Antibiotics in oral and maxillofacial surgery

1. Dr. Firas Kassab

2. Dr. Firas Kassab

3. • HISTORY & INTRODUCTION
• CLASSIFICATION
• PRINCIPLES OF ANTIBIOTIC
THERAPY
• ANTIBIOTIC SIDE EFFEECTS
• ANTIBIOTIC RESISTANCE
• ANTIBIOTIC FAILURES
• MISUSE OF ANTIBIOTICS
• ANTIBIOTIC PROPHYLAXIS
• INDIVIDUAL DRUGS
- Chemistry
- Mechanisms of action
- Spectrum
- Sensitive organisms
- Resistance
- Adverse effects
- Uses
• SPECIAL CONDITIONS-
Pregnancy
- Chronic renal failure
- Hepatic failure
- Diabetes mellitus
- Head and neck infections in
immunocompromised state
• NEWER ANTIBIOTICS
• ANTICANCER DRUGS
• SHOULD ANTIBIOTICS BE
USED?
• CONCLUSION
• REFERENCES
Dr. Firas Kassab

4. ANTIBIOTIC TERMINOLOGY
DEFINITION: SUBSTANCES DERIVED FROM MICROORGANISMS
WHICH SUPPRESS THE GROWTH / KILL THE
MICROORGANISMS AT A VERY LOW CONCENTRATION
OR
A CHEMICAL SUBSTANCE PRODUCED BY
MICROORGANISMS HAVING THE PROPERTY OF INHIBITING
THE GROWTH OF OR DESTROYING OTHER
MICROORGANISMS IN HIGH DILUTION
CHEMOTHERAPY :TREATMENT OF SYSTEMIC INFECTIONS WITH
SPECIFIC DRUGS THAT SELECTIVELY SUPPRESS THE
INFECTING MICROORGANISM WITHOUT SIGNIFICANTLY
AFFECTING THE HOST.
Dr. Firas Kassab

5. • Antimicrobial - This term refers to both antibiotics and
synthetic agents active against microbes.
• Microcidal - (Bacteriocidal. Vincidal, Fungicidal) The
organism is lysed or killed by direct damage on
susceptible cell targets.
• Microstatic - (Bacteriostatic, Virostatic, Fungistatic)
• The organism is reversibly inhibited at specific
metabolic processes.
• action and host defense mechanisms. Multiplication of
the organism is inhibited.
• Narrow Spectrum Antimicrobial - An antimicrobial that
acts on a limited number of microbial species, e.g.
Nitroimidiazole derivatives etc
• Broad Spectrum Antimicrobial - An antimicrobial that acts
on a wide range of species, e.g., erythromycin for Gram
positive. Gram negative, Legionella, Mycoplasma, etc.
Dr. Firas Kassab

6. • (A) The period of emperical use South American Indians used the
bark of the cinchona tree to extract quinine to control malaria
and mercury was known to cure syphilis in the late
1400's,‘mouldy curd’ by Chinese on boils, mercury by Paracelsus
(16th century) for syphilis, Cinchona bark (17th century) for fevers.
• (B) Ehrlich’s phase of dyes & organometallic compounds (1890-
1935): methylene blue, tryptan red, etc.
He coined the term ‘Chemotherapy’
Dr. Firas Kassab

7. • (C) The Modern Era of chemotherapy was ushered in by Domagk
in 1935 by demonstrating the therapeutic effect of prontosil , a
sulfonamide dye in pyogenic infection.
Other pioneers in the field of antibiotics were Louis Pasteur,
Alexander Fleming, Chain Florey , Waksman.
All received Nobel prizes for their discoveries.
Dr. Firas Kassab

8. BASED ON TYPE OF ORGANISM THEY ACT UPON:
1. Antibacterial – penicillin
amino glycosides
erythromycin
2. Antifungal - griseofulvin
amphotericin
ketoconazole
3. Antiviral- acyclovir
amantidine
zidovudine
4. Antiprotozoal- metronidazole
chloroquine
Dr. Firas Kassab

9. BASED ON MECHANISM OF ACTION:
1. Inhibit cell wall synthesis: penicillins
cephalosporins
cyclosporins
2. Leakage from cell membrane:
polypeptides-polymixin, bacitracin
polyenes- amphotericin B
,nystatin
3. Inhibits protein synthesis: tetracyclines,
chloramphenicol,
erythromycin,
clindamycin.
4. Causes misreading of m.RNA: aminoglycosides
5. Inhibits DNA gyrase: fluoroquinolones
6. Interfere with DNA function : rifampin,
metronidazole.
7. Interfere with DNA synthesis: acyclovir,
idoxuridine.
Dr. Firas Kassab

10. Dr. Firas Kassab

11. Sulfonamides and related drugs :
• Sulfones – Dapsone (DDS)
• Para amino salicylic acid (PAS)
Diaminopyrimidines
• Trimethoprim, pyrithamine
Quinolones
• Nalidixic acid, Norfloxacin, Ciprofloxacin etc
β - lactam antibiotics
• Penicillins, cephalosporins, monobactams, carbapenems
Tetracyclines
• Oxytetracycline, Doxycycline etc
Nitrobenenzene Derivative
• Chloramphenicol
Aminoglycosides
• Streptomycin Gentamycin, Neomycin etc
Dr. Firas Kassab

12. - Macrolide antibiotics
• Erythromycin, Roxithromycin, Azithromycin etc
• Polypeptide antibiotics
• Polymyxin – B, colistin, Bacitracin, Tyrothricin etc
• Glycopeptides
• Vancomycin, Teicoplamin
• Oxazolidinase
• Linezolid
• Nitrofuran derivatives
• Nitrofurantoin, Furazolidine
• Nitroimidazoles
• Metronidazole, Tinidazole
• Polyene antibiotics
• Nystatin, Amphotericin – B, Hamycin
• Azole derivatives
• Miconazole, clotrimazole, ketoconazole, fluconazole
Dr. Firas Kassab

13. • Narrow spectrum
Penicillin G, streptomycin and erythromycin.
• Broad spectrum
Tetracyclines, chloramphenicol.
• Extended spectrum
Semi synthetic Penicillins, new cephalosporins,
aminoglycoside.
Dr. Firas Kassab

14. • Antibacterial
Penicillins, Aminoglycosides, erythromycin etc
• Antifungal
Griseofulvin, amphotericin B, ketoconazole etc
• Antiviral
Idoxuridine, Acyclovir, Amantadine, Zidovudine etc
• Antiprotozoal
Chloroquine, pyrimethamine, metronidazole etc
• Antihelminthic
Mebendazole, nicosamide, diethyl carbamazine etc
Dr. Firas Kassab

15. (v) TYPE OF ACTION:
Primarily Bacteriostatic Primarily
Bactericidal
Sulfonamides
Tetracyclines
Chloramphenicol
Erythromycin
Ethambutol
Penicillins , Cephalosporins,
Aminoglycosides,
Vancomycin,
Ciprofloxacin, Isoniazid ,
Rifampin, Cotrimoxazole,
Dr. Firas Kassab

16. • Fungi
• Penicillin, Cephalosporin, Griseofulvin.
• Bacteria
• Polymyxin B, Colistin, Bacitracin, Tyrothricin Aztreonam.
• Actinomycetes
• Aminoglycosides, Tetracyclines, Chloramphenicol, Macrolides, Polyenes.
Dr. Firas Kassab

17. PRINCIPLE 1: TO DETERMINE THE SEVERITY OF
INFECTION
PRINCIPLE 2: TO EVALUATE STATE OF PATIENT’S HOST
DEFENSE MECHANISMS
PRINCIPLE 3:TO DETERMINE WHETHER PATIENT SHOULD
BE TREATED BY GENERAL DENTIST OR SPECIALIST
PRINCIPLE 4:TO TREAT INFECTION SURGICALLY
Dr. Firas Kassab

18. PRINCIPLE 5 :TO SUPPORT THE PATIENT MEDICALLY
PRINCIPLE 6 : CHOOSE AND PRESCRIBE APPROPRIATE
ANTIBIOTIC
PRINCIPLE 7 : PROPER ANTIBIOTIC ADMINISTRATION
PRINCIPLE 8 :MONITORING THE PATIENT
Dr. Firas Kassab

19. • Complete history-Time of onset
-Duration of infection
-Rapidity of progress
• Eliciting patient’s symptom
• Physical examination
Dr. Firas Kassab

