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Basic information about antibiotics and generic drugs | MPO training 17

Curious about antibiotics and generic drugs before starting your MPO journey? This post covers the basic information about antibiotics and generic drugs with real-world context tailored for future Medical Promotion Officers.

Basic-information-about-antibiotics-and-generic-drugs

It’s written in plain language, so you can read and understand it in one go. From definitions to examples, this article helps you connect the dots easily. Whether you're preparing for an interview or just learning, this resource is made for you.

Table of contents: Basic information about antibiotics and generic drugs

Take a look at everything you can know about antibiotics and generic drugs-

Basic information about antibiotics and generic drugs

Every Medical Promotion Officer (MPO) needs a clear idea of how antibiotics work and why generic drugs matter. This article breaks down the basic information about antibiotics and generic drugs into simple points with examples.

READ MORE: Basic concept of infectious diseases | MPO training 16

You’ll learn how these medicines are used in real practice and why understanding generics gives you an edge in pharma sales. Designed for beginners, this guide helps you start strong in your MPO career.

What are antibiotics?

*Antibiotics are medicines that fight infections caused by bacteria. They either kill the bacteria or stop them from growing.

*Antibiotics are substances produced by microorganisms, or similar products produced by bacterial chemical synthesis and are able to inhibit or kill microorganisms without affecting the host.

History of Antibiotic

In 1929, Sir Alexander Fleming, a Scottish bacteriologist, went on a vacation and left a petri dish of staphylococci bacteria uncovered. When he returned, he noticed that there was mold growing on it. Upon further examination, he saw that the area around the mold had no bacteria growing.
History-of-Antibiotic
He named the mold Penicillium, and the chemical produced by the mold was named penicillin, which is the first substance recognized as an antibiotic.

What are some common types of antibiotics?

Some commonly used antibiotic classes include penicillins, cephalosporins, macrolides, tetracyclines, and fluoroquinolones.

Now we will learn all the details about antibiotics and generic names below.

Classification of Antibiotic

  1. Chemical Classification (Group of Antibiotic)
  2. Classification on the basis of Mechanism of Action
  3. Classification on the basis of Way/Nature/Effects of Activity
  4. Classification on the basis of Spectrum of Activity

1. Chemical Classification (Group of Antibiotic)

a. Beta-lactam antibiotics 
  • a. Penicillin
    • Natural Penicillin i.e. Phenoxymethyl Penicillin
    • Semi synthetic Penicillin i.e. Amoxicillin ((Moxilin)
  • b. Cephalosporin
  • c. Carbapenem : Imipenem, Meropenem (Fulspec)
b. Macrolides : Erythromycin (Erocin), Azithromycin (Azin)

c. Fluoroquinolones : Ciprofloxacin (Cipro-A), Levofloxacin (Leo)

d. Tetracycline : Doxycycline (Doxy-A), Oxytetracycline.

e. Aminoglycosides : Amikacin, Gentamicin

f. Sulfonamides : Co- Trimoxazole (sulfamethoxazole and trimethoprim)

g. Polypeptides : Polymyxin B Sulphate, Colistimethate Sodium (Xylistin)

h. Amphenicol : Chloramphenicol (A-Phenicol)

2. Classification on the basis of Mechanism of Action (Antibiotics)

A. Cell wall Synthesis Inhibitor
  • Beta Lactam
B. Protein Synthesis Inhibitor
  • Tetracycline
  • Aminoglycoside
  • Macrolide
  • Amphenicol
C. Nucleic Acid Synthesis Inhibitor
  • Fluoroquinolone
  • Sulfonamide
  • D. Cell Membrane Disruptor
  • Polypeptides
Examples:
A. Inhibit Cell Wall Synthesis

1. Beta Lactam Antibiotics:
  • a. Penicillin:
    • i. Natural Penicillin : Phenoxymethyl Penicillin
    • ii. Semisynthetic Penicillin : Flucloxacillin (A-Flox)
  • b. Cephalosporin:
    • 1st generation: Cephradine (Sefril), Cephalexin.
    • 2nd generation: Cefaclor(Alclor), Cefuroxime (Famicef)
    • 3rd generation: Ceftriaxone (Trizon), Cefixime (Fix-A)
    • 4th generation: Cefepime (Superpime)
  • C. Carbapenem:
    • Meropenem (Fulspec), Imipenem
B. Inhibit Protein Synthesis

1. Tetracycline:
  • Oxytetracycline
  • Doxycycline (Doxy-A)
2. Aminoglycoside:
  • Amikacin
  • Gentamicin
3. Macrolide:
  • Erythromycin (Erocin)
  • Azithromycin (Azin)
4. Amphenicol:
  • Chloramphenicol (A-Phenicol)
C. Inhibit Nucleic Acid Synthesis

1. Fluoroquinolone:
  • Ciprofloxacin (Cipro-A)
  • Levofloxacin (Leo)
D. Cell Membrane Disruptor

1. Polypeptides:
  • Polymyxin B Sulphate
  • Colistimethate Sodium (Xylistin)

3. On The Basis of Way/Nature/Effects of Activity

Bactericidal: Antibiotics that kill the bacteria. Examples: Penicillin, Cephalosporins, Carbapenem, Fluoroquinolones, Colistimethate Sodium etc.

