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penicillin in dentistry (ANTIBIOTICS) - by shefali jain

penicillin in dentistry (antibiotics)

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penicillin in dentistry (ANTIBIOTICS) - by shefali jain

  1. 1. INTRODUCTION Greek word Anti - against Bios - life  Antibiotics are substances produced by microorganisms, which suppress the growth of or kill other microorganisms at very low concentrations (K.D Tripathi- 5TH Edition)  Antibiotics are chemical substances produced by microorganisms having the property of inhibiting the growth or destroying other microorganisms in high dilution (by Waksman)
  3. 3. PERIOD OF EMPERICAL USE  In 17th and 18th century, there were no proper treatment for diseases.  Chinese use plant and moulds to treat infected wounds.  In india,Chalmugra oil is used to treat leprosy.  Chinchona bark for fever.  Egyptian use honey + lint used for dressing wound.
  4. 4. EHRLICH’S PHASE OF DYE AND ORGANOMETALLIC COMPOUND  Ehrlich toyed with idea that if certain dyes could selectively stain microbes ,they could selectively toxic to these organism,tried methylene blue,trypan red etc.  He developed arsenicals-Atoxyl for sleeping sickness, Arsphenamine for syphilis.
  5. 5. MODERN ERA.  In 1935, Domagk demostrate the therapeutic effect of Prontosil, a sulfonamide dye, in pyogenic infection.  Sulfapyridine was first sulfonamide to be marketed in 1938 Gerhard Domagk
  6. 6.  Penicillin was discovered by chance in 1928  Flemings (1929) found that a diffusable substance was elaborated by Penicillium mould which destroy staphylococcus on culture plate.  He named this substance PENICILLIN but could not purify it. Alexander Fleming
  7. 7.  In the 1940s Waksman and his colleagues undertook a systematic search of Actinomycetes as a source of antibiotics and discovered Streptomycin in 1944. All three groups of scientists Domagk,Fleming -chain- Florey and Waksman recieved Nobel Prize for their discoveries. Selman Waksman
  8. 8.  1948- chlortetracycline  In 1957- Nystatin  In 1970- new 4 Quinolones  In 1980- Norfloxacin  In 1998- Smithkine beecham patented Amoxicillin/clavunate potassium tablets .
  9. 9. CLASSIFICATION… DEPENDING ON CHEMICAL STRUCTURE 1.Sulfonamides and related drugs ( dapsone) 2.Diaminopyrimidines( trimethoprim) 3.Quinolone ( norfloxacin, ciprofloxacin) 4.β-lactum antibiotics ( penicillin, cephalosporin) 5.Tetracyclines ( doxcycycline) 6. Nitrobenzene derivative ( chloramphenicol) 7. Aminoglycosides ( gentamycin, neomycin) 8. Macrolide antibiotics ( erythromycin,Azithromycin) 9. Polypeptide antibiotics ( polymyxin- B) 10.Nitrofuran derivatives (furazolidine) 11.Nitroimidazoles (metronidazole) 12. Polyene antibiotics (nystatin, Amphoterin–B)
  11. 11. TYPE OF ORGANISMS AGAINST WHICH PRIMARILY ACTIVE a) Antibacterial- penicillin, Aminoglycosides b) Antifungal- Griseofulvin, Amphotericin B etc c) Antiviral- Acyclovir, Zidovudine d) Antiprotozoal- Chloroquine, metronidazole. e) Anthelmintic- Niclosamide, Mebendazole.
  12. 12. SPECTRUM OF ACTIVITY a) Narrow Spectrum – Penicillin–G, Streptomycin, Erythromycin b) Broad Spectrum - Tetracycline , Chloramphenicol. TYPE OF ACTION a) Primarily Bacteriostatic- Sulfonamide, Tetracycline. b) Primarily Bactericidal- Penicillin, Cephalosporin. SOURCE OF ANTIBIOTICS a) Fungi- Penicillin, Griseflovin b) Bacteria- polymyxin B, Bacitracin c) Actinomycetes- Aminoglycosides, Macrolides.
