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1. INDIAN DENTAL ACADEMY
Leader in continuing dental education
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PRINCIPLES OF SURGICAL AND ANTIMICROBIAL INFECTION
MANAGEMENT
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2. DEFINITIONS
Antibiotics:
These are the substances produced by the
microorganisms , which suppress the growth or
kill other microorganisms at very low
concentrations
Chemotherapy :
Treatment of systemic infections with specific
drugs that selectively suppress the infecting
microorganisms without significantly affecting
the host
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3. HISTORY
THE PERIOD OF EMPIRICAL USE
Mouldy curd by chinesechinese on boils
Chaulmoogra oil by hindus for leprosy
Chenopodium by aztecs for intestinal worms
Mercury by paracelsus for syphilis
Cinchona bark for fevers
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4. EHLIRCHS PHASE
Animal dung was used for wound dressing
Paul ehlrich initiated work on magic bullet 1900
Dyes and organometallic compounds
Atoxyl for sleeping sickness
Arsphenaramine for for syphilis
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5. MODERN ERA OF CHEMOTHERAPY
1932 Dogmak protonsil red dye for streptococci
1928 Alexander Fleming pencillium
1885 Fredrick Dennis similar findings
Ernst chain original preparations of penicillin
Giuseppe brotzu in 1948 cephalosporin
Selman Waksman 1953 Streptomycin
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6. PRINCIPLES OF THERAPY
Presence
State
of an infection
of host defenses
Physiological depression
Disease states
Defective immune systems
Variety of therapeutic drugs
Surgical incision and drainage
Decision
to use antibiotic therapy
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7. PRESENCE OF INFECTION
Determine presence of infection
Pain, swelling , surface erythema,
pus formation, limitation of motion
Fever, lymphadenopathy, malaise
Toxic appearance, increased WBC count
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8. PRESENCE OF INFECTION
Patient does not present with all symptoms
Could just be a inflammation
Ex: 1) Pulpitis
2) 3rd molar extraction
3) Patients undergoing maxillofacial
procedure under GA
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9. STATE OF HOST DEFENSES
PHYSIOLOGICAL
Inability to deliver the defending agents
Ex:- Shock
- Reduced circulation due to age,
Obesity, fluid imbalances
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10. STATE OF HOST DEFENSES
DISEASE
STATES
Malnutrition syndrome
Cancers
Leukemia
Poorly controlled diabetes
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11. STATE OF HOST DEFENSES
DEFECTIVE
IMMUNE SYSTEMS
Multiple myeloma
Total body radiotherapy
Agammaglobulinemia
Splenectomy children
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12. STATE OF HOST DEFENSES
VARIETY OF THERAPEUTIC AGENTS
Cytotoxic agents and Corticosteroids
Glucocorticoids,
Azathioprine,
cyclosporine
depresses T- cell B-cell counts
Antibiotic prophylaxis
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13. SURGICAL INCISION DRAINAGE
Presence of pus
Drain the pus (Dental considerations)
Tissue pressure relieved
Better vascular flow established
Prevention of deeper penetration
Cellulitis – incision – pressure relieved
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14. DECISION TO USE ANTIBIOTIC
THERAPY
Minor infections with depressed immunity
- Aggressive treatment
Normal immunity with minor infection – No
treatment
Ex: penicillin
Benefit V/S Risk
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15. PRINCIPLES FOR CHOOSING THE
APPROPRIATE ANTIBIOTIC
Organism related
Identification of the causative organism
Determination of antibiotic sensitivity
Patient related
Age
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Kinetics of drug in the body
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16. PRINCIPLES FOR CHOOSING THE
APPROPRIATE ANTIBIOTIC
Drug related
Use of narrow spectrum antibiotics
Use of least toxic antibiotic
Use of bactericidal rather than static drug
Use of antibiotic with proven history of success
Cost of antibiotic
Pharmacokinetic and dynamic properties
Encourage patient compliance
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18. IDENTIFICATION OF CAUSATIVE
ORGANISM
Identify
organism and treat
Culture
and sensitivity
Initial
empirical therapy
- Site and features of infection have been well
defined
- Circumstances leading to infection are well known
- organisms which commonly cause infection are known
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19. IDENTIFICATION OF ORGANISM
• Bacterial gram stain and culture
– Sterile samples (CSF, blood, urine, surgical tissue)
– Non-sterile samples (sputum, wound, stool)
• Antigen detection & nucleic acid hybridization
– Group A Streptococcus, N. gonorrheae, Legionella
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26. PATHOBIOLOGY OF
ODONTOGENIC INFECTIONS
Entry – aerobic organisms
Invasion – Acidosis, Hypoxia – anaerobes
Antibiotics helpful in odontogenic infections –
(streptococcal/ anaerobes)
In cellulitis – Antistreptococcal activity
In Abscess – antianaerobic activity important
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27. FOCAL INFECTION
FOCUS OF INFECTION:
Refers to circumscribed area of tissue which is infected
with exogenous pathogenic microorganisms and which is
usually located near mucous or cutaneous surface.
