INTRODUCTION CHEMISTRY CLASSIFICATION DURATION OF ACTION

 In 1930, G.Domagk Use  The Basic Element OR Basic 1) Short Acting  Short Acting
Prontosil (Dye) To Treat Chemical Entity Is Sulfanilamide. (Sulfadiazine) 4-8 Hours
Septicemia.  N1 → Antibacterial Action. 2) Intermediate Acting
 In 1939, He Awarded Nobel  Intermediate Acting
 N4 → Pharmacokinetics And (Sulfamethoxazole)
8-12 Hours
Prize. Potency.
 Pioneer Antibiotic To Treat 3) Long Acting
(Sulfadoxine)  Long Acting
Bacterial Infections.
7 Days
 Sulfonamides Antibiotics Are 4) Other
Synthetic And Bacteriostatic. (Mafenide)
(Sulfacetamide)

MECHANISM OF ACTION USES SIDE EFFECTS

Sulfonamide Inhibit Folate Synthase (Enzyme), Stop Cell  Urinary Tract Infection  Nausea And Vomiting
Division And Inhibit The Growth Of Bacteria.  Upper & Lower Respiratory  Epigastric Pain
Trimethoprim In Combination With Sulfamethaxazole Tract Infections
(Cotrimaxazole), Inhibit Dihydrofolate Reductase And Inhibit  Bacterial Diarrhea And  Crystallurea
Both Steps In Folic Acid Synthesis Pathway In Bacteria. Dysentery  Photosensitivity
 Prevention Of Pneumonia
MECHANISM OF RESISTANCE  Hepatitis By Unknown
 Vast Used For Typhoid Fever
 Preventing Infection On Mechanism
Change In Affinity Of the Enzyme
Increase PABA (Which Antagonize) Burning Skin  Hemolysis
Alternate Pathway (Bacteria Use Another Pathway To Form  Karnicterus
Folic Acid)
INTRODUCTION CHEMISTRY CLASSIFICATION
 Semi-Synthetic Bacteriocidal.  Fluroquinolones Is Formed By Generation-I:
 Metabolic Pathway Inhibitor Combining Nalidixic Acid, Norfloxacin
Of Cell. Fluoride & Piperazine Ring. Ofloxacin
 First Quinolones Is Nalidixic  Fluoride Ion Attach To Overcome Ciprofloxacin (For Enteric Fever & Typhoid Fever)
Acid Which Have; Quinolones Drawbacks.
 Less Potency Generation-II:
 It Is Most Commonly Prescribed.
Levofloxacin (For RTI & Typhoid Fever)
 Required High Dose  It Is More Advanced Broad
Lomifloxacin
 Develop Rapidly Resistance Spectrum Which Have;
Moxifloxacin (Most Preferred By Doctor)
 Less Penetration Into Tissues /  High Potency
Fluids.  Develop Less Resistance  Ofloxacin & Levofloxacin (Isomer Difference)
 Only Used For Gram -Ve  More Penetration Into Tissues /
Bacteria. Fluids.
MECHANISM OF ACTION USES SIDE EFFECTS
Fluroquinolones (FQ) Inhibit DNA Gyrase In Gram +Ve Bacteria  Urinary Tract Infections  GIT
And Inhibit Topoisomerase-IV In Gram –Ve Bacteria.  Gonorrhea  Nausea
FQ Have Affinity With Topoisomerase-IV And 2A1 Subunit Of  Gastroenteritis  Vomiting
DNA Gyrase, Results In Abnormality In Nicking And Resealing  Typhoid Fever  Anorexia (Loss Of
Of DNA Strand Of Bacteria.  Bone Soft Tissue & Appetite)
Due To The Abnormality In DNA Structure, Cell Releases Gynaecological Womb  CNS
Exonucleases Which Lysis The Cell (Cell Death). Infections  Dizziness, Anxiety
 Respiratory Infections  Headache, Insomnia
MECHANISM OF RESISTANCE  Tuberculosis  Tremors, Seizures
 Gram -Ve Septicemia  Hypersensitivity Reactions
Change In Structure Of Enzyme.
 Meningitis  Photosensitivity
Change In Affinity Of Enzymes.
 Conjunctivitis  Swelling Of Lips
Low Penetration In Any Case.
 Rashes
INTRODUCTION
 In 1941, Penicillin Is Made
Accidentally From a Fungus
"Penicillium Notatum".
 Now, Penicillin Is Largely
Obtained From a Fungus
"Penicillium Crysogenum".
 Penicillin Is Cell Wall
Synthesis Inhibitor.
 Used Mainly Against Gram
+Ve Bacteria.
CHEMISTRY
 Mainly Used Penicillin Is Penicillin-G
Which Is Also Called Benzyl Penicillin.
 The Antibacterial (Bacteriocidal)
Activity Of Penicillin Is Due To β-
Lactam Ring.
 β-Lactam Ring Is Attached To
Thiazolidine Ring (COOH + Na Make
Salt To Achieve More Stability).
 Amidases Substitute The Amide Group
To Achieve Semi-Synthetic Activity.
CLASSIFICATION
1) Acid Resistant
Penicillin-V
2) Penicillinase Resistance
Methicillin, Cloxacillin
3) Extended Spectrum
Amoxicillin, Ampicillin, Carbenicillin, Piperacillin
4) β- Lactamase Inhibitors
Clavulanic Acid, Sulbactam, Tazobactum

