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45 Cards in this Set

  • Front
  • Back
• Bacteriocidal
– kills it – typically go after cell wall, plasmid, Nucleic acid synthesis
• Bacteriostatic
– stops growth – attacks ribosome; specific for G+/G-/aerobic/nonaerobic
• B-lactams – examples and what they treat
a. Inhibitors of cell wall synthesis • B-lactams – Transpeptidase (enzyme) involved in NAM-NAG linking; Penicillin, Methicillin – Staph (now MRSA) – resistant; Cephalosporins (broad spectrum); ampicillin,
• Vancomycin ***
blocks synthesis NAM + NAG
1. G+ specific b/c it can’t penetrate LPS layer
2. Pain at injection site, renal failure, deafness, lowers WBC#
3. Binds AA x-link => prevents it from growing further
WTF? Rickettsia, Chlamydia
a. Inhibitors of cell wall synthesis Mycoplasma pneumoniae (->walking pneumonia; no cell wall)
a. All intracellular bacteria
b. Don’t treat mycoplasma with Vancomycin bc no cell wall
2. Monobactams
a. Inhibitors of cell wall synthesis – only affect aerobic G- (aztrenam)
a. Inhibitors of cell wall synthesis – blocks carrier molecule of NAM+NAG synthesis for cell wall
1. Staph/Strep
2. Topical ONLY d/t toxicity, broad spectrum
Fosfomycins.Cycloserine -
a. Inhibitors of cell wall synthesis - Block enzymes for NAM+NAG synthesis enzymes
1. Good for UTI (E. coli)
cell wall synthesis inhibitor:
For TB, Waxy coat of mycobacterium
Polymyxin B and E
Inhibitors of cytoplasmic membrane - – punches holes in plasma membrane. G- specific. Toxic to kidneys, liver and nervous system.
i. Quinolones-c.
Inhibitor of nucleic acid synthesis
i. Quinolones- (nalidixic acid [G- specific], ciproflaxin [broad spectrum]. side effect: spontaneous tendon rupture);inhibit DNA gyrase
1. DNA gyrase activity after binding to DNA. Targets intracellular pathogens including: Chlamydia rickettsia, Legionella pneumonophilia—Legionnaire’s Disease infected 200 people in Philadelphia in 1976 and killed 34 of them! – bacteria need gyrase to stay alive
(nalidixic acid [G- specific], ciproflaxin [broad spectrum]. side effect: spontaneous tendon rupture);inhibit DNA gyrase
1. DNA gyrase activity after binding to DNA. Targets intracellular pathogens including: Chlamydia rickettsia, Legionella pneumonophilia—Legionnaire’s Disease infected 200 people in Philadelphia in 1976 and killed 34 of them! – bacteria need gyrase to stay alive
ii. Floxacin
inhibitor of nucleic acid synthesis
iii. Nitroimiazoles
inhibitor of nucleic acid synthesis: metronidazole [specific to anaerobic bacteria like bacterioides])
1. Damage DNA - the reason that this type of antibiotic doesn’t damage us too much is b/c the antibiotic itself doesn’t do the breaking, there is an enzyme in extracellular matrix of bacteria that changes it into a DNA breaker.
2. Good for anything anaerobic; Narowish spectrum - good for C. difficiile, Bacteroides
iv. Nalidixic acid
– aerobic G- inhibitor of nucleic acid synthesis
v. Ciprofloxixin
– G+/G-; inhibitor of nucleic acid synthesis
vi. Rifampin
inhibitor of nucleic acid synthesis: - low toxicity, standard of care for mycobacterium (TB)
1. RNA polymerase blocker; long term liver damage
vii. Sulfonamides and trimethoprim
1. Block folate synthesis by the bacteria, which cannot acquire it dietarily like us
2. Block nucleotide synthesis – folate is needed for synthesisinhibitor of nucleic acid synthesis - side effects include nausea, vomiting, kidney failure, crystals in the urine, low WBC count, and sensitivity to light. Effective for UTIs, burn victims.

3. Broad spectrum, good for UTIs; Side effects – crystals in urine, kidney failure, allergic rxns
i. Aminoglycosides - (neomycin, streptomycin, gentimycin, tobramycin)
Inhibitors of ribosome function: misread codon -> protein made incorrectly -> cell won’t survive. good for aerobic Gram- specific. Given IV, IM or topically.
ii. Tetracycline/Doxycycline -
inhibits ribosome function sun - “catch all” broad spectrum, side effects include nausea, sensitivity to light, yellowing of teeth; good for UTI, Resp. inf., Ear inf.
