1. The document discusses various antimicrobial drugs including their classification, mechanisms of action, and pharmacological profiles. It covers sulfonamides, cotrimoxazole, penicillins, cephalosporins, chloramphenicol, and erythromycin. 2. The general principles of chemotherapy are outlined including identifying microorganisms, antimicrobial susceptibility testing, and factors affecting drug selection and administration. 3. Various antimicrobial drugs are classified based on their chemical structure, types of organisms they act on, spectrum of activity, and mechanism of action. Adverse effects and uses of different drugs are also mentioned.

1. Presented by:
Mr. Shaikh Akhil. M.
M.Pharm
Asst. Prof. Dept. of Pharmacology,
BCCO Pharmacy, Naigaon,
S.R.T.M.University, Nanded.
Chemotherapy

2. CONTENT
i. General principle of Chemotherapy
ii. Sulfonamide and cotrimoxazole.
iii. Antibiotics- penicillin, cephalosporins,
chloramphenicol, macrolides, quinolones,
fluoroquinolins, tetracycline and aminoglycoside
2

3. General Principle of chemotherapy
• Chemotherapy-use of chemical to destroy- microorganisms
• Antibiotics- obtained from-microorganisms-inhibit or kill
microorganisms in host
• Selection of antimicrobial agents-
• 1. Identify of microorganisms- a. Sample of body fluid b.
staining
• 2. Antimicrobial susceptibility- a. static-cidal b. MIC-Cup-
plate
• 3. site of infection(BBB)- a. Lipid solubility b. M.W
c. P. Binding
• 4. patient factor- a. Immune system b. Renal dysfunction
c. hepatic dysfunction d. Pregnancy- lactation
• 5.safety agent 6. cost of therapy 7. Route of administration
3

4. Classification
1. Chemical Structure- sulfonamide, quuinolones, Beta-
lactum etc
2. Types of organisms- Bacteria, fungal, viral, protozoa
3. Spectrum of activity- narrow spectrum, broad
spectrum
4. Type of action- Bacteriostatic, Bacteriocidal
5. Source of antibiotics- funge, bacteria, actinomycetes
6. MOA- cell wall, protein synthesis decreases, DNA
synthesis decreases
4

5. Antimicrobial drugs- Classification
A. Chemical Structure-
1. Sulfonamides- sulfadiazine, paraaminosalicylic acid
2. Diaminopyrimidine- trimethoprim, pyrimethamine
3. Quinolones- norfloxacin, ciparofloxacin, nalidixix acids
4. Beta-lactum- penicilline, cephalosparine, monobactams
5. Tetracyclines- oxytetracycline, doxycyclines
6. Nitrobenzene derivative- chloramphenicol
7. Aminoglycoside- streptomycine, gentamycin, neomycin
8. Macrolides- erythromycine, clarithromycine,
azethromycine
5

6. Conti......
9. lincosamide- lincomycine, clindamycin
10. Nitroimadazole- metronidazole, tinidazole
11. Nicotinic acid derivative- isoniazid, pyrazinamide
12. Azole derivatives- miconazole, cotrimazole,
ketokonazole
B. Types organisms- a. Antibacterial-penicillins
b. Antifungal-ketoconazole c. Antiviral- acyclivir,
amantidine
d. Antiprtozoal- chloroquine, metronidazole
C. Spectrum activity- a. Narrow-penicilline-G
b. Broad- Erythromycine
D. Types of Action- a. Bactriostatic- tetracycline,
b. Bactreiocidal- penicillines, isoniazid
6

7. 7

8. 8

9. Antimicrobial drugs-Sulfonamides
Class-Interfere with intermediary metabolism-
bacteriostatic
Sulfonamide= structural analog of paraaminobenzoic acid
Classification
1. Short acting- sulfadiazine, sulfisoxazole
2. Intermediate acting- sulfamethazole
3. Long acting- sulfadoxine, sulfamethopyrazine
4. Poorly absorbed- sulfasalazine
5. Topical- sulfacetamide, mafenide, silver sulfadiazine
Antibacterial spectrum- anarobic- not susceptible
9

10. Conti....
• Inhibit many gram positive and few gram negative
bacteria
• Treat – streptococci, H. Influenza, E. Coli, salmonella,
v. Cjlorae, staplylococci, meningococi
• Presence of- pus, blood, tissue brekdown products
makes sulfonamide inettaetive because these are rich in
PABA
10

