1. ANTIMICROBIAL AGENTS ANTIBIOTICS:  NATURAL COMPOUNDS PRODUCED BY MICROORGANISM WHICH INHIBIT THE GROWTH OF OTHER. CHEMOTHERAPY:  SYNTHETIC COMPOUNDS.

2. SELECTIVE TOXICITY:  THE ABILITY TO KILL OR INHIBIT THE GROWTH OF MICROORGANISM WITHOUT HARMING THE HOST CELLS.

3. BACTERICIDAL: KILLS BACTERIA BACTERIOSTATIC: PREVENTS MULTIPLICATION. SPECTRIM OF ACTIVITY:  BROAD SPECTRUM: G+VE& G-VE  NARROW SPECTRUM: SELECTIVE ORGANISM.

4. 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

5. MECHANISMS OF ACTION OF ANTIMICROBIALS 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.

6. MECHANISMS OF ACTION

7. ANTIMICROBIALS THAT INHIBIT CELL WALL SYNTHESIS  BETA LACTAMS  PENICILLINS  CEPHALOSPORINS  CARBAPENEMS  MONOBACTAM  VANCOMYCIN  BACITRACIN

8. FIG. 1

9.  - LACTAM ANTIBIOTICS:  BETA LACTAM RING &ORGANIC ACID.  NATURAL &SEMISYNTHETIC  CIDAL ACTION  BIND TO PBP, INTERFERES WITH TRANSPEPTIDATION REACTION TOXICITY:  HYPERSENS.  ANAPHYLAXIS,  DIARRHOEA,..ETC.

11. PENICILLINS: BENZYLE PENICILLIN:  PENIC. V,  PROCAINE PEN.,  BENZATHIN PEN. 6-AMINOPENICILLANIC ACID: CLOXACILLIN STAPH. AMOXYCILLIN ENTEROBACTERIA PIPERACILLIN PSEUDOMONAS

12. CEPHALOSPORINS: FIRST GENERATIONS: CEPHRADINE SECOND GENERATIONS: CEFUROXIME,CEFOXITIN THIRD GENERATIONS: EXPANDED SPECTRUM  THIRD GEN:  GRAM –VE ONLY  CEFTRIAXONE  CEFTAZIDIME FOURTH GEN:  CEFEPIM  CEFEXIME

13. VANCOMYCIN:  GLYCOPEPTIDE  CIDAL ON G +VE BACTERIA ONLY.  INHIBIT CELL WALL SYNTHESIS  INJ. ONLY.  USED FOR MRSA S.EDIDER. PESUDOMEM.COLITIS.  NEPHROTOXIC & OTOTOXIC.

14. ANTIBIOTICS THAT ALTER CELL MEMBRANES  POLYMYXIN B  PEPTIDE ACTIVE AGAINST G –VE  BACTERICIDAL  ONLY USED LOCALLY DUE TO SERIOUS NEPHROTOXICITY

15. ANTIBIOTICS THAT INHIBIT PROTIEN SYNTHESIS  AMINOGLYCOSIDES  TETRACYCLINES  CHLORAMPHENICOL  MACROLIDES

16. 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

17. TETRACYCLINES  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

18. CHLORAMPHENICOL  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.

19. 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

20. ANTIMICROBIALS THAT ACT ON NUCLEIC ACID  RIFAMOICIN  QUINOLONES  METRONIDAZOLE

21. 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

22. QUINOLONES :  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

23. Fig. 3

24. 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

25. ANTITUBERCULOUS AGENTS FIRST LINE: INH  RIFAMPICIN  ETHAMBUTOL  PYRAZINAMIDE SECOND LINE:  STREPTOMYCIN  PASA  CYCLOSERINE,  CAPREOMYCIN

26. ISONIAZIDE (INH)  BATERICIDAL  INTRA& EXTRA CELLULAR MYCOBACTERIA  TREATMENT & PROPHYLAXIS  PREPHERAL NEURITIS

27. ETHAMBUTOL  CIDAL  CONC.IN PHAGOLYSOSOME OF ALVEOLI  OPTIC NEURITIS PYRAZINAMIDE  ACID ENVIRONMENT OF MACROPHAGES  HEPATITIS & ARTHRALGIA

28. ANTIBIOTIC RESISTANCE IN BACTERIA  INDISCRIMINATE USE OF ANTIMICROBIALS  SELECTIVE ADVANTAGE OF ANTIBIOTICS TYPES OF RESISTANCE: PRIMARY:  INNATE eg. STREPT. &ANAEROBES RESISTANT TO GENTAMICIN

29. 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

30. MECHANISMS 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. PABAFOILC ACID BY PLASMID MEDIATED DFR.

31. PRINCIPLES OF ANTIMICROBIAL THERAPY:  INDICATION  CHOICE OF DRUG  ROUTE  DOSAGE  DURATION  DISTRIBUTION  EXCRETION  TOXICITY  COMBINATION  PROPHYLAXIS: SHORT TERM:  MENINGITIS LONG TERM:  TB, UTI, RHEUMATIC FEVER

32. CRITERIA FOR IDEAL ANTIMICROBIAL:  SELECTIVE TOXICITY  NO HYPERSENSITIVITY  PENETERATE TISSUES QUICKLY  RESISTANCE NOT DEVELOP QUICKLY  NO EFFECT ON NORMAL FLORA  BROAD SPECTRUM

33. ANTIFUNGAL AGENTS:  NYSTATINLOCAL  AMPHOTERICIN BSYSTEMIC ANTIVIRAL AGENTS  IODOXURIDINE  VIDARABINE  AMANTADINE  INTERFERON