Download - Anti Microbial Therapy
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Venus Eisha L. BarteMedicine 2A
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Drugs against pathogenic microorganisms without affecting the host cell
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Spectrum of bacterial activity Narrow: (Selective, gm + or gm -)
PCN Aminoglycoside Macrolides
Broad: (All) Chloramphenicol Tetracycline Quinolone
Effect on Microorganisms Cidal: Kills pathogenic microorganism Static: Inhibits growth and multiplication of pathogenic
microorganism Examples:
Vermicidal – Kills the intestinal border Vermifuge – paralyze the parasite
Source From living source - Antibiotics Non living source – Chemotherapetic agents (Sulfur, INH,
minerals)3
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1. Interference with wall synthesis2. Altering the permeability of the cell
membrane3. Interference with CHON synthesis4. Interference with nucleic acid and
metabolism
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Bacitracin Cephalosporin – A B lactam antibiotic Cycloserine Penicillin – A B lactam antibiotic Resticetin Vancomycin – Not an aminoglycoside
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Amphoterecin B – anti fungal Colistin Imidazole – anti fungal Nystatin Polymyxin
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Aminoglycoside Chloramphenicol – original
Bactericidal / static to a few organisms Lincomycin (Clindamycin) – for anaerobic
microorganisms Macrolides (Thromycin)
Original: Erythromycin Static, but with max. dose can be cidal Latest: Claricid (Expensive cidal drug) Claricin: SARS
Tetracycyline - static
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Chloramphenicol Lincomycin Macrolides
Aminoglycoside Tetracycline
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Act on 50s sub unit of bacterial ribosomes
Act on 30s sub unit of bacterial ribosomes
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Clofazimine - cidal Griseofulvin Metronidazole – cidal, anerobic Nalidixic acid Novobiocin Pyrimethamine Quinolone – cidal, acts on DNA gyrase enzyme Rifampin – RNA acting, cidal, anti TB,
meningococcemia prophylactic agent Sulfonamides – a chemotherapeutic agent
Sulfamethoxazole + Trimethoprim = Cidal effect Sulfadoxine + Pyrimethamine (Fancidar) = For malaria,
cidal Trimethoprim
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Identify the causative organism Choose the best, the most appropriate
drug use if only when necessary Consider the nature of illness and health
status of patient Given an adequate dose so that blood
level shall either be cidal or static Evaluate the clinical response and
maintain blood level for sometime even after s/sx have disappeared
Have an adequate knowledge of the drug to use
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To provide broad coverage (In mixed bacterial infections)
For initial (Blind) therapy when patient is seriously ill and results of culture are pending
To provide synergism when organisms are not eradicated with any single agent
To prevent the emergence of resistance – Multi drug therapy
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Cidal + Static = Antagonism 1+1 = 0 Cidal acts on rapidly multiplying bacteria while
static prevents multiplication Static + Static = Additive or same
1+1 = 1 Cidal + Cidal = Synergism
1 + 1 = 3
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Microorganisms produce enzymes that destroy the active drug
Microorganism develop and altered enzyme that can still perform its metabolic function but less affected by the drugs
Microorganism changes their permeability to the drug
Microorganism develop an altered structural target for the drug
Microorganism develop and altered pathway that bypasses the reaction inhibited by the drug
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MIC (Minimum Inhibitory Concentration) – Lowest concentration of drug that inhibits visible growth after an overnight concentration
MBC (Minimum bactericidal concentration) – Lowest concentration of drug that kills at least 99.9% of the original bacterial inoculum
Bacteriostatic – MBC > MIC Bactericidal – MBC = MIC PAE (Post antibiotic effect) – Time period after
an exposure to and removal of an antimicrobial agent during which inhibition of bacterial growth persists 14
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Inhibits Nucleic Acid Synthesis (Quinolone)
Inhibitors of CHON synthesis (Aminoglycosides)
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Natural Penicillin Penicillinase resistant Aminopenicillins Extended spectrum
Living source of PCN: Penicillium notatum arizegenum?