READ MORE: Concept microbiology guide | MPO training 15

Bacteriostatic: Antibiotics that inhibit the growth of the bacteria. Examples: Tetracyclines, Sulfonamides, Trimethoprim, Macrolides, etc.

Cephalosporin Generation

Cephalosporin-Generation

1) 1st Cephalosporin Generation
  • Cephradine (Sefril) 
  • Cefadroxil (Twicef)
2) 2nd Cephalosporin Generation
  • Cefaclor (Alclor) 
  • Cefuroxime (Famicef
3) 3rd Cephalosporin Generation

(Oral):
  • Cefixime (Fix-A) 
  • Cefpodoxime (CP) 
  • Ceftibuten (Logibac)
Parenteral:
  • Ceftriaxone (Trizon) 
  • Ceftazidime (Trizidim)
4) 4th Cephalosporin Generation
  • Cefepime (Superpime)

Beta-lactam

Beta-lactam:
  • It is a chemical ring.
  • This ring is present in Penicillin, Cephalosporin & Carbapenem.
  • This ring is responsible for the bactericidal (kill bacteria) action.
Beta-lactamase:
  • An enzyme.
  • Produced by bacteria.
  • Helps bacteria to destroy Beta-lactam rings in Penicillin, Cephalosporin and Carbapenem.

Beta Lactam Antibiotics

Antibiotics having Beta lactam ring in their structure are called Beta Lactam antibiotics.

Example:
  • Penicillin: Amoxicillin, Flucloxacillin
  • Cephalosporin: Cephradine, Ceftriaxone
  • Carbapenem: Meropenem

Understanding the Mechanism of Action of Antibiotics

Mechanism-of-Action-of-Antibiotics
Diagram: Mode of action of antibiotic
This image provides a simplified overview of how antibiotics disrupt essential biological processes in bacteria to kill or inhibit their growth.

Here’s an easy-to-understand breakdown:

1. Inhibition of Cell Wall Synthesis:
  • Examples: Beta-lactams, Glycopeptides, Bacitracin, Isoniazid.
  • How they work: These antibiotics prevent bacteria from forming their protective cell wall, making them vulnerable and eventually causing cell death.
2. Disruption of Cell Membrane:
  • Example: Lipopeptides.
  • How they work: These antibiotics damage the bacterial cell membrane, leading to leakage and cell death.
3. Inhibition of DNA Gyrase (DNA Replication):
  • Examples: Quinolones, Novobiocin.
  • How they work: They block enzymes involved in DNA replication, stopping bacterial reproduction.
4. Inhibition of RNA Synthesis:
  • Examples: Ansamycins, Pleuromutilins, Oxazolidinones.
  • How they work: These antibiotics block the transcription process, so the bacteria cannot make essential proteins.
5. Inhibition of DNA-dependent RNA Polymerase:
  • Example: Rifamycins.
  • How they work: They prevent the enzyme that converts DNA into RNA from functioning properly.
6. Inhibition of Protein Synthesis (30S and 50S Ribosomal Subunits):
  • Examples: Tetracyclines, Aminoglycosides, Macrolides, Clindamycin.
  • How they work: They target bacterial ribosomes and stop protein production, which is crucial for survival.
7. Inhibition of Folate Synthesis Pathway:
  • Antibiotics interfere with the conversion of PABA → DHF → THF, a pathway necessary for DNA and RNA synthesis.
Mechanism-of-Action-of-Antibiotics1
This diagram illustrates how different antibiotics target essential components and processes within bacterial cells to stop their growth or kill them.

Here's a clear and simple breakdown:

1. Inhibition of Cell Wall Synthesis
  • Antibiotics: Glycopeptides, Beta-lactams.
  • Mechanism: These antibiotics prevent bacteria from forming their protective cell wall, making them weak and leading to cell death.
2. Inhibition of DNA Replication
  • Antibiotic: Quinolones.
  • Mechanism: Quinolones block the bacterial enzymes responsible for DNA replication, stopping the bacteria from multiplying.
3. Interference with RNA Base Pairing
  • Target: RNA base-pairing
  • Mechanism: Disruption of RNA synthesis prevents proper genetic instructions from forming, which is essential for protein production.
4. Disruption of Protein Synthesis (Ribosome 30S Subunit)
  • Antibiotic: Spectinomycin.
  • Mechanism: This antibiotic binds to the 30S subunit of bacterial ribosomes and stops protein production, which is vital for bacterial survival.
5. Damage to Cytoplasmic Membrane Structure
  • Target: Cytoplasmic Membrane.
  • Mechanism: Antibiotics targeting the cell membrane cause leakage of cell contents, leading to cell death.
In Summary:

The image shows that antibiotics attack bacteria by:
  • Breaking down the cell wall,
  • Blocking DNA and RNA synthesis,
  • Interfering with ribosome function,
  • Damaging the cell membrane.
Each mechanism ultimately prevents the bacteria from growing or causes it to die — making antibiotics powerful tools in fighting infections.
Mechanism-of-Antibiotic-action
This diagram explains how antibiotics work by targeting key structures and functions in bacteria to stop their growth or kill them.