1. Bind 30S ribosome – block tRNA entry
iii. Chloramphenicol -
inhibitor of ribosome function, broad spectrum G+/G-, cheap (used worldwide)
1. Bind 50S subunit – block peptide bond
iv. Macrolides (erythromycin)
inhibitor of ribosome function: block translocation
v. Licosamides
1. Clindamycin (MRSA
inhibitor of ribosome function; blocks peptide bond formation; C. difficile growth
vi. Lincinoids
1. Block peptide bond formation
Antibiotics functions (4)
inhibit cell wall synth (7),
inhibit cytoplasmic membr (2),
inhibit nucleic acid synthesis (8),
inhibit ribosome function (6)
a. β-lactamase
bacterial resistance to antibiotics – degrades β-lactam antibiotics (penicillin, cephalosporins)
i. G+ secrete into environment (S. aureus, MRSA)
ii. G- keep it contained in cell wall (ex: haemophilus influenza, 35%)
Resistance to Vancomycin
antibiotic resistance by changing its NAM-NAG aa link sequence
innate immune response (5)
Innate Immune Response: WBC/Leukocytes
Granulocytes – NON-SPECIFIC
1. Neutrophils – 55-90% WBC (25 billion), 1o phagocytosis
2. Eosinophils – 1-3% WBC, eliminates eukaryotic pathogens (fungi, protozoan), key in allergic reaction
a. High eosinophil #: indicative of eukaryotic pathogens
b. squirts digestive enzymes on the pathogen
c. Parasite/fungal/worm/allergy
3. Basophils (“mast cells”) – rapid response for inflammation, secretes histamine causing vasodillation and recruiting others
ii. Agranulocytes – 20-30% WBC
4. Monocytes (immature phagocytes) – 3-7% WBC
->a. Macrophage – spec/non-spec phagocytosis, considered a step up from the neutrophil for their abilities
i. Chemotactic, can get out of control
->b. Dendritic cells – messengers; phagocytosis solely for antigen presentation, engulfs and leaves to train more at the Th cells, i.e
i. Signal btwn innate and adaptive immune response; take info to T helper cells
5. Natural killer – 1st killers of human cells for intracellular pathogens, enter the battle before the Tc – i.e.
Secrete perforin or granzymes
Can lead to autoimmune diseases
adaptive immune response
i. Lymphocytes
1. T-cells – T Helper (CD4)= commander
a. cell destruction and activation of immune cells
b. Th cells – (helper cells) Use chemotaxis (chemokines, lymphokines, interleukins) to recruit immune cells
i. CD4 extracellular receptor
ii. HIV kills these off by binding to the CD4, leading to a reduced immune response
c. Tc cells (CD8) – cytotoxic=intracellular, kills ‘em, i.e. especially useful for intracellular pathogens >> the cell puts a little of the virus outside the cell >> Tc finds infected cell,
i. Effector cell = attack and kill it
ii. Memory T-cell
2. B-cells – antibody production and antigen presentation
a. High specificity; extracellular
b. Memory B cell/Plasma B cell -> antibodies
5. Blood -> Reticulendothelial system -> Lymph -> Blood
complement cascases (3)
1. classical (adaptive) 1st exposure (days 12+)/2nd exposure 3+ days efficient - C1, C2a+C4b, C3b, C5b, C6, C7, C8, C9
2. alternative -(innate) inefficient and slow, antibacterial: C3b, C5b, C6, C7, C8, C9, but not dependent on antibody to start
3. iii. Lectin –a protein that binds sugars, efficient and rapid, antifungal
Starts with MBL instead of C1 and then C2-5.
Substituted: (Antibody=mannose, C1= MBL.)
Primarily for fungi. Eosinophil also attacks fungi.
Part of innate immune response (day 1). Classical cascade can attack this as well.
general innate response -> interferons
protein secreted from your cells (part of intracellular immune system and NK cells.)
a. Step 1: Virus enters 1st cell and makes double-stranded RNA.
b. Step 2: The presence of dsRNA signals 1st cell to make interferon proteins
c. Step 3: The interferons are secreted as a warning signal.
d. Step 4: Interferon presence stimulates neighboring 2nd cells to make antiviral proteins,
e. Step 5: Virus kills 1st cell and infects next 2nd neighboring cells,
f. Step 6: BUT when virus enters interferon-prepared 2nd cells and makes dsRNA, the dsRNA now ACTIVATES the antiviral proteins, who then block translation. NET RESULT: Cell still dies, BUT the virus dies too.
