antimicrobial, antifungal, antiviral

1. ANTI INFECTIVE
AGENTS
Kkaled shurrab

2. WHAT IS AN
ANTIBIOTIC?
Antibiotics a chemical substance produced by
a microorganism that inhibits the growth of or
kills other microorganisms.
Antimicrobial agents a chemical substance
derived from a biological source or produced
by chemical synthesis that kills or inhibits the
growth of microorganisms.

3. CLASSIFICATION OF
ANTIBIOTICS
Chemical structure
Mechanism of action
Typed of organisms which primarily
active
Spectrum of activity
Types of action
Obtained from

4. SOURCE OF
ANTIBACTERIAL AGENTS
 Organisms develop resistance faster to the natural antimicrobials
 Natural antibiotics are often more toxic than synthetic antibiotics
 Benzylpenicillin and Gentamicin are natural antibiotics
 Ampicillin and Amikacin are semi-synthetic antibiotics
 Moxifloxacin and Norfloxacin are synthetic antibiotics

5. ROLE OF ANTIBIOTIC
 To inhibit multiplication
Antibiotics have a bacteriostatic effect.
At which drug concentration is the bacterial
population inhibited?
Minimal Inhibitory Concentration = MIC
 To destroy the bacterial population
Antibiotics have a bactericidal effect.
At which drug concentration is the bacterial
population killed?
 Minimal Bactericidal Concentration = MBC

7. CHOOSING THE RIGHT
ANTI-INFECTIVE
 Is an antibiotic indicated?
 Use empirical therapy routinely
 Narrow spectrum
 Avoid toxicity and side effects
 Bactericidal vs bacteriostatic
 Cost
 Avoid allergies

8. MAIN DIFFERENCE
BETWEEN HUMAN CELL
AND MICROBIAL CELL
Human cellMicrobial cell
It is dependent on other cells .Cell is isolated and Independent.
The wall is absentThick protective cell wall is present .
Cytoplasmic bridges are present which
help in inter-cellular transport in
between neighboring cells.
Cell membrane : No cytoplasmic
bridges as there is only one cell.
Absent mostly. Except for ciliated cells
in respiratory tract & gut.
Flagella for movement, pili for sexual
reproduction.
Prominent nucleus with nuclear
membrane. So called as an eukaryote
type.
Nucleus is Absent. Instead nuclear
content like DNA are present in
cytoplasm. No distinct nucleus, so
called as prokaryote
80 s type with 60 s and 40 s sub units.RNA : 70 s type with 50s and 30s type
sub units.

10. ODONTOGENIC
INFECTIONS
 are caused by oral pathogens that
inhabit the surface of the teeth and
oral mucous membranes and are
also found in the gingival sulcus
and saliva
 12% of antibiotics in the outpatient
setting are given for odontogenic
infections

11. Microorganisms
ivolved in mixed
bacterial infections of
the oral cavity

12. WHAT PATHOGENS ARE WE
DEALING WITH?
Gram Positive?
Gram Negative?
Mixed Infection?
Aerobes?
Facultative?
Anaerobes?

14. ODONTOGENIC
INFECTIONS
 300-700 species of which more than 50%
cannot be cultured
 Aerobic - anaerobic infections
Aerobes only (7%)
Mixed (60%)
Anaerobes only (33%)
Average isolates per specimen - 4
 Gram + Aerobic & Facultative Streptococci
Common pathogen and most numerous
 Produce hyaluronidase and streptokinase

18. WHAT TYPE OF
ANTIBIOTIC SHOULD WE
USE?
Bacteriostatic?
Bactericidal ?
Narrow Spectrum?
Broad Spectrum?

19. BACTERIOSTATIC VS
BACTERICIDAL
 Bactericidal action necessary in endocarditis,
meningitis, osteomyelitis,neutropenia
 Disadvantage of bactericidal: rapid bacterial lysis in
meningitis with overwhelming inflammatory
response with increased mortality
 Advantage of bacteriostatic: clindamycin in staph
TSS( toxic shock syndrome) effective in inhibiting
TSST-1( toxic shock syndrome toxin) production
without excessive inflammatory response
 Cidal and static should not uses together

20. STRUCTURES OF
BACTERIAL CELL
MEMBRANE
Natural Resistance
Enterococcus- PBP’s are different from other Gram-positives (also higher
lipid content in cell wall), which causes a low level resistance to penicillins
and resistance to C1G.