  13. 13. SELECTION OF ANTIMICROBIAL AGENTPateint factor • Age • Renal and hepatic function. • Local factor. • Drug allergy. • Imapired host defence. • Pregnancy Organism related factor • Bacteriological sensitivity testing. • Minimum inhibitory concentration, • Minimum bactericidal concentration. • Postantibiotic effect Drug factor • Spectrum of activity. • Type of activity. • Sensitvity of the organism • Relative toxicity • Pharmokinetic profile • Route of administration.
  14. 14. IDENTIFICATION OF CAUSATIVE ORGANISM ANAEROBIC BACTERIAAEROBIC BACTERIA Gram- positive cocci Gram- negative bacilli Gram- positive cocci Gram negative bacilli sterptococcs staphylococc s Viridians b-hemolytics Haemophilus influenzae Escheria coli Klebsiella Eikenella corroden streptococcus Porphyromonas Fusobacteria provetella
  15. 15. ORGANISMS RESPONSIBLE FOR APICAL ABSCESS 1. Streptococci species 2. Streptococci intermedius 3. Streptococci angiosus 4. Streptococci constellatus 5. Bacteroides species
  16. 16. ORGANISMS RESPONSIBLE FOR PERIODONTAL DISEASE 1. Porphyromonas gingivalis 2. Actinobacillus actinomycetecomitans 3. Borrelia vicenti 4. Prevotella intermedia 5. Fusobacterium (Mainly gram negative bacteria)
  17. 17. ORGANISMS RESPONSIBLE FOR DENTAL CARIES 1. Strep. Mutans group 2. Strep. Salivarius 3. Actinomyces species 4. Lactobacilli
  18. 18.  Aerobic bacteria plays an important role in the origin of odontogenic infections.  Anaerobic gram-positive cocci are seen 1/3 of all odontogenic infections.  Gram-negative rods comprises of 50% of odontogenic infections.
  19. 19. ORGANISM RELATED FACTORS  Clinical diagnosis  Bacteriologic examination 20 Cont…
  20. 20. Minimum Inhibitory Concentration (MIC) 21 MIC- The lowest concentration of an antibiotic which prevent visible growth of a bacterium determined in microwell culture plate FOR THERAPEUTIC PURPOSES :- 1. Peak concentration of antibiotics should be three to four times of the MIC. 2. Therefore the dosage prescribed must be capable of establishing a concentration of three to four times the MIC.
  21. 21. Minimum bactericidal Concentration (MBC) 22 MBC- of antibiotics is determined by subculturing from tubes with no visible growth A small difference between MIC and MBC indicate antibodies is primary bacteriocidal, Large difference indicate bacteriostatic action. If sufficient drug is not given to reach therapeutic levels, sub therapeutic levels may mask the infection without killing the microbes.
  22. 22. DRUG FACTORS  Spectrum of activity  Type of activity  Sensitivity of organism  Relative toxicity  Route of administration  Evidence of clinical efficacy  Cost  Pharmacokinetic profile 23 Cont…
  23. 23. SPECTRUM ANTIBIOTIC  Narrowest antibacterial spectrum should be chosen. 1. It minimizes the risk of superinfection. 2. Broad-spectrum antibiotic develop resistant against many bacteria. 3. Use of narrow-spectrum antibiotics allow larger proportion of the host flora to be maintained, by reducing superinfection to minimum.
  24. 24. Type of activity  Use of bactericidal rather than a bacterostatic drug .  Bactericidal drugs are used for patients who are pathologically immuosuppresed.  Bacterostatic they inhibit growth and reproduction of bacteria by inhibiting protein synthesis.  Bactericidal they penetrate into bacterial cell and kill them.
  25. 25. Why we use bactericidal drug ? 1. Host resistance 2. Destroying microbes by antibiotic itself 3. Better than bacterostatic drugs 4. Greater flexibility in dosage
  26. 26. Eg:-  Bactericidal drugs such as penicillin or cephalosporin should be used in immunodeficient patients instead of bacteriostatic drugs, erythromycin or clindamycin.  If bacteriostatic drugs are given then bacteria in immunocompromised patients will not be killed and there will be chances for them to develop resistance.
  27. 27. PROPER TIME INTERVAL  Frequency of dosing is very important.  Each drug has its specific plasma half-life (t1/2), during which one half of the absorbed dose is absorbed.  Usual and divided dosages is maintained.