MECHANISM OF ACTION USES SIDE EFFECTS

Inhibit The Transpeptidases Which Is Involved In Stability &  Pharyngitis & Laryngitis
Rigidity Of Cell Wall Of Bacteria.  Rheumatic Fever
Inhibit The Suppression Of Autolysis (Promote The Autolysis).  Pneumococcal Infection
Increase Cell Wall Deficient (CWD).The Cell Becomes  Gonorrhea
Hyperosmotic & Cell Swells, Burst & Dead.  Syphilis
 Diphtheria & Tetanus
MECHANISM OF RESISTANCE  Gas Gangrene
Change In Affinity Of Transpeptidases.  Rat Bite Fever
Change In Structure Of Transpeptidases.  Anthrax
Most Bacteria Produce OR Formed Pencillinase (β-Lactamase) Prophylactic Use
To Develop Resistance.  Agranulocytosis
Decreased In Permeability Of Cell Wall.  Bacterial Endocarditis
 Rheumatic Fever
 Local Irritating
 Pain At Site Of Injection
 Thrombophlebitis
 Muscular Twitching
 Convulsions
 Bleeding (By Interfering
With Platelets)
 Hallucinations
 Hypersensitivity Reactions
 Rashes
 Allergy
 Photosensitivity
INTRODUCTION CHEMISTRY CLASSIFICATION
 Semi-Synthetic Bacteriocidal.  Having a β-Lactam Ring Combined With Thiazide Ring. 1st Generation
Derived From Cephalosporin-C Cefazolin, Cephalexin
(Fungus).
2nd Generation
 Cell Wall Synthesis Inhibitor
Cefaclor, Cefoxitin
Spectra Entirely Different From
Penicillin. 3rd Generation
 Most Commonly Prescribed Ceftriaxone, Cefixime
Antibiotics.  At Position-7 Of β-Lactam Ring, Amidases Breakdown The
 Having Four Generations 4th Generation
Place For Further Substitution To Achieve Different Potency,
Depending Upon Spectra. Cefepime
Efficacy And Pharmacokinetics Parameters.

