First Aid Antibiotics

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Penicillin

Back 1

Mechanism- Bind PBPs, Block transpeptidase cross-linking of cell wall, activate autolytic enzymes.
Clinical use- GP, syphilis
Toxicity- Hypersensitivity hemolytic anemia

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Methicillin, nafcillin, dicloxacillin

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Mechanism- Same as penicillin but penicillinase resistant because of bulkier R group.
Use- S. aureus (NAFCILLIN!!!)
Toxicity- Hypersensitivity. Methicillin causes interstitial nephritis

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Ampicillin, Amoxicillin

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Mechanism- Same as penicillin, penicillinase resistant, wider spectrum. Amoxicillin > ampicillin oral bioavailability.
Use- Extended-spectrum (GP, GN- H. flu, E. coli, L. monocytogenes, Proteus, Salmonella, enterococci), neonatal infections and UTIs!!
Toxicity- Ampicillin rash, pseudomembranous colitis

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Ticarcillin, Carbenicillin, Piperacillin

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Mechanism- Same as penicillin. Extended spectrum.
Use- PSEUDOMONAS and GNRs, anaerobes
Toxicity- Hypersensitivity

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Beta-lactamase inhibitors (clavulanic acid, sulbactam, tazobactam)

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Added to penicillin antibiotics to protect against destruction by beta-lactamase.

Front 6

Cefazolin, Cephalexin

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1st generation cephalosporins
Use- PEcK (Proteus, E. coli, Klebsiella) + GPC
Toxicity- Hypersensitivity with penicillins, nephrotoxicity with aminoglycosides, disulfiram-like reaction with ethanol.

Front 7

Cefoxitin, Cefaclor, Cefuroxime

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2nd generation cephalosporins
Use- HEN PEcK- H. Flu, Enterbacter, Neisseria, Proteus, E. coli, Klebsiella. + GPC
Toxicity- Hypersensitivity with penicillins, nephrotoxicity with aminoglycosides, disulfiram-like reaction with ethanol.

Front 8

Ceftriaxone, Cefotaxime, Ceftazidime

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3rd generation cephalosporins
Use- Serious GN infections resistant to other beta-lactams; cefriaxone is for meningitis and gonorrhea, ceftazidime is for pseudomonas. NOT LISTERIA.
Toxicity- Hypersensitivity with penicillins, nephrotoxicity with aminoglycosides, disulfiram-like reaction with ethanol.

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Aztreonam

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Mechanism- Monobactam resistant to beta-lactamases; Binds to PBP3 to inhibit cell wall synthesis, synergistic with AGs. NO cross-allergy with penicillins.
Use- GNRs ONLY- used in patients who are allergic to penicillin and those with renal insufficiency who cannot tolerate AGs.
Toxicity- GI upset

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Imipenem/cilastatin, meropenem

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Mechanism- Beta-lactamase resistent carbapenem. Imipenem is always administered with cilastatin (inhibits renal dihydropeptidase I) to decrease inactivation of drug in the renal tubules.
Use- GPC, GNR, ANAEROBES (wide-spectrum). Empiric.
Toxicity- GI distress, skin rash, CNS toxicity (not meropenem)

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Vancomycin

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Mechanism- Inhibit cell wall mucopeptide formation by binding to D-ala-D-ala.
Use- GP ONLY; serious multi-drug resistant organisms (MRSA, enterococci, C. difficile oral, coag negative endocarditis)
Toxicity- Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing (red man syndrome- pretreat with antihistamines). Resistance by D-ala-D-lac

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Gentamicin, Neomycin, Amikacin, Tobramycin

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Aminoglycosides
Mechanism- Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake so are INEFFECTIVE against anaerobes.
Use- Severe GNR infections. Synergistic with Beta-lactam antibiotics. Use neomycin for bowel surgery.
Toxicity- Nephrotoxicity (esp with ceph), Ototoxicity (esp with loop diuretics), Teratogen, neuromuscular paralysis
Resistance- Transferase enymes inactivate by phosphorylation, acetylation, or adenylation.