  28. 28. PROPER ROUTE OF ADMINISTRATION  Drugs can be administered by variety of routes but its choice depends on both drugs as well as patient related factors.  Routes divided into:- 1. Local routes 2. Systemic routes
  29. 29. USE OF LEAST TOXIC ANTIBIOTIC • Antibiotics are used for killing living bacteria but some antibiotics kill bacteria's existing in normal flora and thus are highly toxic.  Less toxic drug must be used which are equally effective.
  30. 30.  Eg:- Bacteria which cause odontogenic infections are usually sensitive to penicillin and chloramphenicol Hence, penicillin is preferable because of lower toxicity. • Second choice of drug. 1) Clindamycin 2) Erythromycin
  31. 31. COMBINED USE OF ANTIBIOTICS  Synergism  Reduction in adverse effects  Prevents emergence of resistance  Broadens the spectrum antimicrobial action 32 DISADVANTAGES  Casual outlook  Increased chances of superinfections  Emergence of resistance  Increased cost of therapy
  32. 32. PENICILLIN
  33. 33. History  1928 - Alexander Fleming  Bread mold (Penicillium notatum) growing on petri dish  1939 - Florey, Chain, and Associates  Began work on isolating and synthesizing large amounts of Penicillin.  1941 – introduced in antibacterial therapy
  34. 34. PENICILLINS  Beta- lactam antibiotics  Narrow spectrum antibiotics  Bactericidal  These have the greatest activity against gram-positive organisms, gram-negative cocci, and non- lactamase-producing anaerobes. However, they have little activity against gram-negative rods.  They are susceptible to hydrolysis by lactamases. 35
  35. 35. STRUCTURE
  36. 36.  The penicillins are classified as -lactam drugs because of their unique four- membered lactam ring.  All penicillins have the basic structure shown A thiazolidine ring (A) is attached to a -lactam ring (B) that carries a secondary amino group (RNH–). can be attached to the amino group.  Structural integrity of the 6-aminopenicillanic acid nucleus is essential for the biologic activity of these compounds.  If the -lactam ring is enzymatically cleaved by bacterial -lactamases, the resulting product, penicilloic acid, lacks antibacterial activity.
  37. 37. PENICILLINS Natural Semi synthetic 38
  38. 38. CELL WALL SYNTHESIS IN BACTERIA. The first stage, precursor formation, takes place in the cytoplasm. The product, uridine diphosphate (UDP)- acetylmuramyl-pentapeptide, called a “Park nucleotide” accumulates in cells.  The PEPTIDOGLYCAN residues are linked together forming a long strand and UDP is split off.  The final step is cleavage of terminal D-aniline of peptide chain by transpeptidase; energy so released is utilised for establishment of cross linkage between peptide chains of neighbouring strands.  This cross linking provide stablity and rigidity to the cell wall.
  39. 39. Comparison of the structure and composition of gram-positive and gram-negative cell walls.
  40. 40. Mechanism of action.  Peptidoglycan synthesis(in last step) is inhibited by beta lactam antibiotics.  Penicillin bind at the active site of the transpeptidase enzyme that cross – links the peptidoglycan strands.  It does this by mimicking the D-alanyl-D-alanine residues that would normally bind to this site.  Penicillin irreversibly inhibit the enzyme transpeptidase.  For the action of penicillin and cephalosporin ;these are collectively termed Penicillin-binding protein (PBS) are present on cell membrane of bacteria.