20. CHARACTERISTIC CELLULITIS ABSCESS
Duration Acute Chronic
Pain Severe and generalized Localized
Size Large Small
Localization Diffuse borders Well circumscribed
Palpation Doughy to indurated Fluctuant
Presence of pus No Yes
Bacteria Aerobic Anaerobic
Dr. Firas Kassab

21. • Uncontrolled metabolic diseases
e.g. – uremia, alcoholism, malnutrition, severe diabetes
(decreased function of leucocytes, decreased chemotaxis,
decreased phagocytosis, decreased bacterial killing)
• 2- Immuno Suppressing diseases
Interfere with host defense mechanism
e.g.- leukemias, lymphomas, malignant tumours
• 3- Immuno Supressing drugs
e.g.- cancer chemotherapeutic drugs
Immunosuppressive agents
Dr. Firas Kassab

22. • Criteria for referral to a specialist :
1.Rapid progressive infection
2.Difficulty in breathing
3.Difficulty in swallowing
4.Fascial space involvement
5.Elevated temperature(>101 degree F)
6.Severe jaw trismus(<10mm)
7.Toxic appearance
Dr. Firas Kassab

23. GOALS :
1.To remove the cause of infection
2.To provide drainage of accumulated
pus and necrotic debris
MODES :
1.Endodontic treatment
2.Extraction
3.Incision and drainage
+extraction endodontic treatment
Drainage of pus
Reduction in tissue tension
Improved local blood supply and increased
delivery of host defenses
Dr. Firas Kassab

24. Odontogenic infection
Pain and swelling
No adequate fluid and nutritional
intake
Depressed host defenses
Adequate analgesics and fluid intake
Dr. Firas Kassab

25. PRINCIPLES FOR CHOOSING
APPROPRIATE ANTIBIOTIC
Identification of causative organism
• Scientifically determined either in the laboratory, where
the organism can be isolated from pus, blood or tissue
or
• Empirically based upon the knowledge of the pathogens
and clinical presentation of specific infection.
Dr. Firas Kassab

26. (I) IDENTIFICATION OF THE CAUSATIVE ORGANISM:-
• Scientifically - laboratory
• Emperically – knowledge of
the pathogenesis & clinical
presentation.
• Initial emperical therapy
instituted with a fair degree of reliability.
Dr. Firas Kassab

27. • Typical odontogenic infection is caused by a mixture of aerobic
& anaerobic bacteria (70%)
• Aerobic bacteria – 5% (gm positive cocci)
• Pure anaerobic bacteria – 25% (gm positive cocci – 30% & gm
negative rods – 50%)
• All are sensitive to penicillin & penicillin like drugs, but
Fusobacterium frequently resistant to erythromycin (apprx. 50%)
Dr. Firas Kassab

28. TYPE OF INFECTION MICROORGANISMS
ODONTOGENIC
CELLULITES/ABSCES
S
STREPTOCOCCUS MILLERI GROUP
PEPTOSTREPTOCOCCI
PREVOTELLA AND PORPHYROMONAS
FUSOBACTERIA
RHINOSINUSITIS ACUTE STREPTOCOCCUS PNEUMONIAE
HAEMOPHILUS INFLUENZAE
HEAD AND NECK ANAEROBES
(PEPTOSTREPTOCOCCI, PREVOTELLA
PORPHYROMONAS, FUSOBACTERIA)
GROUP A BETA-HEMOLYTIC STREPTOCOCCI
STAPHYLOCOCCUS AUREUS
MORAHELLA CATARRHALIS
VIRUSES
CHRONIC HEAD AND NECK ANAEROBES
FUNGAL ASPERGILLUS
RHIZOPUS SP. (MUCOR)
NOSOCOMIAL
(ESPECIALLY IF
INTUBATED)
ENTEROBACTERIACEAE (ESPECIALLY
PSEUDOMONAS, ACINETOBACTER,
ESCHERICHIA COLI)
S. AUREUS
YEASTS (CANDIDA SPECIES)
Major pathogens of head and neck infections
Dr. Firas Kassab

29. Pathobiology of mixed odontogenic infection:-
Entry of organisms (aerobic)
Effects underlying
tissues
Cellulitis develops Condtion resolves on
treatment
Hypoxic acidotic condition
Tissue destruction and abscess
formation (anaerobic)
Production of
enzymes and toxins
Dr. Firas Kassab

30. CULTURES SHOULD BE PERFORMED:-
1. Pt. with an infection has compromised host defenses
2. Received appropriate treatment for 3 days without
improvement
3. Postoperative wound infection
4. Recurrent infection
5. Actinomycosis is suspected, or
6. Osteomyelitis is present
Dr. Firas Kassab

31. (II) DETERMINATION OF ANTIBIOTIC SENSITIVITY:-
• Not responded to initial antibiotic therapy or a postoperative
wound infection – causative agent identified & the antibiotic
sensitivity determined.
Dr. Firas Kassab

32. DISK DIFFUSION METHOD
RATIONALE :
• Antibiotics diffuse into the agar and inhibit the growth
of sensitive bacteria in a semicircular zone around the disc.
• When the resistance to a given agent is present, the
zone radius will be reduced or these will be no zone at all.
Dr. Firas Kassab

33. Advantages :
• Simple to perform
• Inexpensive
• Provides data within 18 to 24 hours
Disadvantages :
• It is only semi quantitative and is not useful for many flow
growing or fastidious organisms.
• It has not been adequately standardized for anaerobic
bacteria.
Dr. Firas Kassab

34. • The result of these studies provide the information needed to
prescribe the most appropriate antibiotic.
• Penicillin is excellent for treatment of streptococcus infection & is
good to excellent for the major anaerobes of odontogenic
infections.
• Erythromycin - Streptococcus, Peptostreptococcus & Prevotella
but is ineffective against Fusobacterium.
Dr. Firas Kassab

35. • Clindamycin – streptococcus & major anaerobic groups.
• Cephalexin – moderately active against streptococcus & is good to
excellent against anaerobes.
• Metronidazole – no activity against streptococcus but has excellent
activity against anaerobes.
Dr. Firas Kassab

36. (III) USE OF A SPECIFIC, NARROW SPECTRUM ANTIBIOTIC:-
Advantages -
• less chances of developing resistant organisms.
E.g. streptococcus sensitive to penicillin , cephalosporin and
tetracycline.
• Minimizes the risk of super infections.
E.g. moniliasis and gram negative pneumonias
Dr. Firas Kassab

37. (IV) USE OF THE LEAST TOXIC ANTIBIOTIC:-
• Equally effective but less toxic drugs have to be used.
E.g. bacteria causing odontogenic infection susceptible to both
penicillin and chloramphenicol.
• More toxicity present with the latter drug.
Dr. Firas Kassab

38. (V) PATIENT DRUG HISTORY:-
• Previous allergic reactions
• Previous toxic reactions
• Allergy rate to penicillin - 5 %
• Cross sensitivity Penicillins and cephalosporins.
• Toxic reactions - identify the drug and precise reaction
• Likely to happen again.
Dr. Firas Kassab

39. (Pharmacologic factors in antibiotic selection)
(VI) USE OF A BACTERICIDAL RATHER THAN A BACTERIOSTATIC
DRUG:-
Advantages:
1. Less reliance on the host resistance
2. killing of the bacteria by the antibiotic itself
3. Faster results
4. Greater flexibility with dosage intervals.
•Used especially when the host defenses are low.
Dr. Firas Kassab

40. (VII) USE OF THE ANTIBIOTIC WITH A PROVEN H/O SUCCESS:-
•Critical observation of the clinical effectiveness over a prolonged
period -----assessment of
• Frequency of treatment success and failures
•Frequency of adverse reactions
•Frequency of side effects
•Standards for use
Dr. Firas Kassab

41. (VIII) COST OF THE ANTIBIOTIC:-
• Difficult to place a price tag on health.
• In some situations, more expensive antibiotic is the drug of
choice.
• In other situations, there may be a substantial difference in price
for drugs of equal efficacy.
• Surgeon should consider the cost of the antibiotic prescribed.
Dr. Firas Kassab

42. (IX) ENCOURAGE PATIENT COMPLIANCE:-
• Dosage interval that encourages compliance
OD 80%
BID 69%
TID 59%
QID 35%
• Non-compliant start feeling better
3-5 days 50%
>7 days 20%
• Antibiotic that would have the highest compliance would be the
drug given OD for 4 or 5 days.
Dr. Firas Kassab

