
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(HR) after the b-cell is activated what happens? |
b-cells differentiate into plasma and memory cells |
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(HR) lastly, in the first exposure, what happens after b-cells differentiate |
plasma cells create IgM antibodies |
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(HR) what happens during second exposure? |
don't need T helper cells and memory cells differentiate into plasma cells with the IgM antibodies |
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what type of antigen does cell mediated respond to? |
endogenous |
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t lymphocyte are created in where and mature in where |
bone marrow and thymus |
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(CM) during first response after exposure to an endogenous Ag what happen? |
colonial selection of t-cell with right TCR |
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(CM) after colonial selection what happens? |
T-cell are activated by TH1 memory cells |
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(CM) after t cells are activated what do they do? |
make perforin which makes holes and then granzyme kill cell |
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(CM) during second exposure what happens? |
don't need TH1 cells memory cells will be activated to use perforin and granzyme |
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what is colonial deletion? |
deleting the antibodies that we make to our own antigens which we don't need |
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what happens if colonial deletion fails? |
autoimmunity |
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what is an example of a exogenous antigen |
protein in outer membrane capsule |
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what is an example of an endogenous Ag |
HIV |
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what is an example of a auto Ag? |
auto immune disease |
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what is a Ab protein called? |
immunoglobin |
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in an Ig the heavy and light chains are held together by what bond? |
disulfide |
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what is the constant region of an Ig? |
Fc stem |
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what type of Ig is found most predominantly in blood and can cross the placenta? |
IgG |
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what type of Ig is found in secretions? breast milk tears.... |
IgA |
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what type of Ig is the first class of antibodies made? |
IgM |
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what cell receptor is required for cell activity? |
CD4 |
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production of Ab |
Hummoral |
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activation of Tc cells |
cm |
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t helper cell required |
both |
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memory response |
both |
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death of infected cell |
cm |
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important role of CD4 receptor |
both |
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specificity toward extracellular pathogen toxin |
hummoral |
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what is a natural way to get active immunity? |
infection from a pathogen |
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what is a way to get active immunity artificially ? |
vaccine |
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what is a way to get passive immunity naturally? |
Ab that cross the placenta of through great milk |
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what is a way to get passive immunity artificially? |
getting Ab from antitoxin or antivenin |
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what to antigens do? |
stimulate an immune response |
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as size increases, antigenicity? |
increases |
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as heterogeneity increases, antigenicity? |
increases |
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how is the antigen recongnized? |
by the antigenic determinant that has a certain molecular shape |
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how does cell mediated response kill infected cells? |
T cytotixic lymphocytes |
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where do b lymphocytes mature? |
bone marrow |
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one b cell can make only ____ type of Ab? |
one |
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what is the basis of diagnostic test? |
agglutination |
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what is the term for when phagocyte has a receptor of the Fc stem of the Ab and now has a capsule that makes phagocytosis easier? |
opsonization |
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what is another way to opsonize bacterial cells? |
generate oxidants |
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what is a classical pathway that has antibody dependent cell toxicity? |
activate complement |
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what carries out antibody dependent cell cytotoxity? |
natural killer lymphocytes |
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what is a Ig that is involved in allergies? |
IgE |
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what is a Ig that is the receptor on B cells function? |
IgD |
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how do mothers avoid their babies from getting tetanus at birth? |
vaccinate so that the mother can pass IgG antibodies can cross fetus |
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how can B cells recognize different Ags that they have never seen before? |
each B cell has a different Ig receptor on its cell surface |
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if B cells reconginze self Ag and they don't go through colonial deletion what happens? |
autoimmune disease |
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what is a response that is relatively slow, IgM to x level, and short lived? |
primary |
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what response is immediate, IgG xxxx level, and long lived? |
memory |
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what is a increased resistance to disease by stimulation of immune system or passive transfer of Ab? |
immunization |
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what type of immunization is: disease or colonization induces immunity |
natural active |
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what type of shot is: administration of vaccine to induce protective immune response? |
artificial active |
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shot that: immunity from one host passed naturally to another |
natural passive |
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shots that: immunity from one host artificially passed to another |
artificial passive |
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what are 6 effective things for ideal vaccine? |
1) low levels of side effects 2) protect against natural form of pathogen 3) stimulation of both immune responses 4) provide long term lasting effects 5) shouldn't require lots of booster 6) inexpensive |
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vaccine where virulence is eliminated or reduced but anigenicity remains? |
live attenuated |
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what are advantages to live attenuated vaccine? 4 |
1) replicate inside host 2) strong antigenicity 3) stimulates both immune response 4) requires few booster |
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vaccine where: virus/ antigen is killed but sill same antigenicity? |
killed pathogen |
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advantage to killed pathogen vaccine? |
can never revert to virulent form |
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disadvantage to kill pathogen vaccine? (3) |
1) only stimulates humoral response 2) antigenically weak 3) need boosters |
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vaccine: antigen is present but not pathogen? |
purified antigen from pathogen |
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what are the advantages from purified antigen from pathogen and genetically engineered vaccine? |
take away bad component of pathogen |
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what are the disadvantage from purified antigen from pathogen and genetically engineered vaccine? |
only humoral response is stimulated |
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vaccine: plasmid with gene that codes for Ag |
genetically engineered vaccine |
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vaccine: nontoxic but If similar to exotoxin? |
toxoid |
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what are the advantage of toxoid? |
take purified chemical eight less risk of side effects |
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what are disadvantages to toxoid? |
often need booster |
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what is the most favorable vaccine and why? |
live attenuated because is has strong antigenicity and stimulates both immune responses |
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what causes tuberculosis? |
Mycobacterium tuberculosis |
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how is tuberculosis transmitted? |
through inhalation of respiratory droplets |
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is it highly contagious? |
no |
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if untreated does it have a high mortality rate? |
yes 60% |
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what are virulence factors of tuberculosis? (4) |
1) intracellular growth- phagosome lysosome fusion prevented 2) waxy mycolic acid- provides resistant to drying 3) slow growth rate- synthesis of mycolic acid very slow 4) cord factor- inhibits migration of phagocytes |
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what is the primary stage of TB? |
mild fever, slight cough |
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does the disease enter a latent period after the primary stage? is the patient contagious? how long could it last? |
yes no years |
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what are symptoms of the secondary progression of disease? |
difficulty breathing, chest pain, fatigue, couch (with blood), anorexia |
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during this second stage who is the mycobacteria spread? and where? |
rupture of tubercle to the upper resp tract and into bronchiole |
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t/f TB is the common cause of death in people with HIV? |
true |
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what is it called when macrophages carry mycobacteria via blood to many areas of the body? |
disseminated |
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what is the treatment for TB? |
rifampin |
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what inhibits synthesis of mycolic acid required for the cell wall? |
isoniazid |
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what is a major concern with TB? |
multiple drug resistant strains |
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why does a TB test not tell much? |
because one could be a chronic carrier having been exposed and not infected or not a active infection |
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coagulase, hyaluronidase, staphylokinase, lipase, b lactamsase, transpeptidase are all what kind of virulence factors for Staph? |
enzymes |
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what coagulates plasma and blood to make a fibrin clot around itself making it hard for phagocytosis = protective barrier? |
coagulase |
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what destroys hyaluronic acid "glue" binding connective tissue? |
Hyaluronidase |
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what digest blood clots? |
Staphylokinase |
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what aids in colonization of oily skin, destruction of lipids for nutrients? |
lipase |
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what protects from penicillin? |
B lactamase |
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what causes it to not bind to methicillin in MRSA? |
transpeptidase |
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what are structural defenses does Staph have? |
capsules and protein A |
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how does protein A work? (2) |
blocks Fc stem from binding to PMN no Ab induced opsonization inhibits complement cascade |
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what toxins are associated with staph a ? 3 |
Leucocidins Toxic shock syndrome toxin exfoliative toxins |
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folliculitis, furuncle (boil), carbuncle, sty are all staph a infections associated with? |
pyogenic infections |
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what causes scalded skin syndrome staph a ? |
exfoliative toxins A and B enter the blood and spread throughout the body which causes epidermal shedding |
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what virulence factors are associated with staph p? |
DNAS hyaluronidase (allowing tissue invasion) |
