1. Antibiotics are chemical substances produced by microorganisms like fungi, actinomycetes and bacteria that suppress or destroy other microorganisms. 2. Alexander Fleming discovered penicillin in 1929 after noticing that a mold growing in one of his petri dishes had prevented bacteria from growing nearby. Penicillin revolutionized medicine as the first widely used antibiotic. 3. Antibiotic resistance has become a major problem as bacteria have increasingly developed resistance, even to formerly powerful antibiotics like penicillin. Proper antibiotic stewardship including only using antibiotics when necessary and completing prescribed treatment courses can help address this growing threat.

2. DEFINATION
 Antibiotics are chemical substance
elaborated by various species of micro-
organism such as fungi, actinomycetes and
bacteria. They suppress the growth of other
micro-organism and may ultimately destroy
them in low concentration.

4. Early history
 3500 BC the Sumerian doctors would give patients
beer soup mixed with snakeskins and turtle shells.
 Babylonian doctors would heal the eyes by using an
ointment made of frog bile and sour milk.
 The Greeks used many herbs to heal ailments.
 All of these "natural" treatments contained some sort
of antibiotic.

5. Modern history
 Louis Pasteur was one of the first recognized physicians
who observed that bacteria could be used to kill other
bacteria.
 In 1929 Sir Alexander Fleming a Scottish
bacteriologist, went on a vaction and left a petri dish of
staphylococci bacteria uncovered. When he returned, he
noticed that there was mold growing on it. Upon further
examination, he saw that the area around the mold had no
bacteria growing. He named the mold Penicillium, and the
chemical produced by the mold was named
penicillin, which is the first substance recognized as an
antibiotic.

6.  Almost immediately after penicillin was
introduced, resistance in certain strains of
staphylococci was noticed.
 In 1935, Domagkdiscovers synthetic antimicrobial
chemicals (sulfonamides).
 During World War II, because of need for antibiotic
agents, penicillin was isolated and further tested by
injection into animals. It was found to be extremely
useful in curing infections, and to have extremely low
toxicity to the animals. Because of these findings, use
of penicillin greatly increased. This also spurred a
search of other chemical agents of similar use.

7.  the late 1940's through the early
1950's, streptomycin, chloramphenicol, and
tetracycline were discovered and introduced as
antibiotics.
 In 1953, during a Shigella outbreak in Japan, a certain
strain of dysentery bacillus was found to be resistant to
chloramphenicol, tetracycline, streptomycin, and the
sulfanilamides.
 By the 1950's it was apparant that tuberculosis bacteria
was rapidly developing resistance to
streptomycin, which had commonly been used to treat
it.

9. Classification of antibiotics
Classification based on chemical structure & proposed
mechanism of actions as fallows
1. Agents that inhibits synthesis of bacterial cell wall
these includes
a) penicillin & cephalosporin which are structurally simillar
b) Cycloserine vancomycin bacitracine & the azole
antifungal agent ( e.g clotrimazole, fluconazole &
itraconazole which are structurally dissimilar agent

10. 2.Agent that act directly on the cell membrane of
the micro organism affecting permeablity &
leading to leakage of intercelluar compound
e.G polymyxin & polyene antifungal agent nystatin
Amphotericin B which bind to cell wall sterolls

11. 3 .Agent that affect the function of 30 s or 50 s ribosomal
subunit to cause or reversible inhibition of protein
synthesis
e.G chloramphenical
Tetracycline
Erythromycin
Clindamycin

12. 4 .agent that bind to 30s ribosomal subunit &alter
protein synthesis which eventually lead to cell death
E.g. aminoglycosides
5.agent that affect bacterial nucleic acid metabolism
such as rifamycin (e.g. rifampin ) which inhibit RNA
polymerase & the quinilones which inhibit
topoisomerase

13. 6 . agent that block essential enzymes of folate
metabolisum
E.g. trimethoprim& sulfonamide
7 . Antiviral agent which are of several classes including
a) Nuclic acid analog such as acyclovir or gancyclovir
that selectively inhibit viral DNA polymerase and
zidovidine which inhibit reverse transcriptase
b) Non nucleoside reverse transcriptase inhibitors such
as nevirapine
c) Inhibitor of other essential viral enzyme. E.g.
inhibitors of HIV protease or influenza neuraminidase