43. • Rapidly progressive swelling
• Diffuse swelling
• Compromised host defenses
• Involvement of facial spaces
• Severe pericoronitis
• Osteomyelitis
Dr. Firas Kassab

44. • Chronic well localized abscess
• Minor vestibular abscess
• Dry socket
• Mild pericoronitis
Dr. Firas Kassab

45. INDICATIONS OF EMPIRICAL ANTIBIOTIC THERAPY :
• The site and feature of the infection have been well defined.
• The circumstances leading to the infection are well known.
• Organisms that most commonly cause such infections.
Dr. Firas Kassab

46. EMPIRIC ANTIBIOTIC TREATMENT
Early infection (first 3 days of symptoms and mildly
immunocompromised)
• Penicillin
• Clindamycin
• Cephalexin
Late infection (After 3 days of symptoms or moderately to severely
immunocompomised)
• Clindamycin
• Revicillin and metranidazole.
• Ampicillin and sulbactam.
• Cephalosporin (first or second generation).
-Mild, moderate and severe compromised based on CD4 / viral
loads, glycemic control, and the degree of alcoholic related disease.
Dr. Firas Kassab

47. • Proper dose.
• Proper time interval.
• Proper route of administration.
• Combination antibiotic therapy.
• It is indicated in few situations like in:
• Situations of life threatening situations of unknown cause.
• To increase the bactericidal effect of a specific organism.
• Prevention of the rapid emergence of resistant bacteria.
- Empiric therapy of certain odontogenic infections like when the
infection progresses to the lateral and retropharyngeal spaces and
caused by aerobes and anaerobes.
Dr. Firas Kassab

48. • GOAL :
1.To aid the body’s defenses to clear the tissues of
microbial pathogen by achieving antibiotic levels in the
infected area to or greater than the MIC
Dr. Firas Kassab

49. • PHARMACOKINETIC FACTORS
Diffusion to the site of action
1.Tissue pH.
2.Lipid and water solubility
3.Plasma protein binding
• INOCULUM EFFECT- It is defined as a laboratory
phenomenon that results in significantly increased MIC
required of an antibiotic. When the number of inoculated
organisms increases. It generally occurs in case b-lactum
antibiotics and b-lactamase producing bacteria
(review of infectious diseases vol.2 number.3 may- june 1989)
• SURFACE AREA TO VOLUME RATIO
Dr. Firas Kassab

50. Lipophilic antibiotics
Tetracyclines,macrolides,fluoroquinolones
Pass better through tissue barriers
Effective against intracellular pathogens
Drug depot within macrophages
Dr. Firas Kassab

51. Hydrophilic antibiotics
Beta-lactams,vancomycin,aminoglycosides
Confined to ECF
Poor diffusion through capillaries
Dr. Firas Kassab

52. Limited plasma protein binding
Diffuse easily through capillary walls
and
other barriers
Dr. Firas Kassab

53. (I) PROPER DOSE:-
• Dose – 3 to 4 times the MIC
for e.g. penicillinase producing staphylococcus -
MIC 6 µg/ ml , plasma level - 18µg /ml
• Administration of doses above this level – increases the
likelihood of toxicity & is wasteful.
• Sub therapeutic levels - mask the infection ,recurrence.
Dr. Firas Kassab

54. • BASED ON BODY SURFACE AREA
Individual dose = BSA[m2] x adult dose
1.7
• BASED ON BODY WEIGHT
Individual dose = BW[kg] x average
70 adult dose
Dr. Firas Kassab

55. YOUNG’S FORMULA :
CHILD DOSE = Age x adult dose
Age + 12
DILLING’S FORMULA :
CHILD DOSE = Age x adult dose
20
Dr. Firas Kassab

56. • Greater percentage of body weight compared with
body water
Greater volume of distribution
Increased serum half lives
• Reduced gastric emptying
• Reduced plasma protein binding
• Reduced GFR
Dr. Firas Kassab

57. • Reduced host defenses
• Underlying illness
• Reduced total body water
• Lean body mass
• Reduced cardiac output
• Reduced gastric emptying time
• Decreased renal function
Dr. Firas Kassab

58. • LOADING DOSE; This is a single or few quickly repeated
doses given in the beginning to attain target concentration
capacity.
• MAINTAINANCE DOSE: This is the dose repeated at specific
interval after attainment of target cycles per second
Dr. Firas Kassab

59. • INDICATIONS :
1.The half-life of the antibiotic is longer than 3-hours.
2. A delay of longer than 12-hours to achieve
therapeutic blood levels is unacceptable.
Because most acute orofacial infections
begin and peak rapidly
Dr. Firas Kassab

60. • The ideal antibiotic duration is the shortest time that will
prevent both clinical and microbiological relapse.
Clinical improvement of the patient
Remission of infection.
Dr. Firas Kassab

61. • Prolonged antibiotic therapy destroys resistant bacteria.
• Prolonged antibiotic therapy is necessary to prevent rebound
infections.
• The dosage and duration of therapy can be extrapolated from
one infection to another.
• The prescriber knows how longer the infection will last.
Dr. Firas Kassab

62. (II) Proper time interval:-
• Established plasma t 1/2 – one half of the absorbed dose is
excreted.
• Usual dosage interval for therapeutic use of antibiotics - Four
times the half life.
E.g. cefazolin t 1/2 - 2 hours.
Dr. Firas Kassab

63. (III) Proper route of administration:-
•In some infections , only the parenteral route produces necessary
serum level of antibiotic
For e.g. Penicillin V oral - 2 gm
Plasma level - 4 µG/ mL
•Oral route - variable absorption.
•Serious well established infection - parenteral route
Dr. Firas Kassab

64. (IV) Consistency in Route of Administration:-
•After initial response , immediate discontinuation of parenteral
route - Recurrence
•Maintenance of peak blood levels of antibiotic for an adequate
period is important – max. tissue penetration & effective
bactericidal action.
•After the 5th day of parenteral administration, the blood levels
achievable with oral administration are usually sufficient.
Dr. Firas Kassab

65. (V) Combination Antibiotic therapy:-
• Life threatening sepsis of unknown cause
• Increased bactericidal effect against a specific µorg is desired.
E.g. treatment of infections caused by enterococcus
• Prevention of rapid emergence of resistant bacteria
E.g. tuberculosis
• Empiric treatment of certain odontogenic infections
E.g. Penicillin G & Metronidazole
Dr. Firas Kassab

66. Combination therapy with two or more antibiotics is used in
special cases:
• Prevent the emergence of resistant strains
• To treat emergency cases during the period when an etiological
diagnosis is still in progress
• To take advantage of antibiotic synergism
Dr. Firas Kassab

67. • Broad antibacterial
spectrum
• Reduced dose for each
agent.
• Antibiotic synergism
• Decreased adverse drug
reactions
• Greater likelihood of
adverse reactions
• Antibiotic antagonism
• Increased financial costs
• Greater microbial resistance
• Resistance genes
• Increased risk of
superinfection
Dr. Firas Kassab

68. • Cell wall inhibitors and aminoglycosides
• Beta-lactams with beta-lactamase inhibitors
• Beta-lactams that act on different PBPs
• Sulfonamides and trimethoprim
Dr. Firas Kassab

69. • Should be avoided when not specifically indicated.
• Usual result – broad spectrum exposure that leads to depression
of the normal host flora & inc opportunity for resistant bacteria to
emerge.
• For routine infections, the disadvantages of combination therapy
outweigh the advantages.
Dr. Firas Kassab

70. • Minimal Inhibitory Concentration
• Post-antibiotic effects
• Microbial persistence and regrowth.
• Dosing and resistance
• Antibiotic loading dose
• Duration of antibiotic dosing
• Incision and Drainage
• Special conditions
Dr. Firas Kassab

71. • Is the lowest antibiotic concentration that prevents growth of
microorganism after an incubation period of 18 – 24 hours
incubation period with a standard inoculum of 104 to 105 cfu/ml
MINIMAL BACTERICIDAL CONCENTRATION
• Is the lowest concentration of drug that causes the complete
destruction of the organisms or permits survival of less than 0.1% of
the inoculum
Dr. Firas Kassab

72. • DETERMINES:
1.The ratio of the peak drug concentration in the
serum to the MIC
2.The duration of the time the serum drug
concentration exceeds the MIC
3.The ratio of the 24-hour area under the curve
[AUC] to the MIC
The AUC is the measure of the drug
exposure to the bacteria over time
Dr. Firas Kassab