Here's a breakdown in simple terms:
1. Inhibition of Cell Wall (Peptidoglycan) Synthesis
  • Antibiotics: β-lactams (Penicillins, Cephalosporins, Carbapenems, Monobactams) Bacitracin, Glycopeptides, Cycloserine.
  • How it works: These antibiotics block the formation of the bacterial cell wall, weakening the bacteria and causing them to burst.
2. Disruption of Membrane Integrity
  • Antibiotics: Polymyxin B, Daptomycin.
  • How it works: These drugs damage the bacterial membrane, causing leakage of cell contents and leading to cell death.
3. Inhibition of Nucleic Acid Synthesis (DNA/RNA)
  • Antibiotics: Fluoroquinolones, Rifamycins, Metronidazole.
  • How it works: They stop the bacteria from making DNA or RNA, preventing reproduction and survival.
4. Inhibition of Protein Synthesis
  • 30S Subunit Inhibitors: Aminoglycosides, Tetracyclines.
  • 50S Subunit Inhibitors: Chloramphenicol, Macrolides, Clindamycin, Streptogramins
  • How it works: These antibiotics block the bacterial ribosome, stopping protein production needed for growth and function.
5. Inhibition of Metabolic Pathways (Folate Synthesis)
  • Antibiotics: Sulfonamides, Trimethoprim
  • How it works: These drugs interfere with the production of folate, an essential nutrient for bacterial survival.
In Summary:

Antibiotics fight bacteria by:
  • Breaking down their protective wall,
  • Damaging their membrane,
  • Stopping their genetic copying process,
  • Blocking protein production, And interrupting their nutrient pathways,
  • This multi-target strategy makes antibiotics highly effective in treating bacterial infections.

Mechanism of Cell Wall Synthesis Inhibitor

Mechanism-of-Cell-Wall-Synthesis-Inhibitor
  • Antibiotics (e.g., β-lactams) bind to the bacterial enzyme called transpeptidase.
  • This blocks the transpeptidation process, which is essential for forming peptidoglycan, a major component of the bacterial cell wall.
  • As a result, peptidoglycan synthesis is stopped, and the cell wall becomes weakened.
  • This leads to leakage of cellular contents.
  • The cell wall swells and eventually ruptures.
  • Finally, this causes bacterial cell death.
The diagram on the right visually shows how failure of peptidoglycan cross-linking leads to the breakdown of the cell wall — this is referred to as the bactericidal effect.

Mechanism of Protein Synthesis Inhibitor

Mechanism-of-Protein-Synthesis-Inhibitor
This image explains how bacterial protein synthesis is inhibited. (Simple Explanation)

Protein Synthesis Inhibitor:
  • Certain antibiotics such as Macrolide, Tetracycline, and Aminoglycoside act on the bacterial ribosome.
Binding to the 50S Ribosomal Subunit:

  • These antibiotics bind to the 50S subunit of the bacterial ribosome.
Inhibits Protein Synthesis:

  • As a result of this binding, the bacteria are unable to produce essential proteins.
Leads to inhibition of bacterial growth and reproduction:
  • Since proteins are not produced, the bacteria stop growing and multiplying.
On the right side of the image, various parts of the ribosome are shown, such as the A site, transferase site, mRNA template, and tRNA, and their roles are illustrated.
  • Bacteria also make their own food – they produce a type of food called protein which helps them survive and grow.
  • These medicines (like macrolides and tetracyclines) enter the bacteria's "kitchen"!
  • The bacteria's "kitchen" is a part of their body called the 50S ribosome.
  • The medicines shut down this kitchen, so the bacteria can no longer make their food (proteins).
  • Without food, the bacteria become weak and eventually die.
This is how medicine protects our body from illness.

Mechanism of Nucleic Acid (DNA & RNA) Synthesis Inhibitor

Mechanism-of-Nucleic-Acid-Synthesis-Inhibitor
This image illustrates the mechanism of action of a class of antibiotics called Quinolones, which are Nucleic Acid (DNA & RNA) Synthesis Inhibitors.

Main Parts of the Image

Structure of Quinolones: On the left side, a chemical structure is shown, which represents a quinolone antibiotic.

Mechanism of Action: Quinolones inhibit the topoisomerase enzyme in bacteria.

On the right side, the image shows how quinolones affect bacterial DNA:
  • Quinolones inhibit an enzyme called topoisomerase in bacteria, which is essential for uncoiling DNA.
  • Inhibition of this enzyme causes DNA damage and accumulation of Reactive Oxygen Species (ROS).
As a result, the bacteria die.

Contribution to Antibiotic Resistance:
  • The use of quinolones leads to the selection of bacteria that are resistant to them.
  • It can also induce resistance to other types of antibiotics.
  • In summary, this image explains how quinolones destroy bacterial DNA and how they can contribute to the growing problem of antibiotic resistance.
Mechanism-of-Nucleic-Acid-Synthesis-Inhibitor1
This image explains how a medicine kills bacteria by stopping the production of nucleic acid (DNA and RNA) in a simple way.

Let’s explain it in simple language:

Medicine Name: Moxifix

1. Moxifix blocks two important enzymes in bacteria-
  • Topoisomerase II (DNA Gyrase)
  • Topoisomerase IV
2. When these two enzymes are blocked, the bacteria cannot produce their DNA.