11. Sulfonamides - MOA
11

12. Adverse Effect
• Urinary irritation, haematurea, albuminiurea,
crystallurea,
• Hypersensitivity- rashes, fever, photosensitivity
• Anorexia, nausea, andominal pain
• Haemolytic, anaemia
• Uses- UTI, Nocardiosis, toxoplasmosis, malaria, U.
Colitis, topical
12

13. Antimicrobial drugs- cotrimoxazole
• Cotrimoxazole - trimethoprim + sulfamethoxazole 1:5 ratio
• Trimethoprim- effective against many gram +ve and –ve
• Antibacterial spectrum – alone- static, combination- cidal
• Staphococcus aureus, streptococci, E.coli, slmonella
proteus, h. Influenzae.
• Mechanism of Action
ADR- Nausea, vomiting, headache, allergic skin rashes,
megaloblastic anaemia, AIDS patient face more ADR of
cotrimoxazole
contraindicated- in pregnancy- teratogenicity
Use- UTI, respiratory tract infection, typhoid, chanceroid
13

14. MOA
14

15. Antimicrobial drugs- Penicillins-
 Class- beta lactam antibiotics & Cell wall inhibitor
 Penicillins- fleming-1928- from- penicillium notatum
 Therapeutic use penicillium chrysogenum.
 Classification
A. Natural – 1. regular- penicillin G – Narrow antibacterial spectrum
2. repository penicillin – procaine penicillin, benzathine
penicillin
B. Semi synthetic-
1. Acid resistance – penicillin V.
2. Penivillinase resistance- methacillin, oxacillin, cloxacillin
3. Amino penicillin- ampicillin, bacampicillin, talampicillin,
rivampicillin, amoxicillin
4. Antipseudomonal penicillin- penicilline+aminopenicillin activity
5. Carboxypenicillin- carbenicillin,carbenicillin,
6. Ureidoprnicillin- azlocillin, mezocillin, piperacillin
15

16. Antimicrobial drugs- penicillins- beta lactum
 Cell wall- integrity-shap-prtotection from lysis
 Peptidoglycon- complex polymer-cell wall
1. Consist of- glycan chain, cross linked by peptide chain
2. Glycan chain is madeup of- alternating sugars- a. N. Acetyl
clucosamine and b.N- acetylmuramic acid
3. Glycan chain is gross linked to-peptide chain.strength wall
4. Synthesis of peptidoglycan-requires enzyme called-
transpeptidase
5. Transpeptidase- help in the process of cross –linking of
above step
6. Transpeptidase – penicilline binding protein
16

17. Conti....
1. PBP- enzyme present cell membrane-helps in cross
linkage
2. Beta lactum antibiotics bind covalently to PBP –
decrease peptidoglycan synthesis
3. Inhibiting of peptidoglycan- formation of cell wall
deficient bacteria
4. Bacteria without cell wall- undergo lysis- bactericidal
5. Gram +ve- more susceptible for penicillin because
Increase peptidoglycine
6. Peptidoglycan id unique to bacteria. Not found in
higher animal
7. MOA= Beta lactum---bind PBP---decrease
crosslinkage---decrease cell wall ---cell death
17

18. 18

19. Penicillin-G – pharmacological profile
 Penicillin-G= benzyl penicillin
 Antibacterial spectrum- narrow spectrum
 Effective for- streptococci, pnemococci, gonococci, clostridia
meningococci, c.diptheriae, listeria
 Pk- 1. destroyed by- gastric juice-acid labile
2. It has low bioavailability- hence given by – parentrally
3. Food affect is absorption –should be given before or after 2hr
4. Generally does not cross BBB but in inflammation it may cross
5. Rapidly eliminated by kidney- a.10% by – G filtration, b.90%-T.
secretion
6. Resistance- those bacteria which produce - penicillinase
19

20. Conti...
 Adverse effect – penicillin is highly safe drug
 Use- pnemococccal, streptococci, gonococci, clostridia
meningococci, c.diptheriae, listeria
20

21. Semisynthetic penicillin- pharmacological detail
 Acid resistance penicillin-
1. Penicillin V- phenoxymethyl penicillin-acid stable- orally
2. Used in- mild infection, low B.A, short action, narrow spectrum -
Treat- sreptococcal pharyngits and sinusits.
 Penicillinase resistant penicillin –
1. Resistant to hydrolysis by penicillinase produced by bacteria
2. Less effective to- non penicillinase producing microorganism
3. Methacillin- staphylococcal penicillinase resistant but acid labile
4. Oxacillin- cloxacillin-dicloxacillin-acid stable but affectd by food
5. Naficillin- highly resistant to penicillinase and activity used against
non-penicillinase producing bacteria. Given parentral route.
21

