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Lecture

Infectious Disease Management.docx

15 Pages
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Department
Nursing
Course Code
NURS 2050
Professor
Cynthia Barkhouse Mckeen

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Infectious Disease Management Selection of Antibiotics: 1. Empiric Therapy- when you treat an infectious disease on what you think the cause is but you don‟t have proof. 2. Culture and sensitivity- when you identify the infecting organism and what drugs are susceptible. i.e Pneumonia: listen to lungs and fluids, take an x-ray and do a C&S. Start Empiric therapy based on it. i.e. Strep throat: wait for C&S Classification of Antimicrobials 1. By susceptible organism 2. By mechanism of action (groups/families) Antimicrobials – Can impact: 1. Cell wall synthesis 2. Protein synthesis 3. Metabolism 4. Viral enzymes 5. Synthesis of nucleic acids 6. Cell membrane permeability Classification of Penicillin’s 1. Spectrum – narrow vs. broad 2. Sensivity to pencillinase (Penicillins are known as Beta-lactam antibiotics because they have a beta lactam ring). Mechanism of Action: How does penicillin weaken the cell wall? 1. Molecular targets of penicillin’s – - targets are called penicillin binding proteins (PBP) - binding must happen for antimicrobial effect - only present during growth and division 2. 8 penicillin binding proteins (here are a few) • Transpeptidase (penicillin inhibit these) • Autolysins (penicillin activate these) Autolysins: cleave cell wall bonds • Break down segments of the cell wall to permit growth and division • Exposure to penicillins activates autolytic enzymes that degrade the bacteria. • If these autolytic enzymes are not activated, e.g., in certain strains of Staphylococcus aureus, the bacteria are not killed and the strain is said to be tolerant. • By activating these, penicillin‟s promote active destruction of the cell membrane Penicillins – “beta lactams” • Mechanism – weaken cell wall  Oversimplification – does not always cause death • Bacteria take in water, cells rupture, which is bacteriacidal • Penicillin‟s tend to only affect cells during cell growth and therefore are most active during the log phase of cell growth Why Penicillin’s don’t directly hurt the host: 1. Selective toxicity 2. Mammalian cells lack cell walls 3. Target enzymes that affect wall integrity Mechanisms of resistance 3 mechanisms account for clinically significant bacterial resistance to penicillins, & other β- lactam antibiotics as well: 1. Destruction of antibiotic by β-lactamase (destroys ring and renders inactive) 2. Failure of antibiotic to penetrate the outer membrane of gram-negative bacteria to reach PBP targets, 3. Low-affinity binding of antibiotic to target PBPs. Bacterial resistance: B- Lactamase destruction of antibiotic is the most common mechanism of resistance, which is gram negative bacteria, and Psuedomonas aeruginosa in particular, is often accompanies by efflux. Beta lactamase inhibitors • Have no antimicrobial activity when used alone • Combined with antimicrobials – Clavulanic acid (combined with amoxicillin) *More effective* – Tazobactam (piperacillin) – Sulbactam (ampicillin) MRSA: • Methicillin Resistant Staph Aureus • Resistant to penicillin/beta lactam AB Mechanism of Action: bacteria, through genetic mutation, developed PBP‟s with a low affinity for beta lactam antibiotics Penicillin Classification: 1. Affinity for PBPs 2. Resistance to penicillinase 3. Ability to penetrate Gr –ve cell envelop 4. Affect of stomach acid on bioavailability 5. Pharmacokinetic properties Penicillin **Imporant 1. Natural penicillins, penicillinase sensitive - bacteria that form penicillinase won‟t work on them (e.g. Penicillin G and Penicillin V) - Work on gram positive 2. Narrow-spectrum penicillins, penicillinase resistant (antistaphylococcal penicillins) - kill gram positive (e.g. cloxacillin/methacillin) - will work against staph 3. Aminopenicillins, penicillinase sensitive - broad spectrum- will kill gram positive & gram negative (e.g. ampicillin, amoxicillin) 4. Extended-spectrum, penicillinase sensitive *cannot kill S.Aureus 5. Beta lactamase inhibitor combinations – amoxicillin-clavulanic acid, ticarcillin/Clavulanic acid piperacillin/Tazobactam ** Clauvanic acid is for staph! Penicillin Allergies: • Most common allergy • Immediate, accelerated or late (hives, anaphalaxis) • Cross sensitivity (other penicillins, cephalosporins 1%) Cephalosporins 1. Same mechanism as penicillins (∆ wont give with penicillin allergy) 2. Bactericidal 3. Have a beta lactam ring and therefore can be susceptible to beta lactamases 4. Classified as 1st, 2nd, 3rd, 4 generation cephalosporins st th • In general from 1 to 4 generation: 1. ↑ activity vs gram negative bacteria & anaerobes 2. ↑ resistance to destruction by beta lactamases (#1 gen more susceptible to beta lactamase) 3. ↑ penetration into CSF Classification of Cephalosporins: **learn names, but not Trade names 1. First generation: Cefazolin (Ancef) **no gram negative 2. Second generation: Cefaclor (Ceclor), Cefuroxime (Ceftin) 3. Third generation: Cefixime (Suprax), ceftriaxone (Rocephin)= tazmanian devil- pseduo 4. Fourth generation: Cefepime **Not all cephalosporins are created equal! Adverse Effects: 1. Hypersensitivity 2. Cross reactivity with penicillins 3. There are also specific adverse effects with each agent Vancomycin (MRSA TX, ensure to use other drugs First) 1. Mechanism of Action: Disrupts cell wall synthesis promoting lysis and death 2. Spectrum: Bactericidal vs most gram positive bacteria (except enterococcus - needs to be combined with an aminoglycoside for synergy) – Resndved for severe infections, those resistant to clox or penicillins – 2 line for c. diff diarrhea 3. Huge molecule - poor penetration into certain tissues (e.g. CSF) – Not dialyzable (unless high flux membrane) 4. Given IV as not absorbed orally (no bioavailability) – Oral: infections of intestine such as c. diff where it can act “locally” acts locally in the bowel 5. For prolonged treatment courses– e.g. staph osteomyelitis – home IV programs 6. Therapeutic drug monitoring (especially in those with renal dysfunction) – Troughs (and peaks) narrow spectrum of use, troughs most useful – Ensure to record times: infusion start/stop, when pre/post draws were drawn 7. Renally eliminated (Creatinine clearance, monitor renal function) *low creatinine clearance, look for toxicity b/c half life accumulates and peaks increase. 8. Depending on the institution: Pharmacokinetic monitoring (by pharmacists), protocols tell when to draw levels and dosage adjust. Trough is almost always 30 minutes prior to next dose. Peak 1 hour after a 1 hour infusion. Adverse Effects: 1. Ototoxicity: often irreversible (Rare), associated with drug levels of greater than 60-80 micrograms/L. Caution with concurrent ototoxins (e.g. aminoglycosides, high dose IV furosimide (loop diuretic). 2. Thrombophlebitis 3. Hypersensitivity reactions: (Rare), drug fever or allergic rash 4. Infusion related effects: (more common), „Red Man syndrome‟ realated to histamine release. 1. Slow infusion time (usually given over an hour so prolong this). 2. Pre medicate- diphenhydrinate (Benadryl) 5. Nephrotoxicity: (Rare), but caution with other drugs that cause this. Protein Synthesis Inhibitors: 1. Target the bacterial ribosome (Bacteria- 70S (50S/30S), Mammalian- 80S (60S/40S)) *High levels may interact with mammalian ribosomes 2. 50 S binders (macrolides, Clindamyacin, Chloramphenicol 3. 30 S binders (aminoglycosides, tetracyclines) Types: 1. Tetracyclines 2. Macrolids 3. Clindamycin 4. Aminoglycosides 5. Sulfamethoxazole, trimethoprim 6. Fluoroquinolones 7. Metronidazole Drugs: impact 50S or 30S ribosomal subunit Addition of AA to growing peptide chain is prevented 1. Tetracyclines (bacteriastatic) • Tetracycline, doxycycline, minocycline • Activity versus gram positive bacteria (not always predictable), gram negative bacteria Uses 1. Chlamydia (STD) 2. Acne, 3. H. Pylori (Peptic Ulcer Disease) 4. Traveler's diarrhea Side effects (not tolerated well) 1. GI upset, esophageal ulcers 2. Photosensitivity 3. Hepatotoxicity – fatty infiltration of liver (high dose) 4. Effects on bones and teeth (not given to children during development) Bind to calcium in developing bones and teeth – yellow or brown discoloration – do not use in children less than 8 years **yellow/brown teeth Drug Interactions: 1. Chelate with Ca 2. Fe supplements 3. Mg laxatives 4. Antacids (most) 5. Oral contraceptives 2. Macrolides- * drug of choice in those with penicillin allergy • Antibacterial coverage similar to penicillin 1. Erythromycin: • Has 4 forms: Base (which is unstable in stomach acid), and 3 derivatives of the base:
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