FOCAL INFECTION :
Refers to metastasis from the focus of infection of
organisms or their toxins that are capable of injuring
tissue.
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28. ORAL FOCUS OF INFECTION
Infected periapical lesions
granuloma, cyst, abscess
Teeth with infected root canals
Periodontal disease with respect manipulation
and extraction of teeth
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30. CULTURE SENSITIVITY
No improvement after 3 days
Postoperative infection
Infection is recurrent
Actinomycosis is suspected
Osteomyelitis is present
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31. DETERMINATION OF
ANTIBIOTIC SENSITIVITY
Causative organism should be precisely defined
Development of resistance
Penicillin – streptococcus/ anaerobes
Clindamycin – streptococcus, five anaerobes
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33. CHOICE TO BE BASED ON
BACTERIOLOGICAL
EXAMINATION
Bacteriological services not available: empirical
therapy to cover all likely organisms
Bacteriological services available, but treatment
cannot be delayed:
Bacteriological
services
are
available
and
treatment can be delayed
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35. MINIMUM BACTERICIDAL
CONCENTRATION (MBC)
Subculturing from tubes with no visible growth.
Organism killed : No growth
If inhibited grow on subcultures
MBC kills 99.9% of the bacteria.
Small difference between
indicates bactericidal,
Large difference indicates bacteriostatic action.
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MIC
and
MBC
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36. POSTANTIBIOTIC EFFECT
Lag period between growth of organism in antibiotic
free medium after brief exposure to antibiotic
Long postantibiotic effect
Fluoroquinolones,
Aminoglycosides
β-lactam antibiotics.
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38. CHOICE OF AN ANTIBIOTIC
PATIENT FACTORS
AGE
Kinetics of AMA
Conjugation and excretion of chloramphenicol
Blood brain barrier V/S sulfonamide
Elderly pts t1/2 of aminoglycosides
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39. EVEN IN MILD RENAL FAILURE
Cephalosporins
Metronidazole
Vancomycin
Amphotericin B
Ethambutol
Flucytosine
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41. DRUGS TO BE AVOIDED
DOSE REDUCTION NEEDED
IN LIVER DISEASES
DRUGS TO BE AVOIDED
DOSE REDUCTION
NEEDED
Erythromycin
estolate Chloramphenicol
Tetracyclines
Isoniazid
Pyrazinamide
Metronidazole
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42. LOCAL FACTORS
The conditions prevailing at the site of infection greatly
affect the action of AMAS.
(a) Pus and secretions
(b) Necrotic material or foreign body : eradication of infection
(c) Haematomas foster bacterial growth
(d) Lowering of pH : macrolide and aminoglycoside antibiotics.
(e) Anaerobic environment aminoglycosides in the bacterial cell.
(f) Penetration barriers
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46. PATEINTS DRUG HISTORY
Allergic reaction
Toxic reaction
Cross reaction
H/O minor or major side effects
Potential drug interaction
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48. USE OF SPECIFIC NARROW
SPECTRUM ANTIBIOTIC
Development resistance
Many different bacteria are exposed
Reduced super infections
Host flora affected – overgrowth of resistant
strains
Moniliasis to gram –ve pneumonias
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49. USE OF LEAST TOXIC
ANTIBIOTIC
To
prevent the host cell damage
Ex : penicillin / chloramphenicol
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50. USE OF BACTERICIDAL RATHER
THAN BACTERIOSTATIC DRUG
Less reliance on host defense
Killing of bacteria by antibiotic it self
Faster results
Greater flexibility with dosage intervals
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51. USE OF ANTIBIOTIC WITH
PROVEN HISTORY OF SUCCESS
Subtle toxicities are not proven
Initially sensitive organisms become resistant
Resistance slowed down by limiting the use
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52. WHEN TO USE THE NEWER DRUG
Only effective drug
Active at low concentration, less toxic,
Less bothersome side effects
Less expensive
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53. COST OF ANTIBIOTIC
High
cost antibiotic is the drug of choice
Administration
costs
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54. PATIENT COMPLIANCE
ENCOURAGE PATIENT COMPLIANCE
Compliance decreased with increasing no of
pills/ day
Once a day for 4-5 days
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55. DRUG FACTORS
Pharmacokinetic
profile:
Present at the site of infection :
In sufficient concentration
Adequate length of time.