73. • Is only a point in time and tells nothing about the true antibiotic
activity at the locus of infection
• The concentration of organisms at the site of infection is 108-
1010 cfu/ml – greater than that used to determine the MIC in
the laboratory.
• Exponential growth in vitro
• Differing variables- temperature, inoculum Size, pH and growth
period.
Dr. Firas Kassab

74. • The concentration of the antibiotic in the
blood should exceed the MIC by a factor
of 2-8 times to offset the tissue barriers
that restrict access to the infected site.
Dr. Firas Kassab

75. • CONCENTRATION
DEPENDENT
• TIME DEPENDENT
ANTIBIOTICS
1. Aminoglycosides,
metronidazole,
fluroquinolones
2. Bactericidal activity
depends on the drug
concentration
1. Beta-lactams and
vancomycin
2. Long time of exposure of
the organisms
3. Better the bactericidal
concentration
4. Require organisms in the
process of cell division
Dr. Firas Kassab

76. • Is the persistent supression of microbial growth after short time
exposure to an antimicrobial agent.
• MECHANISM :
Is the time necessary to recover from sublethal structural
and metabolic alterations that prevents resumption of bacterial
regrowth.
Dr. Firas Kassab

77. • The particular organism
• Inoculum size
• Growth medium
• Organism growth phase
• Mechanism of action of antibiotic
• Duration of exposure to the drug
Dr. Firas Kassab

78. • The subpopulation of organisms that is not inhibited
or killed during a given dose interval which can then
reestablish themselves and continue growth.
• FACTORS DETERMINING :
1.Initial inoculum size
2.Bactericidal activity
3.Organism MIC
4.Post-antibiotic effects
5.Antibiotic pharmacokinetics
6.Doubling time of the organism.
Dr. Firas Kassab

79. 1)Response to treatment.
Reasons for treatment failure:
-Inadequate surgical treatment.
-Depressed host defences.
-Presence of foreign body.
-Antibiotic problems – Drugs not reaching infection.
Dose not adequate
Wrong bacterial
diagnosis.
Wrong antibiotic.
2)Development of adverse reactions:
3)Superinfection and recurrent infection:
Dr. Firas Kassab

80. ANTIBIOTIC SIDE EFFECTS
Side effects are unwanted but often unavoidable
pharmacodynamic effects that occur at therapeutic doses.
1) HAEMATOLOGIC EFFECTS
a) Leucopenia and thrombocytopenia: Beta lactams
sulfonamides(Cotrimazole)
b) Anaemia: Beta lactam- Autoimmune anaemia
Cotrimazole- Folate deficiency- Megaloblastic anaemia
Chloramphenicol- Aplastic anaemia.
c) Platelet dysfunction: Anti pseudomonal penicillins- Impaired
platelet aggregation.
d) Clinical bleeding: Moxalactam- Interferes with vit.K depended
clotting factor synthesis.
Trovafloxacin- Increases prothrombin time.
Dr. Firas Kassab

81. Drug fever: 10-15% of unexplained fever in hospitalized patients.
Beta lactams, Sufonamides.
Drug rashes: Itching, urticaria, maculo popular rashes.
Beta lactams, sulfonamides.
Anaphylactic reactions: Beta lactams, rare in Sulfonamides.
Serum sickness: Develops 2 weeks after exposure- Beta lactams.
Photosensitivity reactions: Tetracycline, Sparfloxacin
Rare with Doxycyclin, minocycline
Drug induced Systemic Lupus Erythematosus(SLE):
Minocyclin, Isoniazide, Nitrofurantoin, Griseiofulvin.
Dr. Firas Kassab

82. a) Encephalopathy: Trovafloxacin- Mental confusion
Clarithromycin
b) Seizures: Ciprofloxocin, Imipenem, Trovafloxacin.
It depends on seizure threshold of patient.
c) Neuromuscular blockade: Aminoglycosides
d) Peripheral neuropathy: Isoniazide, Griseiofulvin
e) Muscular tremors and myalgias: Trovafloxacin
f) Ototoxicity: Aminoglycisides, Parenteral
Erythromycin
g) Blindness: Ethambutol, Chloroquine.
Dr. Firas Kassab

83. 4) PULMONARY EFFECTS
a) Acute pulmonary reactions: Rifampicin- Flu like illness.
Nitrofurantoin: Varying degrees of respiratory
Insufficiency, Pleural effusion.
b) Chronic pulmonary reaction: Nitrofurantoin-
Pulmonary fibrosis.
5) CARDIAC EFFECTS
a) Ventricular arrhythmias: Erythromycin
b) Hypotension: Trovafloxacin, Amphotericin-B
Dr. Firas Kassab

84. a)Nausea and vomiting
Clarithromycin,Amoxicillin/Clavulanate,Azithromycin,
Doxicycline,Minocycline.
b) Non-clostridium difficile diarrhea:
Macrolides,Ampicillin, Trovafloxacin
c)Cl. Difficile diarrhoea
Beta lactums, Quinolones
d)Anti pancreatitis
Trovafloxacin.
Dr. Firas Kassab

85. a) drug induced hepatitis
-Isoniazide- elevates serum transaminas, Trovafloxacin,Oxacillin
b) Cholestasis
-Erythromycin,Nitrofurantoin
c) Hepatic necrosis
-PAS, Ketoconazole or Trovafloxacin
8)NEPHROTOXIC SIDE EFFECTS
a) Nephrotoxicity
Aminoglycosides-Tubular toxicity.
Tetracyclines, Polymyxin –B
b) Interstitial nephritis
Beta lactamase therapy.
Dr. Firas Kassab

86. • The organisms continue to multiply even in the presence of
antibiotic.
• Resistance to an antimicrobial can arise
(1) Mutation in the gene that determines
sensitivity/resistance to the agent or
(2) Acquisition of extrachromosomal DNA
(plasmid) carrying a resistance gene.
(3) Bacteriophages.
(4) Mosaic genes
Mutation: random, undirected, heritable variation caused by an alteration in the
nucleotide sequence at some point of the DNA of the cell
Dr. Firas Kassab

87. CROSS RESISTANCE
Single mechanisms confers resistance to multiple
antimicrobial agents
MULTIPLE RESISTANCE
Multiple mechanisms
Cross resistance - closely related antimicrobial agents
Multiple resistance - unrelated antimicrobial agents.
Dr. Firas Kassab

88. 1.ENZYMATIC ANTIBIOTIC INACTIVATION
a.Beta-lactams - beta lactamases
b.Aminoglycosides - aminoglycosides
modifying enzymes
c.Chloramphenicol - acetyl transferases
2.MODIFICATION PROTECTION OF TARGET SITE
a.Beta-lactams-altered PBPs
b.Fluoroquinolones:altered DNA gyrases
c.Rifampin:altered RNA polymerase
d.Sulfonamides: altered dihydropteroate
synthaseDr. Firas Kassab

89. 4.ACTIVE ANTIBIOTIC EFFLUX
5.FAILURE TO ACTIVATE ANTIBIOTIC
Metronidazole - flavodoxin production
Dr. Firas Kassab

90. 6.USE OF ALTERNATE GROWTH REQUIREMENTS
7.OVERPRODUCTION OF TARGET SITES
a.Sulfonamides:overproduction of
PABA
b.Entericbacilli:overproduction of beta-
lactamases
Dr. Firas Kassab

91. Common reasons for antibiotic failure:
1.Failure to surgically eradicate - source of
infection
2.Too low - blood antibiotic concentration
3.Inability to penetrate the site of infection
4.Impaired host defenses
5.Patient failure to take the antibiotic
Dr. Firas Kassab

92. 6.Inappropriate choice of antibiotic
7.Limited vascularity or blood flow
8.Decreased tissue ph or oxygen tension
9.Antibiotic resistance
10.Delay or incorrect diagnosis
11.Antibiotic antagonism
Dr. Firas Kassab

93. • 1) Treatment of untreatable infections
• 2) Therapy of fever of unknown origin
• 3) Improper dosage
• 4) Inappropriate reliance on chemotherapy alone
• 5) Lack of adequate bacteriological information
Dr. Firas Kassab

94. • Refers to unresponsiveness of a microorganism to an AMA
• Natural Resistance
• Acquired Resistance
.
Dr. Firas Kassab

