Anitbiotics in dentistry- a brief presentation

1. ANTIBIOTICS
Presented by
Department of Oral Medicine and radiology
Dr Sarah Nazeer

2. CONTENTS
 Introduction
 History
 Classification
 Mechanism of action
 Principles of antibiotic administration
 Individual antibiotics
 Clinical implications
 Conclusion

3. Coined by Walksman in 1942
Ancient Greek
ἀντί- Anti - against
βίος -Biotic - Life
Antibiotics are substances produced by microorganisms
which suppress the growth of or kill other microorganisms at
very low concentrations.
Both synthetic +microbiologically produced
drugs=ANTIMICROBIAL AGENT.

4. Antibiotics
HISTORY

5. 1877 Louis Pasteur Inhibition of some microbes
by others; anthrax(Bacillus anthracis)

8. CLASSIFICATION

9. Classification of Antibiotics
Inhibitors of Cell
Wall Synthesis
Protein Synthesis
Inhibitors
Inhibitors of Nucleic
Acid Synthesis and
Function
Others:
Vancomycine
Bacitracin
ß-lactam
antibiotics
Monobactams
Chloramphenicole
Carbapenems Cephalosporins
Clindamycine Macrolides
Penicillins
Tetracyclines
Antistaph:
Methicillin
Natural:
Penicillin G
Penicillin V
Extended
spectrum:
Amoxicillin
Ampicillin
Erythromycine
Azithromycine
Clarithromycin
e
Quinolones
Metronidazole
Doxycycline
Minocycline
Tetracycline
Ciproflaxicine
Flagyl

10. Antibiotics
A. CHEMICAL STRUCTURE
Sulfonamides- Sulfadiazines, Sulfones, Dapsone,
Paraaminosalicylic Acid(pas)
Diaminopyrimidines- Trimethoprim
-Lactam Antibiotics- Penicillins, Cephalosporins,
Monobactums
Tetracyclines- Oxytetracycline, Doxycycline

11. Antibiotics
 Nitrobenzene Derivative- Chloramphenicol
 Aminoglycosides- Streptomycin, Gentamycin,
Neomycin
 Macrolide Antibiotics- Erythromycin,
Roxithromycin
 Polypeptide Antibiotics- Polymixin-B , Colistin,
Bacitracin

13. Antibiotics

14.  Interfere With D.N.A Synthesis- Acyclovir
 Interfere With Intermediary Metabolism- Sulfonamides, Sulfones,
Ethambutol
C. TYPE OF ORGANISMS AGAINST WHICH
PRIMARILY ACTIVE
 Antibacterial- Pencillins, Aminoglycosides, Erythromycin
 Antifungal- Griesofulvin, Ketoconazole
 Antiviral- Acyclovir, Zidovudine
 Antiprotozoal- Chloroquine, Metronidazole
 Antihelminthic- Mebendazole

15. Antibiotics
D. SPECTRUM OF ACTIVITY
NARROW SPECTRUM BROAD SPECTRUM
- Penicillin –G - Tetracyclines
- Streptomycin -Chloramphenicol
- Erythromycin
E. TYPE OF ACTION
PRIMARILY BACTERIOSTATIC
- Sulphonamides
- Tetracyclines
- Chloramphenicol
- Erythromycin

16. Antibiotics
PRIMARILY BACTERIOCIDAL
-Penicillin
-Cephalosporins
-Aminoglycosides
-Polypeptides
-Ciprofloxacin
F. ANTIBIOTICS ARE OBTAINED FROM
 Fungi
- Penicillin
-Cephalosporin
-Griesofulvin

17. Antibiotics
Bacteria
-Polymyxin – B
-Colistin
-Bacitracin
Actinomycetes
-Aminoglycosides
-Tetracyclines
-Chloramphenicol
G. RAPID KILLING ANTIBIOTICS
-Penicillins
-Cephalosporins
-Metronidazole (Flagyl)