14. classification
 According to spectra
1.Antibiotic effective against gram positive bacteria
a.For systemic
infection, erythromycin, lincomycin, novobiocin.
b. Those employed topically
e.g. bacitracin
2.Antibiotic mainly against gram negative bacteria
a.For sylstemic infection
e.g. strepomycin & other aminoglycosides
b.Those used locally in intestine
e.g.paromomycin

15. 3.Antibiotic mainly effective against gram –ve &
+ve bacteria
a.Used for systemic infection
e.g. ampicillin, amoxycillin, cephalosporin
b.For topical application
e.g. neomycin
4. Effective against rickettsial & chlamydia
e.g. tetracycline & chloramphenicol
5.Effective against acid fast bacilli
e.g. steptomycin, rifampicin & viomycin

16. 6.Effective against protozoa
e.g. paramomycin & tetracyclin
7.Effective against fungi
e.g.nystatine, amphotericin B
8.Effective against malignancy
e.g. actinomycin, mitomycin

18.  Following are the points by which the clinician can
make a decision of when to use antibiotic, which are to
select, and how to use both therapeutic and
prophylactic situations. To do this one should atleast
know about the following
1. Bacterial flora causing most odontogenic
infections
2. The basic mechanism of host defenses
3. The variety of contemporary antibiotics and
principles to choose

19. Bacterial flora causing most
odontogenic infections
 The indigenous microbial flora of the mouth is
bacteria, which are almost always the cause of
odontogenic infections. The usual flora is both aerobes
and anaerobes

20. The basic mechanism of host
defenses
 Host defense mechanism is the most important factor in
the final outcome of a bacterial insult.Each patient has
many defenses against infections.
1. Physiologic depression of host defence,
Shock
Disturbances of circulation caused by advanced age
Obesity
Fluid imbalance
2. Diseases and disease state that may inhibit host defense
Malnutrition syndrome
Patient with cancer and leukemia
Poorly controlled diabetics

21.  3 Congenital defect which causes defective host
mechanism
Agammaglobulinemia
Multiple myeloma
Total body radiation therapy
Children who have had splenectomy
 4. Therapeutic drugs that impares host defense
mechanism
Cytotoxic drugs
Immunosuppressive drugs

22. principles to choose Antibiotics
 Once the decision has been made to use antibiotics as
an adjunct to treating infection the antibiotics should
be properly selected. The followingguide lines are
useful
1. Identification of causative organism
2. Determination of antibiotic sensitivity
3. Choice of antibiotics

23. 1. Identification of causative organism
Causative organism can be isolated from pus
blood, or tissue fluids. Based upon the knowledge of
pathogenesis and clinical presentation of specific
infection,antibiotic therapy will be either initial or
definitive depending upon whether or not the
organism is diagnosed previously.

24. 2. Determination of antibiotic sensitivity
When treating an infection that has not
responded to initial antibiotic therapy or when
treating a postoperative wound ,the causative agent
must be previously identified and the antibiotic
sensitivity must also be determined.

25. 3 Choice of antibiotics
Upon receipt of the culture and sensitivity
report, there may be a choice of four or five antibiotics.
Selection should be based on consideration of several
factors like
1. Patients previous history of allergy
2. Antibiotics with narrow spectrum
3. Drug that cause fewest adverse reactions.
4. Drug which is least toxic
5. The well established still effective antibiotics
6. Bactericidal rather than bacteriostatic drug
7. The less expensive still effective antibotic
8. Combination antibiotics

26.  1. Patient`s history of allergy
Allergic reaction to drugs should be considered
first. When it exists, alternative drugs must be used.
Example erythromycin or clindamycin is usually use if
the patient is allergic to penicillin

27.  2. Antibiotics with narrow spectrum
The only majour indication for use of broad
spectrum antibiotics coverage is in severe life
threatening infection where identification of causative
agent is obsure. Each time bacteria are exposed to
antibiotics, the opportunity for development of
resistant strains is present. If narrow spectrum
antibiotics is used ,fewer organisms have the
opportunity to become resistant.

28.  3. Drug that cause fewest adverse reactions
The goal of antibiotic therapy is to provide an
effective Drug that causes least problem to the patient
 4. Drug which is least toxic
Toxicity reactions are those that occur as a result
of excessive dose or duration of therapy, but can occur
in individual patients with normal doses.

29.  5. The well established still effective antibiotics
Since its initial availability, penicillin, has been
used for oral infection and it has been very
effective, with low incidence of adverse reaction.
Newer antibiotics should be used only when they have
proved advantage over the older ones .