3 Without making DNA, the bacteria cannot survive or grow.

4 As a result, Moxifix quickly kills the bacteria (Rapid Bactericidal Activity).

In short:

*Moxifix stops bacterial DNA production, so the bacteria die very quickly.

*The Magic Medicine That Kills Bacteria: Moxifix

READ MORE: Basic medical terminology with dosage forms and packaging types | MPO training 14

*Imagine bacteria have a tiny copy machine that helps them make copies of themselves.

*To run this machine, they need two buttons — one called DNA Gyrase and the other called Topoisomerase IV.

*A medicine named Moxifix comes in and turns off both of these buttons!
  • As a result, the bacteria can no longer make copies of themselves.
  • If they can’t copy themselves, they can’t grow.
  • Eventually, they become weak and die.
This is how Moxifix quickly kills bacteria and keeps us healthy.

Mechanism of Cell Membrane Disruptor

Mechanism-of-Cell-Membrane-Disruptor
This image explains the mechanism of action of Colistimethate Sodium (Xylistin) or Colistin, an antibiotic belonging to the Cell Membrane Disruptor class.

Main Content of the Image:

Colistimethate Sodium (Colistin): It is an antibiotic of the polymyxin class.

Step-by-step Mechanism:
  • Colistin binds to the lipopolysaccharides of the bacterial cell membrane.
  • It then destabilizes the lipopolysaccharide structure.
  • As a result, the cell membrane is disrupted.
Mode of Action in Short: Colistimethate Sodium has a high binding affinity for lipopolysaccharides, which leads to the disruption of the bacterial cell membrane and ultimately kills the bacteria.

In summary, the image shows how Colistin destroys the bacterial cell membrane and explains its mechanism in a step-by-step manner.

Therapy-Resistance-Carrier Stage

Switch Therapy

  • Switching from intravenous (IV) to Oral dosage form is called Switch Therapy. 
  • Example: Ceftriaxone (Trizon) —> Switching to —> Cefixime (Fix-A)
Switch-Therapy

Antibiotic Resistance

Antibiotic resistance is the ability of a bacterial cell to resist the harmful effect of an antibiotic.

Two types of bacterial resistance:
  • Plasmid Resistance
  • Enzymatic Resistance

Plasmid Resistance

Acquisition of antibiotic resistance occurs when genetic material is taken up by the bacterial cell and either incorporated into the chromosome, or, that is able to exist in a stable form independent of the chromosome.

Such stable genetic elements that can not only exist but that can replicate (reproduce) independently of the chromosome, are known as plasmids.

If the genetic information encoded (fixed) by a plasmid leads to resistance against a particular antibiotic, this plasmid is known as a resistance plasmid. Example: MRSA.

Enzymatic Resistance

Enzymatic inactivation of the antibiotic is called enzymatic resistance.

The best known example of enzymatic inactivation of antibiotics is that of the B-lactamases.

These enzymes render B-lactam antibiotics inactive by cleaving the lactam ring of susceptible antibiotics via an irreversible hydroxylation of the amide bond.

b-lactamases are a common resistance mechanism among Gram-positive and Gram-negative organisms, both aerobic and anaerobic.

Cross-resistance

Microorganisms resistant to one drug may also show resistance to a second drug that has a similar mode of action or with similar structure even without being exposed to the second drug. Such a phenomenon is called cross-resistance.

Carrier Stage

It is a condition where a person harbors a pathogenic organism but does not show any symptoms of disease.

After suffering from typhoid many people become carriers of typhoid and spread the disease. 
That is why typhoid should receive sufficient treatment to eradicate the typhoid bacilli.

Methicillin Resistant Staphylococcus aureus

MRSA stands for Methicillin-Resistant Staphylococcus aureus, a type of bacteria that is resistant to several antibiotics.

These strains are resistant to penicillin, amoxicillin and beta lactam agents including cephalosporin.

Delafloxacin is effective against MRSA.

Post-Antibiotic Effect

PAE is the effect of the antibiotic during the period between removal of the antibiotic and the complete recovery of normal bacterial growth.
  • PAE = T - C 
PAE (Post-antibiotic effect): Time required for culture to return to logarithmic growth.

T = time required for the viable count to increase 10X above the count at the time the drug is removed from the culture.

C = time required for the count to increase 10X in an untreated culture.

Properties of an Ideal Antibiotic

The properties of an ideal antibiotic are divided on the basis of 4 (four) factors:
  1. Efficacy: The ability to produce an effect.
  2. Safety: The level of side effects / adverse effects of a drug.
  3. Convenience: The flexibility and comfort to take the medicine.
  4. Cost: How much is the expense of treatment with the medicine.

1. Efficacy 

  • Should be broad spectrum, which means able to kill or inhibit both gram-positive and gram-negative pathogens.
  • Should be bactericidal rather than bacteriostatic.
  • Absorption and distribution of the drug should be rapid.
  • Should be excreted through urine in an active unchanged form to be effective in UTI.
  • MIC against culprit pathogens must be lower than that of Peak plasma concentration (Cmax).
  • Microorganisms should not be able to develop resistance.
  • Absorption should be independent of the presence of food in the stomach.
  • Should have antibacterial efficacy that is not reduced by body fluids, exudates, plasma proteins or tissue enzymes.
  • Achieve and maintain bactericidal levels in blood, tissue and body fluids. I.e. CSF.
  • Should not be contraindicated with other drugs.