MECHANISM OF ACTION USES SIDE EFFECTS

It's Mechanism Of Action Is Same As Penicillin, But Binding  Alternative To Penicillin  Pain At Injection Site
Proteins Are Different.  Upper Respiratory Tract  Thrombophelibitis
Inhibit The Transpeptidases. Infections  Diarrhea
Promote The Autolysis.  Urinary & Soft Tissue  Hypersensitivity Reactions
Increase Cell Wall Deficient (CWD). Infection  Rashes
 Septicemia  Shock
MECHANISM OF RESISTANCE  Pharyngitis & Meningitis  Photosensitivity
Change In Affinity Of Transpeptidases.  Gonorrhea  10% Penicillin Allergic
Change In Structure Of Transpeptidases.  Typhoid Fever Patients Show Cross Reactions
Most Bacteria Produce OR Formed Pencillinase (β-Lactamase)  Mixed Aerobic & Anaerobic With Cephalosporins
To Develop Resistance. Cancer  Hemolysis
Decreased In Permeability Of Cell Wall.  Hospital Acquired Infection  Nephrotoxicity
 For Surgical Prophylaxis  Homocytopenia
INTRODUCTION Monocyclic CHEMISTRY
 Monobactams Are Monocyclic  The Four-Membered Ring At The Bottom Is The β-lactam.
Naturally Occurring Antibiotic  There Is a Second Thiazole Ring, But It Is Not Fused To The
Isolated From `Chromobacterium β-lactam Ring.
spp`.
 The β-lactam Ring Is Not Fused To DRUGS NAME
Another Ring, In Contrast To Most o Aztreonam
Other β-lactams. o Tigemonam
 Monobactams Are Effective Only o Carumonam
Against Aerobic Gram-negative o Nocardicin A
Bacteria (e.g. Neisseria,
Pseudomonas). o
MECHANISM OF ACTION USES SIDE EFFECTS
Monobactams Work Only Against Aerobic Gram-  Hospital Acquired Infections  Skin Rash
Negative Bacteria. Originating From Urinary,  Occasional Abnormal Liver
Inhibit Synthesis Of Peptidoglycan Layer Of Bacterial Cell Wall Biliary, Gastrointestinal And Functions
By Binding To And Inhibiting PBPs,a Group Of D-Alanyl-D- Female Genital Tracts.  Cross Sensitivity With
Alanine (Transpeptidases)  Cystic Fibrosis Cephalosporins Allergic
 Skin Infections  Nausea
MECHANISM OF RESISTANCE  Pyelonephritis (Severe  Vomiting
Change In Affinity Of Transpeptidases. Kidney Infection)  Diarrhea
Change In Structure Of Transpeptidases.  Septicemia  Abdominal pain
Most Bacteria Produce OR Formed β-Lactamases To Develop  Peritonitis  Abnormal Taste In
Resistance.  Endometritis The Mouth
INTRODUCTION CHEMISTRY STRUCTURE CLASSIFICATION
 Thienamycin Was The First  The Carbapenems Are Very Group 1
Carbapenem To Be Similar To The Penicillins Ertapenem
Discovered in 1976. (Penams).
 Carbapenems Are Notable  The Sulfur Atom In Position-1 Group 2
For Their Ability To Inhibit Of The Structure Has Been Imipenem
Beta-Lactamase Enzymes. Replaced With a Carbon Atom. Meropenem
 It Is An Extremely Potent  An Unsaturation Has Been
Bacteriocidal And Broad- Introduced, Hence The Name Doripenem
Spectrum β-Lactam Of The Group, The
Antibiotic. Carbapenems

MECHANISM OF ACTION USES SIDE EFFECTS

It Is Resistant To Most β-Lactamases; Inhibits Penicillinase  Nosocomial infections Like  Seizures At Higher Doses
Producing Staphylococci And Some MRSA.  Septicaemia  Diarrhea
It Penetrates The Cell Wall Of Bacteria And Bind To Protein  Febrile Neutropenia  Vomiting
Binding Target Sites.  Skin Rashes
Interfering With The Synthesis Of Vital Cell Wall Components,
 Intraabdominal
 Pelvic Infections  Cross Sensitivity With
Which Leads To Cell Death.
Respiratory Tract Infections Penicillin Allergic
MECHANISM OF RESISTANCE ENT  Headache
Genitourinary Infections  Loss Of Apetite
Decreased In Permeability Of Cell Wall.
For Multi-Drug Resistant  Tiredness
Modifications Of Target Sites Through Genetic Mutations.
Infections  Pruritis
Modifications In β-Lactamases Enzymes.
INTRODUCTION CLASSIFICATION ANTI-MICROBIAL
 First Isolated From Soil Bacteria 1) Short Acting (6-8 Hours) SPECTRUM
(Actinomycetes). Tetracycline  Cocci (Gram+Ve & Gram -
 It Is Observed That It Is Very Chlortetracycline Ve)
Broad Spectrum Even Against Oxytetracycline  Bacilli
Protozoa And Anaerobes etc. 2) Intermediate Acting (12 Hours)  Spirochaetes
 The Semi-synthetic Tetracycline Demeclocycline  Mycoplasma
Is Water Soluble And Bitter In Methacycline  Actinomyces
Taste. 3) Long Acting (16-18 Hours) Doxycycline
 It Is Broad Spectrum (Gram +Ve Minocycline
& Gram -Ve) Bacteriostatic. Tigecycline

