Bacteriostatic include clindamycin, macrocodes, sulfonamides, and tetracyclines. Most bacterial protein synthesis inhibitors are bacteriostatic except streptogramins which is bactericidal Bactericidal include the aminoglycosides, beta-lactams, fluoroquinolones, metronidazole, most antimycobacterial agents, streptogramins, and vancomycin Bactericidal drugs are preferred for the treatment of endocarditis and meningitis and for most infections in patients with impaired defense mechanisms, especially immunocompromised patients. Some bactericidal agents (aminoglycosides, fluoroquinolones) cause concentration-dependent killing. Maximizing peak blood levels of such drugs increases the rate and the extent of their bactericidal effects. This is one of the factors responsible for the clinical effectiveness of high-dose, once-daily administration of aminoglycosides. Other bactericidal agents (beta-lactams, vancomycin) cause time-dependent killing. Their killing action is independent of drug concentration and continues only while blood levels are maintained above the minimal bactericidal concentration (MBC). Inhibition of bacterial growth that continues after antibiotic blood concentrations have fallen to low levels is called the postantibiotic effect (PAE). The mechanisms of PAE are unclear but may reflect the lag time required by bacteria to synthesize new enzymes and cellular components, the possible persistence of antibiotic at the target site, or an enhanced susceptibility of bacteria to phagocytic and other defense mechanisms including postantibiotic leucocyte enhancement. PAE is another factor contributory to the effectiveness of once-daily administration of amino glycosides and may also contribute to the clinical efficacy of the fluoroquinolones. DRUG ELIMINATION MECHANISMS Erythromycin, clindamycin, chloramphenicol, rifampin, and ketoconazole are notable exceptions, requiring no change in dosage in renal failure Drugs contraindicated in renal impairment include cidofovir, nalidixic acid, long-acting sulfonamides, and tetracyclines Dosage adjustment may be needed in patients with hepatic impairment for drugs including amprenavir, chloramphenicol, clindamycin, erythromycin, indinavir, metronidazole, and tigecycline. Dialysis, especially hemodialysis, may markedly decrease the plasma levels of many antimicrobials; supplementary doses of such drugs may be required to reestablish effective plasma levels after these procedures. Drugs that are not removed from the blood by hemodialysis include amphotericin B, cefonicid, cefoperazone, ceftriaxone, erythromycin, nafcillin, tetracyclines, and vancomycin. di several drug interactions with sulfonamides are based on competition for plasma protein binding; these include excessive hypoglycemia with sulfonylureas and increased hypoprothrombinemia with warfarin disulfiram-like reactions to ethanol occur with metronidazole, with TMP-SMZ, and with several cephalosporins TO ACHIEVE SYNERGISTIC EFFECTS
Several mechanisms, discussed next, may account for synergism. The combined use of drugs may cause inhibition of 2 or more steps in a metabolic pathway. For example, trimethoprim and sulfamethoxazole (TMP-SMZ) block different steps in the formation of tetrahydrofolic acid. Clavulanic acid, sulbactam, and tazobactam inhibit penicillinases and are often used with penicillinase-sensitive beta-lactam drugs. Increased permeability to aminoglycosides after exposure of certain bacteria to cell wall-inhibiting antimicrobials (eg, beta-lactams) is thought to underlie some synergistic effects. ref
 Bacterial Protein Synthesis Inhibitors: Chloramphenicol, Tetracyclines, Macrolides, Clindamycin, Streptogramins, & Linezolid MOA
 Bacterial Protein Synthesis Inhibitors: Amino-glycosides Aminoglycosides are bactericidal inhibitors of protein synthesis. Their penetration through the bacterial cell envelope is partly dependent on oxygen-dependent active transport, and they have minimal activity against strict anaerobes. Aminoglycoside entry can be enhanced by cell wall synthesis inhibitors, which may be the basis of antimicrobial synergism. Inside the cell, aminoglycosides bind to the 30S ribosomal subunit and interfere with protein synthesis in at least 3 ways: (1) they block formation of the initiation complex; (2) they cause misreading of the code on the mRNA template; and (3) they inhibit translocation (reference). Aminoglycosides may also disrupt polysomal structure, resulting in nonfunctional monosomes. Sulfonamides, Trimethoprim, & Fluoroquinolones Antimycobacterial Drugs Gram Positive Organisms: 5 Major groups
Gram Negative Organisms : 5 groups of antibiotics
Anaerobic Organisms: 5 antibiotics
Pulmonary Infection and Antibiotics GI Infection and Antibiotics C. DIFF COLITIS - NAP1/BI/027 or not - Initial episode / 1st or 2nd recurrence - Mild / Moderate / Severe / Severe Complicated - Improving / Worsening - Treatment plan
      Clinical Infectious Diseases 2010;50:133–64 Clinical Infectious Diseases 2010;50:133–64C. Diff
KUB Infections and Antibiotics   SSTI and Antibiotics Anti-fungal Therapy      DOI: 10.1093/cid/civ482 HCAP / VAP / HAP Guidelines for hospital-acquired pneumonia and health-care-associated pneumonia: a vulnerability, a pitfall, and a fatal flaw. Lancet Infect Ds 2011   Nosocomial Meningitis Infection Hospital acquired Gm -ve rods SPACE organisms
Aspiration
Isolation in hospital Contact precautions: GNR with > 3 class resistance
Droplet Precautoin
Airborne Precaution |
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