95. • Single step mutation
E.g. Enterococci to Streptomycin, E.coli & Staphylococci to rifampin
• Multistep mutation
E.g. resistance to erythromycin, tetracyclines & chloramphenicol by
many organisms.
Dr. Firas Kassab

96. • Gene Transfer:- from organism to another can occur by,
(i) Conjugation:-
E.g. Chloramphenicol – typhoid bacilli,
Streptomycin – E.coli, Penicillin – Haemophilus & Gonococci
(ii) Transduction:-
E.g. Penicillin, Erythromycin & Chloramphenicol
(iii) Transformation:-
E.g. pneumococcal resistance to Penicillin
Dr. Firas Kassab

97. It is the use of antibiotics before, during, or after a
diagnostic, therapeutic, or surgical procedure to
prevent infectious complications.
ADVANTAGES:
1.Prevention of infection.
2.Decrease patient morbidity and mortality.
3.Decrease hospital stay.
4.Decreased medical cost.
5.Decreased total antibiotic usage.
6.Decrease numbers of resistant bacteria – because of short term
course.
Dr. Firas Kassab

98. DISADVANTAGES
• No reduction of infection.
• Development of increased number of resistant bacteria.
• Delay in onset of infection.
• Adverse effect on surgical technique
Dr. Firas Kassab

99. • Increased risk of significant bacterial contamination and
a high incidence of infection.
• Organism must be known.
• Antibiotic susceptibility must be known.
• To be effective and to minimize adverse effects the
antibiotic must be in the tissue at the time of
contamination (operation) and it must be continued for
not more than 4 hours after cessation of contamination.
• Four times the MIC of the causative organisms.
• Timing the antibiotic correctly.
• Shortest effective antibiotic exposure.
Dr. Firas Kassab

100. 1.Bacterial inoculum of sufficient size
2.Extensive and prolonged surgery
3.Insertion or presence of foreign body
4.Depressed host resistance
Dr. Firas Kassab

101. Dr. Firas Kassab

102. Type I. Clean wounds (no opening of mucosa in the oral cavity): Confirmed
infection rate of 1 to 4%. Antibiotic prophylaxis not required.
Type II. Clean-contaminated wounds (opening of mucosa in the oral cavity,
insertion of dental implants or intervention on inflammatory pathology):
Confirmed infection rate of 5 to 15%. These require antibiotic prophylaxis
with drugs covering Gram positive and anaerobic micro-organisms.
Type III. Contaminated wounds (oncological pathology in which there is
simultaneous action on the oral cavity and the neck): Confirmed infection rate
of 16 to 25%. Antibiotic prophylaxis must be carried out to cover Gram
negative organisms whose coverage in clean and cleancontaminated
surgeries is disputed.
Type IV. Dirty and infected wounds. Confirmed infection rate of above 26%.
These always need adequate antibiotic treatment.
CLASSIFICATION OF SURGICAL WOUNDS
Dr. Firas Kassab

103. 1.Effective against the most likely organism
2.Narrow spectrum antibiotic
3.Least toxic antibiotic
4.Bactericidal antibiotic
Dr. Firas Kassab

104. • To ensure diffusion of antibiotic into all fluid and tissue components
• USUAL RECCOMENDED DOSE: Two times the usual therapeutic
dose
Dr. Firas Kassab

105. • Antibiotic must be administered before the surgery begins
Prolonged surgery
Additional antibiotic is required
Intraoperative dose intervals should be one half the usual
therapeutic dose interval
Dr. Firas Kassab

106. • Continued antibiotic administration - no benefit once the
surgical procedure is complete
• Hence the final dose of the antibiotic - after surgical
operation
Procedure lasts for Short procedure
more than two hours
2nd dose of antibiotic is Single preop dose is
required adequate
Dr. Firas Kassab

107. • GOALS :
1.To reduce the intensity of bacteremia.
2.Assist the RES in killing the bacteria.
3.Decrease the bacterial adherence to the damaged heart
valves and vegetations.
Dr. Firas Kassab

108. • Antibiotic prophylaxis recommended :
High risk condition
1.Prosthetic cardiac valves
2.Bioprosthetic valves
3.Previous bacterial endocarditis
4.Complex congenital CHD
Moderate risk condition
1.Acquired valvular dysfunction
2.Hypertrophic cardiomyopathy
3.Other congenital cardiac malformation
Dr. Firas Kassab

109. • LOW RISK CONDITION:
1.Isolated atrial septal defect
2.Previous coronary artery bypass graft surgery.
3.Mitral valve prolapse without valvular
regurgitation
4.Cardiac pacemakers and defibrillators
5.Previous rheumatic fever without valvular
regurgitation
Dr. Firas Kassab

110. • PROPHYLAXIS RECOMMENDED :
1.Extractions
2.Periodontal surgery
3.Implants placement
4.Endodontic surgery
5.Subgingival antibiotic fiber strips
6.Intraligamentary LA injections.
• NOT RECOMMENDED :
1.Restorative dentistry
2.LA injections
3.Intracanal endodontic treatment
4.post-op suture removal
5.Oral radiographs
Dr. Firas Kassab

111. Dr. Firas Kassab

112. ANTIBIOTICS USEFUL FOR OROFACIAL INFECTIONS:
• Penicillins.
• Cephalosporins.
• Erythromycins.
• Clindamycin and Lincomycin.
• Metronidazole.
• Aminoglycosides.
• Fluoro quinolones – ciprofloxacin.
• Sulfonamides and trimethoprim
Dr. Firas Kassab

113. • Discovered in 1929, it was first antibiotic drug to be used.
• The drug of choice for the initial empirical management of
odontogenic infections remains penicillin
• Bactericidal
• Narrow but appropriate spectrum
• Little or no toxicity
Dr. Firas Kassab

114. CLASSIFICATION OF PENICILLIN
I) Natural penicillins :
Penicillin G (Benzyl penicillin)
II) Acid resistant penicillins :
Phenoxymethyl penicillin (penicillin V)
III) Penicillinase – resistant penicillins :
Acid labile : Methicillin, nafillin, cloxacillin, dicloxacillin
IV) Penicillins effective against gram +ve and some gram –
ve organisms :
Ampicillin
V) Extended spectrum penicillins :
Carboxypenicillins : Carbenicillin, tiocillin
Dr. Firas Kassab

115. -Narrow spectrum activity
Spectrum of activity- Streptococci except enterococci, Staph.
aureus, N. gonorrhoea, N. meningitides, Anthracis, C.diphtheriae,
Clostridia, Listeria.
PHARMACOKINETICS: PnG is acid liable destroyed by gastric acid.
-Absorption of sodium PnG from i.m. site is rapid and complete.
-Distributed extracellularly, penetration into serous cavity and CSF
is poor.
-Plasma T1/2 is 30 min.
-Extreted through kidneys by glomerular filtration.
Dr. Firas Kassab

116. • PREPARATION AND DOSE: 1) Sod. PnG or Crystallin penicillin
injection: 0.5-5 MU i.m. 6-12 hrly
• Repository PnG injections: These are insoluble salts must be
given deep i.m. never given i.v. Drug is released slowly from the
injection site.
• Procaine PnG: 0.5-1MU i.m.12hrly
• Fortified Procaine PnG : Contains 3lakhU
• Procaine PnG and 1lakhU Sod. PnG
• Benzathine PnG : 0.6-2.4MU i.m. every 2-4 weeks. It releases
drug very slowly and effective for prophylactic purposes.
Dr. Firas Kassab

117. Semi synthetic penicillin belongs to aminopenicillins.
Spectrum: Active against all organisms sensitive to PnG,
H.Influenza, E.Coli, Proteus, Salmonella, Shigella, Strepto.
Viridans, Enterococci, Pseudomonas, Klebsiella.
Kinetics : Not degraded by gastric acid.
Oral absorption is incomplete but adequate.
Food interferes with absorption.
Plasma T1/2 is 1 hr, excreted through kidneys.
Dose: 0.5-2g oral /i.m. /i.v. every 6th hrly.
Children 25-50mg /kg /day.
Dr. Firas Kassab

118. Uses: Urinary tract infections, Respiratory tract infections, Meningitis,
Gonorrhoea, Typhoid fever, Bacillary dysentery, Cholecystitis,
SABE.
Adverse effects: Diarrhea is frequent after oral administration,
rashes
Avoided in patients with a H/O hypersensitivity to PnG.
AMOXICILLIN
It is a close congener of Ampicillin, similar to it
except
- Oral absorption is better food does not interferes
- Incidence of diarrhea is less.
- Less active against Shigella, H.Influenza.
Dose: 0.25-1g orally /i.m /i.v. TDS.
Dr. Firas Kassab

