This ppt describes General principals od Chemotheray of infectious diseases

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2.  Review the classification of antimicrobials
 Define pharmacokinetic and pharmacodynamic principles and their
relationship to effective antimicrobial therapy
 Review relevant microbiologic information as it relates to choosing an
antimicrobial
 Discuss patient and drug related factors that influence the selection of the
appropriate antimicrobial agent
 Identify monitoring parameters to evaluate antimicrobial therapy
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3. Chemical & Therapy (drug treatment)
 Cell Killing
Cancer Chemotherapy
Antimicrobial
Chemotherapy
Bactericidal
Bacteriostatic
1. Antibacterial
2. Antifungal
3. Antiviral
4. Antiprotozoal
Chemotherapy
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4. Antibiotics are anti-infective substances
(byproducts) derived from microbes and used
against microbial infections.
Bactericidal: kill the bacteria
Bacteriostatic: prevents the growth of
bacteria
MIC
MBC
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ANTIBIOSIS
SELECTIVE TOXICITY

5. Prophylaxis – prevention of serious infection at-
risk situation
Empiric therapy - management before confirming
the presence of infection or its cause
Directed-therapy – aim of treatment at micro-
organisms which have been confirmed
Narrow spectrum antibiotics
Extended spectrum
Broad spectrum , TETRACYCLINE,
CHLORAMPHENICOL.
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6. Inhibit cell wall synthesis-Penicillins,
Cephalosporins
Damage to cell membrane-Polymyxins
Inhibit protein synthesis- Tetracyclines
Inhibit DNA synthesis- Ciprofloxicin
Interference with RNA function-
Aminoglycossides
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8. ANTIBIOTIC INHIBITS THE CELL WALL
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10. Appropriate spectrum of activity for the clinical
setting.
No toxicity to the host, be well tolerated.
Low propensity for development of resistance
No hypersensitivity in the host
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11. USED WHEN NO ALTERNATIVE
Polymyxin B : neurotoxicity, nephrotoxicity
Vancomycin : Ototoxicity, nephrotoxicity
Amphotericin B : neurotoxicity, bone marrow
depression, nephrotoxicity,
Low therapeutic index
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High Therapeutic index- Penicillin,
Cephalosporins.

12. Used carefully
Low therapeutic index
Aminoglycosides: Ototoxicity, nephrotoxicity
Tetracyclines: hepatotoxicity, nephrotoxicity,
antianabolic effect
Chloramphenicol: bone marrow depression
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13. Hypersensitivity reactions
Penicillin, cephalosporin, sulfonamides etc.
ORGAN TOXICITY
Drug Resistance
Natural : G-ve bacilli resistance penicillins
: M.tuberculi resistance to
conventional antimicrobials.
Acquired : Mutation or gene transfer
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14.  Natural resistance, Pen- -VE , METRO-
AEROBIC
 Acquired – TB
 Mutation- SM
 Gene transfer- Conjugation, Transduction
(Bacteriophage ), Transformation- DNA .
 Drug destruction. –Beta lactamase.
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15. Causes for resistance:
DRUG TOLERANT : deviation of metabolic path e.g.
Sulfonamide
DRUG DESTROYING: beta-lactamase by staphylococci,
gonococci etc. Chloramphenicol acetyl transferase by
resistant E.coli, H.influenzae.
DRUG IMPERMEABILITY; Closure of porin (channel)
CROSS RESISTANCE: Erythromycin = Clindamycin
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16. Avoid overuse or misuse of antimicrobials
Select rapidly acting selective drugs
Reserve the use of broad spectrum antimicrobials
Use antimicrobial-combination for prolonged use.
Follow intensive treatment for resistance
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17. Normal Flora, commensal organisms, opportunistic
Bacteriocins
Non-susceptible pathogens
Susceptible pathogens
Broad-spectrum
Antimicrobials
Emergence of
Superinfection
Prevention of infections
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18. Candida albicans: monilial diarrhea, thrush,
vulvovaginitis
Nystatin or clotrimazole
Staphylococci (resistance)
Cloxacillin
Clostridium difficile: Pseudo-membraneous
enterocolitis. common after colorectal surgery -
enterotoxin damages gut mucosa forming
plagues
Metronidazole and vancomycin.
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19. Proteus: UTI, enteritis.
Carbenicillin/piperacillin + gentamicin.
Pseudomonas: UTI, enteritis.
Carbenicillin/piperacillin + gentamicin.
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20. Local reaction at the site of administration
Oral: Gastric irritation
Local: Dermal/corneal
Intramuscular: abscess
Intravenous: thrombophlebitis
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21. 1. Synergism:
Sulfonamide with trimethoprim
Betalactamase inhibitor with penicillins
2. To reduce incidence of adverse effects:
Drug combination reduce the individual doses;
therefore side effects reduced
3. To reduce the duration of the course
Amphotericin B + flucytosine will reduce the
duration of the course
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22. 4. To prevent emergence of resistance:
Drug regimen in the treatment of
tuberculosis
5. To broaden the spectrum of antimicrobial
action:
Essential in mixed & severe infections.
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23. Rheumatic fever (streptococci): Peniciilin G
choice
Tuberculosis: Isoniazid with or without
rifampicin
Meningococcal meningitis (epidemic):
rifampicin/sufadiazine
Gonorrhoea/syphilis (before & after contact):
procaine penicillin
Malaria (endemic): chloroquine/mefloquine
Influenza A2 (epidemic): amantadine
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24. Dental extract, tonsillectomy, endoscopies
Catheterization
Surgical prophylaxis
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25. Improper selection of drug, dose, route or
duration
Late treatment
Poor host defense
Lack of adjuvant measures: drainage of
abscesses, control of diabetes, adjustment of pH
in UTI.
Dormant stage of organisms
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26.  Identifying organism
 Organisms susceptibility
 Site of infection
 Patients factor, immunity,renal, hepatic,age
 Safety of antimicrobial
 Cost of therapy
 Pregnancy
 Post antibiotic effect
 Empirical therapy.02/28/19 PATKI 26