MECHANISM OF ACTION USES SIDE EFFECTS

Tetracycline Enter Into Bacterial Cell By Passive Diffusion And  First Choice Drug For;
Active Transport.  Atypical Pneumonia,
It Bind To 30S Ribosomal Unit And Inhibit The Binding Of Cholera, Brucellosis,
Aminoacetyl-tRNA To The Acceptor Site On The mRNA- Plaque, Relapsing Fever,
Ribosome Complex. Dropping Mountain
As a Result, Cell Is Unable To Grow Or Further Replication. Fever
 Second Choice Drug For;
MECHANISM OF RESISTANCE  Tetanus, Anthrax,
Bacteria Modify EDTS To Prevent The Entry Of Tetracycline. Gonorrhea, Syphilis,
Efflux Of Tetracycline To Reduce Cytoplasmic Concentration. Pneumonia
Mutations At Ribosomal Subunit Site.  Imperial Therapy
Monooxygenase Enzyme Inactivate The Tetracycline By  Prophylactically Use For
Hydroxylation Reaction. COPD
 Jaundice, Hepatic Cell
Necrosis, Superinfection
 Epigastric Pain, Nausea,
Diarrhea
 Oesophagial Ulcer
 Odynophagia
 Fanconi Syndrome (Kidney
Failure)
 Antianabolic Action
 Nystagmus, Ataxia, Vertigo
 Diabetes Insipidus
 Hypersensitivity
 Photosensitivity
INTRODUCTION CHEMISTRY CLASSIFICATION USES
 In 1943, The First  Polybasic Amino Acid Are Systemic Aminoglycosides  Empiric Therapy For;
Aminoglycoside Antibiotic Glycosidically Linked With Streptomycin  Endocarditis
Discovered Is Streptomycin. Amino Sugars.  Sepsis
 It Is First Obtained From Soil  Polybasic Aminoacids In Sulfate Gentamicin  Intrabdominal
Microorganism `Actinomycetes`. Salt Form Are More Stable. Kanamycin Infections
 It Is a Protein Synthesis Inhibitor.  It Is Alkaline In Nature And
Tobramycin SIDE EFFECTS
 It Is Bacteriocidal And Now, Neutralized In Acidic Medium.
Synthesize Semi-synthetically In  Active In Alkaline Medium. Topical Aminoglycosides  Ototoxicity
Laboratory.  Actual Structure Remain Empi  Nephrotoxicity
 Mainly Used Against Gram -Ve Unchanged When Excreted Neomycin
 Neuromuscular
Bacteria. Through Urine. Framycetin Blockage
MECHANISM OF ACTION MECHANISM OF
Aminoglycisides Majorly Bind At 30s Ribosomal Subunit But Also Have Affinity For 50s And Interface RESISTANCE
Site And Inhibit Protein Synthesis. Cell Membrane
Its Mechanism Is Multistep. Attached Enzymes
In First Step, AGs Moves Through Bacterial Porins And Stuck In Periplasm Space. Then, Move Into (Adenylate,
Cytoplasm By Energy Dependent Phase-I Mechanism In Which ATP And Oxygen Is Required. Phosphorylate) Attach
Then, AGs Bind To 30s Ribosomal Subunit And Inhibits Polysome Formation And Degraded The Groups To
Polysome Due To Misleading Codon. Aminoglycisides And
As a Result, Chain Formation Of Functional And Structure Proteins Don't Not Take Place. Change Its Structure.
The Non-Structural Proteins Incorporate Into Cell Wall And Loss Its Integrity. Decrease In Penetration
As a Result, Energy Dependent Phase-II Starts In Which More Aminoglycisides And Other Toxins Of Aminoglycisides.
Move Inside Of Cell And Accumulate Because, Energy Is Not Needed. Decrease In Affinity Of
As a Result, Cell Lysis Of Bacterial Cell Takes Place. 30s Ribosomal Subunit.
INTRODUCTION
 Chloramphenicol Was Initially
Obtained From Soil Bacteria
"Streptomyces Venezuelae".
 Now, It Is Synthetic And
Commercially Synthesized.
 It Is Bacteriostatic But
