CC1 & L1 Intro Flashcards
3 obligate intracellular bacteria
Mycobacterium Leprae
Chlamydiae spp.
Rickettsia spp.
3 important encapsulated bacteria
Niesseria meningitidis
streptococcus pneumoniae
Hemphoulis influenza
5 Facultative intracellular bacteria
salmonella spp. shigella spp. listeria monocytogenes legionella spp. mycobacterium tuberculosis
also most fungi and protozoa are fac. intracellular
Extracellular 3 bact., 1 fungi, 1 parasite
Most gram+ (except listeria)
vibrio cholerae
treponema pallidum
fungi: cryptococcus spp.
parasites: giardia
Gram Neg LPS and antigens
LPS - inflammations and causes disease
- Lipid A - endotoxin - O-antigen - variability, complement resistance, bile resistance - enteric bacteria - Core - LOS - no O antigen - not usually enteric - still has the Lipid A endotoxin - gram + super antigen are similar that cause shock - H-antigen - flagella - K- antigen - capsule
bacteristatic antibiotics
tetracyclines, macrolides (azithromycin, erythromycin) clindamycin, linezolids, tigecycline
bactericidal
penicillins, cephalosporins, aminoglycosides, vancomycin, fluoroquinolones, monobactams, daptomycin
B-lactam categories, mech of action, resistance
- penicillin, cephalosporin, carbapenems, monobactams, vancomycin (glycopeptide), fosfomycin
- Mechanism: resemble D-ala D-ala that is usually bound by PBP and then is crosslinked by PBP
- Penicillin is bound by PBP isntead, inhibiting it, - cidal activity (except against enterococcus)
- Resistance:
- alter target: PBP - they don’t bind penicllin anymore
- staph, strep, enterococcus (gram +)
- increase efflux pumps
- loss of porins
- B-lactamases - staph
- in periplasmic space of gram -, outside membrane gram+
- alter target: PBP - they don’t bind penicllin anymore
Antibiotic cell wall inhibitor categories
B-lactams
vancomycin
fosfomycin
Vancomycin -mech, resistance, target, toxicity
Mech: binds D-ala to prevent cross linking, 1 step before B-lactams
Resistance: altered binding site -D-ala D-lac
- really thick cell wall so it can’t get in and do job
Target: Gram + (including MRSA, and non VRE enterococcus, ) and C.diff
Tox: red man rash
- nephrotoxicity
Fosfomycin - mech, target
- inhibits formation of peptidoglycan precursors
- well tolerated
- gram + - staph, strep, entero
gram neg - E. coli and others - no pseudomonas - only used for first line for uncomplicated UTI (TMP/SMX resistance
6 Protein synthesis inhibitor antitbiotics and mech
Types: aminoglycosides, macrolides (azithromycin, clarithramycin, erythramycin), tetracyclines, linezoild, clindamycin, tigecycline
Mechanism:
Block 50S - inhibit translation, block the translocation/elongation part
Block 30S: black tRNA access to ribosome, or bind rRNA
4 Antibiotics categories that inhibit DNA/RNA synthesis
- TMP/SMX - block 2 steps in purine formation
- 100,000x more effective against bact
- resistance - target site mutation
- Rifamycins (rifampin)
- block DdRp - inhibit RNA synthesis
- target site mutation
- Fluoroquinolones
- block topoisomerases
- Resistance: abx mod enzymes, target mutation, efflux pumps
- Ciprofloxacin
- Levofloxacine
- Moxifloxacine
- Fidazomicin
- inhibits transcription of RNA pol
2 DNA damaging antibiotics
- Nitrofurantoin
- reduced to form ROS damage DNA
- resistance: mutation of reductase that makes the ROS from it
- Metronidazole
- pro-drug, is reduced to radiacals the damage DNA - anaerobic nitro-reduction
- resistaance - rare, multiple
2 antibiotics that damage cell membranes
- Daptomycin
- bind to membrane, cause depolarization/efflux K+
- cell death
resistance - thick cel wall/altered binding site (still studied)
- Polymyxin (colistin)
- inserts into membrane than acts as a detergent that dissolves membranes
Non-renal elimination (unlike most that requires renal dosing
- Cetriazone*
- Moxifloxacin*
- azithromycin
- clindamycin
- rifampin
- tetracycline
- fidaxomicin