  41. 41. Penicillin Bind (PBP) on the cell wall of susceptible bacteria Inhibits transpeptidation Prevents peptidoglycan synthesis Cell wall deficient forms spheroplasts & filamentous forms Autolysis Cell death (bactericidal action)
  42. 42. CLASSIFICATION- PENICILLIN- Natural Penicillins • Penicillin G Semi synthetic Penicillins • Acid-resistant alternative to penicillin G • (Penicillin V); • Penicillinase-Resistant Penicillins • (cloxacillin, Oxacillin, Methicillin) • Extended-spectrum penicillins • 1. Aminopenicillin- Ampicillin and Amoxycillin • 2.Carboxypenicillin • Carbenicillin, Ticarcillin • 3.Ureidopenicillins- • Piperacillin,Mezlocillin. B-lactamase inhibitors- • Clavlanic acid • Sublactam
  43. 43. CLASSIFICATION  NARROW SPECTRUM PENICILLINS β-lactamase sensitive Acid resistant -Penicillin V (oral) Acid labile - Penicillin-G (benzyl penicillin)(I.M,IV) - Procaine penicillin-G(I.M,depot inj) - Benzathine penicillin-G(I.M, depot inj)
  44. 44. β-lactamase resistant Acid resistant - Cloxacillin - Dicloxacillin - flucloxacillin Acid labile - Methicillin (I.M,I.V) - Nafcillin (I.M,I.V)
  45. 45.  EXTENDED SPECTRUM PENICILLINS Acid resistant • Aminopenicillins: Ampicillin, Amoxicillin, Bacampicillin, Talampicillin Acid labile (ANTIPSEUDOMONAL PENICILLINS) • Carboxypenicillins: Carbenicillin, Ticarcillin • Ureidopenicillins: Piperacillin, Mezlocillin, Azlocillin  BETA LACTAMASE INHIBITORS • Sulbactam, Tazobactam, Clavulanic acid
  46. 46. Natural penicillins  Penicillin G is a narrow spectrum antibiotic; activity is primarily to gram positive bacteria and few other.  Obtained from fermentations of the mold Penicillium chrysogenum  Penicillin G (benzylpenicillin) Penicillium
  47. 47.  Cocci- streptococci (except enterococci) staphylococcus aureus, (gram negative cocci) Neisseria gonorrhea N. meningitis  Bacilli- B.anthracis Corynebacteriumm diptheria, Clostridium tetnai. Actinomyces israelli(moderately sensitive) Gram negative bacilli- E coli. proteus. Activity against these Microrganism-
  48. 48. Pharmacokinetics  It is relatively unstable in acid, thus the bioavailability is low.  There is poor penetration into the cerebrospinal (CSF), unless inflammation is present.  Active renal tubular secretion results in a short half-life.
  49. 49. Pharmacokinetics Oral administration of Penicillin G:  Acid labile  About one-third of an orally administered dose of PnG is absorbed from the intestinal tract under favorable conditions.  Gastric juice at pH 2 rapidly destroys the antibiotic. Parenteral Administration of Penicillin G:  From I.M site absorption is rapid and complete  Peak plasma levels attained in 30min
  50. 50. DISTRIBUTION Penicillin G is distributed widely, but the concentration differs in various fluids and tissues. Its apparent volume of distribution is ~0.35 L/kg. Approximately 60% of penicillinG in plasma is reversibly bound to albumin. Significant amounts appear in liver, bile, kidney, joint fluid, and lymph.
  51. 51. Cerebrospinal Fluid  Penicillin does not readily enter the CSF but penetrates more easily with meningeal inflammation.  The concentration attained usually reaches 5% of the value in plasma and thus is therapeutically effective against susceptible microorganisms.
  52. 52. EXCRETION Normally, penicillin G is eliminated rapidly from the body, mainly by the kidney. Approximately 60–90% of an intramuscular dose of penicillin G in aqueous solution is eliminated in the urine, largely within the first hour after injection. The remainder is metabolized to penicilloic acid.  The t1/2 for elimination of penicillin G is ~30 minutes in normal adults. Approximately 10% of the drug is eliminated by glomerular filtration and 90% by tubular secretion
  53. 53. Unitage of Penicillin  The IU of penicillin is the specific penicillin activity contained in 0.6 microgram of the crystalline sodium salt of penicillin G.  Thus 1g= 1.6 million units  1 million unit= 0.6g
  54. 54. DOSES-  1. Sod.Penicillin G inj- 0.5-5 MU i.m./i.v. 6-12 Hourly ( BENZYL PEN 0.5-1MU in  Repository Penicillin G inj- these are insoluble salts of PnG which must be given by deep i.m (Never i.v.) slowly at the site of inj. 2. Procaine Penicillin G inj- 0.5-1 MU( i.m) 12-24 hourly as aqueous suspension. ( PROCAINE PENICILLIN-G 0.5 MU dry powder in vial)  It is a form of penicillin which is a combination of benzylpenicillin and the local anaesthetic agent procaine. Following deep intramuscular injection, it is slowly absorbed into the circulation and hydrolysed to benzylpenicillin — thus it is used where prolonged low concentrations of benzylpenicillin are required.  This combination is aimed at reducing the pain and discomfort associated with a large intramuscular injection of penicillin. It is widely used in veterinary settings.
