Antibiotics for AECOM

Drugs: Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

Mechanism: PABA antimetabolite that inhibits dihydropteroate synthetase (enzyme necessary for folic acid production)

Clinical use: Gram(+), gram(-), Nocardia, Chlyamydia. Triple sulfas or SMX for simple UTI

Toxicity: Hypersensitivity, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace drugs from albumin (e.g., warfarin)

Resistance: Altered enzyme, decrease uptake, increased PABA synthesis.

Drugs: Trimethoprim, pyrimethamine

Mechanism: Inhibits bacterial dihydrofolate reductase

Clinical: Used in combination with sulfonamides (TMP-SMX) causing sequential block of folate synthesis. Combination used for recurrent UTIs, Shigella, Salmonella, Pneumocystis jiroveci pneumonia.

Toxicity: Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid [leucovorin rescue]).

Trimethoprim = TMP: "Treats Marrow Poorly"

Drugs: Penicillin G (IV), Penicillin V (PO)

Mechanism: Bind penicllin-binding proteins, block transpeptidase cross-linking of cell wall, and activate autolytic enzymes

Clinical: Mostly used for gram(+) organisms (S. pneumoniae, S. pyogenes, Actinomyces) and syphilis (Treponema pallidum). Bactericidal for gram(+) cocci, gram (+) rods, gram(-) cocci and spirochetes. Not penicillinase resistant

Toxicity: Hypersensitivity reactions, hemolytic anemia

Drugs: Methicillin, nafcillin, dicloxacillin

Mechanism: Same as penicillin. Narrow spectrum; penicillinase resistant because of bulkier R group.

Clinical: S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

Toxicity: Hypersensitivity reactions; methicillin - interstitial nephritis.

"Use naf (nafcillin) for staph."

Drugs: Ampicillin, amoxicillin

Mechanism: Same as penicillin. Wider spectrum; pencillinase sensitive. Combine with clavulanic acid to enhance spectrum (b-lactamase inhibitor). AmOxicillin has greater Oral bioavailability than ampicillin.

Clinical: Extended-spectrum penicillin - certain gram(+) bacteria and gram(-) rods (Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci).

Toxicity: Hypersensitivity reactions; ampicillin rash; pseudomembranous colitis

AMPed up penicillin

Coverage: ampicillin/amoxicillin HELPS kill enterococci

Drugs: Ticarcillin, carbenicillin, piperacillin

Mechanism: Same as penicillin. Extended spectrum

Clinicail: Pseudomonas spp. and gram(-) rods; susceptible to penicillinase; use with clavulanic acid.

Toxicity: Hypersensitivity reactions

TCP: Takes Care of Pseudomonas

Drugs: Clavulanic acid, sulbactam, tazobactam

Clinical: Added to penicillin antibiotics to protect the antibiotic from destruction by b-lactamase (penicillinase)

CAST

Drugs: Cefazolin, cephalexin

Mechanism: B-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal

Clinical: Gram(+) cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.

Toxicity: Hypersensitivity, vitamin K deficiency. Cross-hypersensitivity with penicillins occurs in 5-10% of patients. Increased nephrotoxicity of aminoglycosides; disulfiram-like reaction with ethanol (in cephalosporins with a methylthiotetrazole group, e.g., cefamandole)

PEcK

Drugs: Cefoxitin, cefaclor, cefuroxime

Mechanism: same as 1st generation

Clinical: gram(+) cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens

Toxicity: Hypersensitivity, vitamin K deficiency. Cross-hypersensitivity with penicillins occurs in 5-10% of patients. Increased nephrotoxicity of aminoglycosides; disulfiram-like reaction with ethanol (in cephalosporins with a methylthiotetrazole group, e.g., cefamandole)

HEN PEcKS

Drugs: Ceftriaxone, cefotaxime, ceftazidime

Mechanism: same as 1st generation

Clinical: Serious gram(-) infections resistant to other b-lactams

Toxicity: Hypersensitivity, vitamin K deficiency. Cross-hypersensitivity with penicillins occurs in 5-10% of patients. Increased nephrotoxicity of aminoglycosides; disulfiram-like reaction with ethanol (in cephalosporins with a methylthiotetrazole group, e.g., cefamandole)

Ceftriaxone - meningitis and gonorrhea

Ceftazidime - Pseudomonas

Drug: Cefepime

Mechanism: same as 1st generation

Clinical: Increased activity against pseudomonas and gram(+) organisms

Toxicity: Hypersensitivity, vitamin K deficiency. Cross-hypersensitivity with penicillins occurs in 5-10% of patients. Increased nephrotoxicity of aminoglycosides; disulfiram-like reaction with ethanol (in cephalosporins with a methylthiotetrazole group, e.g., cefamandole)

Drug: Aztreonam

Mechanism: Inhibits cell wall synthesis by binding PBP3 (only), and is resistant to pencillinase.