119. • Clavulanic acid- streptomycet clavuligerous-inhibiting β
lactamase enzymes
• Broaden antibacterial spectrum of amoxicillins
Dr. Firas Kassab

120. • Semisnythetic betalactamase inhibitor
• Related chemically in activity to clavulanic acid
• Progressive inhibitor ,highly active against
betalactamase
• 2-3 times < potent
• Oral absorption- inconsistent,preferably im/iv
• Sulbactam+ ampicillin=Dicapen
• SULBACIN, AMPITUM
1g+ 0.5g per vial im/iv 6-8hourly
1g+500mg tab
Dr. Firas Kassab

121. • ADVERSE EFFECTS :
a) Local irritancy and direct toxicity
b)Jarisch-Herxheimer reaction
c) Hypersensitivity or drug allergy(1-10%)
Defn: An allergic drug reaction is defined as any noxious, unintended, and
undesired effect of a drug that occurs at doses used in humans for prevention,
diagnosis, or treatment.
2types predictable
unpredictable
PENICILLIN ALLERGY SKIN TESTING
Reagents: Concentration
-Penicilloate 0.01 mol/L
-Penilloate 0.01 mol/L
-Penicillin G 10,000U/ml
-Ampicillin/Amoxicillin 1-20mg/ml
PROCEDURE:
1) Epcutaneous or (scratch or prick)
2) Intradermal test
Dr. Firas Kassab

122. • Administration of a penicillin to a allergic patient, who
requires penicillin for clearly defined medical reasons.
Ex; Endocarditis, meningitis.
-Done in Intensive care setting…
-Penicillin doses of 1,5,10,100 and 1000U
administered intradermally ,60 mints interval b/n doses.
-well tolerated- 10000U-50,000U given s.c.
Dr. Firas Kassab

123. Therapeutic Uses :
• Streptococcal infections
• Pneumococcal infections
• Meningococcal infections
• Staphylococcal infections
• Gonorrhoea
• Syphilis
• Diphtheria
• Tetanus and gas gangrene
• Antibiotic prophylaxis
Dr. Firas Kassab

124. • These are a group of semisynthetic antibiotics derived
from "cephalosporin – C" obtained from a fungus
cephalosporium.
• They are chemically related to penicillins, the nucleus
consists of a β-lactam ring fused to a dihydrothiazine
ring.
Dr. Firas Kassab

125. 1ST GENERATION CEPHALOSPORINS
Good against methicillin sensitive S. aureus,
streptococci and many Enterobacteriaceae.
Members include: Cephalexin (Keflex), Cefazolin
(Ancef), Cephapirin (Cefadyl) and Cephalothin (Keflin)
Cefadroxil.
2ND GENERATION CEPHALOSPORINS
More stable to Gram negative b-lactamase and less
active against S. aureus.
Members include: Cefuroxime (Ceftin [oral] and
Zinocef), Cefotetan (Cefotan), and Cefoxitin (Mefoxin).
Dr. Firas Kassab

126. 3RD GENERATION CEPHALOSPORINS
Broader activity against Gram negatives.
Members include: Cefdinir (Omnicef),
Cefoperazone (Cefobid), Ceftazidime (Fortaz), and
Ceftriaxone (Rocephin), and Cefotaxime (Claforan).
4TH GENERATION CEPHALOSPORINS
More resistant to destruction by chromosomal b-
lactamases, but not completely resistant to the b-lactamases of
Serratia, Enterobacter and Pseudomonas.
Cefepime (Maxipime).
Dr. Firas Kassab

127. Adverse effects :
• Pain
• Diarrhoea
• Hypersensitivity
• Nephrotoxicity
• Neutropenia
• Thrombocytopenia
Dr. Firas Kassab

128. USES :
• As alternatives to PnG in patients developing rashes or other allergic reactions
with PnG.
• Respiratory, urinary and soft tissue infections caused by gram negative
organisms.
• Penicillinase producing staphylococcal infection.
• Septicaermias caused by gram negative organisms : an aminoglycotide may be
combined with a cephalosporin.
• Surgical prophylaxis; surgical prosthesis such as artificial heart valves, artificial
joints etc. The first generation drugs are used.
• Meningitis caused by H.influenzae, enterobacteriaceae.
• Gonorrhoea caused by penicillinase producing organisms.
• Typhoid : as alternative to fluoroquinolones (specially in children)
• Mixed aerobic – anaerobic infections seen in cancer patients those undergoing
colorectal surgery, obstetric complications.
• Prophylaxis and treatment of infections in neutropenic patients.
Dr. Firas Kassab

129. • Bind to the 50s ribosomal subunit.
• Block chain elongation.
• Bacteriocidal or bacteriostatic depending upon the organism.
Dr. Firas Kassab

130. USES
Gram positive organisms.
Used to treat Legionella, Mycoplasma,
syphilis, diphtheria carriers and pertussis.
Safe in pregnancy.
SIDE EFFECTS
Erythromycin estolate - cholestatic
hepatitis (1/1000).
Ototoxic in high doses.
Dr. Firas Kassab

131. A.Uses
Spectrum is similar erythromycin and
respiratory Gram-negative pathogens
Clarithromycin can be used - H. pylori and
atypical mycobacteria infections.
B.Side Effects
Teratogenic.
Ototoxic in high doses.
Dr. Firas Kassab

132. • A.USES
Used against Gram positive cocci and anaerobes, both
Gram-positive and Gram-negative rods.
• B.SIDE EFFECTS
Significant risk of pseudo- membranous colitis due to the
overgrowth of C. difficile.
Dr. Firas Kassab

133. • MECHANISM :
Works by binding to a specific protein,
S12, on the 30s ribosomal subunit.
Blocks normal activation of the initiation
complex.
At low concentrations - the mRNA is misread and
the wrong amino acid is inserted.
At higher concentrations - inhibit translation.
Dr. Firas Kassab

134. • Excreted by glomerular filtration.
• Aminoglycosides have a low toxic to therapeutic ratio. Blood
levels need to be monitored to insure safety and efficacy.
• If the GFR falls below 70mL/min, the daily dose must be
reduced to prevent toxicity.
Dr. Firas Kassab

135. • Ototoxicity
• Nephrotoxicity
• Very high concentrations - neuromuscular blockade.
Dr. Firas Kassab

136. • It is effective against gram positive and negative bacteria including penicillinase
resistant staphylococci.
• Gentamicin and ampicillin should be administered separately because
gentamicin gets destroyed.
• It is indicated in severe anaerobic infections.
• Dose – Adult – 3-7mg/kg/day in 2-3 divided dose.
Child – 1-3mg/kg/day in 2-3 divided dose.
• Toxicity – It causes ototoxicity (vestibular and cochlear). If serum concentrations
exceeds 10mg/ml transient tinnitus may occur.
• When used over a weak, nephrotoxicity occurs.
• Allergic reactions – not recommended in lactating mothers.
Dr. Firas Kassab

137. CLASSIFICATION
First generation: Cinoxacin, Oxalinic acid,
Nalidixic acid.
Second generation: Ciprofloxacin,
Ofloxacin, Norfloxacin, Levofloxacin
Third generation: Gatifloxacin,
Sparfloxacin, Tosulfioxacin
Fourth generation: Gemifloxacin,
Moxifloxcin, Torvafloxacin.
Dr. Firas Kassab

138. • Mechanism
Interfere with the activity of DNA
gyrase.
Prevent winding of the DNA helix
into the supercoiled form.
Actions are bacteriocidal.
Dr. Firas Kassab

139. • Used against Enterobacteriaceae.
• Ciprofloxacin most active against
Pseudomonas.
• Fluoroquinolones used for
UTIs
Pneumonia
Atypical pneumonia and
Bacterial gastroenteritis.
Dr. Firas Kassab

140. • High drug levels are neurotoxic.
• Prolonged use leads to tendon damage (rupture of Achilles
tendon).
• Not approved for children causes cartilage damage.
• Safety in pregnancy is not established
Dr. Firas Kassab

141. Belongs to Nitroimidazole group.
Mechanism
-In a reducing environment, metronidazole is reduced to a substance
- inhibits bacterial DNA synthesis.
-Its action is broadspectrum bacteriocidal
-Its use is limited to anaerobic organisms.
* Plasma t1/2 is 8hrs.
Dr. Firas Kassab