  55. 55. Fortified procaine penicillin G inj- contain 3 lac U procaine penicillin and 1 lac U sod. Penicillin G to provide rapid as well as sustained blood level. 3. Benzathine benzylpenicillin- Dose- Penidure LA12 Inj (12 lac unit) It is the drug-of-choice when prolonged low concentrations of benzylpenicillin are required and appropriate, allowing prolonged antibiotic action over 2–4 weeks after a single IM dose
  56. 56. USES 58  Streptococcus pneumoniae infections  Meningococcal infections  Syphilis  Prophylaxis against Group A Streptococci in patients with history of rheumatic heart disease  Actinomycosis  Trench mouth
  57. 57. Therapeutic uses-  Gingivostomatitis, produced by the synergistic action of Leptotrichia buccalis and fusospirochetes that are present in the mouth, is readily treatable with penicillin.  For simple “trench mouth,” 500 mg penicillin V given every 6 hours for several days is usually sufficient
  58. 58. Streptococcal Infections  Pharyngitis is the most common disease produced by S. pyogenes. Penicillin-resistant isolates of this organism have yet to be observed.  The preferred oral therapy is with penicillin V, 500 mg every 6 hours for 10 days. Equal results are produced by the administration of 600,000 units of penicillin G procaine intramuscularly once daily for 10 days or by a single injection of 1.2 million units of penicillin G benzathine
  59. 59.  Streptococcal Toxic Shock and Necrotizing Fascitis  These life-threatening infections are best treated with penicillin plus clindamycin (to decrease toxin synthesis).
  60. 60. Pneumococcal Infections Penicillin G is the drug of choice for infections caused by sensitive strains of S. pneumoniae, but resistance is an increasing problem. Thus, for pneumococcal pneumonia, a third-generation cephalosporin or high-dose penicillin G (i.e., 20–24 million units daily by continuous intravenous infusion or in divided boluses every 2–3 hours) should be used until sensitivities are determined. For parenteral therapy of sensitive isolates, penicillin G or penicillin G procaine is favored. Therapy should be continued for 7–10 days, including 3–5 days after the patient is afebrile
  61. 61.  Streptococcal Pneumonia, Arthritis, Meningitis, and Endocarditis  These uncommon conditions should be treated with penicillin G; daily doses of 12–20 million units are administered intravenously for 2–4 weeks (4 weeks for endocarditis
  62. 62. Infections with Anaerobes  Many anaerobic infections are polymicrobial, and most of the organisms are sensitive to penicillin G.  An exception is the B. fragilis group, 75% of which may be resistant. Pulmonary and periodontal infections usually respond well to penicillin G.  Mild-to-moderate infections at these sites may be treated with oral medication (either penicillin G or penicillin V 400,000 units four times daily).
  63. 63. Staphylococcal Infections  The vast majority of staphylococcal infections involve penicillinase-producing organisms.  Patients with staphylococcal infection should receive penicillinase-resistant penicillins (e.g., nafcillin or oxacillin).  Staphylococcal infections increasingly involve methicillin-resistant staphylococci, which are resistant to penicillin G,
  64. 64. Meningococcal Infections  Penicillin G is the drug of choice for meningococcal disease. Patients should be treated with high doses of penicillin given intravenously
  65. 65. Syphilis  Therapy of syphilis with penicillin G is highly effective. Primary, secondary, and latent syphilis of<1 year’s duration may be treated with penicillin G procaine (2.4 million units per day intramuscularly),plus probenecid (1.0 g/day orally) to prolong the t1/2, for 10 days or with 1–3 weekly  Intramuscular doses of 2.4 million units of penicillin G benzathine (three doses in patients with HIV infection)
  66. 66. Adverse effects  Hypersensitivity Reactions: The basis of which is the fact that degradation products of penicillin combine with host protein and become antigenic.  Jarisch- Herxheimer reaction: Penicillin injected in a syphillitic pateint (secondary syphillis) may produce shivering , fever,myalgia, exacerbation of lesions, even vascular collapse. This is due to sudden release of spirochetal lytic products and last 12-72 hrs. It does not recur and doesnot need inertuption of therapy.