30.  6. Bactericidal rather than bacteriostatic drug
Bactericidal drugs are effective during the log
phase of bacterial growth the time . If growth is
slowed or brought to stop,cidal drugs have a greately
diminished effect. As a result, in these situations,
when combination drug therapy is to be used,cidal
and static combination should not be used in
combination.

31.  7. The less expensive still effective antibotic
Most effective but less expensive drug should be
considered first.
 8. Combination antibiotics
There are situations in which the use of antibiotic
combination is clearly indicated. Example is when it is
necessary to increase the antibacterial spectrum in
patients with life threatening sepsis of unknown cause.

32. Bacterial resistance to antibiotic
1. When the drug does not reach it’s target
2. The drug is not active
3. Target is altered.

33. Selection of antibiotics
 When an antibiotic is indicated the goal is to
choose a drug that is selectivley active for the
most likely infecting micro-org.& that has least
potential to cause toxicity or allergic reaction in
individual being treated.
 Antibiotic are used in three general ways
 as empirical therapy
 as definative therapy
 As prophylactic or preventive therapy

34. Pharamacokinetic factor that affect
the selection of antibiotic
 Location of the infection
 access of antibiotic to sites of infection
e.g. if the infection in the CSF the drug must
pass the blood brain barrier

35. Host factors
 Host factor for the selection of antibiotics
1. Host defense mechanisms
a. action in the immunocompetant host can be cure
mearly by halting multiplication of micro
organism { bacteriostatic effect}
b. if host defense are impaired bacteriostatic
activity may be inadequate and a berteriocidal
agent may be required for cure
e.g. pt with bacterial endocarditis
pt with AIDS

36. Local factors
 Antimicrobial activity may be significantly
reduces in pus
 Large accumulation of Hb in infected
hematomous cab bind penecillin and
tetracycline & thus may reduce the
effectiveness of other drug
 Penetration of antibiotic into infected areas
such abscess is imparied because vascular
supply is reduce
 Presence of the foreign bodies reduces the
effectiveness of antibiotic

37. Genetic factors
 A no. of drug (e.g.
sulfanamides, chloramphenicol and
nalidixic acid ) may produces acute
hemolysis in pt with glucose 6-
phosphate dehydrogenase deficiency

38. pregnancy
 Pregnancy may impose an increased risk of
reaction to antibiotic for both mother & fetus
 Hearing loss in child with administration of
streptomycin to the mother during pregnancy
 Tetracycline can affect bones & teeth of fetus
, may develop fatal acute fatty necrosis of liver
pancreatitis & associated renal damage.

39. Drug allergy
 A antibiotics especially- B-lactum are
notorious or provoking allergic reaction
 Sulfonamides trimethoprim nitrofurapterin
and erythromycin also has been associated
with hypersentitivity reaction especially
rash.
 Antimicrobial agent like othe drugs can
caused drug fever

40. Therapy with combined
antimicrobial agent
 Indication
 Empirical therapy of severe infections in which a cause
is unknown
 Treatment of polymicrobial infection
 Enhancement of antibacterial activity in the treatment
of specific infection.

41. Disadvantage of combination of
antimicrobial agents
 Risk of toxicity from two or more agent
 The selection of multiple drug resistance
 micro organism
 Increased cost to the patient

42. Some commonly used antibiotics
Penicillin
It is the extract from mould
penicilium notatum
Belonging to group called beta
lactum antibiotics

43. Classification
 1. natural penicillin
 E.g. penicillin g benzyl penicillin
 Procaine penicillin
 Benzedrine penicillin
 2.acid resistant penicillin
 Phenoxymethyl penicillin
 3.penicillinase resistant penicillin
 Methicillin
 Oxacillin
 cloxacilline
 Flucloxacilline
 nafcillin

44.  4.penicillin effective against gram +ve
&some gram -ve organism
 Ampicillin
 Amoxicillin
 Talampicin
 5.extended spectram penicillin
 a.carboxypenicilin
 Carbenicillins
 b.amidinopenicillin
 Mecillinam
 pivmecilliam

45. Mechanism of action
 Act by inhibiting cell walll synthesis in
bacteria. they prevent sythesis &
crosslinkage of peptidoglycans which is the
integral part of bacterial cell wall.

46. Antibacterial spectrum of penicillin
 Effective mainly against gram +ve & gram –
ve cocci &and some gram +ve bacilli.