2. Safety

  • Should be suitable for all age groups and sex.
  • Bacterial resistance in target pathogens should be no or very low.
  • Should be safe for pregnant or lactating mothers.
  • Side effects of the drug should be as low as possible.

3. Convenience

  • Should be long acting rather than short acting.
  • Should not have unpalatable after taste of the drug.
  • Should be available both in oral and parenteral form.
  • Should possess a short duration of therapy.

4. Cost

  • Drugs should be cost effective.

Minimum inhibitory and bacterial concentration

MIC (Minimum Inhibitory Concentration)

Minimum Inhibitory Concentration is the lowest concentration of an antibiotic in the plasma that inhibits the growth of target pathogens.

Example: MICg0S (µg/ml) of Ciprofloxacin against E.coli is 0.03, which means that 0.03 µg/ml concentration of ciprofloxacin is effective to inhibit 90% growth of the E. coli.

MBC (Minimum Bactericidal Concentration)

Minimum Bactericidal Concentration is the lowest drug concentration in the plasma that kills the target pathogen.

Example: The MBC of Ciprofloxacin against E.coli is 0.004 (mg/l), which means that 0.004 mg/l concentration of ciprofloxacin is effective to kill 99.9% of the E. coli.

Penicillin antibiotics explain in details

Classification of Penicillin

A. Natural Penicillin: Phenoxy methyl Penicillin (Pen-V)

B. Semisynthetic Penicillin
  • Beta lactamase resistant penicillin : Flucloxacillin 
  • Non Beta lactamase resistant penicillin : Amoxicillin

Strengths of Penicillin

  • Broad spectrum of activity
  • Higher safety profile in children and pregnant mothers
  • Lesser side effects
  • Convenient dosage schedule

Weakness of Semisynthetic Penicillin

  • Penicillin is inactivated by beta lactamases and are therefore not effective against most Staphylococcal infections.
  • Inactive against Pseudomonas aeruginosa.
  • Cross-allergenicity exists between all types of penicillins.
  • Amoxicillin is not useful in the treatment of Shigella and Salmonella infections.
  • Hypersensitivity reactions.

Cephalosporins generations antibiotic explain in details

Cephalosporins are semisynthetic antibiotics that are derived from fungi cephalosporium (Cephalosporium acremonium).

Side chain modifications to the nucleus of beta lactam ring offers:
  • An improved spectrum of antibacterial activity.
  • Pharmacokinetic advantages.

Strength of Cephalosporins

  • Broad spectrum of antimicrobial activity. 
  • Increasing resistance to destruction by beta-lactamases. 
  • Outstanding safety profile in children and pregnant women. 
  • Very good tissue penetration. 
  • Lesser side effects than other antibiotics. 
  • Convenient dosage schedule. 
  • Both oral and parenteral dosage forms are available. 
  • Less allergic than that of penicillin.

Weakness of Cephalosporins

  • Inadequate cerebrospinal fluid penetration of 1 ^ (st) and 2 ^ (nd) generation cephalosporins.
  • Limited activity against enterococci and pseudomonas.
  • Gram positive coverage diminishes with each successive generation of cephalosporins.
  • Diarrhoea has more common side effects with 2 ^ (nd) and 3 ^ (rd) generation.
  • Patients who have a history of penicillin allergy should avoid cephalosporins.

Difference between Generation of Cephalosporins

Generation of Cephalosporins Activity against gram Positive organisms Activity against grame negativelorganisms
1st generation ++++ ++
2nd generation +++ +++
3rd generation ++ ++++
4th generation +++ ++++

Here,
  • Higher coverage = ++++
  • Moderate coverage = +++
  • Lesser coverage = ++

First Generation Cephalosporins

Strengths:
  • Good activity against staphylococci, streptococci, pneumococci, some anaerobic cocci.
  • Prophylaxis of wound infections following surgery, SSTI.
  • Used as Alternative to penicillin in penicillin-allergic individuals.
Weakness:
  • Weaker gram negative coverage.

Second Generation Cephalosporins

Strengths:
  • Extended gram negative coverage against Klebsiella, Proteus, Haemophilus, E.coli and Moraxella.
  • Used to treat abdominal and gynecological infections, UTI & Lower RTI.
Weaknesses:
  • Poor activity against P. aeruginosa.
  • Not active against Salmonella typhi, atypical pathogen and anaerobic bacteria.

Third Generation Cephalosporins

Strengths:
  • Extended activity against gram negative bacilli, particularly enterobacteriaceae & H. influenzae.
  • Few side effects and less allergenic than penicillin.
  • Important drugs for treating bacterial meningitis.
  • Ceftazidime is active against P. aeruginosa and safe for neonates from day one.
  • Can be used in renal dysfunction without any dose adjustment.
  • Ceftriaxone is the safest treatment option for paediatric patients in typhoid/enteric fever.
Weaknesses:
  • Reduced activity against S. aureus.
  • More resistant to non-Staphylococcus ẞ-lactamase.

Fourth Generation Cephalosporins

Strengths:
  • Increased gram positive cocci activity against S. viridians and penicillin resistant pneumococcus.
  • More effective against Enterobacteriaceae.
  • Improved resistance to beta lactamases compared to the third generation.
Weaknesses:
  • Not indicated in children.
  • Not active against Klebsiella.
  • Need to combine with aminoglycoside to cover P. aeruginosa.