22. Conti....
Amino penicillin- extended spectrum antibiotics.
 Cover Wider antibacterial spectrum including many –
gram –ve
 Orally effective sensitive to betalactamase.
 Ex.- Ampicillin – very effective against – E.coli proteus,
enterobacteria, salmonella, shigella 2. activity increase by
adding beta lactamase inhibitor 3. a stable, absorb orallay
 Adverse effect- 1. diarrhoea- due to irritation of unabsorbed
drugs 2. skin rashes to – AIDS patient and person taking
allopurinol
22

23.  Use
1. Respiratory tract infection- bronchotis, sinusits, otitis media
2. UTI = Ampicillin was drug of choice earlier. Now resistant
3. Meningitis- ampicillin with – cephalosporin/
chloramphenicol
4. Typhoid- alternative to- cephalosporin and chloramphenicol
5. Septicemia- due to gram –ve- given IV with aminoglycoside
6. Bacillary dysentry- caused by singella
 Amoxicillin- similar to ampicillin but ditter in
1. Amoxicillin better absirbed orally
2. food does not affect absorption
3. Attain high blood level after oral, less protein bound
4. Diarrhoea is rare because well absorbed
23

24. Beta lactamase Inhibitors - pharmacology
 Beta-lactam – enzyme produced by – bacteria- open up
betalactam ring and inactive beta-lactam antibiotics.
1. Beta lactamase inhibitors- bind to and inactive beta
lactamase
2. Increase antibiotic spectrum of penicillin by preventing
distruction Ex. Clavulanic acid, sulbactam, tazobactum.
3. These are themself beta lactam compounds but no
significant antibacterial activity.
4. Beta lactamse inhibitors are no effective against beta
lactamase produced by- pseudomonas, enetrobacter and
methicillin resist styphylococus aurus
Note- Each beta lactamse inhibitor or combined with penicillin
of choice
24

25. Cephalosporin- introduction & classification
 Cephalosporin- semisynthetic antibiotics. Having beta-
lactam ring
 Derived from- cephalosporin-c obtained from-
Cephalosporium
 Having wider spectrum of activity than penicillin.
 Mechanism- inhibition of cell wall synthesis – bactericidal
 Resistance- a. alteration in target protein (PBP) – decrease
antibiotic activity b. Impermiability of antibiotics to site of
action c. Due to cephalosporinase
25

26. Classification
 Generation- chromological sequience – spectrum-potency
1. First generation- parentral- cetazolin, oral-cephalixin,
cefadroxil.
2. 2nd generation- p-cefuroxim, o-cefactor,cefprozil
3. 3rd genration- p- cefuroxim, seftizoxim,ceftriaxone o-
cefixime, cefdinir, ceftibuten
4. 4th generation- p- cefepime, cefpirone
5. 5th generation- p- sefitaroline, tosamil, ceftibiprole,
medocaril
26

27. Cephalosporin-generation with example
A. 1 st generation- 1960 high activity – gram +ve. Weaker –ve
 Sefazolin- p00rototype 1st gen. 2. given – IM ( mild pain) & IV
 Longer t1/2- 2hrs, due to slower tabular secretion
B. 2nd generation- more active against – gram –ve bacteria 2. useful
of resistant strain of some 1st gen. 3. as compare to 1st gen. weaker
for gram positive bacteria sefprozil -1.good oral
absorption 2.use –bronchitis, ENT, skin
C. 3rd generation- 1980. highly active against-gram –ve
enterobacteriaceae
 1. some membrane have BBB penetration properly- useful in
meningitis
 Sefdine- good activity against many beta-lactamase producing
agent
27

28. Conti.....
A. 4th generation- cefepime - highly resistant against-
beta lactamase-highly effective
B. 5th generation- kill MRS+ and other penicilin resistant
bacteria. Useful in resistant and hospital acquired
infection
• ADR of cephalosporine- pain after IM, diarrhoea due
to gut , increase sensitivity, disulfiram like action
28