47. Adverse effect of penicillin
 Intolerance
 Thrombophlebitis
 Allergy with manifestation like
 1.skin rash
 2.serum sickness like syndrome
 3.renal disturabane
 4.haemopoitic disturabance
 5.anaphylaxis

48.  Jarish herxiheimer reaction on syphilitic pt
treated with penicillin
 Superinfection e.g. candida
 hypermia

49. Activity against oral
 Classification pathogens
Usual adult
Gm+ve gm+ve gm–ve
resgimen Arobes anarobes anarobes
 Natural penicillin 250-500mg +ve +ve + -ve
vk QID
 Penicillinase
resistance
Dicloxacillin
250mg 6 hrly stap.only -ve -ve
 Nafcillin 500mg QID stap & -ve -ve
strepto
 Amoxicilline 250-500mg +ve +ve -ve
 Amox/ 8hrly +ve +ve -ve
potassium 250-500mg
clavulanate 8hrly
(augmantin)
 Ampicillin 250-500mg QID +ve -ve -ve

50. AMINOGLYCOSIDES
 These are group of natural & semisynthetic
drugs having polybasic amino groups &
linked glycosidically to two or more amino
sugars.

51. Mechanism of action
 The drugs combine with the bacterial
ribosomes & interfares with m-RNA
ribisomes combination which ultimately
prevents protien synthesis.

52. Absorbtion fate and excreation
 It is excreted mainly by glomerular filtration
&asmall portion in bile

53. spectrum
 Vibrio comma
 Proteus
 E-colli
 Enterobacteria
 Klebsiella
 H- influenza

54.  This group includes drug like
 Streptomycine
 Gentamycine
 Kanamycine

55. Tetracycline
 They are naphthalene derivatives
 it’s nucleus is made up by the fusion of foci
partialy unsaturated cyclohexiane radius
and hence named tetracycline

56. Mechanism of action
 Interfer with protein synthesis by blocking
the attachment of amino acyl transfer rna to
acceptor site on m-RNA ribosome complex.

57. Absorption fate & excretion
 Tetracycline form insoluble complexes
by chelation with calcium ,magnesium
& aluminium
 Iron interferes with absorption
excreted mainly in urine

58. Spectrum
 Includes both gram +ve & -ve orgamism
 Dose –
 orally-250-500mg TDS
 Parantally- 1-2gms in two equal doses 12hrly
interval.
 Newer drug are-
 Doxycycline
 Demeclocycline
 Methacycline
 Minocycline
 lymecycline

59. Disadvantages
 GI system
 Diahrroea
 Nausea
 Vomiting
 Suprinfection
 Candida infectionis comman
 Fetal hepatic disfuction
 Azotemia may be agrevated to renal
impairment
 Chelating effect in teeth & bone

60. Cephalosporins
 1st generation
 They are highly effective against gram +ve
but weaker against gram _ve bacteria
 These are
 cephalexim
 Cephalethin
 Cephaloridine
 Cephradine
 cefadroxil

61. Cephalexin
 Only orally active first generation cephalosporin with
spectrum
 Strptococcus
 Staphylococci
 Gonococci
 Closridia
 C. diptheria
 Actinomyces
 Klebshiella
 Protease
 Salmonella
 shingella

62. Dose
 Adult – 25mg to 1gm 6 to 8 hrly.
 children – 25mg to 100mg/kg/day

63. Cefadroxil
 A it is close congener of cephalexim& has
good tissue penetration
 B can be given 12 hrly
 C spectrum is same as cephalexim
 Dose 0.5gm -1gm BD.

64. SECOND GENARATION
 They are newer to first genaration.
 They have more activity against gram –ve
organisms.
 E.g. cefuroxime – it is higher activity
against penicilliase producing organisms
and all ampicillin resistant H-influenzae.

65. Other spectrum
 More active against klebsiella, E-
coli, enterobacter, indole positive protiens.
 Dose – a. 0.75 – 1.5 gms/ IM or IV/9 hrly
b.30- 100mg/kg/day.
 Available as- supacef.