18. Bactericidal- the ability to kill the bacteria
Bacteriostatic- the ability to inhibit or
retard the growth of bacteria
BACTERIOSTATIC V/S BACTERICIDAL
Aminoglycosides
Bacitracin
Cephalosporins
Metronidiazole
vancomycin
Penicillins
ciprofloxacin
streptomycin
cotrimoxazole
Chloramphenicol
Clindamycin
erythromycin
Sulfonamides
Tetracycline
trimethoprim

19. ANTI - MICROBIAL DRUG TARGETS

20.  Erythromycin 250-500 Mg Qid
 Clindamycin 150-300 Mg Qid Or 300-450 Mg Qid
 Cephalosporins
 Tetracyclines 250-500 Mg 2-4 Times Daily.
 Doxycycline 100 Mg Every 12 Hours First Day Then
100 Mg Daily
 Ciprofloxacin 250-500 Mg , 12th Hourly
 Metronidazole ( Flagyl) Loading Dose - 1 Gram IV,
maintainence Dose 500 Mg Qid, Oral Dose 500 Mg Qid.

21. MECHANISMS OF ANTIBACTERIAL
RESISTANCE (1)
 Structurally modified antibiotic target
site, resulting in:
 Reduced antibiotic binding
 Formation of a new metabolic pathway preventing
metabolism of the antibiotic

22. STRUCTURALLY MODIFIED ANTIBIOTIC TARGET
SITE
Interior of organism
Cell wall
Binding Target site
Antibiotic
Antibiotics normally bind to specific binding
proteins on the bacterial cell surface

23. STRUCTURALLY MODIFIED ANTIBIOTIC TARGET
SITE
Antibiotics are no longer able to bind to modified
binding proteins on the bacterial cell surface
Interior of organism
Cell wall
Modified target site
Antibiotic
Changed site: blocked binding

24. MECHANISMS OF ANTIBACTERIAL
RESISTANCE (2)
 Altered uptake of
antibiotics, resulting in:
 Decreased permeability
 Increased efflux

25. ALTERED UPTAKE OF ANTIBIOTICS: DECREASED
PERMEABILITY
Interior of organism
Cell wall
Porin channel
into organism
Antibiotic
Antibiotics normally enter bacterial cells via
porin channels in the cell wall

26. ALTERED UPTAKE OF ANTIBIOTICS: DECREASED
PERMEABILITY
Interior of organism
Cell wall
New porin channel
into organism
Antibiotic
New porin channels in the bacterial cell wall do
not allow antibiotics to enter the cells

27. ALTERED UPTAKE OF ANTIBIOTICS: INCREASED
EFFLUX
Antibiotics enter bacterial cells via porin
Interior of organism
Cell wall
channels in the cell wall
Porin channel
through cell wall
Antibiotic
Entering Entering

28. ALTERED UPTAKE OF ANTIBIOTICS: INCREASED
EFFLUX
Once antibiotics enter bacterial cells, they are
Interior of organism
Cell wall
immediately excluded from the cells
via active pumps
Porin channel
through cell wall
Antibiotic
Entering Exiting
Active pump

29. MECHANISMS OF ANTIBACTERIAL
RESISTANCE (3)
 Antibiotic inactivation
 bacteria acquire genes encoding
enzymes that inactivate antibiotics
Examples include:
 -lactamases
 aminoglycoside-modifying enzymes
 chloramphenicol acetyl transferase

30. ANTIBIOTIC INACTIVATION
Interior of organism
Antibiotic
Cell wall
Binding Target site
Enzyme
Inactivating enzymes target antibiotics

31. ANTIBIOTIC INACTIVATION
Enzymes bind to antibiotic molecules
Enzyme Binding Target site
Interior of organism
Antibiotic
Cell wall
Enzyme
binding

32. ANTIBIOTIC INACTIVATION
Enzymes destroy antibiotics or prevent binding to target sites
Enzyme Target site
Interior of organism
Antibiotic
Cell wall
Antibiotic
destroyed
Antibiotic altered,
binding prevented

33. PRINCIPLES OF ANTIBIOTIC
ADMINISTRATION

34. PROPER DOSE
 Prescribe or administer sufficient amounts to achieve the
desired therapeutic effect, but not enough to cause injury to
the host.
o Relationship between antibiotic dose/ concentration.
o Relationship between dose and body weight
Individual dose = BW(kg)/70 x avg adult dose
 Under-dosing – emergence of bacterial resistance.