29. 29

30. 30

31. Chloramphenicol- Introduction & Mechanism
 In 1947 obtained from – streptomyces venezualae
 Class 1. nitrobenzene derivative 2. broadd spectrum 3.
bacteriostatic 4. protein synthesis inhibitor
 Mechanism- inhibit bacterial protein synthesis
 Interfere- Transfer of elongated peptide chain to the newly attach
aminoaceyl + RNA of the ribosome m-RNA complex
 Specially attaches to 50s ribosomes near the acceptor (A) site.
 Prevent bond formation between the newly attached amino acid
and nascent peptide chain
 At high dose- inhibit mammalian mitochondrial protein synthesis
 Note- choloramphenicol bends to 50s subunit – interropeptide
bond formation – decrease transfer of peptide chain from p site
31

32. 32

33. Spectrum – ADR- USE
 Antibacterial spectrum-
 Broad spectrum- treat- gram +ve, some –ve, anaerobic bacteria,
rickettsia, salmonella, shigella, gonococci meningococci,
streptococci, clostridium
 It is bactericidal for- neissria meningitidis, influenzae
 Resistance due to- inactivating enzyme 2. reduce permiability
 Adverse reaction-
 GIT distrubance- nausea, vomiting, diarrhoea
 Bone marrow depression- by anaemia due to inhibition of protein
synthesis
 Grey baby syndrom- new born baby given high dose may develop
 GBS- vomiting, hypothermia, abdominal distension etc.
 Drug intraction- increase toxicity- phenytoin, warfarin,
tolbutamide
33

34. Macrolides Antibiotics- Erythromycin
 Macrolides- Antibiotic having macrocyclic lactone ring with
attached sugars. Erythromycin 1st discovered in-1950s
 Ex.- roxithromycin, clorothromycin, telithromycin,
azithromycin
 Erythromycin- obtained from- streptomyces erythreus.
 Water solubility is limited remain stable in cold water only.
 Spectrum- 1.bacteriostatic- at low conc. 2. bacteriocidal-high
 Use.- streptococci, pnemococci, gonococci, legionella,
mycoplasma, & some atypical mycobacteria.
 Activity is enhanced several time at alkaline medium.
34

35. MOA
 Act by- inhibiting bacterial protein synthesis
 Combine with 50s ribosome submit and interfere with
translocation of growing peptide chain from A site to p site.
 By this A site is not available for next Amino acid ( brought by t
RNA) – protein synthesis stop.
 Not. – to be combined with- chloramphenicol & clindamycin.
 Erythromycin- pharmacology
 Anti-microbial resistance-
1. Impsired permiability of antibiotic
2. Efflux of the drug by active transport mechanism
3. Formation of macrolide inactivating enzyme.
4. Protection of ribosomal subunit-prevent binding
5. Chromosomal mutation-mutation of 50s subunit
35

36. 36

37. Conti....
 Pharmacokinetic-
1. Erythromycin base is acid liable – given as enteric coating
enters into – abscesses, placenta but cannot cross BBB
 Use- A. as an alternative to penicillin-
1. Steptococcal phyringitis, tonsillitis, community acquired
respiratory infection, 2. diptheria , 3. tetanus, 4. gonorrhoea
2. B. 1st choice of drug- atypical pnemonia caused by –
mecoplasma 2. woofing of drug 3. chancroid
ADR-
1.Hearing impairment 2. hypersensitivity 3. arythmia
4. decrease hepatic oxidation 5. increase plasma level of some
dry - toxicity
37

38. Qunolons – pharmacology and Mechanism
 Quinolones- synthetic antimicrobial agents- decrease DNA gyrase
 Ex.- nalidixic acid, oxalic acid, cinoxacin
 Nalidixic acid- bacteriocidal agent, many gram –ve bacteria
 Like- E.coli, Shigella, Enterobacter, proteus
 Well absorbed orally but plasma concentration of free drug is
insufficient to produce systemic effect.
 Attains high concentration in urine-useful in UTI
 ADR- (mostly incommon)- Haemolytic anaemia, allergic reaction
headche, drowsiness, visual distrubance
 Use- UTI- urinary antiseotic in uncomplited UTI due to E Coli,
Shigella and proteus.
 Diarrhoea - due to E coli, Shigella & proteus
 MOA- 1. nhibiting DNA Gyrase 2. INHibiting “Topoisomarase-IV
 Affect – bacterial DNA replication , transcription, repair &
recombination
38