  67. 67. Other adverse effects  Very high doses of penicillin G can cause seizures in kidney failure.  Pain at I.M injection site  Nausea on oral ingestion  Thromboplebitis of injected vein
  68. 68.  The major draw backs of benzylpenicillin are:  Inactivation by gastric acid  Short duration of action  Poor penetration into the CSF  Narrow spectrum of activity  Susceptibility to Penicillinase  Development of resistance  Possibility of anaphylaxis
  69. 69. Penicillin V ( acid resistance to Penicillin –G)  Orally active  Used for the treatment of bacteremia and oral infections  Higher minimum bactericidal concentration. • DOSE: • 250-500 mg. Given 6 hourly. • Infants:60mg • Crystapen-V, kaypen, 125, 250mg tab.
  70. 70. Penicillinase-resistant penicillins (antistaphylococcal penicillins)  These congeners have side chains that protect the beta lactam ring from attack by staphylococcal penicillinase  Indicated in infections caused by penicillinase producing staphylococci (drugs of choice, except in MRSA)  Methicillin, Cloxacillin  Oxacillin, Nafcillin, Dicloxacillin
  71. 71. Penicillinase-resistant penicillins (antistaphylococcal penicillins) Methicillin:  Acid labile  Not used clinically, except to identify resistant strains  MRSA is susceptible to Vancomycin/linezolid and rarely Ciprofloxacin  It is highly penicillin resistant but not acid resistant- must be injected.  Adverse reaction- haematuria, albuminuria, reversible interistial nephritis.
  72. 72. Penicillinase-resistant penicillins … Cloxacillin:  Highly Penicillinase and Acid resistant  More active than methicillin  Less active against PnG sensitive organisms: should not be used as its substitute  Incompletely but dependably absorbed (oral route)  >90% protein bound, eliminated primarily by kidney, also partly by liver  Plasma half life is about 1hr  Given in staphylococcus infection resistant to benzyl penicillin  Active against a variety of gram-negative bacilli as well.
  73. 73.  Dose- 0.25, 0.5 g orally every 6 hourly, For severe infections 0.25-1g may be injected i.m or i.v. BIOCLOX , CLOCILIN 0.25, 0.5g CAP. 0.5g/ vial injection Ampicillin + cloxacillin – Ampoxin- (ampicillin 125mg + cloxacillin 250mg) Roscilox- (ampicillin 125mg + cloxacillin 250mg)
  74. 74. Extended spectrum penicillins. Aminopenicillins: Ampicillins:  Active against all organisms sensitive to PnG; in addition, many gram- negative bacilli
  75. 75. Extended spectrum penicillins Cont…
  76. 76. Extended spectrum penicillins Cont… Pharmacokinetics:  Acid resistant  Oral absorption is incomplete but adequate  Primary excretion is kidney, partly enterohepatic circulation occurs  Plasma half life is 1hr Uses:  UTI, RTI, Meningitis, Gonorrhoea, typhoid fever, bacillary dysentery, Cholisystitis, Subacute bacterial endocarditis and Septicemias
  77. 77. Extended spectrum penicillins Adverse effects:  Diarrhoea(it is incompletely absorbed – the unabsorbed drug irritates the lower intestine as well as causes marked alteration of bacterial flora)  Rashes  Hypersensitivity Interactions:  Hydrocortisone –inactivates ampicillin if mixed in the I.V solution  Oral contraceptive –failure of oral contraception  Probenecid –retards renal excretion