35. AGE
The dose of drug for children is often calculated from the
adults dose
Young’s formula
Age
Child dose = x adult dose
Age +12
Dilling’s formula
Age
20
Child dose = x adult dose

36. PROPER TIME-INTERVAL
 The frequency of dosing is also important
 Plasma half life (t 1/2)
 The usual dosage interval for the therapeutic use of
antibiotics is four times the t ½.

37. PROPER ROUTE OF ADMINISTRATION
 Oral route - most common route
 But some of the bacteria are not susceptible to the drug
plasma concentrations produced by oral route and hence,
parenteral routes are chosen.
 Timing of administration

38. CONSISTENCY OF ROUTE OF
ADMINISTRATION
 Severity of the infection
 After an initial response has been achieved immediate,
discontinuation of parenteral therapy should not be done,
since this can lead to a fall in therapeutic blood levels,
causing recrudescence of the infection.
 Bacteria are usually eradicated when the antibiotic is given
for 5 to 7 days.

39. Antibiotic drug-combination therapy -
Rationale
• Minimize the emergence of antibiotic-resistant microorganisms.
• To increase the certainty of a successful clinical outcome.
• To treat mixed bacterial infections & severe infections of unknown
etiology.
• To prevent suprainfection.
• To decrease toxicity without decreasing efficacy.

40. Indications :
 In the patients with life threatening sepsis of unknown etiology.
 When increased bactericidal effect against a specific organism is
desired. e.g.: treatment of Enterococcus infection
(penicillin & aminoglycoside)
 Prevention of rapid emergence of resistant bacteria .
e.g.: Tuberculosis
 Treatment of odontogenic infections which could progress to
more serious like retropharyngeal space infections.
(penicillin and metronidazole)

41. Rules
1) 2 bactericidal drugs produce, supra-additive effects, but not
antagonism i.e. (1+1>2)
2) The combination of a bacteriostatic and a bactericidal drug
generally results in diminished effects i.e. (1+1<2)
3) 2 bacteriostatic drugs are never inhibitory i.e. (1+1=2)

42. PATIENT MONITORING
 Adjunctive surgery
 Fluid balance
 Nutritional support
CARE MUST BE TAKEN SPECIFICALLY ON
1. Response to treatment
2. Development of adverse drug reactions

43. RESPONSE TO TREATMENT
 Most commonly, the response begins by the 2nd day and
initially produces a subjective sense of feeling better.
 There after, objective signs of improvement occur
including a decrease in temperature, swelling, pain and
lessening of trismus.
 Duration of therapy
(omfscna vol. 15 Feb 2003)

44. Antibiotics

46.  Penicillin was first antibiotic to be used clinically in
1941.
 It was miracle that the least toxic drug of its kind was the
first to be discovered.
 It was originally obtained from the fungus Penicillium
notatum, but the present source is a high yeilding mutant
of P.chrysogenum.
 Penicillinase is a beta lactamase developed by most
staphylococci and many gram negative organisms, that is
responsible for the breakdown of beta lactam ring

47. BASED ON THE SUSCEPTIBILITY TO PENICILLINASES
AND SPECTRUM OF ACTION, PENICILLINS ARE
CLASSIFIED AS:

48. DOSAGE
PHENOXY METHYL PENICILLIN (OR) PENICILLIN (V)
 Oral loading dose of 1000 mg followed by 500 mg every six hours for 6 –
10 days.
 For severe infections antibiotics is taken every 4 hours to maintain more
constant serum level
CLOXACILLIN
 250mg to 500 mg orally every 6 hours.
AMOXICILLIN
 500 mg every 8 hours for 6 – 10 days.
CARBOXY PENICILLIN’S
 125 to 250mg TID (or)
 200 to 1000 mg IM /IV

