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ANTIMICROBIAL AGENTS
ANTIBIOTICS:
NATURAL COMPOUNDS PRODUCED BY MICROORGANISM WHICH INHIBIT THE GROWTH OF OTHER .
CHEMOTHERAPY:
SYNTHETIC COMPOUNDS.
SELECTIVE TOXICITY:SELECTIVE TOXICITY:
THE ABILITY TO KILL OR INHIBIT THE GROWTH OF MICROORGANISM WITHOUT HARMING THE HOST CELLS.
BACTERICIDAL: KILLS BACTERIA
BACTERIOSTATIC: PREVENTS MULTIPLICATION.
SPECTRIM OF ACTIVITY:
BROAD SPECTRUM: G+VE& G-VE NARROW SPECTRUM: SELECTIVE ORGANISM.
THERAPEUTIC INDEX:THERAPEUTIC INDEX:
THE RATIO OF THE DOSE TOXIC TO THE HOST TO THE EFFECTIVE THERAPEUTIC DOSE.
EXAMPLES:
PENICILLIN: HIGH AMINOGLYCOSIDES: LOW POLYMYXIN B: THE LOWEST
MECHANISMS OF ACTION OF MECHANISMS OF ACTION OF ANTIMICROBIALSANTIMICROBIALS
1) INHIBITION OF CELL WALL SYNTHESIS.
2) ALTERATION OF CELL MEMBRANES
3) INHIBITION OF PROTEIN SYNTHSIS
4) INHIBITION OF NUCLEIC ACID
5) ANTIMETABOLIC OR COMPETITEVE ANTAGONISM.
MECHANISMS OF ACTIONMECHANISMS OF ACTION
ANTIMICROBIALS THAT INHIBIT ANTIMICROBIALS THAT INHIBIT CELL WALL SYNTHESISCELL WALL SYNTHESIS
BETA LACTAMS
PENICILLINS CEPHALOSPORINS CARBAPENEMS MONOBACTAM
VANCOMYCIN BACITRACIN
FIG. 1
- LACTAM ANTIBIOTICS:- LACTAM ANTIBIOTICS:
BETA LACTAM RING &ORGANIC ACID. NATURAL &SEMISYNTHETIC CIDAL ACTION BIND TO PBP, INTERFERES WITH TRANSPEPTIDATION
REACTION
TOXICITY: HYPERSENS. ANAPHYLAXIS, DIARRHOEA, ..ETC.
PENICILLINS:PENICILLINS:
BENZYLE PENICILLIN:
PENIC. V, PROCAINE PEN., BENZATHIN PEN.
6-AMINOPENICILLANIC ACID:
CLOXACILLIN STAPH.
AMOXYCILLIN ENTEROBACTERIA
PIPERACILLIN PSEUDOMONAS
CEPHALOSPORINS:
FIRST GENERATIONS:
CEPHRADINE
SECOND GENERATIONS:
CEFUROXIME ,CEFOXITIN
THIRD GENERATIONS:
EXPANDED SPECTRUM
THIRD GEN: GRAM –VE ONLY CEFTRIAXONE CEFTAZIDIME
FOURTH GEN: CEFEPIM
CEFEXIME
VANCOMYCIN:VANCOMYCIN:
GLYCOPEPTIDE
CIDAL ON G +VE BACTERIA ONLY.
INHIBIT CELL WALL SYNTHESIS
INJ. ONLY.
USED FOR MRSA S.EDIDER. PESUDOMEM.COLITIS.
NEPHROTOXIC & OTOTOXIC.
ANTIBIOTICS THAT ALTER CELL ANTIBIOTICS THAT ALTER CELL MEMBRANESMEMBRANES
POLYMYXIN B
PEPTIDE ACTIVE AGAINST G –VE
BACTERICIDAL
ONLY USED LOCALLY DUE TO SERIOUS NEPHROTOXICITY
ANTIBIOTICS THAT INHIBIT PROTIEN ANTIBIOTICS THAT INHIBIT PROTIEN SYNTHESISSYNTHESIS
AMINOGLYCOSIDES
TETRACYCLINES
CHLORAMPHENICOL
MACROLIDES
AMINOGLYCOSIDES:
BACTERICIDAL
GRAM –VE BACTERIA
SRTEPT.& ANAEROBES RESISTANT
ACTION: INTERFER WITH BINDING OF t RNA TO 30 S SUBUNIT
GENTAMICIN, AMIKACIN, NEOMYCIN
INJECTABLE
NEPHROTOXIC& OTOTOXIC -DOSE RELATED
TETRACYCLINESTETRACYCLINES
BROAD SPECTRUM, STATIC ORAL ABSORPTION INTRACELLULAR EG. MYCOPLASMA, CHLAMYDIA
BRUCELLA ALSO FOR CHOLERA NOCARDIA
TWO CLASSES: SHORT ACTING: TETRACYCLINE LONG ACTING: MINOCYCLIN ,DOXY.
SIDE EFFECTS: TEETH DISCOLORATION, GIT DISTURBANCE
CHLORAMPHENICOLCHLORAMPHENICOL
BROAD SPECTRUM, CIDAL
BIND TO 50 s RIBOSOMAL SUBUNIT
AFFECT BONE MARROW CELLS AND CAUSE APLASTIC ANAEMIA
SEVERE INFECTIONS: TYPHOID FEVER, HI MENINGITIS, RICKETSIA…ETC.