Bacteriocidal At High
Concentration.
 It Crosses Placenta And Is
Secreted In Bile And Milk
STRUCTURE
CHEMISTRY USES USES
 It Is Yellowish White  Second Line Drug To  As An Alternative To
Crystalline Solid And Intensely 1) Cephalosporins For Clindamycin For
Bitter Taste.  Pyogenic Meningitis  Anaerobic Infections
 Aqueous Solution Is Quite  Meningococcal  Wound Infections, Pelvic
Stable But Needs Protection Meningitis Abscess, Brain Abscess
From Sunlight. 2) Tetracycline For  Intraocular Infection
 The Nitro-Benzene Moiety Of  Brucellosis And  Endophthalmitis
Chloramphenicol Is Rickettsial Infections  Enteric Fever
Responsible For Antimicrobial 3) Erythromycin For  Urinary Tract Infections
Activity.  Whooping Cough  Topically In Congunctivitis
MECHANISM OF ACTION SIDE EFFECTS
It Inhibits Bacterial Protein Synthesis By Preventing Transfer Of  Bone Marrow Suppression
Elongating Peptide Chain To The Newly Attached Aminoacyl-  Aplastic Anaemia,
tRNA At The Ribosome-mRNA Complex. Agranulocytosis, Penia,
It Attaches The 50s Ribosome Subunit Near The Acceptor Site Thrombocytosis.
And Prevents Peptide Bond Formation Between The Newly  Hypersensitivity Reactions
Attached Amino Acid And The Nascent Peptide Chain.  Rashes, Fever, Atropic
Glossitis, Angioedema
MECHANISM OF RESISTANCE  Irritative Effects
Acquisition Of R Plasmid Encoded For An Acetyl -Transferase  Nausea, Vomiting,
Which Inactivate The Chloramphenicol By Acetylation. Diarrhea, Pain At Injection
Change In Affinity At 50S Ribosome Subunit Site. Site
Decrease In Penetration Of Chloramphenicol.  Superinfection
 Gray Baby Syndrome
INTRODUCTION CHEMISTRY CLASSIFICATION
 In 1952, Erythromycin Is First  It Is a Polyketide Class Of Natural Macrolides
Macrolide Obtained From Naturally Occurring
Erythromycin (A To F),Oleandomycin
"Streptomyces erythraeus". Hydrophobic Compounds.
 It Is Protein Synthesis Inhibitor.  It Has Macrocyclic Lactone Spiramycin, Midecamycin
 It Is a Bacteriostatic But At High Ring Which Make Complex
Semi-Synthetic Macrolides
Doses, It Is Bacteriocidal For Only With Deoxy Sugars.
Very Sensitive Bacteria.  It Has 90% Same Spectra As Clarithromycin, Roxithromycin
 Used As an Alternative To Penicillin Penicillin.
Or Cephalosporin's Allergic Patients. Azithromycin
 Quinolidomicin A1 Is The
 Mainly Used Against Gram +Ve Rokitamycin, Miokamycin
Largest Macrolide (60 Rings).
Bacteria.
MECHANISM OF ACTION USES SIDE EFFECTS
Macrolides Penetrate Through The Bacterial Cell Wall Into The Cytoplasm Mainly Used For Increased In Motilin
By Energy Dependent And PH Dependent Mechanisms. Respiratory Tract Production Which Lead
It Binds To 50s Ribosomal Subunit And Inhibt The Relocation Of Polysome Infections. To;
From Acceptor Site To Peptide Site And Stop Protein Synthesis. As An Antiseptic For  Increase Motility Of
As a Result Protein Is Synthesized But Not Completely. Urinary Tract Intestine
Infections.  Disturb Normal Flora
MECHANISM OF RESISTANCE Skin Infections (In  Gastric Disturbance
Decrease Penetration By Efflux Pump. Which Mixed  Diarrhea
Decrease Binding Or Affinity With 50s Ribosomal Subunit. Microorganisms Are  Nausea
Inactivation Of Macrolides By Esterases Enzyme. Not Involve)  Vomiting
 Abdominal Pain