49. TRADE NAMES
AMOXICILLIN- 250/500mg EVERY 8 HOURS
ACTIMOX
AXL
BLUEMOX
MOX
NOVAMOX
WITH LACTOBACILLUS SPORES
AMOLAC 500
NODIMOX LB
NOVAMOX LB
SWIMOX LB

51. BENZYL PENICILLIN (PENCILLIN G)
•PnG is a narrow spectrum antibiotic; activity is limited primarily to
gram positive bacteria
•Is available in the form of water soluble sodium and potassium salts
•This salts in a dry state are stable at room temperature for years.
•The aqueous solution requires refrigeration and deteriorates
considerably with in 72 hours.
Antibacterial activity
• Most potent, inhibits the growth of susceptible organism.
• Mainly gram +ve, gram –ve cocci and some gram +ve bacilli with
exception of enterococci.
•Cocci – Highly sensitive – Streptococci, Pneumococci, Staph.
aureus, N. gonorrhoeae, N. meningitis
•Bacilli – B. anthracis, Corynebacterium diphtheriae, clostridium
tetany and spirochetes .
•Actinomyces israelii is moderately sensitive

52. Absorption fate and excretion :
• About 1/3 of drug is activated on oral administration.
• Absorbed from the duodenum.
• Because of the inadequate absorption the oral dose should be
4/5 times larger than the intramuscular dose.
• As food interferes with its absorption PnG should be given
orally atleast 30 min after food or 2 to 3 hours before food.
• B. Pencillin in aqueous solution is rapidly absorbed after SC
or IM administration.
• Peak plasma level of 8 to 10 units per ml is reached with in 15
to 30 min and drug disappears from plasma with in 3-6 hours.

53. • Widely distributed in the body and significant amounts
appear in liver, bile, kidney, jointfluid and intestine.
• PnG is excreted mainly by the kidney but in small part in
the bile and other routes.
• 50% drug is eliminated in urine with in first hour.

54. ADVERSE REACTIONS :
a) Miscellaneous reactions :
• Nausea and vomiting on oral PnG
• Sterile inflammatory reaction at the site of IM inj.
• Prolonged IV administration may cause thrombophlebitis
• Accidental IV administration of procaine PP cause anxiety,
mental disturbances paraesthesia and convulsions
b) Intolerance :
• Major problem with PnG includes idiosyncratic,
anaphylactic and allergic reactions

55. c) Other allergic reactions are
• Skin rashes
• Serum sickness
• Renal disturbance
• Hemolytic disturbance
• Anaphylaxis
• Jarisch herxheimer reaction
• Super infection
• Hyperkalemia

56. Uses :
PnG is the drug of choice for infections
1. Streptococcal infections
2. Pneumococcal infections
3. Meningococcal infections
4. Gonorrhoea
5. Syphilis
6. Diphtheria
7. Tetanus and gas gangrene
8. Prophylactic uses

57. SEMI SYNTHETIC PENICILLINS
The major drawbacks of benzyl penicillin are :
1. Inactivation by the gastric hydrochloric acid
2. Short duration of action
3. Poor penetration into CSF
4. Activity mainly against gram +ve organism
5. Possibility of anaphylaxis
Attempts therefore have been made to synthesize pencillin free
from such drawbacks.
P.chrysogenum produces natural penicillins which produce the 6
amino-penicillanic acid (6-APA) nucleus.
The attachment of side chains are inhibited and instead various
organic radicals can be substituted.
Thus a variety of semisynthetic resins are produced.

58. I) Acid resistant pencillins :
1. Potassium phenoxymethyl penicillin (penicillin V)
• Similar antibacterial spectrum like benzylpenicillin.
• More active against resistant staphylococci
• Less inactivated by the gastric acid.
• Plasma levels achieved is 2 to 5 times higher than
benzylpenicillin.
• 50-70% is bond to plasma proteins.
• 25% of drug is eliminated in urine
• Available as 60 & 125 mg tablets.
• Administered in the dose of 250 –500 mg at 4-8 hours
intervals, atleast 30 min before food.
• This can be used in less serious infections (pneumocci
and streptococci).