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Penicillin V (Phenoxymethyl Penicillin) Narrow spectrum Acid stable Penicillinase sensitive Give PO since
Penicillin G (Benzylpenicillin) Narrow spectrum Acid labile (Sensitive to HCl) Penicillinase sensitive Parenteral (IM, IV, intrathecal) Vial
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Methcillin (Staphcilin) Acid labile with narrow spectrum
Isoxazolyl Drugs:
Cloxacillin (Tegopen) Dicloxacillin Flucloxacillin – A staphlotoxin, can also be parenteral /
capsule Oxacillin (Bactocill)
Narrow spectrum, acid stable, Highly protein bound: 90-97% (High protein bound = Reduced frequent administration)
Nafcillin (Uripin) Penicillinase resistant Narrow spectrum, poorly absorbed 88% protein
bound only 18
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Drugs Ampicillin
The parent compound Less absorbed
Amoxicillin – q8o, most widely used Better penetration even with purulent sputum, can be
taken with food, and also parenteral Bacampicillin – a prodrug in the liver Epicillin
Has gm + and – activity Acid stable Penicillinase sensitive 19
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Drugs Azlocillin Carbenicillin Mezlocillin Piperacillin – Most expensive Ticarcillin
More on gm (–) activity, acid labile, penicillinase sensitive
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Due to penicilloic acid – antigenic substance from penicillin, common in expired products
There is a release of Ag-Ab reaction
Drug Organism
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Type Incidence Ab Time after PCN
exposure
Immediate (Anaphylactic)
0.02-0.2% IgE 0-30 mins
Accelerated (Parenteral)
1-3% IgE, IgM 30-72hr
Delayed (Serum
sickness)
IgE, IgM/IgG 5-21 days
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S CH3
R—C—NH— CH – CH C—CH3
B A O=C N CH—
COOH
D C
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A = Thiazolidine ring B = B lactam ring
(B lactamase enzyme, destruction site by penicillinase, cephalosporins)
C = Site of salt formation D = Site of penicillinase action R = Side chain
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Drug Preparation Duration
Benzathine Pen G IM 15-30 days
Crystalline Pen G (K or Na)
IM, IV, intrathecal (for meningitis)
4 hrs. Order 4h RTC
Procaine Pen G IM 24h
(One administration/day)
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50-70% of cases of early syphilis and later stages of syphilis
Occurs abruptly after therapy manifested by fever, headache, myalgia, and malaise and may last 24 hrs.
Due to release of toxins of T. pallidum Ask health hx of syphilis
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H2N—CH—HC CH2 5 O
6 C N C—CH2—O—C
O C CH3
COOH
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S
2
3
4#1 and #7 I cannot find
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1 = Dihydrothiazine 2 = B lactam 3 = Site of action of Cephalosporins 4 = Site of salt action 5 and 6 = Site of substitution 7 = Aminocephalosporanic acid
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1st generation drugs Cefa: LZ
loridine zoline
Cepha: DLLP drine lexin lothin pirin
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2nd generation: AAAMOOOOOU Cef:
aclor amandole amezole minox onicid oramide otetan otiam oxitine uroxime
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3rd generation DIOOOTTTT Cef:
diner ixime odizime operazone otaxime tazidime tibuten tizoxime triaxone
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Fourth generation Drugs
Cefditoren Cefepime Cefpirome
Has more anaerobic activity
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1st gen 2nd gen 3rd gen 4th gen
Gm (+) +++ +++ + +++
Gm (--) + ++ +++ +++
Anaerobes (--) (+)/(--) (+)/(--) ++++
Enterococci (--) (--) (--) (--)
Bbrain distribution
(--) (+) [Cefuroxime only]
+++ +++
Dosing interval
q6-8hr q8-12h q6-24h (For brain abscess)
q12hr
Elimination Kidney Kidney K / Liver K
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Suspected bacteremia (Most likely the gm --) especially in debilitated and immunosuppressed patients. Usually given with an aminoglycosides
Surgical prophylaxis: Given 2-6hrs before and 12-24hrs after a surgical procedure having more than 5% risk of infection
Mixed infections especially those including anaerobes involving chest, abdomen, or pelvis
Penicillinase producing N. gonorrhea Gm (--) rod bacterial meningitis – 3rd gen is
DOC
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Monobactam Aztreonam (Azactam) Active against Gm (--) aerobes only No activity against gm (+) organisms and
anaerobes Ex:
E. coli K. pneumoniae H. influenza N. meningitides N. gonorrhea
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Carbapenens Imipenem (Primaxin) – Widest spectrum B
lactam antibiotic Cilastatin – Given in combination with
imipenem A potent selective enzyme inhibitor Ensures urinary antibiotic concentration Nephroprotective effect
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- Drugs in combination of PCN and B lactamase inhibitors
- Drugs:1. Clavulanic acid
1. From Strep. clavuligerus2. Sulbactam
1. Semi synthetic copound derived from 6-APA2. By forming a complex with the B-lactamase,
they render the enzyme inactive so that a B lactam antibiotic can destroy the organism
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Amoxicillin + Clavulanic acid (Augmentin) = PO
Ticarcillin + Clavulanic acid (Timentin) = IV For gm (--)
Ampicillin + Sulbactam (Uripin) = IV
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THE END God bless you