Macrolides generations antibiotic explain in details

Macrolides are a large group of antimicrobials derived from Actinomycetes (soil bacteria) or semi synthetic derivatives of them.

Macrolides are characterized chemically by a large "macrocyclic" ring structure.

The structural differences in Macrolides make them ideal alternatives to penicillin in patients who have penicillin allergies.

READ MORE: Basic pharmacology for medical promotion officers | MPO training 13

Pseudomonas, E.coli and Klebsiella strains are resistant to erythromycin.

Pneumococci that are resistant to penicillin are resistant to macrolides.

Erythromycin does interact adversely with drugs oxidized by Cytochrome p-450 eg, Simvastatin, Theophylline.

Macrolides Generations

  1. First generation : Erythromycin (Erocin)
  2. Second generation : Azithromycin (Azin), Clarithromycin (Claricin), Roxithromycin 
  3. Third generation : Telithromycin, Cethromycin and Solithromycin.

Advantages of Azithromycin over Erythromycin

The addition of Nitrogen at position 9a of the lactone ring gives azithromycin:
  • Decrease GI side effects
  • Increase Spectrum of activity
  • Fewer drug interactions
  • Less frequent dosing (increase compliance)
  • Better tissue penetration

Fluoroquinolone generations antibiotic explain in details

The fluoroquinolones are a series of synthetic antibacterial agents that are used in the treatment of a variety of bacterial infections. All fluoroquinolones accumulate within bacteria very rapidly.

Classification:
  1. First generation : Nalidixic acid (Naligram)
  2. Second generation : Ciprofloxacin (Cipro-A)
  3. Third generation : Levofloxacin (Leo)
  4. Fourth generation : Moxifloxacin (Moxifix), Delafloxacin (Delaflox).

Strengths of Fluoroquinolones

  • Potent activity against gram negative pathogens.
  • Long acting than penicillin / erythromycin / cephalosporins.
  • Suitable for treatment of bacterial infections due to multidrug resistant organisms.
  • Excellent activity against S. typhi and all strains of Enterobacteriaceae.
  • Patients who are allergic to the penicillin, cephalosporins, sulfonamides, erythromycin can shift to fluoroquinolones.
  • Able to be active against plasmid mediated resistance of bacteria in case of MRSA.
  • Superb synergistic effect with metronidazole.

Weakness of Fluoroquinolones

Fluoroquinolones are not recommended for children, pregnant or breastfeeding mothers due to bone development problems.

Not useful against infections caused by anaerobes.

Fluoroquinolones may cause phototoxicity from exposure to sunlight.

Bioavailability of all quinolones is impaired by di and trivalent cations in stomach (eg. Al+++, Ca++, Mg++, Fe++, Zn++, as in vitamins with zinc or iron or in antacids).

First Generation Fluoroquinolones

Strengths:
  • Activity against gram negative organisms.
Weaknesses:
  • More frequent dosing.
  • Susceptible more to development of bacterial resistance.
  • Minimum serum level is achieved, so use of drugs has been restricted in UTI.

Second Generation Fluoroquinolones

Strength:
  • Very active against aerobic gram-negative bacilli.
  • Has excellent oral bioavailability.
  • Excellent activity against S.typhi and all strains of Enterobacteriaceae.
  • Able to be active against plasmid mediated resistance of bacteria in case of MRSA.
  • Increase gram negative, gram positive and atypical pathogen coverage.
  • Because of good penetration into the bone, orally administered ciprofloxacin is a useful alternative to parenterally administered antibiotics for osteomyelitis.

Second Generation Fluoroquinolones

Limitations:
  • Is not active against anaerobes.
  • Has only limited activity against streptococci and staphylococci.
  • S. pneumoniae is frequently resistant to this class.

Third Generation Fluoroquinolones

Strength:
  • Expanded activity against gram-positive organisms, particularly penicillin-sensitive and penicillin-resistant S. pneumoniae, and atypical pathogens such as Mycoplasma pneumoniae and Chlamydia pneumoniae.
  • Treatment of community-acquired pneumonia, acute sinusitis and acute exacerbations of chronic bronchitis - primary FDA-labeled indications.
Limitation:
  • Less active against P. aeruginosa species
  • Significant risk of phototoxicity.

Fourth Generation Fluoroquinolones

Strengths:
  • Significant antimicrobial activity against anaerobes while maintaining the gram-positive and gram-negative activity of the third-generation quinolones.
  • Retains activity against Pseudomonas species comparable to that of ciprofloxacin.
  • Originally labeled by the FDA for the treatment of a wide spectrum of infectious diseases.

Aminoglycosides antibiotics explain in details

Aminoglycosides are a group of antibiotics that are used to treat certain bacterial infections.

This group of antibiotics includes:
  • Amikacin
  • Gentamicin
  • Kanamycin
  • Neomycin
  • Streptomycin
  • Tobramycin

Aminoglycosides antibiotics Mechanism of action

  • Aminoglycoside attaches to a bacterial cell wall and is drawn into the cell via channels made up of the protein, porin.
  • Once inside the cell, the aminoglycoside attaches to the cell's ribosomes.
  • This attachment either shuts down protein production or causes the cell to produce abnormal, ineffective proteins.
  • And the bacterial cell eventually destroys.