22. STRUCTURES OF BACTERIAL
CELL MEMBRANE
Natural Resistance- Many Gram-negative organisms are naturally
resistant to penicillin G and oxacillin because the drug is
prevented from entering the cell by the LPS which blocks the
porins.
Gram-negatives are naturally resistant to vancomycin.

25. WHAT TYPE OF
ANTIBIOTIC SHOULD WE
USE?
Bactericidal ?
Bacteriostatic?
Narrow Spectrum?
Broad Spectrum?

28. INHIBITORS OF CELL
WALL SYNTHESIS
Beta-lactams
• Penicillins
• Cephalosporins
• Monobactams
• Carbapenems
Glycopeptides
Fosfomycins

29. BETA-LACTAMS
 There are about 50 different Beta (ß)-lactams.
 They are all bactericidal.
 They are non-toxic.
 They are relatively inexpensive.
 organic acids and most are soluble in water.
 inactivation by beta-lactamases
• Some more common Beta-lactamase enzymes include:
• Penicillinases
• Cephalosporinases
• ESBL’s
• Cephamycinases
• Carbapenemases

30. BETA-LACTAMASE
INHIBITORS(BLI)
 have a beta(ß)-lactam ring, but have weak or poor
antibacterial activity.
 They have a very high affinity for ß-lactamases
 They act as a trap, and are hydrolyzed in preference
to the ß-lactam drug.
 The drug is left intact to act on the bacteria (cell
wall)
 Should be called penicillinase inhibitors, because
they are active against: ƒStaph penicillinase,
Penicillinase of K. pneumoniae

31. BETA-LACTAMASE
INHIBITORS(BLI)
 ESBL (to a greater or lesser degree)- if the
penicillinase is being overproduced, the
inhibitor effect may be diluted (Inoculum
Effect)
 Inhibitors are active against all penicillinase
but never on cephalosporinase
 NEW ISSUE- BLI can act as inducers and actually
stimulate enzyme (betalactamase) production. It
ispossible to see the following:
Pseudo monas Ticarcillin = S Ticarcillin/Clavulanic = R
Enterobacteriaceae Piperacillin = S Piperacillin/Tazobactam =
R

38.  Beta-lactams
 Penicillins
 Cephalosporins
 Monobactams
 Carbapenems
 Glycopeptides
 Fosfomycins
INHIBITORS OF CELL WALL
SYNTHESIS

40. aztreonam differs from those of other β-lactam
antibiotics and more closely resembles that of an
aminoglycoside.
Aztreonam has activity only against gram-negative
bacteria

41. Inhibitors of Protein
Synthesis
 Aminoglycosides
 MLSK
(Macrolides, Lincosamides, Streptogramins, Ketolides)
 Tetracyclines
 Glycylcyclines
 Phenicols
 Oxazolidinones
 Ansamycins

42. Aminoglycosides:
Spectrum of Action
 Rapid bactericidal effect
 Broad spectrum of action
 Gram-negative infections
 Gram-positives, except Streptococus and
Enterococcus. Must combine an aminoglycoside
(Gentamicin or Streptomycin) with a penicillin,
ampicillin or vancomycin for severe enterococcal
infections (Synergy Testing).
 In serious infection, used in association with beta-
lactams or fluoroquinolone
 Nephrotoxic and toxic for ears

43. AMINOGLYCOSIDE
Mode of action:
• Target = Ribosome in cytoplasm
• Aminoglycosides are positively charged molecules
• The negative charge of bacteria is due to LPS in
the outer membrane and the peptidoglycan
(notably the teichoic acid).
• The drugs cross the cytoplasmic membrane via
respiratory enzymes(involved in aerobic
respiration).

44. AMINOGLYCOSIDE
Aminoglycosides bind to the RNA of the
30S ribosomal sub-unit.
Release of incomplete, toxic proteins
The bactericidal activity of aminoglycosides
ultimately stops protein synthesis and
dramatically damages the cytoplasmic
membrane.