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Tetracycline, Doxycycline, Demeclocycline, Minocycline

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Mechanism- Static; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration. Doxy is fecally eliminated and can be used in patients with renal failure. DONT TAKE WITH DIVALENT cations (prevent absorption)
Use- Vibrio, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma, Tularemia, H. pylori, Borellia burgdorferi, Rickettsia (can accumulate intracellularly)
Toxicity- GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. CX in pregnancy! Minocycline can cause blue pigmentation of skin
Resistance- Decreased uptake into cells or increased efflux out of cell by plasmid-endcoded transport pumps

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Erythromycin, Azithromycin, Clarithromycin

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Macrolides
Mechanism- Block translocation by binding 23S of the 50S ribosomal subunit. Static
Use- Pneumonia (mycoplasma, chlamydia, legionella), URIs, STDs, GPC, Neisseria
Toxicity- Prolonged QT interval (erythromycin), GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines and oral anticoagulants
Resistance- Methylation of the 23S rRNA binding site

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Chloramphenicol

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Mechanism- Inhibits 50S peptidyltransferase activity. Static
Use- Meningitis (H. flu, Neisseria, S. pneumo).
Toxicity- Anemia, aplastic anemia, gray baby syndrome (lack liver UDP-glucuronyl transferase)
Resistance- Plasmid-encoded acetyltransferase inactivates drug

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Clindamycin

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Mechanism- Blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic
Use- ANAEROBIC (above diaphragm- B. fragilis, C. perfringes) in aspiration pneumonia, skin infection due to MRSA
Toxicity- Pseudomembranous colitis, fever, diarrhea

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Sulfonamides (SMX, Sulfdiazine, fulfisoxazole)

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Mechanism- PABA antimetabolites that inhibit Dihydropteroate synthetase.
Use- Hypersensitivity, hemolysis if G6PD deficient, nephrotoxicity (TIN), photosensitivity, kernicterus in infants, displace other drugs from albumin (warfarin)
Resistance- altered enzyme, decreased uptake, increased PABA synthesis

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TMP

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Mechanism- Inhibits bacterial DHFR
Use- TMP-SMX used for UTIs, Shigella, Salmonella, PCP pneumonia
Toxicity- Megalobastic anemia, leukopenia, granulocytopenia (alleviate with leucovorin rescue)

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Ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin (fluoroquinolones), nalidoxic acid (quinolone)

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Mechanism- Inhibit DNA gyrase (Topo II). Cidal. Dont take with antacids.
Use- GNRs of UTI and GI tracts. PSEUDOMONAS, Neisseria, GP
Toxicity- GI upset, superinfections, rash, headache, dizziness, CX in pregnant women and children because damage to articular cartilage. Tendonitis and rupture in adults (dont run), leg cramps, myalgias
Resistance- Chromosome-encoded mutation in DNA gyrase

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Metronidazole

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Mechanism- Forms free radical toxic metabolites in the bacterial cell that damage DNA. Cidal, antiprotozoal
Use- Giardia, Entamoeba, Trichomonas, Gardnerella, ANAEROBES (below diaphragm), H. Pylori
Toxicity- Disulfiram reaction with alcohol, headache, metallic taste, parasthesias, dizziness, GI

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Polymyxins- Polymyxin B, Colistimethate (E)

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Mechanism- Bind to cell membranes of bacteria and disrupt their osmotic properties. Catatonic and act like detergents (basic).
Use- Resistance GN infections. ONLY TOPICAL, PSEUDOMONAS skin infections
Toxicity- Neurotoxicity, ATN

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Pyrazinamide

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Mechanism- Only effective in acidic pH of phagolysosomes where TB engulfed by macrophages is found.
Toxicity- Hepatotoxicity

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Ethambutol

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Mechanism- Decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
Toxicity- Optic neuropathy

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Isoniazid

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Mechanism- Decreased synthesis of mycolic acids. Bacterial catalase-peroxidase needed to convert INH to active metabolite. Similar in structure to B6 (competes in the synthesis of GABA and increases B6 excretion). Different INH half-lives in fast vs. slow acetylators
Use- MTB. Can be used as solo prophylaxis if the person has no evidence of clinical disease.
Toxicity- Neurotoxicity (peripheral neuropathy- Prevent with pyridoxine, B6), hepatotoxicity, lupus.

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Rifampin

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Mechanism- Inhibits DNA-dependent RNAP
Use- MTb, delays resistance to dapsone for leprosy, meningococcal prophylaxis and chemoprophylaxis in contacts of children with H. flu
Toxcity- Increases P450, orange body fluids

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Amphotericin B

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Mechanism- Binds ergosterol and forms membrane pores to allow leakage of electrolytes.
Use- Serious systemic mycoses, Crypto, Blasto, Cocci, Aspergillus, Histo, Candida, Mucor. Intrathecally for funal meningitis (does not cross BBB)
Toxicity- Fever/chills, hypotension, nephrotoxicity (dec GFR- hydration reduces this), arrhythmias (dec K and Mg), anemia, IV phlebitis. Liposomal Amphotericin B reduces toxicity.