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what are structural defense for staph p? |
M protein |
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what prevents phagocytosis by inhibiting C3b |
M protein |
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with M protein can opsonization still occur? |
yes, b plasma cell can make Ab to M protein to enhance phagocytosis |
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with staph p what toxin stimulate macrophages and TH cells to release cytokines? |
pyrogenic |
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what toxic assoc with staph p that causes toxemia and tissue damage? |
exotoxin |
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what toxin assoc with staph p kills host cell |
streptolysin |
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what is a form of staph that is associated with: exfoliative toxins A and B skin flakes from epidermis and peels off not serious but contagious |
impetigo |
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what form of staph is associated with: impetigo infection spread to the lymph nodes intrusion to dermis via opening edema redness at port of entry fever chills |
erysipelas |
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what staph is associated with: trauma subtle injury to dermis several days fro signs to develop pain, tenderness, swelling, fast spreading red line progressing |
cellulitus |
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what staph is associated with: microbe introduced with a cut intense pain toxins kill epidermal and dermal cells infection spread to muscles may result in amputation and death |
necrotizing fascitis |
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what is another skin infection due to neuropathy painless that can become infected and aren;t easily treated with antibiotics? |
diabetic foot ulcer |
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what infection is caused by fecal contamination of urethra by normal flora of the GI tract? |
UTI |
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are men more susceptible then women to UTIs? |
not women |
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what is a bacterial infection caused by Treponema pallidum?
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syphillus |
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can syphilus grow in cell free culture? |
no |
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what are the virulence factors of syphilus? |
adhesions hydaluronidase capsule |
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what is the primary stage of syphilus? |
appearance of chancre which is painless and then disappears very infection on this stage |
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what is the secondary phase of syphilus? |
rash all over torso still infectious and then disappears |
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does syphilus enter a latent stage after the secondary stage? |
yes |
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what is the latent phase of syphilus? |
no symptoms, anitbodies present difficult to diagnose |
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do a majority of cases advance past the latent phase? |
no due to antibiotics |
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what is a result of inflammation and hyperimmune response not T. palladium but shows a Gumma a rubbery lesion a key feature? |
tertiary |
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what can the tertiary phase lead to? |
lead to dementia blindness and death |
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do antibiotics work in tertiary phase? |
no |
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can T palladium cross the placenta at any time? |
yes |
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what can congenital syphilis lead to ? |
death rate and if lives tooth and bone CNS disorders |
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Neisseria gonorrhoea is the causative agent of what? |
Gonorrhoea |
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what are the virulent factors of Gonorrhoea? |
fimbriae capsule IgA protease |
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what is the cause of pelvic inflammatory disease and can lead to sterility? |
can attach to sperm cells and travel to fallopian tubes |
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what are symptoms following infection of gonorrhoea? (3) |
1) pus discharge 2) painful urination 3) 50% of females are asymptomatic 25% develop PID Males generally ave symptoms |
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what is the causative agent in Chlamydia? |
Chlamydia trachomatis |
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does chlamydia have a cell wall or motility? |
obligate intracelluar parasite no cell wall or non motile |
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what can chlamydia infect? |
eyes, urinary tract, lungs, and genital tract anus and rectum |
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who are highly susceptible to chlamydia |
females less then 20 |
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what are signs of chlamydia ? |
discharge and painful urination |
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what is the causative agent in AIDS? |
HIV |
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what is the ultimate result of HIV infection? |
decrease in T helper lymphocyte |
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how is HIV infection spread? |
by exposure to body fluid |
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can HIV cross the placenta and be present in breast milk? |
yes |
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what are the targets for antiviral drugs in HIV? |
reverse transcriptase a protease |
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what is the occurence of herpes? |
1 and 6 people between the ages of 14 and 69 years old |
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what is the cause of genital herpes? |
type 2 |
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what type of virus is herpes? |
ds DNA enveloped |
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what can cause genital warts and cancers? |
human papilloma virus |
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what are genital warts a concern to human health? |
can cause cancer by crossing into the human genome |
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what can the fetus contract with contact of HPV? |
recurrent respiratory papilomatosis |
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what does gardicell prevent against what warts |
6, 11 |
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what does gargle prevent against what cervical cancers? |
16,18 |
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:) |
:) |