g. α and β - antiviral
h. Interferons can be used as anti-cancer b/c they’ll inhibit tumor growth
i. γ – immune stimulation – completely different function
11. Specific immunity
a. Lymphocyte development and differentiation
b. Presentation of antigen (ex: dendritic cells)
c. Challenge of B and T cells by antigen – in response to dendritic cells, they seek and destroy
d. B cell response – Humoral (Bone marrow) response – antibody production
e. T cell response – from thymus - cell mediated response – intracellular killing
clonal selection theory
a. About 1020 different B-cells for antigen recognition initially in a human, occurs developmentally through recombination events
b. Through clonal deletion, the 1020 is reduced to 1015 b/c all “self” Ag’s are deleted (an inaccurate process here results in an autoimmune disease- ie body attacks self if it’s close to pathogen sequence)
c. B, D and J genomic reassortments
i. B1D1J1, B1D1J2, B1D2J2…… etc.
d. Genomically DNA of B cells is mostly same, sometimes slightly different
i. Have B cells to respond to pathogens even if haven’t been exposed
e. Stem cell -> B cell -> B1/B2/B3/B4…. All recognize different antigens
i. Groups of whatever B cell recognized pathogen (B4 for ex) replicate and together become plasma cells -> fight infection (~1% of B cells activated) and a few -> memory cells (1/2 life 5-10yrs) => have + B4s even after infection is gone & respond to pathogen more quickly
f. Design B and t cells for every pathogen that exists, present and future
three functions of immunoglobulins
that serve in (1) opsonization (bacteria), (2) direct neutralization (viruses) and (3) agglutination (which clumps the bacteria together)
1. IgM –
in bloodstream Antibody produced from the plasma B cells upon 1st exposure to an antigen, takes 7-10d; (also low IgG produced)
2. IgG –
in bloodstream Antibody produced from the memory cells upon 2nd exposure, (2-4d); (also low IgM)
i. IgA –
Secretory Antibody; deals w/ pathogens on the mucosal surface, not in the bloodstream.
iii. IgE –
allergies and parasitic infections, can bind to basophils upside down to create a specific-response capability and better histamine release to prolong inflammatory response; these bound basophils become integral in quick allergic responses because they don’t die
1. Can coat basophil w IgE for different pathogens -> respond more rapidly bc know what it’s looking for
a. Problem = allergies, ie histamine, leukotriene release etc. (body learned things as foreign)
i. Example: Pollen -> dendritic cell -> Thelper -> Activated B cell -> made IgM/IgE -> attacked infection
ii. Can delete B cells that we recognize as foreign/ increase exposure and build up tolerance
iv. IgD –
surface of all B-cells, receptor for antibodies
1. B cells take sample of antibody -> put of surface -> IgD =id marker for B cell
2. Can bind antigen directly/ act as antigen presenting cell (like dendritic cell) ie show to Thelper -> tells B cell to make antibodies
e. Gamma globulin treatment
Ie immunoglobulins, Ig-S.
ii. Uses: Respiratory – Syncytial virus, Hep, Rh factor
purpose of Th1=> and what IL, INF, TNFs activate it
anti-viral; indicative of intercellular infection
i. ->IL2 -> NK recruitment
ii. ->IL3 -> hematopoiesis
iii. INFa -> general Th1 response
iv. INFg -> acting a cytokine to induce Th1 response -> MHC class I & II (markers on cell) expression
v. TNFb -> direct killing of cell
vi. Activates Tcytotoxic cells
b. Th2 =
indicative of extracellular issue; GENERAL; bacterial -> B-cell
i. Secretes cytokines and IL4 (B-cell -> IgG/IgE), IL5 (B-cell/IgA/IgM), IL6 (B-cell), IL9, IL13 (B-cell)
ii. Stimulates mass B-cell scattering in search of the bacteria and the B-cells then bring the antigen back to a Th cell to start making antibodies
c. Th17 -
Macrophages, Neutrophils, autoimmunity, arthritis, allergies
IL10 -> shut everything down once infection done
iii. Interleukins:
1. Ag -> Macrophage
* -> IL18, IL15, Il12 -> more NK cells, Neutrophils
pyrogenes -> fever

* 2. Ag -> DC
* IL1a, IL1B, IL8 ->attractant for Th
What is the specific role of Tcytotoxic cells?
(cytotoxic, intracellular infections ie viruses)
i. Specific antigen on surface
ii. CD8
iii. Secretes perforin (makes holes) and granzymes (enters and kills)
iv. Designed to recognize and attack cancer (like NK cell going after abnormal cell. specifically trained)
15. MHC I & II
a. Self vs non-self protein
i. On all nucleated cells (i.e. not on RBCs)
1. Can do blood transfusions bc no MHCI
ii. Intracellular antigens
i. On antigen presenting cells
ii. Extracellular antigens
iii. Must be complimentary for transplants