Penetration site of infection : pharmacokinetic
properties
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56. PHARMACOKINETIC PROFILE
Distribution and protein binding
breakdown and excretion
Distribution
GI absorption
First pass metabolism
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57. PRINCIPLES OF ANTIBIOTIC
ADMINISTRATION
PROPER DOSES
Proper time interval(T1/2)
Proper route of administration
Consistency in route of administration
Combination antibiotic therapy
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58. PROPER DOSE
Proper amount to achieve therapeutic effect
Sensitivity tests help to select the dose
Minimum inhibitory concentration(3-4 times)
Blood levels to be achieved
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59. PROPER DOSES
Therapeutic levels / toxicity levels
High doses justified when site of infection sealed
off blood supply
Sub therapeutic doses mask only infection
Clinician fears of toxicity
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60. PROPER TIME INTERVAL
Adjust dose according to established plasma t 1/2
4 times the t1/2 is taken as the dosage
Preexisting disease states
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62. CONSISTENCY IN ROUTE OF
ADMINISTRATION
Severe infection – start i.v antibiotic
Decision to shift to oral antibiotic
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63. COMBINATION ANTIBIOTIC
THERAPY
Avoid when not necessary
Depression of normal host flora
Opportunistic bacteria emerge
When to use combination therapy
Life threatening sepsis
Infection due to enterococcus
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64. COMBINED USE OF
ANTIMICROBIALS
To achieve synergistic
To reduce severity or incidence of adverse
effects
To prevent emergence of resistance
To broaden the spectrum of antimicrobial action
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Treatment of mixed infection
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65. DISADVANTAGES OF
ANTIMICROBIAL COMBINATIONS
They foster a casual rather than rational outlook
in the diagnosis of infections and choice of AMA.
Increased incidence and variety of adverse
effects.
Toxicity of one agent may be enhanced by
another failure.
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66. DISADVANTAGES OF
ANTIMICROBIAL COMBINATIONS
Increased chances of superinfections.
If inadequate doses of nonsynergistic drugs are
used
-emergence
of
resistance
may
be
promoted.
Increased cost of therapy.
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68. LOCAL IRRITANCY
Site of administration
Gastric irritation
Pain and abscess - i.m. injection
Thromboflebitis – i.v
Practically all AMAS irritants
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69. SYSTEMIC TOXICITY
Some have a high therapeutic index
Doses over nearly 100 fold range administered
Penicillins, some cephalosporins erythromycin.
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70. SYSTEMIC TOXICITY
Others have a lower therapeutic index –
Doses individualized and toxicity watched for,
Aminoglycosides 8th cranial nerve and kidney toxicity.
Tetracyclines liver and kidney damage, antianabolic
effect.
Chloramphenicol bone marrow depression.
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71. SYSTEMIC TOXICITY
Still others have a very low therapeutic index use highly restricted
Polymyxin B - Neurological and renal toxicity.
Vancomycin - Hearing loss, kidney damage.
Amphotericin B neurological toxicity.
Kidney,
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bone
marrow
and
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73. RESISTANCE
It refers to unresponsiveness of a microorganism
to an AMA and is akin to the phenomenon of
tolerance seen in higher organisms
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74. NATURAL RESISTANCE
Some are always resistant to AMAS.
They lack the metabolic process
The target site - affected by drug.
Gram negative bacilli‘ are - penicillin G
M. tuberculosis – Tetracyclines
not pose significant clinical problem .
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75. ACQUIRED RESISTANCE
Resistance by an organism over period of time.
Major clinical problem.
Dependent on microorganism and drug
Some bacteria rapid resistance
Staphylococci, Strep. pyogenes penicillin
Gonococci resistance to sulfonamides
Slowly and low grade resistance to penicillin.
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76. RESISTANCE
MUTATION
stable and heritable genetic change
microorganisms higher concentration of the AMA for
inhibition.
These are selectively preserved
(i)Single step
A single gene mutation may confer high degree of
resistance
Emerges rapidly
e.g. enterococci to streptomycin, E. coli and
Staphylococci to rifampin.
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77. RESISTANCE
(ii) Multistep.
A number of gene modifications are involved
sensitivity decreases gradually in a stepwise
manner
erythromycin, tetracyclines and chloramphenicol
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78. GENE TRANSFER
Can occur by
Conjugation Sexual contact through bridge orsex pilus
Transduction
It
is
the
transfer
by
bacteriophage
Transformation release DNA into the medium :
imbibed another organism
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80. CROSS RESISTANCE
Resistance to one
resistance to other
antibiotic
They should be Chemically or mechanically
similar
EXAMPLES: sulfonamide , Tetracycline
Aminoglycosides may not extend to another
Partial cross resistance
Tetracyclines and chloramphenicol,
Erythromycin and lincomycin.
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conferring
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81. PREVENTION OF DRUG
RESISTANCE
No indiscriminate and inadequate or
unduly prolonged use
This
would
Minimise
the
selection
pressure
Resistant strains get
less chance to
propagate
Prefer rapidly acting and selective AMAs
Combination of AMAs
Infection by Notorious organisms : Treat
intensively.
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82. INTOLERANCE
It
is the appearance of characteristic
toxic
effects
of
a
drug
in
an
individual at therapeutic doses.
It is the converse of tolerance and
indicates
a
low
threshold
of
the
individual to the action of a drug.
One tablet of Chloroquine may cause
vomiting and abdominal pain in an
occasional patient.
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83. IDIOSYNCRASY
It is genetically determined abnormal
reactivity to a chemical.
Certain adverse effects of some drugs
are largely restricted to individuals with a
particular genotype
In addition, certain uncharacteristic or
bizarre drug effects due to peculiarities
of an individual (for which no definite
genotype has been described)
Quinine/ quinidine cause cramps ,
diarrhoea, purpura, asthma and vascular
collapse in some patients.
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84. SUPERINFECTION
(SUPRAINFECTION)
Appearance of new infection as a result
of new treatment
This is because of Normal microbial flora
altered
As they provide Defence by bacteriocins
For ordinary pathogen Competition lost
with the normal flora
Due to Incomplete absorption
Higher
amounts reach the lower bowel
Inhibit colonic bacteria and cause they
cause Diarrhoeas
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85. COMMON SUPERINFECTIONS
Corticosteroid therapy
Leukemias and other malignancies
Treated with anticancer drugs
Acquired immunodeficiency syndrome
(AIDS)
Agranulocysis
Diabetes
Disseminated Lupus erythematosus
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86. MINIMISE SUPERINFECTIONS
Use specific (narrow spectrum)
Avoid
in
trivial,
self
limiting
or
untreatable (viral) infections.
Do not unnecessarily prolong treatment
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87. NUTRITIONAL DEFICIENCIES
B complex and Vit K synthesized by the
intestinal flora
prolonged use cause eliminates flora
thus causes deficiency
Neomycin
abnormalities
of
intestinal
mucosa
It
may
cause
Steatorrhoea
Malabsorption syndrome
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88. MASKING OF AN INFECTION
A short course briefly suppress one
infection but can not suppress another one
contracted concurrently.
The other infection will be masked initially
will manifest later in a severe form
Syphilis masked by penicillin which is
sufficient to cure gonorrhea.
Tuberculosis
masked
by
streptomycin
given for trivial respiratory infection.
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89. PROPHYLACTIC ANTIBIOTICS
The difference between
treating
and
preventing
infections is that treatment is
directed against a specific
organism
infecting
an
individual
patient,
while
prophylaxis is often against all
organisms capable of causing
infection
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91. PROPHYLAXIS AGAINST
SPECIFIC ORGANISMS
d) Gonorrhea /syphilis: procaine penicillin.
e) Rickettsial infections : Tetracyclines.
f) Malaria: endemic :chloroquine
pyrimethamine.
g) Influenza A2 :Epidemic or Contacts:
amantadine.
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92. PREVENTION OF INFECTION IN
GENERAL
(a) Neonates, specially after prolonged or
instrumental delivery.
(b)To prevent postpartum infections in the
mother after normal delivery.
(c)Viral upper respiratory tract infections: to
prevent secondary bacterial invasion.
(d)To
prevent
respiratory
infections
in
unconscious patients or in those on
respirators.
(e) Clean elective surgery.
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93. PRINCIPLES OF
PROPHYLACTIC ANTIBIOTICS
TIMING, PRE-OP:
present at therapeutic levels at the
site time of contamination
If given orally: 1 hour pre-op.
If given intravenously IV: "on-call" to
the
operating
room
or
shortly
BEFORE anesthetic induction.
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94. PRINCIPLES OF
PROPHYLACTIC ANTIBIOTICS
TIMING, PRE-OP
Therapeutic levels maintained for the
duration of the procedure.
extended procedures (over 6 hours)
may require a second dose
since contamination re-occurs at skinclosure.
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95. PRINCIPLES OF
PROPHYLACTIC ANTIBIOTICS
Post-op:
Post-operatively have little effect on
wound infections.
After 24 hours : Not protective.
Some
continue
until
wound
drainage
Incision-line leakage has stopped
Packing is removed from wounds
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96. FAILURE OF ANTIBIOTIC
THERAPY
Improper selection of drug, dose, route
or duration of treatment.
Treatment begun too late.
Failure to take necessary adjuvant
measures,
Improper treatment of underlying cause
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97. FAILURE OF ANTIBIOTIC
THERAPY
Poor host defense
Infecting
organism
present
behind
barriers
Trying to treat untreatable infections
Presence
of
dormant
or
altered
organisms
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99. CHEMICAL STRUCTURE
1.SULFONAMIDES AND RELATED DRUGS:
Sulfadiazine and others,
Sulfones-Dapsone (DDS),
Paraaminosalicylic acid
(PAS).
2. DIAMINOPYRIMIDINES:
Trimethoprim, Pyrimethamine.
3.QUINOLONES:
Nalidixic acid, Norfloxacin,
Ciprofloxacin etc.
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100. CHEMICAL STRUCTURE
4. Β-LACTAM ANTIBIOTICS:
Penicillins, Cephalosporins,
Monobactams,Carbapenems
5. TETRACYCLINES:
Oxytetracycline, Doxycycline etc.
6. NITROBENZENE DERIVATIVE:
Chloramphenicol.
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101. CHEMICAL STRUCTURE
7.Aminoglycosides:
Streptomycin, Gentamicin, Neomycin etc.
8.
Macrolides antibiotics:
Erythromycin, Roxithromycin, Azithromycin
etc.
9.
Polypeptide antibiotics:
Polymyxin-B, Colistin, Bacitracin, Tyrothricin.
10. Nitrofuran derivatives:
Nitrofurantoin, Furazolidone.
11.Nitroimidazoles:
Metronidazole, Tinidazole.
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108. ANTIBIOTICS ARE OBTAINED FROM
FUNGI
BACTERIA ACTINOMYCETES
Penicillin
Polymyxin B
Aminoglycosides
Cephalosporin
Colistin
Polyenes
Griseofulvin
Aztreonam
Chloramphenicol
Bacitracin
Tetracyclines
Tyrothricin
Macrolides
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109. ANTIBIOTICS THAT INHIBIT
CELL WALL SYNTHESIS
ß-lactam Antibiotics
Major Classes
Penicillins
Cephalosporins
Carbapenems.
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110. MECHANISM OF ACTION OF ßLACTAM ANTIBIOTICS
Inhibit cell wall synthesis blocking
the action of transpeptidases, also
known as penicillin binding proteins
(PBPs)
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111. PREPARATIONS
Sodium penicillin (crystalline penicillin) 0.5-5 MU
i.m/i.v 6-12 hourly It is available as dry powder in
vials to be dissolved in sterile water at the time of
injection.
BENZYL PEN 0.5, 1 MU inj.
Repository
penicillin
G
injections
These
are
insoluble salts of PnG which must be given by
deep i.m. (never i.v.) injection. They release PnG
slowly at the site of injection, which then meets the
same fate as soluble PnG.
1.Procaine penicillin g inj.
hourly
as
aqueous
concentrations
0.5-1 MU i.m. 12-24
suspension.
attained
are
lower,
Plasma
but
are
sustained for 1-2 days; PROCAINE PENICILLIN-G
0.5, 1 MU dry powder in vial.
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112. PREPARATIONS
A- Fortified procaine penicillin G inj:
contains 3 lac U procaine penicillin and 1
lac U sod. penicillin G to provide rapid as
well as sustained blood levels.
FORTUMD P.P. INJ 3+1 lac U vial.