MACROLIDES:
ERYTHROMYCIN & CLINDAMYCIN
BACTERIOSTATIC
LEGIONELLA, CAMPYLOBACTER, G +VE INFECTIONS IN PTS. ALLERGIC TO PEN.
CLINDAMYCIN ACT ON ANAEROBES
GIT DISTURBANCE, PMC (CLIND)
NEW MACROLIDES:
AZITHROMYCIN , CLARITHRIMYCIN
ANTIMICROBIALS THAT ACT ON NUCLEIC ACIDANTIMICROBIALS THAT ACT ON NUCLEIC ACID
RIFAMOICIN
QUINOLONES
METRONIDAZOLE
RIFAMPICIN:
SEMISYNTHETIC , CIDAL G +VE COCCI
RESERVED FOR TB
INHIBIT DNA DEP.RNA POLYMERASE
RESISTANCE DEVELOP QUICKLY
USED IN COMBINATION
DISCOLORATION OF BODY FLUIDS
HEPATOTOXIC
QUINOLONESQUINOLONES::
SYNTHETIC ,CIDAL, INHIBIT DNA GYRASE
NALIDIXIC ACID : OLD,G _VE ONLY
FLOUROQUINOLONES: CIPROFLOXACIN, NORFLOXACIN
SYSTEMIC INFECTIONS, UTI
BROAD EPECTRUM
BETTER PHARMACOLOGICALLY
AFFECT CARTILAGE IN ANIMALS
Fig. 3
ANTIMETABOLITES:ANTIMETABOLITES:
SULFONAMIDES
TRIMETHOPRIM
COMBINATION: BACTRIM/ SEPTRIN
BLOCK SEQUENTIAL STEPS IN FOLIC ACID SYNTHESIS
NOCARDIA,CHLAMYDIA,PROTOZOA,P.CRANII
UTI LRTI, OM..
GIT.HEPATITIS, BM DEPRESSIN, HYPERSENSITIVITY
ANTITUBERCULOUS AGENTS
FIRST LINE: INH RIFAMPICIN ETHAMBUTOL PYRAZINAMIDE
SECOND LINE:STREPTOMYCIN PASA CYCLOSERINE,CAPREOMYCIN
ISONIAZIDE (INH)
BATERICIDAL
INTRA& EXTRA CELLULAR MYCOBACTERIA
TREATMENT & PROPHYLAXIS
PREPHERAL NEURITIS
ETHAMBUTOL CIDAL CONC.IN
PHAGOLYSOSOME OF ALVEOLI
OPTIC NEURITIS
PYRAZINAMIDE ACID
ENVIRONMENT OF MACROPHAGES
HEPATITIS & ARTHRALGIA
ANTIBIOTIC RESISTANCE IN BACTERIAANTIBIOTIC RESISTANCE IN BACTERIA
INDISCRIMINATE USE OF ANTIMICROBIALS SELECTIVE ADVANTAGE OF ANTIBIOTICS
TYPES OF RESISTANCE:
PRIMARY:
INNATE eg. STREPT. &ANAEROBES RESISTANT TO GENTAMICIN
ANTIBIOTIC RESISTANCE IN BACTERIA (Continue)ANTIBIOTIC RESISTANCE IN BACTERIA (Continue)
AQUIRED: 1-MUTATION: MTB R TO SRTEPTOMYCIN
2- GENE TRANSFER: PLASMID MEDIATED OR TRANSPOSONES
CROSS RESISTANCE: R TO ONE GROUP CONFER R TO OTHER OF THE
SAME GROUP EG ERYTHROMYCIN & CLINDAMYCIN
DISSOCIATE R: R TO GENTA. DOES NOT CONFER R .TO
TOBRAMYCIN
MECHANISMS OR RESISTANCEMECHANISMS OR RESISTANCE
1-PERMIABILITY CANGED
2-MODIFICATION OF SITE OF ACTION, EG. MUTATION
3-INACTIVATION BY ENZYMES.EG. BETA LACTAMASE, AMINOGLYCOSIDES INACTIVATING ENZYMES
BYPASSING BLOCKED METABOLIC REACTION EG. PABA FOILC ACID BY PLASMID MEDIATED
DFR.
PRINCIPLES OF ANTIMICROBIAL THERAPY:PRINCIPLES OF ANTIMICROBIAL THERAPY:
INDICATION CHOICE OF DRUG ROUTE DOSAGE DURATION DISTRIBUTION EXCRETION TOXICITY COMBINATION PROPHYLAXIS:
SHORT TERM: MENINGITISLONG TERM: TB, UTI , RHEUMATIC
FEVER
CRITERIA FOR IDEAL ANTIMICROBIAL:CRITERIA FOR IDEAL ANTIMICROBIAL:
SELECTIVE TOXICITY
NO HYPERSENSITIVITY
PENETERATE TISSUES QUICKLY
RESISTANCE NOT DEVELOP QUICKLY
NO EFFECT ON NORMAL FLORA
BROAD SPECTRUM
ANTIFUNGAL AGENTS:
NYSTATIN LOCAL AMPHOTERICIN B SYSTEMIC
ANTIVIRAL AGENTS IODOXURIDINE VIDARABINE AMANTADINE INTERFERON
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