59. Dose : infants 60 mg, children 125-250 mg given 6 hourly
CRYSTAPEN-V, KAYPEN, PENIVORAL 65, 130, 125, 250 mg
tablets125 mg/5 ml dry ser
2. Potassium phenoxyethyl penicillin and
3. Azidocillin
Both have similar properties to penicillin V and no difference in
the antibacterial effect

60. II) Pencillinase resistant pencillins :
1. Methicillin
1. Effective in staphylococci
2. It is given IM or IV (slow) in the dose of 1 gm every 4-6
hours.
3. Haematuria, albuminuria and reversible interstitial nephritis
are the special adverse effect of methicillin.
2. Cloxacillin
1. Weaker antibacterial activity.
2. Distrubuted thro out the body, but highest s concentration in
kidney and liver. 30% excreted in urine.
3. Oral dose for adults 2-4 gm divided into 4 portions children
50-100mg/kg/day.
4. IM adults 2-12 gm/day, children 100-300 mg/kg/day every
4-6 hours.
BIOCLOX, KLOX, CLOCILIN 0.25, 0.5 gm cap, 0.5 gm/vial.

61. Oxacillin, Dicloxacillin, Flucloxacillin are other isoxazolyl
penicillins, similar to cloxacillin, but not marketed in India.
Nafcillin :
More active than methicillin and cloxacillin but less active than
PnG
80% of drug bonds with plasma proteins excreted by liver in
patients with renal failure.
Dose is similar to cloxacillin.

62. III) Extended spectrum pencillins :
1. Amino pencillins
1. Ampicillin –
• Antibacterial activity is similar to that of PnG that is more
effective than PnG against a variety of gram-ve bacteria
• Drug is effective against H.influenzae strep.viridans,
N.gonorrhea, Salmonella, shigellae, Klebsilla and
enterococci.
Absorption, fate and excretion :
• Oral absorption is incomplete but adequate
• Food interferes with absorption
• Partly excreted in bile and partly by kidney

63. Dose : 0.5-2 gm oral/IM or IV depending on severity of infection
every 6 hours
Children : 25-50 mg/kg/day
AMPILIN, ROSCILLIAN, BIOCILIN – 250, 500 mg cap
100mg/ml ped drops, 250 mg/ml dry syr, 1 gm/vial inj.
USES :
• Urinary tract infections
• Respiratory tract infections
• Meningitis
• Gonorrhoea
• Typhoid fever
• Bacillary dysentry
• Septicaemias
• SBE

64. Adverse effects :
• Diarrhoea is frequent
• Skin rashes is more common
• Unabsorbed drug irritates lower intestines
• Patient with history of hypersensitivity to PnG should not
be given ampicillin.

65. AMOXYCILLIN :
• This is a semisynthetic penicillin
• (amino-p-hydroxy-benzylpencillin)
• Antibacterial spectrum is similar to ampicillin but less effective
than ampicillin for shigellosis.
• Oral absorption is better; food does not interfere; higher and
more sustained blood levels are produced.
• It is less protein bond and urinary excretion is higher than that
of ampicillin.
• Incidence of diarrhoea is less

66. Dose : 0.25-1 g TDS oral;
AMOXYLIN, NOVAMOX, SYNAMOX, MOX, AMOXIL 250,
500 mg cap, 125 mg/5ml dry syr, 500 mg/vial inj.
USES :
• Typhoid
• Bronchitis
• Urinary infection
• SBE
• Gonorrhoea

67. Carboxy penciillins :
The Carboxypenicillins are extended spectrum penicillins,
because they inhibit a wide variety of aerobic gram-ve bacilli
They are ineffective against most strains of staph. Aureus
They have following properties :
1. Highly active against anaerobes
2. Most useful in infections caused by other gram-ve rods
3. Act synergistically with amino glycoside antibiotics, particularly
enterobacteriacea.
4. Much less active than penicillin G against gram+ve organisms
5. The CNS penetration is about 10% of their serum levels and
hence not recommended for the treatment of meningeal
infections.