2. Benzathine penicillin GI 0.6-2.4 MU i.m.
every 2-4 weeks as aqueous suspension.
It releases penicillin extremely slowlyplasma concentrations are very low but
remain
effective
for
prophylactic
purposes for up to 4 weeks: PENIDLTRELA
(long
acting),
LONGACILLIN,
PENCOM, 0.6, 1.2, 2.4 NW as dry powder
in vial.
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113. PENICILLIN AND RELATED ßLACTAMS
Penicillin, ampicillin (amoxicillin)
Gram positive (eg, S. pneumoniae,
enterococcus)
Extended spectrum penicillins
– Nafcillin: S. aureus
– Piperacillin: P. aeruginosa, other
GNRs
Clearance: predominantly renal
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125. COMMONLY USED PROTEIN
SYNTHESIS INHIBITORS
AMINOGLYCOSIDE(gentamicin,
tobramycin)
– Inhibits protein synthesis but also
disrupts cell permeability (cidal)
– Gram negatives; Synergy with ßlactams
vs
gram
positive
(eg,
Enterococci)
125
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126. USES
Tuberculosis
SABE
Plague
Tularemia
In treating Pseudomonas, Proteus
or Klebsiella infections
Meningitis by gram negative bacilli
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128. PRECAUTIONS AND
INTERACTIONS
(i) Avoid during pregnancy: risk of foetal
ototoxicity.
(ii) Avoid concurrent use of other ototoxic
drugs,
e.g.
high
ceiling
diuretics,
Minocycline.
(iii)
Avoid
concurrent
use
of
other
nephrotoxic drugs, e.g. amphotericin B,
vancomycin,
cephalothin,
cyclosporin
and cisplatin.
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129. (lv) Cautious use in patients past middle age
and in those with kidney damage(v) Cautious use of muscle relaxants in
patients receiving an aminoglycoside
(vi)Do not mix aminoglycoside with any
drug in the same syringe/ infusion bottle.
129
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135. PRECAUTIONS
Not to use in pregnant women
Avoid in pateints with diuretics :
blood urea rises
Renal and hepatic insufficiency
Never use beyond the expiry
Never mix with penicillins
Do not inject intrathecally
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135
139. OTHER INHIBITORS OF PROTEIN
SYNTHESIS
CHLORAMPHENICOL
Broad activity, penetrates CSF
Idiosyncratic and irreversible bone
marrow toxicity limit its use
Active
against
vancomycin
resistant
Enterococcus
faecium
(VRE) but not E. faecalis
139
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143. ANTIBIOTICS THAT AFFECT
NUCLEIC ACIDS
FLUOROQUINOLONES(CIPROFLOXICIN,
GATIFLOXICIN,
LEVOFLOXICIN,,MOXIFLOXICIN)
– Inhibit DNA gyrase and topoisomerase;
not used in children
– Active against enteric gram negative rods
and P. aeruginosa
– “Respiratory quinolones” (levo, gati, moxi,
not cipro) active vs S.pneumoniae; Also
some activity against Staphylococci
– Concentrate intracellularly (eg, versus
Salmonella typhi)
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149. ANTIMETABOLITES
Sulfonamides (Sulfamethoxazole,
sulfadiazine)
Interfere with microbial folic acid
synthesis
Ultimate
effect
is
decrease
in
bacterial nucleotide pool.
Most commonly used drug is a
combination
of
trimethoprim
+sulfamethoxazole
149
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150. TRIMETHOPRIM +
SULFAMETHOXAZOLE
Used primarily in UTI, but E. coli
resistance is increasing
Respiratory tract infections
Typhoid
Bacterial diarrheas and dysentry
Chancroid
Granuloma inguinale
Agranulocytosis
Pneumocystitis carinii infections
150
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151. Adverse effects
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Nausea, vomiting, epigastric pain
Crystalluria
Hypersensitivity reactions
Hepatitis
Bleeding in G6-PD deficiency
Kernicterus
COTRIMOXAZOLE
Folate deficiency
Renal impairment
Bone marrow hypoplasia
Thrombocytopenia when used with
diuretics
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151
152. RIFAMYCINS (RIFAMPIN)
Inhibits
DNA-dependent
RNA
polymerase; bactericidal
Forms a critical part of therapy for
tuberculosis, leprosy
Also used in combination with other
agents to treat
Staphylococcus,
Legionella
and
some atypical pneumonia
Brucellosis along with doxycycline
152
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