142. • Anorexia nausea and abdominal cramps.
• Produces metallic taste in the mouth.
• Peripheral neuropathy, seizures and ataxia have been seen with
prolonged use.
• Thromboflebitis of injected vein occurs if the solution is not well
diluted.
Dr. Firas Kassab

143. -Neurological disease.
-Blood dyscrasias.
-First trimister of pregnancy.
-Chronic alcoholism.
Preparations: Tab Metrogyl 200mg 400mg
200mg/5ml susp
500mg/100ml i.v. infustion
Dr. Firas Kassab

144. • Amoebiasis
• Giardiasis
• Trichomonas vaginitis
• Anaerobic bacterial infections
• Pseudomembranous enterocolitis
• Ulcerative gingivitis, trench mouth
• Helicobacter pylori gastritis/peptic ulcer
Dr. Firas Kassab

145. • These are bacteriostatic agents.
• inactivated by presence of pus.
• They act by inhibition of bacterial synthesis of
folic acid from para amino benzoic acid (PABA).
• The concentration of sulfonamides in the urine is
greater than in blood this leads to formation of
crystals of sulfonamides termed as crystalluria
and leads to renal damage.
Dr. Firas Kassab

146. • Allergic reactions
• Prolonged therapy can lead to macrocytic
anemia
• Also cause kernicterus by displacing bilirubin
from plasma albumin in babies during
intrauterine life. They may also cause foetal
malformation.
• Sulfadizine: It penetrates blood brains
barrier. It is commonly used in traumatic
meningitis.
Dr. Firas Kassab

147. • This agent inhibits the conversion of folic acid to folinic
acid which is important for bacterial synthesis of DNA and RNA.
• It is active against strep pyogens and most staphylococci
and haemophili.
• It is indicated in acute exacerbations in post irradiation
osteomyelitis secondary to osteoradionecrosis. It is also used in
mixed actinomycotic infections along with penicillin.
• Dose 80 mg of Trimethoprim + 400 mg of sulfamethoxazole
2 tablets 12 hourly
Child : 20 mg + 100 mg
Dr. Firas Kassab

148. Cotrimoxazole is widely used
• Urinary tract infections
• Respiratory tract infections
• Typhoid
• Bacterial diarrhoeas and dysentery
• Chancroid
• Granuloma inguinale
• It is an effeictive alternative to penicillin for protecting
agranulocytosis patients and treating respiratory and
other infections in them.
• Pneumocystitis carinii.
Dr. Firas Kassab

149. These are the antibiotics used for external application of drugs to the surface for
local action.
POLYPEPTIDE ANTIBIOTICS
• Low molecular weight cationic drugs.
• Powerful bactericidal
• Toxic when used systemically.
• They are: Polymyxin-B, Colstin, Bacitran, Tyrothricin.
POLYMYXIN-B & COLISTIN
• Active against g-ve bacteria.
• They have a detergent like action on cell membrane causing leak in cell
constituents. No cross resistance with other drugs.
• Adverse effects: No systemic absorption after oral or topical administration.
• Given orally causes G.I.T. disturbances.
• Systemic effects are flushing, paraesthesia, renal and CNS disturbance.
Dr. Firas Kassab

150. Uses: 1. Topically used in combination with other anti microbials for
skin infections, burns, otitis externa, conjunctivitis, corneal ulcers.
2. Orally for g-ve bacillary dysentery, diarrhea in children and
infants.
Preparation and dose: 1. Neosporin powder: 5000u polymyxin with
neomycin sulphate 3400u and bacitracin 400u per g.
• Neosporin eye drops.
• Neosporin-H ear drops.
BACITRACIN
• Discovered from Bacillus Subtilis.
• Active against g+ve organisms like Neisseria, H.Influenza,
Staph, Strepto, Clostridium, Corynebacterium.
• Not absorbed orally and does not penetrate the intact skin.
• Commonly combined with Neomycin and Polymyxin-B.
Dr. Firas Kassab

151. It is an aminoglyciside, obtained from Steptomyces Fradiaea.
Binds to ribosomal 30S subunit to inactivate DNA polymerase cause misreading of
genetic code.
Spectrum: Active against g+ve and g-ve bacteria less active against
Pseudomonas, Strepto. Pyogens.
It is not used systemically because of nephro and ototoxicity.
No systemic absorption from topical and oral administration.
Uses: a) Topical: Combined with Polymyxin-B & Bacitracin for infected
wound, ulcers, burns, external ear infection, conjunctivitis.
• Oral: -For preparation of bowel before surgery to decrease post
operative infection.
In hepatic coma to reduce nitrogen producing bacteria in G.I.T.
Dr. Firas Kassab

152. FOUR CATEGORIES BASED ON HOW SAFE OR RISKY IT IS TO USE ANTIBIOTICS
DURING PREGNANCY.
Category A – No evidence of foetal harm.
Eg : Nystatin
Category B – No known association with birth defects
Eg : Amoxicillin, Augmentin, Metronidazole
Category C – Information only from animal studies
Eg : Bactrim, isoniazid, rifampin
Category D – Clear - cut problems
Eg : Tetracyclines, minocycline, sulfa drugs.
Dr. Firas Kassab

153. Drug Use during
pregnancy
Risk Use during
Breast feeding
Antibiotics
Pencillins YES - YES
Erythromycin YES - Avoid estolate
form
- YES
Cephalosporins YES - YES
Tetracylines AVOID Tooth discoloration
inhibits bone
formation
Avoid
Metronidazole YES - YES
Clindamycin YES - YES
Dr. Firas Kassab

154. • Concentration-dependent antibiotics
Dosage interval should be increased
• Time-dependent antibiotics
Dose is decreased
Dr. Firas Kassab

155. • Aminoglycosides
• Cotrimoxazole
• Cephalexin
• Carbenicillin
• Ethambutol
• Cefotaxime
• Vancomycin
• Norfloxacin
• Amphotenicin –B
• Metronidazole
Dr. Firas Kassab

156. • Cephalothin
• Cephaloridine
• Talampicillin
• Tetracycline (except doxycline).
Dr. Firas Kassab

157. • ATTENTION IN LIVER DISEASE :
• Antimicrobials to be avoided or used at lower dose in liver
disease are :
• Drugs to be avoided Dose reduction
needed
• Erythromycin estolate Chloramphenicol Pyrazinamide
Metronidazole Talampicillin Clindamycin
Tetracycline Isoniazid Nalidixic
acid Rifampin Pefloxacin
• The biliary concentration of ampicillin may be significantly
reduced in patients with hepatic disease, rendering the antibiotic
less effective.
Dr. Firas Kassab

158. • Antibiotic prophylaxis.
• Amoxicillin is better choice.
• Uncontrolled diabetes.
• PRECAUTION;Gatifloxacilin- causes both
hypoglycemia and hyperglycemia.
• Compared with macrolides- Gatifloxacilin
4.3 times higher risk hypoglycemia
16.7times higher risk hyperglycemia
Dr. Firas Kassab

159. • The immunocompromised host has a potential risk for
severe head and neck infections that usually require
aggressive antimicrobial therapy and prolonged
hospitalization.
Dr. Firas Kassab

160. • Airway monitoring and possible surgical airway establishment.
• Comprehensive history and physical examination.
• Obtaining appropriate laboratory and imaging studies.
• Empiric antimicrobial therapy.
• Surgical debridement and irrigation, as needed.
• Culture and antibiotic sensitivity testing of infectious organisms to
appropriately adjust antibiotic therapy.
• Close follow-up to monitor for resolution and recurrence.
Dr. Firas Kassab

161. 1. MEROPENEN
• It is a beta-lactam, belongs to the subgroup of carbapenem.
• Ultra broad spectrum injectable antibiotic.
• Inhibits bacterial cell wall synthesis.
• Action against gram positive and gram negative bacteria and
some anaerobic bacteria.
• Administered intravenously.
Dr. Firas Kassab

162. • Cystic fibrosis
• Infections in immunocompromised patients.
• Intra abdominal infections.
• Urinary tract infections.
• Septicaemia.
• Skin infections
• ADVERSE EFFECTS :
Diarrhoea, Nausea, Vomiting, headache, rash,
thrombophlebitis.
Dr. Firas Kassab