39. Mechanism - Bctericidal
1. Inhibit DNA – Gyrase
2. Inhibit topoisomarse –IV
These O2 are required for DNA replication and transcription
Steps-
1. during DNA replication there is excesassive +ve supercoiling of
DNA
2.Thes is corrected by DNA Gyrase by conti. Introducing –ve
supercoiling
3. this is very important replication.
4. Topoisomarase IV separate daughter cell after replication
5. Drug decrease this process-stop sepration
6. DNA gyrase decrease gram –ve bacteria
7. Topoisomarase decrease – decrease gram +ve bacteria
39

40. 40

41. 41

42. Fluoroquenolones-Pharmacology
 Advantage of fluroquinolones over quinolones-
1. Wider spectrum of activity 2. fewer side effects 3. lesser chance of
resistance 4. better therapeutic blood level
 Classification-
1. 1st generation- nofloxacin, ciprofloxacin, ofloxacin, pefloxacin
2. 2nd generation- levofloxacin, maxifloxacin,
gemifloxacin,prulifloxacin, lomefloxacin, sparfloxacin
 Resistance- 1. mutation in target enzyme – drug loose affinity
2.change in permiability of drug in organism 3.protection of
DNA gyrase by same protein – via plasmid
 Spectrum- A. Gram – ve – gonococci, meningcocci, E. Coli,
salmonella, shigella, enrerobacteria, H.pylori, H. Influenzae
B. Gram + ve- staphylococci, vibreo cholerae are susceptible,
mycoplasm, mycobacterium with M. Tuberculisis
 P’kinetic- absorbed orally, attend by food antacid, ofloxacin BBB
42

43. ADR – Use- Contraindication
 Adverse reaction – Nausea- vomiting- abdominal discomfert
diarrhoea-skin rashes, tandonitis, damage growing cartilage,
headache, dizziness, insomnia, arythmia. Etc
 Use-
1. UTI- very useful, even for multiresistant bacteria
2. Typhoid – ciprofloxacin- drug of choice ( also in carrier state)
3. diarrhoea- due to shigella, almonella, E. Coli, camphybacter
4. Gonorrhoea – single dose 250 mg ciprofloxacin- curative
5. Chanchroid – alternative to – cotrimoxazole, ciprofloxacin
6. Respiratory tract infection- gemifloxacin, moxifloxacin,
gatifloxacin, levofloxacin- respiratory antibiotics.
7. T. B. – ciprofloxacin is one of the Drug in ( MDT)
8. Eye infection- ciprofloxacin. Oflaxacin
 Contraindication- 1. pregnancy 2. age below 18 years 3. arythmia 4.
theophyllin toxicity 5. ca++-Iron preparation- decrease absorption.
43

44. Mechanism - Bctericidal
1. Inhibit DNA – Gyrase
2. Inhibit topoisomarse –IV
These O2 are required for DNA replication and transcription
Steps-
1. during DNA replication there is excesassive +ve supercoiling of
DNA
2.Thes is corrected by DNA Gyrase by conti. Introducing –ve
supercoiling
3. this is very important replication.
4. Topoisomarase IV separate daughter cell after replication
5. Drug decrease this process-stop sepration
6. DNA gyrase decrease gram –ve bacteria
7. Topoisomarase decrease – decrease gram +ve bacteria
44

45. Tetracyclines- general Pharmacology
 Class- ex. Of- 1. broad spectrum 2. protein synthesis decreases
 Obtained from- soil actinomycets. Chlorteracycline- 1st tetra.
 Classification-
1. Short acting ( t1/2= 6H)- tetracycline,chlortetracycline,oxy t.c
2. Intermediate (t1/2=12H)- demeclocycline, methacycline
3. Long acting (t1/2=18H)- doxycycline, minocycline.
4. Newer tetracycline- tigecycline ( t1/2=36H)
 Adminstration-
 Available as – oral topical, parenteral 2. may be given with food –
decrease irritation.
 Contraindicated with – milk dairy product, antacid, iron, sucralfate
 Also not to be given with- chlolestyramine, cholestipol- decrease
absorption
45