(Aminoglycoside + Beta lactam) combination

When Aminoglycocides are given with beta lactam antibiotics, it gives synergistic effects in case of all common gram-positive and gram-negative infections.

Beta-lactamase disrupts the integrity of the bacteria cell wall, making it more porous. The increased porosity allows more of the aminoglycoside into the bacteria cell.

Strength of Aminoglycosides

  • Amikacin - Least susceptible to resistance.
  • Aminoglycosides are often included in combination antibiotic regimens for polymicrobial infections and for prophylaxis in surgery.
  • Active against Pseudomonas aeruginosa klebsiella pneumoniae, enterobacteriaceae, serratia and proteus species.
  • Reserved for serious infection due to aerobic gram negative bacilli.

Weakness of Aminoglycosides

  • Ototoxicity
  • Nephrotoxicity
  • Poor crossing of blood brain barrier
  • Narrow therapeutic range - not greater than 2mcg/ml
  • Not active against Streptococci, Pneumococci, and Enterococci

Tetracycline antibiotics explain in details

The antibiotic effect of tetracycline is based on an inhibition of the ribosomal protein synthesis of the bacteria. The tetracycline ties up at a special connection place of the ribosome. Thus the complete formation of the protein chain is interrupted and prevents the reproduction process of the bacteria.

Examples:
  • Tetracycline
  • Oxytetracycline
  • Doxycycline (Doxy-A)
  • Minocycline

Advantages of Doxycycline over Tetracycline

  • Improved admission in the intestine than tetracycline.
  • Gastro-intestinal side effects are reduced than tetracycline.
  • Increased compatibility than tetracycline.

Weakness of Tetracyclines

  • Tetracyclines may cause yellowish discoloration of the teeth.
  • Many streptococcus and pneumococcus strains have become resistant to tetracyclines.
  • Most S. aureus, most bacteroides, some mycoplasma, and all Pseudomonas aeruginosa strains are resistant.
  • Tetracyclines are contraindicated in pregnancy because of fetal bone growth inhibition.

Cotrimoxazole

Cotrimoxazole is the combination of sulfamethoxazole and trimethoprim. These drugs have a wide range of antimicrobial activity against gram-positive and gram-negative bacteria by providing synergistic action.
MOA-OF-TRIMETHOPRIM-SULFAMETHOXAZOLE
This image explains the step-by-step mechanism of action of the antibiotic combination Trimethoprim-Sulfamethoxazole.

Step-by-step process:
1. PABA (Para-Aminobenzoic Acid) is a component used by bacteria to make folic acid.

2. Sulfonamides (e.g., Sulfamethoxazole)
  • Inhibit the enzyme Tetrahydro Pteroic acid synthase, preventing the formation of;
3. Dihydrofolic acid.
  • This blocks the first step of folic acid synthesis.
4. Trimethoprim
  • Inhibits the enzyme Dihydrofolate reductase, which converts Dihydrofolic acid into Tetrahydrofolic acid.
  • This blocks the next step needed for purine and DNA synthesis.
Summary:
  • Sulfamethoxazole blocks the first step in folic acid production.
  • Trimethoprim blocks the final step in the conversion.
  • As a result, DNA synthesis is disrupted, and the bacteria cannot grow or survive.
  • This combination is very effective in stopping bacterial growth.

Mechanism of action

  • Sulfamethoxazole and trimethoprim both act by inhibiting the synthesis of folic acid.
  • Sulfonamide inhibits the formation of dihydrofolic acid from PABA (Para Amino Benzoic Acid).
  • Trimethoprim inhibits the formation of tetrahydrofolic acid from dihydrofolic acid.
  • Thus they are used in combination to produce great synergistic effects.

Meropenem antibiotics

Meropenem is an antibiotic of Carbapenem Group. Meropenem is used after initial therapy when cephalosporins or penicillins have been ineffective.

Meropenem is useful for the treatment of serious hospital-acquired or mixed infections in which aerobic and anaerobic gram-negative bacilli plus S. aureus might be involved.

Indications

  • Intra-abdominal infections.
  • Septicaemia.
  • Empiric treatment, including initial monotherapy, for presumed bacterial infections in host compromised, neutropenic patients.
  • Meningitis.
  • Lower RTI.
  • Gynecological infections, including postpartum infections.
  • Complicated UTI.

Classification Chart With ACME Brand and Generic

Since I worked at Acme Laboratories Limited, I am providing the names and generic names of Acme Laboratories Limited's antibiotic drugs as examples. You should memorize the antibiotic drugs of the pharmaceutical company in which you will work.