163. • Fourth generation cephalosporin.
• Extended spectrum of activity against gram +ve and gram –ve
microbes compared to third generation cephalosporins.
• Administrated intramuscularly or intravenously dose – 1 gm
to 2 gm every 12 hourly.
PHARMACOKINETICS :
• Peak plasma concentration after i.m. administration is 1.0 to 1.6
hour.
• It is distributed throughout the body tissues and fluids.
• Primarily excreted unchanged in urine.
Dr. Firas Kassab

164. • Lower respiratory tact infections.
• Urinary tract infections.
• Skin and skin structure infections.
• Sepsis and bacteremia
• Febrile neutropenia
• Meningitis.
ADVERSE EFFECTS :
• Headache, nausea, vomiting, rash, diarrhoea,
dizziness.
Dr. Firas Kassab

165. • Synercid is the brand name of combination of quinupristin
and dalfopristin antibiotics.
• These are semisynthetic pistinamycin derivatives.
• Active against methicillius sensitive staphylococcus aureus,
group A streptococci, Enterococcus faecium.
• 500 mg strength of synercid contains 150 mg of quinupristin and
350 mg of Dalfopristin.
• Administration – intravenously.
Dr. Firas Kassab

166. • In life threatening infections and certain skin infections.
• Adverse effects :
• Pain, swelling and irritation at the injection site.
• Muscle and joint pain, nausea, vomiting, rash, diarrhoea,
headache, itching.
Dr. Firas Kassab

167. • New antibacterial drug belongs to class oxazolidones.
• Inhibits protein synthesis – 70s ribosomes.
• Active against methicillin resistant and sensitive
staphylococci, and streptococci enterobacteria faecalis.
• 400 – 600 mg orally twice daily (12 hrly) parenteral
route for severely ill patients. Dosage is same as that
of oral route
• Metabolized by oxidation and hence can safely
used in renal failure.
Dr. Firas Kassab

168. • It is a synthetic fluoroquinolone agent.
• Inhibits topoisomerase II and IV, there by affects the
replication and repair of bacterial DNA.
• It is active against following organisms :
• Step. aureus, staph Epidermides, strepto pneumonias, H.
influenzae, Klebsiella, Enterobacilus, mycobacterium,
Bacillus anthracis.
• Administrated both oral and intravenous route.
• Dose : 400 mg daily orally or i.v. infusion.
Dr. Firas Kassab

169. • Acute sinusitis.
• Acute exacerbation of chronic bronchitis.
• Pneumonia.
• Skin and skin structure infections.
• Second – line agent in T.B.
CONTRAINDICATIONS :
• Known hypersensitivity, in QT prolongation.
• Pregnancy and lactation.
SIDE EFFECTS :
• G.I. disturbances – Nausea vomiting anorexia, bloating.
Dr. Firas Kassab

170. • It is a fourth generation fluro-quinolone agent.
• Greater affinity for topoisomerase IV.
• Active against gram +ve cocci.
• Oral and intravenous route.
• Dose – 200 to 400 mg orally or i.v. once daily (+½
shown)
• Active against – Streptococcus pneumonias.
• Chlamydia pneumonias.
Dr. Firas Kassab

171. • The reversible inclusion of a molecule between two other groups,
most commonly seen in DNA
• Inhibits DNA replication in rapidly growing cells
Dr. Firas Kassab

172. • First anthracycline antibiotics were isolated from
Streptomyces peucetius in 1958
• Interact with DNA by intercalcation and inhibit
topsoimerase
• Some of the most effective cancer drugs available
• Very wide spectrum
Dr. Firas Kassab

173. • Daunorubicin (Cerubidine)
• Doxorubicin (Adriamycin, Rubex)
• Epirubicin (Ellence, Pharmorubicin)
• Idarubicin (Idamycin)
Dr. Firas Kassab

174. • Daunomycin (DNR) for acute lymphocytic and myeloid leukenmia
• Doxorubicin (DOX) for chemotherapy for solid tumors including breast
cancer, soft tissue sarcomes, and aggressive lymphomas
Dr. Firas Kassab

175. • Disrupt DNA
• Intercalate into the base pairs in DNA minor grooves
• Inhibits topoiosomerase II enzyme, preventing the relaxing of supercoiled
DNA, thus blocking DNA transcription and replication
• Cause free radical damage of ribose in the DNA
Dr. Firas Kassab

176. • Causes cardiotoxicity due to free radical formation
• Interference with ryanodine receptors of the sarcoplasmic reticulum in the
heart muscle cells
• Free-radical formation in the heart
• Leads to forms of congestive heart failure, often years after treatment
• Counteract with dexrazoxane
Dr. Firas Kassab

177. • Natural glycopeptidic antibiotics produced by Streptomyces
verticillus
• Efficacy against tumors
• Mainly used in therapy in a combination with radiotherapy or
chemotherapy
• Commonly administered as Blenoxane, a drug that includes
both bleomycin A2 and B2.
Dr. Firas Kassab

178. • First discovered in 1966 by Hamao Umerzawa from Japan
when screening cultures of S. verticullus
• Launched in Japan by Nippon kayaku in 1969
• Initially marketed by Bristol-Myers Squibb under brand
name-Blenoxance
Dr. Firas Kassab

179. Dr. Firas Kassab

180. • Induction of DNA strand breaks
• Medicate DNA strand scission of single and double strand
breaks dependent on metal ions and oxygen
Dr. Firas Kassab

181. • Pulmonary fibrosis and impaired lung function
• Age and dose related
• Capillary changes, atypical epithelial cells
Dr. Firas Kassab

182. • Resistance mechanisms can operate to
• Prevent agents from entering cells, as in loss of plasma membrane
carriers for nucleoside analogs
• Enhance their extrusion, as exemplified by energy-dependent pumps
such as ABC transporters
Dr. Firas Kassab

183. ANTIBIOTICS
NEEDED,NOT
NEEDED
WHAT TO DO
WHAT TO GIVE
HOW TO DOPROBLEMS OF
MISUSE
Dr. Firas Kassab

184. • SURGICAL EXTRACTIONS
• SURGIAL MANAGEMENT OF LESIONS
• SPACE INFECTIONS
• TRAUMA
• ORTHOGNATHIC SURGERY
• OSTEOMYELITIS
Dr. Firas Kassab

185. [ ASIAN J OMFS : VOL 18 : NO. 4 : 272-278 ]
MOST ORAL INFECTIONS ARE ODONTOGENIC IN
ORIGIN
SEQUELAE OF DEEP CARIOUS LESION /
PERIODONTAL / PERICORONAL INFECTIONS
MANAGEMENT
EXTRACTION / ENDO TREATMENT
/ SURGICAL DRAINAGE
WITHOUT ANTIBIOTICS
Dr. Firas Kassab

186. UNCOMPLICATED EXTRACTION,SURGERIES
+
OTHERWISE HEALTHY
LOW INFECTION RATE
ANTIBIOTICS NOT NEEDED
[ JIDA VOL.69 : SEPT-DEC 1998 : 274 – 277]
Dr. Firas Kassab

187. • Antibiotics are used to treat infections and are also responsible
for making them more difficult to treat because of their misuses
and development of resistance. The only way to keep antibiotics
useful is to use them appropriately and judiciously.
Dr. Firas Kassab

188. • NEVER ACCEPT CONCEPT OF ANTIBIOTICS ON DEMAND
• NEVER USE A BROAD SPECTRUM ANTIBIOTICS WHEN NARROW SPECTRUM IS
INDICATED
• NO LONG COURSE OF ANTIBIOTICS
• NO NEED OF ANTIBIOTIC PROPHYLAXIS FOR SIMPLE SURGICAL PROCEDURES or
WHEN THERE IS LESS CHANCE OF POST SURGICAL INFECTION
• WHEN NO SIGNS OF INFECTIONS SUCH AS SWELLING,LYMPHADENOPATHY,
ELEVATED TEMPERATURE
• ALWAYS MAKE SURE THE SOURCE OF INFECTION IS ELIMINATED-EXTRACTION
OF TOOTH
INCISION AND DRAINAGE
Dr. Firas Kassab

189. • Medical pharmacology
- Satoskar
• Medical pharmacology.
- K.D. Tripathi.
• Contemporary oral and maxillofacial surgery.
- Lary J. Peterson 4th Edition.
• Pharmacology and therapeutics and dentistry.
- Yogiela Dowd Neidle
• OMFS Clin N Am -2003
• Oral and maxillofacial infections
Topazian
• Internet
Dr. Firas Kassab

190. Dr. Firas Kassab