  78. 78. Extended spectrum penicillins Bacampicillin –ester prodrug of ampicillin  Talampicillin, Pivampicillin and Hetacillin are other Prodrugs of ampicillin DOSE-  Adult- 250- 500 mg every 6 hr  Child- 50-100 mg/kg given in equally divided doses every 6 hr  Maximum- 2-4 g/ day  Roscillin cap 500mg cap- 250 mg, inj 250 mg, inj 500 mg (ranbaxy) D-syr 125mg/ml, 250mg/ml  Ampillin- Cap 250 mg, Cap 500mg, inj 250mg, 500mg  Ampicillin + cloxacillin – Ampoxin- (ampicillin 125mg + cloxacillin 250mg) Roscilox- (ampicillin 125mg + cloxacillin 250mg)  Ampicillin + sulbactam – Ampitum inj ( ampicillin 1g + sulbactam 0.5g/ml) ( community accguired and hospital accquired pneumonia)
  79. 79. Amoxicillin:  Close congener of ampicillin but not a prodrug  Similar to it in all aspects except:  Better oral absorption  Higher and sustained blood levels are produced  Incidence of diarrhoea is lower  Less effective against Shigella and H. influenzae DOSE-  Amoxylin , 250, 500mg  Novamox 250,500mg  Mox 500mg,500mg  Symoxyl – LB 625 (500mg(amoxicillin )+ 60 million cell( lactobacilli sporogene  Stedmox- Tn(500mg(amoxicillin ) + 500mg( tinidazole)  Moxikind CV- kid (200mg(amoxicillin)+28.5mg( clavunaic acid)  Moxikind CV- 625 (500mg(amoxicillin)+125mg( clavunaic acid)  Agupen LB- (875(amoxicillin trihydrate)+125mg( clavunate K) + 60 million cell( lactobacilli sporogene)  Agupen LB- 625 (500mg(amoxicillin trihydrate)+125mg( clavunate K) + 60 million cell( lactobacilli sporogene)
  80. 80. Extended spectrum penicillins 2. Carboxypenicillins (Carbenicillin, Ticarcillin) and 3. Ureidopenicillins (Piperacillin)
  81. 81. CARBEPENICILLIN  Penicillin conger.  Special feature- its activity against peudomonas aeriginosa and indole positive Proteus.  It has Gram-negative coverage which includes Pseudomonas aeruginosa but limited Gram-positive coverage  Less active against- salmonella, E.coli, Enterobacter.  Klebisella and gram positive cocci are remain unaffected.
  82. 82. Uses-  Burns  Urinary infection.  Septecimia.  Uncomplicated gonorrhea
  83. 83. Pharmacokinetics  It is neither penicillinase resistant nor acid resistant.  Inactive orally.  Excreted rapidly in urine.  t ½ = 1hr  Dose= 1-2 g i.m, 1-5 g i.v.  Trade name-  Pyogen, Carbelin 1g, 5 g per vial inj
  84. 84. Extended spectrum penicillins  These are called antipseudomonal penicillins  Piperacillin is more potent among these  Carbenicillin is less effective against Salmonella, E. Coli and enterobacter but not active against Klebshiella and gram-positive cocci  Piperacillin has good activity against Klebshiella, and is used mainly in neutropenic/ immunocompromised patients having serious gram-negative infections and in burns UREIDOPENICLLINS- (PIPERACILLIN)
  85. 85.  t ½ =1 hr.  Dose = 100-150 mg/kg/day.  Trade name=  Piprapen 1g, 2g vials  Pipracil inj 2g, 4g  Pipracillin+tazobactam ( noscomial infection )- Novacillin plus (pipracillin Na 4g + tazobactam 0.5 g)
  86. 86. Beta-lactamase inhibitors Clavulanic acid, Sulbactam and Tazobactam They contain beta-lactam ring but themselves, do not have significant antibacterial activity. Inactivate bacterial beta-lactamases and are used to enhance the antibacterial actions of beta-lactam antibiotics.
  87. 87. Beta-lactamase inhibitors Cont… Clavulanic acid:  Obtained from Streptomyces clavuligerus.  It has beta lactam ring but no antibacterial activity of its own.  It inhibit wide variety Class II to class V of beta lactamase.  It is a progressive inhibitor : binding with beta lactamase is reversible intially but becomes covalent later – inhibitition increasing with time.  Called a suicide inhibitor , it gets inactivated after binding to enzyme.
  88. 88. Pharmacokinetics-  Rapid oral absorption.  Bioavailability – 60%  t ½ = 1 hr  Pharmacokinetics matches amoxicillin with which it is used.