Classification Chart of ACME's Antibiotic

Classification-Chart-of-ACMEs-Antibiotic

Therapeutic Class - Antibiotic:

1. Beta-lactam
  • Penicillin
  • Cephalosporin
  • Carbapenem
2. Macrolides

3. Fluoroquinolones

4. Tetracycline

5. Polypeptides

Details:
Classification-Chart-of-ACMEs-Antibiotic-in-details

1. Beta-lactam

Penicillin: Cloxacillin (A-Clox), Flucloxacillin (A-Flox), Amoxicillin (Moxilin)

Cephalosporin:
  • 1st generation: Cephradine (Sefril), Cefadroxil (Twicef)
  • 2nd generation: Cefaclor (Alcior), Cefuroxime (Famicef)
  • 3rd generation (Oral): Cefixime (Fix-A), Cefpodoxime (CP), Ceftibuten (Logibec)
  • 3rd generation (Parenteral): Ceftriaxone (Trizon), Ceftazidime (Trizidim)
  • 4th generation: Cefepime (Superpime)
Carbapenem: Meropenem (Fulspec)
Classification-Chart-of-ACMEs-Antibiotic-in-details1

Macrolides

  • Azithromycin (Azin), Clarithromycin (Claricin), Erythromycin (Erocin)

Fluoroquinolones

  • 1st generation: Nalidixic acid (Naligram)
  • 2nd generation: Ciprofloxacin (Cipro-A)
  • 3rd generation: Levofloxacin (Leo)
  • 4th Generation: Moxifloxacin (Moxifix), Delafloxacin (Delaflox)

Tetracycline

  • Tetracycline (A-Tetra), Doxycycline (Doxy-A)

Polypeptides

  • Colistimethate Sodium (Xylistin)

Indication Chart of Antibiotic Generic

Indication-Chart-of-Antibiotic-Generic

URTI: Upper Respiratory Tract Infection

  • Erythromycin
  • Cefadroxil

LRTI: Lower Respiratory Tract Infection

  • Amoxicillin
  • Cefepime
  • Ceftazidime
  • Delafloxacin
  • Colistimethate Sodium

UTI: Urinary Tract Infection

  • Cefuroxime
  • Cefuroxime+Clavulanic Acid
  • Cefepime
  • Ceftazidime

Both URTI & LRTI:

  • Cefradine
  • Cefuroxime
  • Cefuroxime+Clavulanic Acid
  • Cefaclor
  • Ceftibuten
  • Cefixime
  • Cefpodoxime Proxetil
  • Azithromycin
  • Clarithromycin
  • Tetracycline
  • Doxycycline

SSSI: Skin and Soft Structure Infection

  • Cloxacillin
  • Flucoxacillin
  • Cefradine
  • Cefadroxil
  • Cefuroxime
  • Ceftriaxone
  • Ceftazidime
  • Cefpodoxime Proxetil
  • Azithromycin
  • Erythromycin
  • Delafloxacin

Typhoid:

  • Cefuroxime+Clavulanic Acid
  • Ceftriaxone
  • Cefixime
  • Azithromycin

Diarrhoea:

  • Ciprofloxacin
  • Azithromycin
  • Tetracycline
  • Doxycycline

STD: Sexually Transmitted Disease

  • Cefixime
  • Azithromycin
  • Tetracycline
  • Doxycycline

Septicemia:

  • Cefepime
  • Ceftazidime
  • Meropenem

CNS Infections: Central Nervous System Infections

  • Ceftazidime
  • Meropenem
  • Ceftriaxone

Intra abdominal Infections:

  • Ceftazidime
  • Meropenem
  • Cefepime

Oral & Parenteral Antibiotic Brands of ACME Laboratories Ltd.

Only Oral:
  • Cephalosporin Antibiotic: Sefril, Twicef, Famiclav, Alclor, Logibac, Fix-A, CP.
  • Non Cephalosporin Antibiotic: A-Clox, Moxilin, A-Tetra, Doxy-A, Azin, Erocin, Claricin, Leo.
Only Parenteral: Trizon, Superpime, Trizidim, Fulspec, Delaflox, Xylistin.

Both Oral & Parenteral: Famicef, A-Flox, Cipro-A, Moxifix.

Oral-and-Parenteral-Antibiotic-Brands-of-ACME-Laboratories-Ltd

FAQs about basic information about antibiotics and generic drugs

1. Do antibiotics work against viruses?
No, antibiotics do not work against viruses like the flu, cold, or COVID-19. Antibiotics only treat bacterial infections.

2. Can we stop taking antibiotics once I feel better?
No. We should always complete the full course as prescribed by a doctor to make sure all bacteria are fully removed.

3. What happens if antibiotics are overused?
Overuse or misuse can lead to antibiotic resistance, where bacteria stop responding to the medicine.

4. Are there any side effects of antibiotics?
Yes. Common side effects include stomach upset, diarrhea, allergic reactions, and yeast infections.

5. What is a broad-spectrum antibiotic?
It is an antibiotic that works against a wide variety of bacteria, both gram-positive and gram-negative.

6. What are generic antibiotics?
Generic antibiotics have the same active ingredient, strength, and effect as brand-name drugs but are often more affordable.

Conclusion

You’ve just explored the essential basics of antibiotics and generics—two powerful pillars of the pharma world. For any future Medical Promotion Officer (MPO), this knowledge isn't optional—it’s necessary. By learning the basic information about antibiotics and generic drugs, you're already one step ahead. This article aimed to make things simple and practical. Take this understanding forward as you move closer to your pharmaceutical goals.
Sarwar Hossain Himel

Sarwar Hossain Himel

I am Sarwar Hossain Himel, I am a sports lover. Education: BBA & MBA in Accounting. Job: Medical Promotion Officer (MPO) & 5 years of teaching experience. Freelancing: Google blogger & Article Writer. Web Design is my passion.

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