66. Third generation
 These were developed in end of 1980’s.
 They have augmentation activity against –ve
Endobactericeae.
 They are resistant to β lactamase.
 These are-
 Cefotaxamine
 Ceffizoxime
 Ceftriaxone
 Moxalactum
 ceftazidium

67. Cefotoxamine
 Potent action on gram-ve as well as gram+ve
 It is not so active against anaerobic like bact.
Fragillis, Staphylococcous aureus, Pseudomonas
aerugemosa.
 It is very important drug in teratment of
meningitis, hospital acquired diseases septicaemia
and infection in immuno compromised pt.
 Dose –
 A.1-2gms/Imor IV/6- 12hrly
 50-100mg/kg/day

68.  Available as -
 Omnatax
 claforan

69. Ceftizaxone
 Long acing cephalosporin
 One daily dose is good enough and it has good CSF
penetration
 Dose
 Adult - 1-2gms/IM or IV /day
 Child- 75-100mg/kg/day

70. Ceftazidime
 Most prominent feature is high activity againt
pseudomonas.
 It is used in febrile pt including pt with burns.
 It is less effective to staphylococcus aureus.
 Dose
 Adult-0.5-2gms/IM or IV/ every 8 hours
 Child- 30mg/ kg/day

71. Forth generation cephalosporine
 E.g. cefepime(maxipime) and cefpirome
 It is new cephalosporine with properties like those of
3rd generation cephalosporine but more resistance to
some beta-lactumase.
 It is active against streptococci and methyciline
sensetive staphylococci but not against methyciline
resistance staphylococci.

72. Spectrum
 It’s main use is in serious gram –ve infection (H-
influenza, Neisseria- gonorrhoae and Neissera
meningities) including infection of CNS inti which it
has exelent penetration.
 Half life is of 2hrs.
 Dose -2gm I.V. every 12hrs

73. Fifth generation cephalosporine
 Ceftobiprole has been described as "fifth
generation",though acceptance for this terminology is
not universal.
 Ceftobiprole (and the soluble prodrug medocaril) are
on the FDA fast-track. Ceftobiprole has powerful
antipseudomonal characteristics and appears to be
less susceptible to development of resistance.

74.  These cephems have progressed far enough to be
named, but have not been assigned to a particular
generation.
 Cefaclomezine
 Cefaloram
 Cefaparol
 Cefcanel
 Cefedrolor
 Cefempidone
 Cefetrizole
 Cefivitril

75.  Cefmatilen
 Cefmepidium
 Cefovecin
 Cefoxazole
 Cefrotil
 Cefsumide
 Ceftaroline
 Ceftioxide
 Cefuracetim

76. Adverse effect
 Pain after injection.
 Diarrhoea due disturbance in Gut ecology
 Hypersensitivity reaction-
anaphylaxis, angiodema, asthma, urticaria.
 Nephrotoxicity
 Neutropenia or thrombocytopenia
 Hyperprothombinemia
 A flase +ve cmbs test may occur in as many
as 60%of pt or cephalathin therapy.

77. Macrolides
 They are antibiotics having a macrocyclic
lactone ring with attached sugars
 They are bacteriostatic drug

78. Erythromycin
 Used as aternative in penicillin sensitive
individuals
 CONTRAINDICATIONS
 Hypersensiivity
 Liver dieases- ester salt is avoided
 Available as –tablet & syrup
 Dose ADULT- 250-500mgQID
CHILDREN-30-50mg kg/day
in form of divided doses.

79. Adverse reaction
 Nausea
 Vomiting
 Diahrroea
 Hypertention
 Cardiac arrythmias
 Revesible hearing loss
 ONSET OF ACTION- 2to4hrs

80. Azithromycin
 This new azalide longer of erytromicin has
an expanded
spectrum, hyper…, Pharmacokinetics, better
tolerability and drugs interation profile
however it is not effective against
erythromycin resistant bacteria.

81. Indications
Respiratory track infection
Urenary track infection.
Otitis media

82. Contraindications
 Hypersensitivity
 Hepatic impairment
DOSE- ADULT-500mg OD for 3days OR 500mg OD on
days one followed by 250mg OD for 4 days.
CHILDREN- 10mg/kg/ day for 3 days OR
10mg/kg/day followed by 5mg/kg/day OD for
5day.
ONSET OF ACTION- one to two hrs

83. Adverse effect
 Mild gastric upset
 Abdominal pain
 Headache
 Dizziness

84. Imidazoles
 Metronidazole
 Prototype netroimidazole
 Active against anarobes

85. Mode of action
 In anarobic micro-organisms metronidazole
is converted into an active form by reduction
of it’s nitro group.
 This binds to DNA and prevents formation
of nuclic acid.

