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These are the drugs used to suppress the
growth or to kill various microorganism

 ANTIBIOTICS These are the drugs/ chemical substances produced by various species of micro-organisms that kill or suppress the growth of other micro-organisms or cancer cells at very low concentrations .

 Treatment of infections or cancer with specific agents that selectively suppress the infecting microorganism(cancer cells) without significantly affecting the host .

ATP & energy Class II Energy + class I comp → small molecules (amino acids.Biochemical reactions involved in Bact. nucleotides. Cell function: Class I Use of glucose & other “C” sources to produce simple carbon comp. sugars. Phospholipids) Class III Assembly of small mole to form proteins nucleic acids & peptidoglycan .


Biochemical pathway it inhibits/interferes with i-cell wall synthesis ii-protien synthesis iii-nucleic acid synthesis .According to 1-Class & spectrum of microorganism it kills i-antibacterial ii-antiviral iii-antifungal 2.

  chemical structure of drug Macrolides Imidazoles Polypeptides Sulphonamides .


:ii) Protein synthesis inhibionitIBITOR Drugs Tetracyclins Chloramphenicol Aminoglycosides Erythromycin Lincomycin Clindamycin Oleandomycin .

Marry’s hospital London  Penicillin isolated & antibact. (1941) to an old lady --. Chemotherapy History  Male fern & aztes chenopodium → anthalmintic (Greeks)  Chaulmoogra → leprosy (Hindus)  16th century → Mercury → Leprosy  17th century → Cinchona brak →Malaria  19th century → modern chemoth → pioneer → P. Activityshown infected mice  1st Penicillin inj. (1939) by Chain & Florey at Oxford & powerful effects analyzed antibact.  Sulphonamides (1935) by Fletcher  Extracted laboriously form culture of mould of Genus Penicillinum notatum in laboratories of Dunn School of Pathology in Oxford .Anti-bact.  Penicillin (1928) by Alexander Fleming at St. Ehrlich  He used word “Chemotherapy” in 1906.

v) Duration of treatment .  Suitability iv) Route of adm  Severity of inf  Compliance of Pt. Therapy: i) Diagnosis of infection ii) Remove barriers iii) Select best drug  C&S  Kinetics prop.Antibacterial may be: Bacteriostatic Bactericidal ANTIMICROBIALS MAY BE ANTIBIOTICS • Synthetic anti bact: • Principles of anti-bact.

g. cotrimoxazole. Of resistance (e.g TB) To broaden the spectrum Te reduce incidence & severity of side eff. . Penicillin + Gentamycin → enterococcal endocarditis To delay dev. e.Combination Therapy: To get potentiating eff. Disadvantages: False sense of security Broader suppression of normal flora Increase in variety of side eff.

pathogen isolation Suppressive-----------Resolution .Self limiting disease ----no antimicrobials No infection -------Prophylaxis Infection (asymptomatic) -----Pre-empitive Infection (symptomatic) ------Empiric Definitive ----------.

 SELF LIMITING DISEASE influenza non specific diarrhea or Rota virus .

surgical dental Vertical postexposure transmission c .


 Use of antimicrobial agents before the pathogen responsible for a particular illness or the susceptibility to a particular agent (C/S report)  Indication .

APPROACHE TO EMPIRIC THERAPY 1-Formulate clinical diagnosis of microbial disease 2-Obtain specimens for lab exam 3-Formulate microbiological diagnosis 4-Determine the necessity of empiric therapy 5-institute treatment .


serology 3)Formulate a microbiological diagnosis ( history.&immediately available results) . APPROACH TO EMPIRIC THERAPY 1.Formulate a clinical diagnosis(antatomical evidence) 2-Obtain specimen for laboratory examination staining &microscopic exam Send cultures non culture methods antigen testing. physical exam.PCR.

i-significant risk of serious morbidity
ii-public health reason e.g N gonnrhea,
chlamydia trachomatis
iii-immunocompromised /known risk
factors for poor outcome

if no microbial information available
broad spectrum antimicrobial which may cover
most likely pathogens

 The reflex action to associate fever with
treatable infections and prescribe antimicrobial
therapy without further evaluation is irrational
and potentially dangerous because

1-diagnosis may be masked

2- promotes selection of resistant strains

Isolation of pathogen

Susceptibility testing


Specialized assay method
(Betalactamase assay,synergy studies etc )

 Antimicrobial therapy with known etiology 1-ISOLATION OF PATHOGEN specimens properly obtained & processed results properly interpreted 2.SENSITIVITY TEST ADVANTAGES dec chance of resistance. narrow spectrum antibiotic -when ever possible single antibiotic .

BACTERIOSTATIC They arrest the growth and replication of bacteria at serum levels achievable in the patient thus limiting spread of infection BACTERICIDAL They kill bacteria at drug serum levels achievable in the patient .











 surgical prophylaxis--wound infection after surgical procedure in i-dirty or contaminated surgical procedures ii-insertion of a prosthetic implant iii.complications of infection are so drastic iv.high risk of endocarditis .

meningococcal procedures only if there is manipulation of gingival tissue periapical region of teeth. ii. perforation of oral mucosa  Post exposure prophylaxis --- to protect healthy close contacts i.rifampin --.macrolides -----after contact with pts of pertussis iii-gonorrhea or syphilis after contact.HIV .

To prevent Mother-to-child transmission of dis i)syphilis during pregnancy ii)Anti-retroviral therapy for HIV .

post-transplant) . after the initial disease control therapy is continued at a lower dose if i)infection is not completely eradicated ii)immunological or anatomical defect that led to the original infection is still present.(AIDS .

 Delivery of therapy prior to development of symptoms (presymptomatic) i-aborts impending disease ii-Given for a short and defined period iiiUsed as a substitute to universal prophylaxis eg---cytomegalovirus after stem cell transplant .



Time- dependent dependent . Conc.

g aminoglycosides quinolones .g beta-lactam.TIME DEPENDENT KILLING The killing action continues only while blood levels are maintained above MBC /MIC e. vancomycin CONC DEPENDENT KILLING The rate & extent of killing increase with increased conc of drug e.




POST ANTIBIOTIC EFFECT Persistant suppression of bacterial growth after limited exposure to an antimicrobial agent or Antibacterial effect that persists after drug conc falls below MIC PAE= T-C .

T =time required for the viable count in the test culture to inc 10 fold above the count immediately before removal C= time required for the viable count in the untreated culture to inc 10 fold above the count immediately after completion of same procedure used on test culture .

 Mechanism of post antibiotic effect i-persistance of drug at binding site/ periplasmic space ii-slow recovery after reversible non lethal damage to cell structures iii-time taken for synthesis of new enz before growth can resume iv-PALE (postantibiotic leukocyte enhancement) in vivo .

 ROUTE OF ADMINISTRATION Depends upon site of infection  pharmacokinetic properties of drug .

Oral 2-Topical .cannot take orally ii-bacterial endocarditis& meningitis iii-GIT problems----NVD.1.any disease severly impair abs iv-very poor oral abs----aminoglycosides . gastrectomy.endopthalmitis ---ocular cavity 3-Parentral I/V i-critically ill.



synergism 7-dec development of resistance . RATIONALE FOR COMBINATION ANTIMICROBIAL 1-rapid killing of microbe 2-Provide broad-spectrum 3-empiric therapy in seriously ill patients 4-To treat polymicrobial infections 5-dec dose-related toxicity 6.

SYNERGISM(potentiation) Inhibitory or killing effects of two or more antimicrobials used together are significantly greater than expected from their effects when used individually MECHANISM Inc of antimicrobial agent uptake 1) penicillin+gentamycin (G -ive) 2) amphotericin B + flucytosine .

 2) Blockade of sequential steps  e.g trimethoprim & sulphamethoxazole 3)INHIBITION OF ENZYMATIC ACTIVATION inhibition of beta lactamases e.g sulbactam .

g bacteriostatic & bactericidal MECHANISM OF INHIBITION Inhibition of cidal activity with static drugs Penicillins & tetracyclines  Induction of enzymatic activity Ampicillin &piperacillin .ANTAGONISM It occurs when the combined inhibitory or killing effects of two or more antimicrobial drugs are significantly less than observed when the drugs are used individually e.

How bacterial develop resistance:- a) Natural resistance natural selection b) Acquired resistance:- i) Chromosomal muation  MRSA.B mycobact. mycobact. T. leprac ii) Through the genetic material  Gene of resistance is tranferred by:  Plasmid  Transponsons  Gene casettes & intergron .

Mechanisms for transfer of resistance Gene:- a) Conjugation:- b) Transduction: (Bacteriophage) c) Transformation:- Taking naked DNA from enviroment carrying gene for resistance .


chromosomal gene → (Enz inducible) Plasmid gene (Enz constitutively) Many b lactamases are encoded by transposons .Biochemical mechanism of resistance a) Enzymatic inactivation i) b-lactamase: Penicillins Cephalosporins Genes → on plasmid → transduction Staph →Enz in inducible G –ve bact.

ii) Chloramphenicol acetyl trasferase Plasmid mediated (G +ve → inducible & G –ve → constitutive) iii) Aminoglycoside inactivation (Through plasmid & transposons → G +ve & G –ve bact.) Phosphorylation Adenylation Acetylation .

penicillin binding proteins → Methicilhin resistant staph aureus . binding of DNA gyrase → Fluoroquinolones Alt. of protein on 30 s subunit by chromosomal mutation (Aminoglycoside) Alt. of DNA dependent RNA polymerase → (Rifampicin) Alt.b) Alteration of target / binding site Decr. of protein on 50 – s plasmid → (Erythromycin) Alt.

c) Impaired drug accumulation Tetracyclins d) Development of alternative pathway Sulphonamides Trimethoprim .

Ampicillin f) Efflux pump Some b – lactam anti-biotic Tetracyclines Macrolides Anti-cancer drugs .g.e) Impaired penetration through outer membrance (porins) b lactam drugs in G –ve org e.

Imipenem  Meropenem Extapenem Vancomycin Bacitracin Cycloserine .Classification of Anti-microbials: i) According to structure: b lactams Aminoglycosides Tetracycline Macrolides Imidazoles Polypeptides Sulphonamides ii) According to mechanism of action a) Inhibiting bact. Cell wall synth: Penicillins Cephalosporins Monobactams --.aztreonam Carbapenems --.

c) Inhibiting proteins synth: Broad spectrum • Tetracyclines • Chloramphenicol Aminoglycosides Macrolides • Erythromycin • Oleandomycin Mis • Lincomycin • Clindamycin • Spectinomycin .

DNA – polymerase in herpes virus only) .d) Inhibitors of nucleic acid synth: i) Inhibit RNA synth Rifampicin Rifamycin ii) Inhibit DNA synth Nalidixic acid Oxolinic acid Other Quinolones & Fluoroquinolones Actinomycin Mitomycin Acyclovir (inhib.

Inhibiting nucleotide s ynth: Sulphonamides Sulphones PAS Trimethoprim Pyrimethamine .