68. CARBENICILLIN
• Has similar spectrum as other penicillin
• Weaker antibacterial activity than ampicillin
• Active against –pseudomonas, proteus
• < Salmonella , E coli Enterobacter
• Inactive against – klebsiella and gram –ve cocci
• Acid labile and has to be given by parenteral route only
• Peak plasma level is 2hours and excreted in urine

69. Dose : 1-2g im/iv 4-6hours
Adverse effects :
• Cause congestive heart failure
• Bleeding disorders-impaired platelet function
Uses :
• Pseudomonas ,burns, UTI and septicemia
• PYOPEN,CARBELIN 1g,5g per vial

70. UREIDOPENICILLINS –
PIPERACILLIN ( PIPRIL)- antipseudomonal pencillin
Has similar indications of carbenicillin

71. WHAT IF…. PATIENT IS ALLERGIC TO PNC?
patient allergic to
penicilln
early infection
late infection
periodontal infection
clindamycin
erythromycin
metrinidazole
doxycyclin

72. CEPHALOSPORINS
 Group of semi-synthetic antibiotics derived from
cephalosporin, “C” obtained from fungus Cephalosporium.
 Chemically related to penicillins (contain β-lactum ring)
 Have been classified as first, second, third and fourth
generation.
Based on:
When the were introduced
Bacterial susceptibility patterns
Resistance to -lactamase
Pharmacokinetics

73. FIRST GENERATION
These are active against gram-positive bacteria but weaker against gram-negative
bacteria. e.g.Cephalothin, cephalexin.
SECOND GENERATION
More active against gram-negative organisms with some members active
against anaerobes. e.gCefuroxime, Cefaclor
THIRD GENERATION
Very active against gram–negative and gram-positive, but not effective
against anaerobes. e.gCefotaxime, Cefixime
FOURTH GENERATION
Very effective against anaerobes and resistant to beta lactamase
.e.g.Cefipime

74. TRADE NAMES
CEFADROXIL-500mg Every 12 hrs
ACTIDROX
ACUDROX
CEDROX
CEFOXID
CEFUROXIME 125 mg Every 12 hrs
ACTUM
CEFTAZ
CEFEXL
MAXIM

75. CEFIXIME -200-400 mg in a single or two divided
doses
AFIXIM
CEFI
CEFEXY
NOVAFEX
CEFEPIME- 1-2 g 8-12 hourly
BIOPIME
CEPIME
NOVAPIME

76. TETRACYCLINES
 Obtained from soil actinomycetes.
 The first to be introduced was chlortetracycline in 1948 under the
name “Aureomycin’.
 These bind to 30S ribosomal subunit and inhibit the binding of
aminoacyl-tRNA to the A site.
 On the basis of chronology of development they may be divided in
to 3 groups
Group – I Group – II Group – III
Chlortetracycline Domeclocycline Doxycycline
Oxytetracycline Methacycline Minocycline
Tetracycline

77. PRECAUTIONS
 Not used during pregnancy, lactation ,childhood.
 Avoided in patients on diuretics- blood urea levels rise in such
cases
 Used cautiously in renal and hepatic patients.
 Not used with penicillins

78. TRADE NAMES
TETRACYCLINE- 500mg every 8 hrs
ACHROMYCIN
HOSTACYCLINE
TETLIN
DOXYCYCLINE-100 mg every 12 hrs
APIDOX
DOXYN
SWIDOX
TETRADOX
Antibiotics

79. MACROLIDES
 These are antibiotics having a macrocyclic lactone ring with
attached sugars.
 Erythromycin is the first member discovered in 1950s.
 For the past 40 years erythromycin has been the only macrolide
antibiotic.
 Roxythromycin, Clarithromycin, Azithromycin are the next
additions in macrolides.