86. Absoption fate and excretion
 The drug is well absorbed after oral or rectal
administration.
 It is elimanated urine, partly unchanged &
party metabolized

87. Contraindications
 Neurogenic diseases
 Blood dyscrasias
 first trimester of pregnancy

88. Uses
 Acute ulcerative gingivitis
 Dental infections
 Amoebiasis
 Giardiasis
 Trichomoniasis

89. Dose
 Orally 400mg 8hrly
 IV infusion 0.5gms/8hrs.
 Treatment should be continue for 7 days.

90. Adverse effects
 Anorexia
 Nausea
 Metalic taste
 Headache
 Glossitis
 Dryness of mouth
 Thromphlebitis of injected veins

91. Indication for antibiotic used
A. Systemic indications
1. Congnital or acquired heart
a. Rheumatic heart disease
b. Valvular diseases
c. Pt with ventricular defects
2. Severe kidney diseaes
a. chronic glumerulonephritis
b. pt undergoing dialysis

92. 3. Active leukemia, agranulocytosis, aplasia
, anemia
4. Metabolic disturbances – diabetes
5. Pt on chemotherapeutic drugs
6. Pt with vascular graft

93. B. Maxillo- facial trauma
1.Hard tissue trauma-the consensus is that
antibiotic convert should be used for any
mandibular or maxillar fracture compented
into mouth or paranasal sinus through mouth.
2.Soft tissue trauma
3.Orthognathic & recontructive maxillo- facial
surgery.
4.Odontogenig infection
5.Pericoronities
6.Osteomylitis

94. contraindication
 Minor chronic localised abscess.
 Well localised vesibular abscess .
 Localised ostitis
 For sterilizing root canal
 Pt with mild pericoronitis, minor gingival
oedema & mild pain which do not required
antibiotcs

95. Prophylactic antibiotic therapy
 Standard recommendation
 A cephalosporin cefadroxil preferred
 1preoperatively 500 mg orally 1hr before surgery
 2 post operatively 250 mg orally 6hr after initial
dose
 or
 Clindamycin in penicillin allergic pt
 1 pre operatively 300 mg orally 1 hr before surgery
 2 post operatively 150 mg orally 6hr after initial
dose

96. Principles of antibiotic prophylaxis
 1 antimicrobial agent t is chosen on basis of
most likely micro organisum to cause
infection
 2 an antibiotic loading dose should be
employed
 3 antibiotic should present in sufficient
concentration in blood and targate tissue
prior to dissemination of offending micro
organisum

97.  4 antibiotics should be continued only as
long as microbial contamination from
operative site persist
 5 patient benefits from prophylaxis should
out high risk of antibiotic included allergy
, toxicity , superinfection.

98. Dental procedure that require
endocardititis prophylaxis
 Tooth extraction
 Periodontal suergery
 Subgingival dental prophylaxis
 Endodontic surgery
 Incision & Drainage of infection

99. Dental procedures that do not
require endocardiatis prophylaxis
 Supragingival prophylaxis
 Restorative tooth preparation
 Placement of orthodontic appliances
 Conserative endodontic theraphy

100. REASONS FOR ANTIBIOTIC FAILURE
 INAPPROPIATE choice of antibiotics
 Too low blood concentration
 Poor penetration to infected site
 Limited or decreased vascularity
 Impaired host defence
 Unfavourable local factors

101.  Increased plasma protein binding
 Antibiotic antagonism
 Slow microbial growth
 Antibiotic resistant organisms
 Patient failure to take antibiotics
 Failure to eradicate sorce of infection

102. Myths &misconception in
antibiotic th erapy
 Myth- antibiotics cure pt
1 except in immunocompramised pt
antibiotics are not curative but rather
function to provide time for normal host
defence initially overwhelmed by micro
organisum to gain and control &eventually
eliminate the in fectious process

103.  2 .Antibiotics are substitute for surgical
drainage - never are antibiotics a
substituted for eradication of the source of
infection ( extraction, incision, drainage )
unless the infection is too diffuse
(pericoronitis)

104.  3 culture and sensitivity test are required -
orofacial infection are characteristically
acute in nature, polymicrobial in
cause, short in duration with proper
treatment. These infection require
immediate attention and a dealy of 18 to 36
hrs for result of culture & sensitivity tests
prior to initiation of antibiotics therapy is
usually not appropriate because the
microbial cause Is commly such that
common antibiotics are effective, incision
&drainage are relatively easy.