Clinical: Gram(-) rods only [NO activity against gram(+) or anaerobes]. Used in patients that are allergic to penicillin and those with renal insufficiency who cannot tolerate aminoglycosides.

Toxicity: No cross-allergenicity with penicillins or cephalosporins; usually non-toxic; occasional GI upset.

Drugs: Imipenem, meropenem, ertapenem, and doripenem

Mechanism: Broad-spectrum beta-lactamase resistant Abx that is ALWAYS adminstered with cilastatin (inhibits renal dehydropeptidase I) which decreases inactivation in renal tubules

Clinical: Gram(+) cocci, gram(-) rods, and anaerobes. Life-threatening infections only

Toxicity: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

With imipenem, "the kill is LASTIN' with ciLASTATIN." (meropenem does not need cilastatin)

Drugs: Vancomycin and Telavancin

Mechanism: Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal

Clinical use: Gram(+) ONLY, serious multidrug-resistant organisms (S. aureus, enterococci and C. difficile)

Toxicity: Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing--"Red man syndrome" (prevent with antihistamines and slow IV)

Well tolerated in general-- does NOT have many problems

Resistance: Amino acid change of D-ala D-ala to D-ala D-lac

"Pay back 2 D-alas for vandalizing"

Drugs: Ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin, ofloxacin, sparfloxacin, gatifloxacin(X), enoaxin, nalidixic acid (quinolone)

Mechanism: Inhibits DNA gyrase (topoisomerase II). Bactericidal, do NOT take with antacids

Clinical use: Gram(-) rods of urinary and GI tract (includes pseudomonas), Neisseria, and some gram(+)

Toxicity: GI upset, superinfection, skin rash, headache, dizziness, prolong QT interval. Contraindicated in children and women because of damage to cartilage. Tendonitis and rupture in adults; leg cramps and myalgias in kids

FluroquinoLONES hurt attachments to your BONES

Resistance: Chromosome-encoded mutation in DNA gyrase, ATP-requiring efflux pump

Drugs: Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

"Mean" GNATS caNOT kill anerobes."

Mechanism: Inhibit formation of initiation complex (binds 30S & 50S) and cause misreading of mRNA (bactericidal). Requires O2 for uptake; therefore, ineffective against anaerobes.

Clinical use: Severe gram(-) rod infections. Synergism with beta-lactam Abx

Toxicity: Nephrotoxicity (increased when used with cephalosporins), Ototoxicity (increased with loop diuretics), and Teratogenic.

Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation.

A "initiates" the alphabet

Drugs: Tetracycline, doxycycline, demeclocycline, minocycline

Demeclocycline - ADH antagnoist; acts as a Diuretic in SIADH

Mechanism: Binds to 30S and prevents attachment of aminoacyl t-RNA (Bacteriostatic), with limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Must NOT take with milk, antacids, or iron-containing preparations because divalent cations inhibit its absorption in the gut.

Clinical use: Borrelia burgdorferi, M. pneumoniae. Drug's ability to accumulate intracellularly makes it VERY effective against Rickettsia and Chylamydia

Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in children; photosensitivity. Contraindicated in pregnancy (fatty hepatic necrosis)

Resistance: Decrease uptake into cells, or increase efflux by plasmid-encoded transport pumps.

Drugs: Erythromycin, azithromycin, clarithromycin

Mechanism: Inhibit protein synthesis by blocking translocation ("macroSlides"); bind to the 23S rRNA of the 50S ribosomal subunit (Bacteriostatic)

Clinical use: Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), URIs, STDs, gram(+) cocci (pts. allergic to penicillin), and Neisseria

Toxicity: Prolonged QT interval (especially Erythromycin), GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rash. Increases serum concentration of theophyllines and oral anticoagulants

Resistance: Methylation of 23s rRNA binding site.

Drug: Clindamycin

Mechanism: Blocks peptide bond formation at 50S ribosomal subunit (Bacteriostatic)

Clinical use: Anaerobic infections (Bacteroides fragilis, C. perfringens) in aspiration pneumonia or lung abcess

Treats anaerobes "above" the diaphragm vs. metronidazole (anaerobic infections "below" diaphragm)

Toxicity: Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea.