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102 Cards in this Set

  • Front
  • Back
Natural Penicillins
-Benzylpenicillin (Pen G)
-Phenoxymethyl penicillin (Pen VK)
Penicillinase Resistant (Antistaphylococcal) Penicillins
-Carbenicillin indanyl sodium
Natural Penicillins' Activity
-primarily gram (+)
-gram (-) limited to N. gonorrhaea & P. multocida
-Clostridium (not C. difficile)
-T. pallidum
Penicillinase Resistant (Antistaphylococcal) Penicillins' Activity
- < activity vs. streptococci then naturals
- < activity vs. enterococci & gram (-)
-NOT active vs. anaerobic bacteria
-[sacrifice activity for resistance]
Aminopenicillins' Activity
-retain streptococci activity
- > activity to enterococci & L. monocytogenes
-improved gram (-) activity
Carboxypenicillins' Activity
-resembles that of ampicillin
-enhanced gram (-) activity
-minimal activity to enterococci
Ureidopenicillins's Activity
-resembles that of carboxypenicillins
-increased anaerobic coverage
-slightly < activity to streptococci then natural PCN and ampicillin
B-Lactamase Inhibitors
-Clavulanic Acid
B-Lactamase Inhibitors' Activity
"suicide inhibitors" that protect other B-lactams from hydrolytic activity of B-lactamases thus are active vs. B-lactamase producing bacteria (except Richmond Skyes/Bush Class I bacteria)
1st Generation Cephalosporins
1st Generation Cephalosporins' Activity
-very active vs. gram (+) cocci
-moderate activity vs. community acquired infections
-unpredictable activity vs. enterobacteriaceae
-active vs. PCN susceptible oral cavity anaerobes (except B. fragilis)
2nd Generation "True" Cephalosporins
2nd Generation "True" Cephalosporins' Activity
- > activity vs. staphylococci & non-enteric streptococci
-improved activity against gram (-)
2nd Generation Cephamycin Cephalosporins
2nd Generation Cephamycin Cephalosporins' Activity
- < activity vs. staphylococci & streptococci
- > activity vs. selected enterobacteriaceae
- most active cephalosporin vs. Bacteroides sp.
- good anaerobic coverage
3rd Generation Anti-pseudomonal Cephalosporins
3rd Generation Cephalosporins
(No Activity vs. P. aeruginosa)
3rd Generation Cephalosporins' Activity
-most active vs. facultative gram (-) bacilli
-superior activity vs. S. pneumoniae, S. pyognes, & other streptococci (except Ceftazidime)
-modest activity vs. S. aureus (except Ceftazidime)
4th Generation Cephalosporins
4th Generation Cephalosporins' Activity
-similar gram (-) activity as Ceftazidime
-enhanced activity vs. SPICE
-enhanced gram (+) activity compared to Ceftazidime: Streptococci & MSSA
5th Generation Cephalosporins
5th Generation Cephalosporins' Activity
-similar gram (-) activity as Ceftazidime & Cefepime
-enhanced gram (+) activity compared to Cefepime: MRSA
Organisms Cephalosporins Lack Activity Against
-Enterococcus sp.
-MRSA (except 5th generation)
-PCN resistant S. pneumoniae
-Listeria monocytogenes
-Stenotrophomonas maltophilia
-Atypical organisms
drug that blocks the metabolism of Imipenem by inhibiting kidney dipeptidase
Carbapenem's Activity
-gram (-), gram (+), anaerobes
-Ertapenem has NO activity against gram (-) aerobes P. aeruginosa & Acinetobacter sp.
-NOT susceptible to plasmid mediated B-lactamase
-strong inducers that do not alter activity
Organisms Carbapenem Lack Activity Against
-E. faecium
-Stenotrophomonas maltophilia
-Flavobacterium meningoseptium
-Atypical organism
Monobactams' Activity
-limited to gram (-) aerobic bacteria
-similar activity as 3rd Generation Cephalosporins
-poor activity vs. gram (+) & anaerobes
Polypeptide Antibiotics
Cyclopeptide Antibiotics
-Bacitracin A: gram (+)
-Colistin A: gram (-)
-Polymyxin B: gram (-)
-Daptomycin: gram (+)
Polypeptides' Activity
-gram (+)
-NO gram (-) activity
-bactericidal vs. staph & strep sp. including those resistant to B-lactams
-bacteriostatic vs. enterococci
B-Lactam Resistant Pathogens
-Ampicillin resistant enterococcus
Aminoglycosides Naturally Occuring via Streptomyces sp.
Aminoglycosides Naturally Occuring via Micromonospora sp.