105. Myth – antibiotics incresed host
defence to infection
 The followoing condition appear valid at present
 1 antibiotic that can peenetrate into the
mammelion cell (tetracycline , eryt hromycin) are
more likely to affect host defence than those that
can not (beta lactum)
 2 tetracycline may supress white cell chemotaxis
where as betta lactum do not
 3 most antibiotics (except tetracycline) do not
depress phagocytosis
 Tnb lymphocyte transformation may be depressed
by trtracyclines

106. Multiple antibiotics are superior to
as single antibiotics.
 It is often assume that antbiotic combination are
superior to single antibiotic such as not commonly
the case.
 The primary clilical indication for antibiotic
conbination therapy is severe infection in which
ofending organism is unknown and major
conciquences may ensue if antibiotic therapy is
not instituted immediatey before culture and
sensetivity test are available.

107. Antibiotic prophylaxis usually
effective
 It is commonly assume that antibiotics
administered prior to invasive surgical
procedure remain post operative infection.
 The reality based on laboratoru studies is
that antibiotic prophalaxis is only some time
effective.

108. Bacteriocidal agents are always
superior to bacteriostatic agent
 Bacteriocidal antimicrobials are
required in pt with impaier host
defenses (nutropenia, meningitis) but
bacteriostatic agent are uaually
satisfactory, if host defence against
infection are adequqte.

109. Antimicrobials are effective in
chronic infectious disease
 Antimicrobials are never been
successful in the eradication of a
chronic infection because the prolong
exposure of micro-organism to
chemical leads to eventual dominance
of drug resistance organism

110. Antibiotics are safe and non toxic
 Most antimicrobials are among safest drug
yet all are associated with allergy, ecological
damage to human and microbial
environment.


111. Infection require a complete
course of therapy
 There is no such things as predetermine complete
course of antibiotic therapy.
 The only guide for determining the effectiveness of
antibiotic therapy and hence duration of treatment is
related to clinical improvement of pt.

112. Misconceptions
 Prolong therapy destroy resistant micro-organism.
 Prolong therapy is necessary for rebound infection
that recur as organism is suppresed but not
eliminated (orofacial infections do not rebound if
the sourse of infection is properly eliminated)
 Antibiotic doseges and duration of therapy can be
extra polated from one infection to another

113. REFERENCE—
 GOODMAN & GILLMAN
 TEXTBOOK OF PHARMACOLOGY
 BY TRIPATHI
 BY SATOSKAR

115. INTRODUCTION:
 Infections and their consequences are a considerable problem inorthopedic
surgery.
 Despite systemic prophylaxis, infection rates after orthopedic surgery are
above1%.
 Antibiotic loaded PMMA bone cements have been shown to enhance the
efficiency of intravenous prophylactic treatments for total hipreplacement1.
 However, less than 10% of the load is released during the first 5-10 days
ofimplantation2: the remaining antibiotic is released at low levels over many
months3 and could select antibiotic-resistant strains2.
 The recommendations for the use of antibiotic in prophylactic applications are
to obtain high levels, with treatment duration inferior to 48 hours.
 A new HAP/TCP bone substitute loaded with 125 mg of Gentamicin was
designed for prophylactic use in bone filling applications.
 Its aim was to enhance the efficacy of systemic prophylactic treatments by
increasing the local antibiotic concentration without selecting resistant strains.

116. Methods
 A commercial bone substitute composed of 70%
Hydroxyapatite and 30% β- Tricalcium Phosphate4
containing 125 mg of Gentamicin (ATLANTIK
Genta, Medical Biomat, France) was used in this study.
 The release rate of Gentamicin from the bone
substitute was investigated after implantation in the
femoral condyle of 5 sheep. In order to investigate the
local and systemic Gentamicin
concentrations, synovial fluids and blood samples
were assessed by immunoassay over a 5 day period.

117.  There were differences in local Gentamicin
concentrations between individuals but for all
animals, the local Gentamicin concentrations
measured during the first 8 hours were higher than
the minimal bactericidal concentration of the majority
of the germs responsible for infections in orthopedic
surgery, i.e. 6-12 μg/ml. After 48 hours, the
concentration in blood and synovial fluids was less
than 0.5 μg/ml.