46. Conti....
 Intramuscular injection should be avoided – irritation, slow
absorbtion
 Doxycyline and minocycline are the only tetracycline which are
suitable for IV because other cause- thrombo phlebits.
 Spectrum, resistance, ADR
 Spectrum- broad spectrum = decreases all types of microorganism
except fungi
1. cocci- intially for all +/- bacteria. Now strept. Pyogenes,
staph.aureus + MRSA and enterococcci.
2. most gram + ve – clostridia, propionibacterium
3. protoza like – entamoeba histolytica inhibited at high conc.
 Resistance-
1. decrease uptake and efflux of antibiotic by bacteria
2. displacing tetracycline from binding site- tooget ribosome
3. activating enzyme that inactivate tetracyclin
46

47. Adverse effect
• GIT- irritation, burning, oesophagal ulcer, nausea-vomiting,
diarrhoea
• Hepatotoxicity- on large dose may result into-jaundice
• Renal toxicity- increase level of N2 due to antibiotic,
proteinurea, polyurea
• Phototoxicity- skin iritation , dermatitis on exposure to
sunlight
• Teeth-bone- chelate ca++, - orthophosphate, complex deposit
• Superinfection- due to decrease of intestinal flora
• Local – IV infection cause – thrombophlebitis.
47

48. 48

49. Tetracycline- Mechanism of action
 Tetracycline are taken up by susceptible microorganism by active
transport.
 Mammilian cell lack this transport process- selective toxicity.
 Selective targeting-different in ribosome of pro & Eukaryotes
 Bacterial ribosome consist of 50s & 30s subunit.
 Tetracycline binds to 30s subunits
 t-RNA carries amino acid to ribosome for protein synthesis
 Tetracycline- binds to A site and prevent binding of t-RNA
 Result- amino acid can’t added to the growing peptide chain
 Prevent protein synthesis- no protein- bacterioststic effect
 Use- drug choice-Rickettsial injection 2. trachoma 3. inclusion
conjunctivitis 4. urethritis 5. atypical pneumonia 6. cholera 7. plague
 Other use- diarrhoea, STD, Acne, protozoal infection
49

50. 50

51. Aminoglycoside- classification properties
 Aminoglycoside- amino sugars joined by- glycosidic linkage
 Derived from- soil actenomycetes of genes- streptomyces & genus-
micromonospora.
 Classification- 1. systemic – streptomycin, kanamycin, tobramycin,
gentamycin.
 2. topical- neomycin
 Properties-
1. highly water soluble polar compound
2. Polycationic carbohydrate containg amino sugar in glycosidic link
3. Not absorbed orally – given parentrally
4. Elininated unchanged by kidney
5. Act by- inhibiting bacterial protein synthesis
6. Mainly effective against – gram negative bacteria
7. Main ADR- ototoxicity & nephrotoxicity
8. Poor- csf penetration
51

52. Spectrum- resistance- Pharmacokinetic
 Spectrum- aerobic gram –ve bacilli- E.coli, proteus, nocardia, v,
cholerae pseudomonas, bricella, salmonella
 Resistance-
1. Aminoglycoside inactivating enzme – no antibiotic effect
2. Low affinity of ribosomes – acquired by mutation
3. Decrease permiability to the antibiotic
 P’kinetic- 1.poorly absorbed from GIT
2. They don not cross- BBB though they may cross placenta
3. tratogonicity-hearing – loss in children born
 Adverse effect-
 Ototoxicity- most imp toxic effect- vestibular & auditory
dysfunction- auditor nerve dgentrate, vestibular dysfunction may
affect nausea, vomiting, vertigo, headache
 Nephrotoxicity- damage renal tubulis, low GFR ( gentamycin n)
 Neuromuscular toxicity- block neuromuscular transmission
52

53. MOA
 Aminoglycoside- water soluble- penetrate bacterial cell
membrane through aqueus pores and reach periplamic space
 Transported across cell membrane into cytoplsm by – oxygen
dependent active transport- 20times more active in alkaline
PH
 Aminoglycoside- disrupt cell membrane –penetrate drug in
bacterium from periplasmic space
 Inside the cell- aminoglycoside binds to 30s ribosomal
subunit
 Inhibit bacterial protein Synthesis- block initiation of protein
Termination of protein synthesis
 Synthesis of abnormal protein- bacteriocidal – death of
bacteria
53

54. use
• Example-
1. Streptomycin - tuberculosis, plague
2. Gentamycin- a. UTI- used in uncomplicated urinary tract
infection b. Pneumonia c. Meningitis d. Topical-burns,
wounds
3. Kanamycin- due to toxicity, T.B.
4. Amikacin- T.B
5. Neomycin- topical- skin infection, burns, ulcer, wounds, ear,
eye
54

55. 55