Semi-Synthetic Aminoglycosides
Aminoglycosides' Activity
-serious gram (-) infections (used in combo with B-lactam)
-synergy vs. gram (+) infections such as staphylococi, enterococci, & viridans streptococci
-Mycobacterium tuberculosis (1st line: Streptomycin; 2nd line: Amikacin, Kanamycin)
Glycylcycline Tetracyclines
Tetracyclines' Activity
-broad spectrum
Ketolide Macrolides
Atypical Organisms
-Mycoplasma pneumoniae
-Legionella pneumophila
-Chlamydia pneumoniae
Gram (+) Pathogens
-Staphylococcus aureus: MSSA & MRSA
-Enterococcus: VSE & VRE
-Streptococcus pneumoniae: PCN-S & PCN-R
-Group A Streptococus
-S. pyogenes
Gram (-) Pathogens
-Haemophilus influenzae
-Atypical respiratory organisms
Antibiotics that Bind 30S Subunit
-Glycylcycline Tetracyclines
(-Polypeptide Antibiotics)
Antibiotics that Bind 50S Subunit
-Ketolide Macrolides
Causes of Community Acquired Lower Respiratory Tract Infections
-S. pneumoniae
-H. influenzai
Causes of Community Acquired Upper Respiratory Tract Infections
-Group A Streptococcus
Types of Resistant gram (+)
-PCN-R S. pneumoniae
Types of Sexually Transmitted Diseases
-Neisseria gonorrhea
-Chlamydia trachomatis
Types of Peptic Ulcer Diseases
-Helicobacter pylori
Treatment of Community Acquired Repiratory Tract Infections
Treatment of Resistant Gram (+)
-Glycylcylines Tetracyclines
Treatment of Sexually Transmitted Diseases
Treatment of Peptic Ulcer Disease
-Quinupristin/Dalfopristin (Synercide)
Therapeutic Uses of Tetracyclines
Therapeutic Uses of Macrolides
Therapeutic Uses of Ketolide Macrolides
-CAP: mild to moderate severity only
-PCN-R S. pneumoniae
Therapeutic Uses of Lincosamides
-anaerobes (NOT C. difficile b/c actually causes it)
Therapeutic Uses of Oxazolidinones
-PCN-R S. pneumoniae
Therapeutic Uses of Chlorampheicols
-PCN-R S. pneumoniae
Therapeutic Uses of Streptogramins
-MRSA: bacteriocidal
-VRE (E. faecium only): bacteriostatic
Therapeutic Uses of Glycylcycline Tetracyclines
-complicated skin infections & skin structure infections (cSSSIs)
-complicated intra-abdominal infections
-gram (+) including MRSA
-gram (-)
-NO activity vs. Pseudomonas
Treatment of MRSA
-DOC: Vancomycin
-Alternatives: 1.Linezolid 2. Streptogramins 3. Glycylcyline Tetracyclines
-Maybe susceptible: Tetracyclines
Treatment of VRE
-DOC: Linezolid
-Alternatives: Streptogramins (E. faecium only)
-Maybe susceptible: Tetracyclines
Treatment of PCN-R S. pneumoniae
-DOC: Flouroquinolones, Vancomycin
-Alternatives: Ketolide Macrolides, Linezolid, Streptogramins
Macrolide Resistance
-Efflux pump
-Methylase production
Macrolide Resistance due to Efflux Pumps
-mrsA gene in staphylococci
-mefA gene in Group A streptocci
-mefE gene in Streptococcus pneumoniae (NOT with Telithromycin)
Macrolide Resistance due to Methylase Production
-inducible (NOT Telithromycin) or constitutive
-genes: ermA, ermB, ermC
MLSb Resistance
resistance due to methylase production that acts against Macrolides, Lincosamides, & Type B Streptogramins
Tetracyclines Resistance
-plasmid or transposon mediated  efflux pumps
Chloramphenicols Resistance
-chloramphenicol acetyltransferase modifies binding site
Oxazolidionones Resistance
-mutation of ribosomal binding site
Macrolides Alternative Effects
-influence neutrophil cells functions
-anti-inflammatory effects
-decrease production & viscosity of biofilm below MIC levels
Macrolide Effects on Neutrophils Functions
-promotes neutrophil cell degranulation
-decrease neutrophil cell phagocytosis
-increase neutrophil cell migration
MLS (Macrolides, Lincosamides, Streptogramins) MOA
prevents transfer of the growing polypeptide chain from the "A" site to the "P" site
Ketolide Macrolides MOA
blocks protein synthesis by binding to domain II and V of the 23S rRNA of teh 50S subunit
Tetracyclines MOA
reduces the affinity of tRNA for the mRNA ribosome complex
Chloramphenicols MOA
prevents binding of the amino acid containing tRNA to the "A" transferase site
Oxazolidinones MOA
binds to a site on the 50S ribosomal subunit near its interface with the 30S unit  prevents the formation of a 70S initiation complex
Glycylcycline Tetracyclines MOA
binds to 30S subunit & blocks entry of tRNA into the A site of the ribosome
Aminoglycosides MOA
irreversibly binds to the 30S ribsome subunit (bacteriacidal):
-blocks initiation of protein synthesis
-blocks further translation and elicits premature termination
-incorporation of incorrect amino acids
Aminoglycosides Resistance
-decreased AG uptake and accumulation
-ribosomal target modification to decrease affinity for the 30S subunit (esp. with Streptomycin)
-AG modifying enzymes (gentamicin = tobramycin >amikacin)
Decreased Aminoglycoside Uptake & Accumulation Resistance
-instrinsic to species or acquired by chromosomal mutation
-due to membrane impermeability (P. aeruginosa & other non-fermenting gram (-) bacilli)
-efflux pumps
Aminoglycoside Modifyng Enzymes
-AG acetyltransferases (aac)
-AG nucleotidyltransferases (ant)
-AG phosphotransferases (aph)
Vancomycin MOA
inhibits cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan pentapeptides preventing elongation and cross-linking
Vancomycin Resistance
-modifaction of D-Ala-D-Ala terminal  D-Ala-D-Lactate terminal
-3 phenotypes: vanA, vanB, vanC
B-Lactams MOA
-analog of D-Ala-D-Ala N-terminal and thus inhibits bacterial cell wall synthesis by binding to PBP, inducing a bacterial autolytic effect (bactericidal)
B-Lactams Resistance
-inactivation by B-lactamases
-altered permeability to PCN (gram (-) only)
-active efflux
-altered PBP
-Serratia sp.
-P. aeruginosa
-Indole + Proteus sp.
(-Bush 1 enzymes)
-Enterobacter sp.
High Potential for Induction of B-lactamases
-K. pneumoniae
-E. coli
(-Bush 2be enzymes)
(-plasma mediated)
Treatment Options for SPICE
Treatment Options for ESBLs