118.  The mean Gentamicin concentration peak obtained in
blood was 4.2 μg/ml and then mean local Gentamicin
concentration obtained in synovial fluids during the
first 8 hours was305 μg/ml
 The Gentamicin amount remaining in the implant
explanted at day 8 was less than 0.003% of the initial
amount

120.  It is a fact that selection of multi-drug-resistant
bacteria has occurred throughout history.
Unfortunately, however, drug-resistant bacteria have
been met with antibiotics that are nothing more than
recapitulations of earlier drugs. There has been an
urgent need for new avenues of therapeutic
treatment, and a new era of prophalytic (preventative)
treatment has begun. Here the most plausible
approaches are described:
 bacterial interference

121.  bacteriophage therapy
 bacterial vaccines
 cationic peptides
 cyclic D,L-a-peptides

123. One way is to inoculate hosts with
nonpathogenic bacteria.
 Bacterial interference, also known as
bacteriotherapy, is the practice of deliberately
inoculating hosts with nonpathogenic (commensal)
bacteria to prevent infection by pathogenic strains. To
establish an infection and propagate
disease, pathogenic bacteria must find nutrients and
attachment sites (adhesion receptors).
.

124.  Infection by pathogenic bacteria is prevented by
commensal bacteria, which compete with pathogenic
bacteria for nutrients and adhesion receptors or spur
attack through secretion of antimicrobial compounds

125.  This treatment has had promising results in infections
of the gut, urogenital tract, and wound sites. The
major advantage of using bacteria in a positive way to
benefit health, known as “probiotic” usage, is that
infection is avoided without stimulating the host’s
immune system and decreases selection for antibiotic
resistance. Understanding how bacterial species
compete, an essential criterion for research, has been
known for at least 20 years but its practical application
has yet to be realized.

127.  Bacteriophages (commonly called “phages”) are
viruses that infect bacteria and were recognized as
early as 1896 as natural killers of bacteria.
Bacteriophages take over the host’s protein-making
machinery, directing the host bacteria to make viral
proteins of their own. Therapeutically, bacteriophages
were used as a prophylaxis against cholera, typhoid
fever, and dysentery from the 1920s to the early 1940s.

128.  The practice was abruptly stopped when synthetic
antibiotics were introduced after World War II. Now
that there is a plethora of multi-drug-resistant
bacteria, bacteriophage therapy once again has
become of keen interest.

129. Pathogens may be targeted
through manipulation of phage
DNA.
 Bacteriophage therapy is quite attractive for the
following reasons:
 phage particles are narrow spectrum agents, which
means they posses an inherent mechanism to not only
infect bacteria but specific strains

130.  Other pathogens may be targeted through
manipulation of phage DNA
 exponential growth and natural mutational ability
make bacteriophages great candidates for thwarting
bacterial resistance.
 Development of bacterial vaccines has become an
increasingly popular idea with the advent of complete
genomic sequencing and the understanding of
virulence regulatory mechanisms.

132.  Bacterial genomics allows scientists to scan an entire
bacterial genome for specific sequences that may be
used to stimulate a protective immune response
against specific bacterial strains. This approach
expedites the drug discovery process and, more
importantly, provides a more rational, target-based
approach.
 The best targets are essential bacterial genes that are
common to many species of bacteria, which code for
proteins with the ability to gain accesses through lipid
membranes, and possess no homology to human
genes.

133.  Regulatory genes that control virulence protein
production are excellent vaccine candidates for
priming the human immune system or inhibiting
virulence production.
 Bacterial genomics can also detect conserved
sequences from bacterial species and strains
worldwide. This technology will inevitably yield
superior clinical vaccine candidates.

135.  These diverse peptides are natural compounds that
posses both hydrophobic and hydrophilic
characteristics, which means portions of the molecule
are water avoiding or water loving. Cationic peptides
are found throughout nature in the immune systems
of bacteria, plants, invertebrates, and vertebrates

136. Other Peptides are synthetic, and
are engineered to kill bacterial
cells.
 These peptides are not the usual synthetic drugs
encountered in pharmaceutical drug design;
however, they do exhibit antibacterial effects. Cationic
peptides have several mechanisms of action, all of
which involve interaction with the bacterial cell
membrane leading to cell death. From a therapeutic
standpoint, these proteins have great promise, as they
have coevolved with commensal bacteria yet have
maintained the ability to target pathogenic bacteria.

137. Other peptides are synthetic, or
engineered, to kill bacterial cells.
 Unlike cationic peptides, cyclic D,L-a-peptides are
synthetic and amphipathic (molecules having both
water loving and water hating characteristics) cell
membrane disruptors. As the name implies these
peptides are cyclic in nature and are composed of
alternating D and L amino acids. Cyclic D,L-a-peptides
are engineered to target gram-positive and negative
membranes (not mammalian cell membranes).

138.  In contrast to any other known class of peptides, these
peptides can self-assemble into flat ring shaped
conformations forming structures known as
nanotubes, which specifically target and puncture
bacterial cell membranes resulting in rapid cell death