  89. 89. Uses-  Addition of clavunic acid restablises the activity of amoxicillin against beta lactamase producing resistant Staph.aureus, H. inflenza, N.Gonorrhoeae, E coli proteus, klebisella, salmonella and bacteria Fragilis.  Coamoxiclav is indicated for  Odontogenic infection  Skin and soft tissue infection.  Respiratory tract infection.  Intra abdominal and gynaecological infection  Dose- Agumentin- Amoxicillin 250mg + Clavunic acid125mg ( TDS) Agumentin – amoxicillin 1 g & clavunic acid 0.2 g vial. i.m /i.v 6-8 hourly for severe infection.
  90. 90. Adverse effect-  As same as amoxicillin alone.  Poor G.I tolerance.(specially in children)  Other side effect- Candida stomatitis. Vaginitis. Rashes. some cases of hepatic injury have been reported
  91. 91. Sulbactam:  Semisynthetic beta-lactamase inhibitor  Related chemically as well as in activity to clavulanic acid  It is also a progressive inhibitor  Combined with ampicillin.  On the weight basis , it is less potent than clavunic acid for most type of enzymes, but the same level of inhibition can be obtained at the higher concentration achieved clinically.  Oral absorption of sulbactam is inconsistent.  Therefore , it is preferably given parentally. Dose – Sulbacin, Ampitum : Ampicillin 1 g & sulbactam 0.5 g per vial inj. Sulbacin 375 mg tab
  92. 92. Beta-lactamase inhibitors Cont… Tazobactam:  Similar to Sulbactam  Pharmacokinetics matches with Piperacillin with which it is used for used in severe infections like peritonitis, pelvic/urinary/respiratory infections  However, the combination is not effective against piperacillin- resistant Pseudomonas
  93. 93. They are available only in fixed combinations with specific penicillins:  Ampicillin + Sulbactam (1g+0.5g I.V/I.M inj)  Amoxycillin + Clavulanic acid (250mg+125mg tab)  Piperacillin + Tazobactam sodium (2g+0.25g I.V/I.M inj)
  95. 95. DRUG INTER ACTIVITY DRUG POTENTIAL EFEECT MANAGEMENT PENICILLIN CLASS Food Decrease / delayed GI absorption of penicillin GI Administer penicillin at least absorption of oral penicillin's. 2 hours before or after a meal. Tetracyclines (doxycycline, minocycline, oxytetracycline) Decreased effects of penicillin .Avoid combination. Warfarin (Anti coagulant, thrombolytic) Increased the effect of warfarin with larger dose of IV penicillin Decrease warfarin dose if necessary Methorexate (Antineoplastic agent) Increase concentration of methorexate , decrease effect of penicillin, Increase risk of methotrexate toxicity Monitor sign of toxicity, Use of alternative antibiotic (Ceftazidime)
  96. 96. Allopurinol Increased rate of ampicillin associated skin rash use alternative drug if rash develops. Atenolol Decreased effects of atenolol Separate administration times. Monitor blood pressure. Increase atenolol dose if necessary.
  97. 97. Poisioning and overdose- Drug Half life Toxic dose /serum level toxicity Penicillin 30 min 10 million units/d IV, or CSF > 5 mg/L Seizures with single high dose or chronic excessive doses in patients with renal dysfunction Methicillin 30 min Unknown Interstitial nephritis, leukopenia Nafcillin 1.0 h Unknown Neutropenia. Ampicillin, amoxicillin 1.5 h Unknown Acute renal failure caused by crystal deposition Carbenicillin 1.0–1.5 > 300 mg/kg/d or > 250 mg/L Bleeding disorders due to impaired platelet function; hypokalemia. Risk of toxicity higher in patients with renal insufficiency Piperacillin 0.6–1.2 > 300 mg/kg/d “ Ticarcillin 1.0–1.2 > 275 mg/kg/d “ Poisoning and drg overdose, Kent R.Olson. 5th edition.
  98. 98. Refrences-  Essential of medical pharmacology. K D Tripathi. 5th edition  Manual of pharmacolgy and therapeutics. Goodman and Glickman .  Poisoning and drug overdose, Kent R.Olson. 5th edition  Katzung 9th edition.

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penicillin in dentistry (antibiotics)


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