80. ERYTHROMYCIN
 It was Isolated from Streptomyces erythreus in 1952.
 Water solubility of erythromycin is limited and the solution
remains stable only when kept in cold.
 It acts by inhibiting bacterial protein synthesis. It combines
with 50S ribosomes subunits and interferes with translocation.
ANTIMICROBIAL SPECTRUM
It is narrow, includes mostly gram positive organisms and
few gram negative bacteria and overlaps considerably with
that of Penicillin G.

81. DOSAGE
Erythromycin estolate- 250-500mg qid.
ALTHROCIN, E-MYCIN
Erythromycin stearate- 250-500mg qid
ERYTHROCIN, ERYSTER
Erythromycin base - 250-500mg qid.
ERYSAFE, EROMED

82. DRUG INTERACTIONS
1) Interaction with warfarin leads to serious bleeding in patients
undergoing anticoagulation therapy.
2) Interaction with lovastatin, drug given for cholesterol
reduction leads to severe muscle weakness.
3) Interaction with Theophylline, a bronchodilator used for
asthmatic patients leads to toxic concentrations of the same
resulting in cardiac arrhythmias

83. Newer macrolides were made
Azithromycin –loading dose;500mg 1st day
Followed by 250mg daily.
AZID AZEE AZIPAR AZIWIN
Clarithromycin – 250-500mg every 12 hrs for 6-10 days.
CLAR CLARIWIN MACLAR

84. METRONIDAZOLE
 Introduced in 1959 for the treatment of “Trichomonas
Vulgaris”.
 Used especially for serous anaerobic infections, including
those of the orofacial region.
 Distributed well in to bone, saliva, mucosa, and even brain
abscess.
 Bactericidal

85. TRADE NAMES
METRONIDAZOLE-200-400mg every 8 hrs
FLAGYL
METROGYL
MET
METRONIDAZOLE AND AMOXYCILLIN
200mg + 250 mg every 8 hrs
STEDMOX -M

86. PREVENTING RESISTANCE TO DRUGS
 Limit the use of antimicrobial agents to the treatment of
specific pathogens sensitive to the drug being used.
 Notorious-Make sure doses are high enough, and the duration
of drug therapy long enough , combination therapy.
 To be cautious about the indiscriminate, inadequate or unduly
prolonged use of anti-infectives

87. SUPERINFECTIONS:
 During treatment normal host bacteria that are susceptible to the
drugs are eliminated.
 In the normal state, these bacteria live in peaceful coexistence
with the host and by their physical presence prevent bacteria
capable of producing disease from growing in large numbers.
 The normal flora acts as a defense mechanisms, but when the
indigenous flora is altered, the pathogenic bacteria resistant to an
antibiotic may cause a secondary infection, or superinfection.
 Example is of candidiasis with the use of penicillin, which
eliminates the gram-positive cocci (seen after long term high dose
penicillin therapy).

89.  The use of antibiotics has been standard practice
for patients identified as being at risk of developing
endocarditis.
 The link between dental procedures and IE remains
a controversial subject. In 1984, Guntheroth
reported a low incidence of bacteremia associated
with dental procedures and suggested that
meticulous oral hygiene was more important in the
prevention of IE than any antibiotic regimen.

93. Antibiotics should only be prescribed on the basis of a
defined need otherwise their use may present more of a
risk to the patient than the infection being treated or
prevented.
Antibiotics can be responsible for various
adverse effects, including drug interactions, nausea,
gastrointestinal upsets, potentially fatal allergic reactions and
antibiotic associated colitis
The indiscriminate prescribing of antibiotics can also
cause drug resistance which is an emerging
and significant problem

94. CONCLUSION
 Although antibiotics do not prevent all post-operative
infections, they can reduce their incidence significantly when
administered correctly.
 We should prescribe effective, short-course therapies,
directed at improving the outcome of our patients.
 Future treatment strategies will not only include the
aggressive use of traditional management methods but also
the understanding of normal immune system-associated
defects and newer antimicrobials.

95. THANK YOU