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Nystatin

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Mechanism- Same as Amphotericin B. Used topically because it is too toxic for systemic use.
Use- Swish and swallow for oral candidiasis, topical for diaper rash or vaginal candidiasis

Front 28

Fluconazole, ketoconazole, clotrimazole, micronazole, itraconazole, voriconazole

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Azoles
Mechanism- Inhibit fungal sterol synthesis by inhibiting the P450 enzyme that converts lanosterol to ergosterol.
Use- Systemic mycoses: fluconazole for crypo meningitis and candidal infections. Ketoconazole for blasto, cocci, histo, candida albicans, HYPERCORTISOLISM (inhibits desmolase). Clotrimazole and miconazole for topical fungal infections. Itraconazole for Sporothrix.
Toxicity- Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits P450), fever, chills

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Flucytosine

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Mechanism- inhibits DNA/RNA synthesis by conversion to 5-FU.
Use- Systemic fungal infections (candida, crypto) + amphotericin B
Toxicity- N/V/D, BM suppression

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Caspofungin

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Mechanism- inhibits cell wall synthesis by inhibiting synthesis of beta-glucan
Use- Invasive asperillosis
Toxicity- GI, flushing

Front 31

Terbinafine

Back 31

Mechanism- Inhibits squalene epoxidase
Use- Determatophytoses (ESP onchomycosis)

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Griseofulvin

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Mechanism- Interferes with microtubules function to disrupt mitosis. Deposits in keratin containing tissues (nails).
Use- Oral for superficial infections; dermatophytes (tinea, ringworm)
Toxicity- Teratogenic, carcinogenic, confusion , headaches, increases P450 and warfarin metabolism

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Amantadine

Back 33

Mechanism- Blocks penetration/uncoating (M2) and causes DA release from intact nerve terminals
Use- Prophylaxis and treatment for influenza A ONLY; PD
Toxicity- Ataxia, dizziness, slurred speech, anticholinergic
Resistance- Mutated M2 protein (90% influenza A are resistant)
RIMANTIDINE has fewer side effects, but doesnt cross BBB (cant use for PD)

Front 34

Zanamivir, oseltamivir

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Mechanism- Inhibit influenzae NA to decrease the progeny
Use- Influenza A and B, H1N1, H5N1

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Ribavirin

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Mechanism- Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP DH
Use- RSV, chronic hepatitis C
Toxicity- Hemolytic anemia, Severe teratogen

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Acyclovir

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Mechanism- Monophosphorylated by HSV/VZV thymidine kinase and acts as a guanosine analog. Cellular enzymes create triphosphate. Inhibits viral DNA polymerase by chain termination
Use- VZV (use famciclovir), HSV, EBV. No effect on latent forms of VZV and HSV
Resistance- lack of viral TK

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Ganciclovir

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Mechanism- 5'-monophosphate formed by a CMV viral kinase or HSV/VZV TK. Guanosine analog. Triphosphate formed by cellular kinase. Inhibits viral DNAP.
Use- CMV (esp in IC patients)
Toxicity- Leukopenia, neutropenia, thrombocytopenia, renal toxicity.
Resistance- Mutated CMV DNAP or lack of viral kinase

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Foscarnet

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Mechanism- DOES NOT REQUIRE ACTIVATION BY VIRAL KINASE. Inhibits viral DNAP by binding to pyrophosphate site
Use- CMV retinitis when ganciclovir fails.
Resistance- mutated DNAP

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-navir

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HIV Protease inhibitors
Mechanism- Inhibits protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. So maturation of new viruses is halted
Toxicity- Hyperglycemia, GI, lipodystrophy, thrombocytopenia (indinavir), inhibits P450, pancreatitis (Ritonavir), nephrolithiasis (indinavir)

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Zidovudine (ZDV/AZT), Didanosine, Zalcitabine, Stavudine, Lamivudine, Abacavir

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Mechanism- Competitively inhibit nucleotide binding to RT and terminate the DNA chain (lack 3'OH group). Need to be phosphorylated by TK. ZDV for pregnancy
Toxicity- Hypersensitivity (Abacavir), BM suppression (reversed with G-CSF and EPO), peripheral neuropathy (Didanosine, stavudine, zalcitabine), lactic acidosis, megaloblastic anemia (ZDV), GI, hepatic steatosis (didanosine, stavudine)

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Nevirapine, Efavirenz, Declaviridine

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Mechanism- Bind to RT at a site different from NRTIs. DO NOT REQUIRE P-ATION
Toxicity- BM suppression (reversed with G-CSF and EPO), peripheral neuropathy, rash, GI, false positive for cannabinoids and confusion (efavirenz)

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Enfuvirtide

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Mechanism- Bind gp41 to inhibition conformational change required for fusion with CD4 cells, blocking entry and replication. Used in patients with persistent viral replication despite antiretroviral therapy.
Toxicity- Hypersensitivity, reactions at subcutaneous injection site, increased risk of bacterial pneumonia

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Raltegravir

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Integrase inhibitor

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Maraviroc

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CCR5 analog