47. Bacteriostatic
Their spectrum of activity is limited to Gram-positive
cocci such as Streptococci and Staphylococci. These
antibiotics are also active against anaerobes.
Clindamycin used in osteomyelitis of the jaws.
Clindamycin dose not in routine of odontogenic infection

48.  The drugs enter a Gram-positive cell without any problem.
 In Gram-negative bacteria there is no entry because MLSK are lipophilic
molecules.
 They cannot cross the outer membrane which is hydrophilic. “Oil and
water don’t mix”.
 MLSK are also large molecules that cannot pass through the porins (which
are also aqueous channels) – impermeability.
 Most Gram-negatives are naturally resistant to MLSK Antibiotics
 MLSK group are structurally distinct but have a similar mode of action by
binding the 50S ribosomal subunit

51. Inhibitors of Protein
Synthesis
 Aminoglycosides
 MLSK
(Macrolides, Lincosamides, Streptogramins, Ketolides)
 Tetracyclines
 Glycylcyclines
 Phenicols
 Oxazolidinones
 Ansamycins

52. Tetracyclines:
 Spectrum of Action: Broad spectrum,
 resistance is common
 Primarily for treatment of genital infections (chlamydiae) and atypicals
(Rickettsiae, Mycoplasma).Growth promotor in animal husbandry.
Toxicity:
 Diffuse well in cells and bones.
 Not recommended for pregnant women and children (less than 2 years old)
because of the toxicity on bones and teeth of the fetus.

53. TETRACYCLIN
 Tetracycline = Short acting
 Minocycline and Doxycycline = Long acting
 Minocycline and Doxycycline are more
active than Tetracycline.
 Used extensivly in periodontitis and
periodontal disease
 tetracycline exists as a mixture of two forms
- lipophillic and hydrophillic, Helps the
antibiotic gain entry in to the Gram-pos and
neg cel

54. TETRACYCLIN
 it’s target - the 30s ribosome
 Gram-positives have no natural resistance to the
tetracyclines.
 Of the Gram-negative organisms only Proteus mirabilis is
naturally resistant

55. 1st Generation Quinolones: Only for Gram-negatives,
 used to treat urinary tract infections
Fluoroquinolones: Ciprofloxacin,Levofloxacin, Norfloxacin,
Ofloxacin)More effective (lower MIC values).
Spectrum extended to cover Staphylococci, Streptococci and
Pneumococci(sparfloxacin).

60. MAIN ANTIBIOTICS IN
EXODONTOGENIC
INFECTION

62. IMPORTANT
NOTES
• In culture and sensitivity testing on 94 patients with odontogenic
abscesses, penicillin V was the least effective antibiotic for
eradicating bacterial isolates. Despite this, more than 95% of
patients treated with surgical incision and drainage in conjunction
with penicillin V recovered satisfactorily.
• Amoxicillin has a broader spectrum of activity than penicillin V, but
does not provide any better coverage in treating odontogenic
infections. Its dosing schedule and ability to be taken with food may
make it more acceptable for patients, resulting in better compliance.
• Cephalosporins are not a first-line treatment in the management
of odontogenic infections.

63. IMPORTANT
NOTES
• Clindamycin: Clindamycin inhibits bacterial protein synthesis and
is bactericidal at high dosages. Its use has increased in recent
years due to increasing concern over penicillin resistance. For
example, it has replaced penicillin as the recommended
antibiotic for the management of odontogenic infections
• Clindamycin has excellent coverage of gram positive cocci and
anaerobic bacteria. Eikenellais inherently resistant to clindamycin
and alternative antibiotics should be considered if this species is
found to be the causative organism.

64. IMPORTANT
NOTES
Fluoroquinolones: The broad-spectrum antibiotic has excellent
bacterial coverage in the setting of an odontogenic infection. It is
effective against Eikenella and most strains of bacteria that produce
beta lactamase.
It has the highest rate of bacterial susceptibility among all antibiotics
including penicillin and clindamycin for odontogenic infections.
However, given its broad spectrum and high cost, it should be
considered as a secondl ine therapy to penicillin V, metronidazole
and clindamycin.
Penicillin in conjunction with metronidazole provides excellent
bacterial coverage for most odontogenic infections and should be
considered the antibiotic of choice.

76. DO IT , OVERCOME
THE PROBLEM
Bacteria never die
Be happy