Antibiotics Types And Side Effects: History, How it Works, Types

Edited By Team Careers360 | Updated on Jul 02, 2025 05:24 PM IST

Antibiotics are a powerful group of drugs that fight infections and can even save lives if used correctly. They work by stopping the growth of bacteria or killing them completely. But our immune system kills bacteria before they multiply and cause symptoms. While white blood cells attack harmful bacteria that cause symptoms, our immune system usually fights infection. Unable to fight them, sometimes antibiotics are used.

This Story also Contains

History Of Antibiotic
How Do Antibiotics Work?
Type Of Antibiotic
Antibiotic Resistance
Side Effects Of Antibiotics

Antibiotics Types And Side Effects: History, How it Works, Types

If you know what penicillin is, you know that it was the first antibiotic discovered and is used to treat certain infections. There are also a number of topical antibiotics available as OTC ointments and creams.

History Of Antibiotic

Initially, antibiotics were derived from microorganisms. Antibiotics were developed synthetically in late years after advances in synthetic methods.

In the 19th century, German bacteriologist Paul Ehrlich began searching for chemicals that could kill bacteria in both humans and animals, but without affecting health. After conducting some research, he discovered a drug called Arsphenamine, also known as Salvarsan. It is used to treat syphilis caused by spirochetes. He won the Nobel Prize in 1908. The drug had some side effects, but its effect on bacteria was far greater than on humans.

In 1932, another drug called Prontosil was discovered by a group of researchers at the Bayer Institute. It was very similar to salvarsan, which tends to convert to sulfanilamide when ingested.

But the real change in antibacterial treatment came in 1929 when Alexander Fleming discovered a natural antibiotic called penicillin.

How Do Antibiotics Work?

There are many different types of antibiotics, but they work in two basic ways.

1. Some antibiotics, like penicillin, tend to dislodge bacteria when they kill them. They usually do this by interfering with the formation of the bacterial cell contents or cell wall.

2. Other types of antibiotics inhibit the growth of bacteria.

Type Of Antibiotic

Antibiotics is usually classified based on their chemical structure. Antibiotics with the same structural class have similar properties in terms of efficacy, sensitizing and toxicity. Some of them are-

Penicillin
macrolide
Sulfonamide
Cephalosporins
Tetracycline system
Fluoroquinolone
Aminoglycoside

Depending on how they work to prevent bacterial infections, they are classified as:

Bactericidal: Tends to destroy pathogenic bacteria in the body. For example, penicillin and polymyxin are among them.
Bacteriostatic: A drug used to inhibit the growth of microorganisms. Examples include chloramphenicol and tetracycline.

NEET Highest Scoring Chapters & Topics

This ebook serves as a valuable study guide for NEET exams, specifically designed to assist students in light of recent changes and the removal of certain topics from the NEET exam.

Download EBook

Depending on the spectrum of antibiotics, they are divided into two categories:

Wide range:

These are drugs that inhibit or destroy the growth of a wide range of Gram-positive and Gram-negative bacteria. For example amoxicillin

Narrow spectrum:

These types of antibiotics usually attack gram-positive or gram-negative bacteria. For example, penicillin G

Limited spectrum:

These antibiotics are also effective against certain types of organisms and diseases.

Antibiotic Resistance

The emergence of bacterial resistance to antibiotics is a very common phenomenon. The emergence of bacterial resistance reflects the evolutionary processes that occur during antibiotic treatment. Antibiotic therapy may tend to select bacterial strains that are genetically or physiologically enhanced to tolerate higher doses of antibiotic drugs. Under some conditions, the growth of resistant bacteria may be favourable, while the growth of sensitive bacteria is inhibited by antibiotics.

Side Effects Of Antibiotics

Antibiotics are usually tested several times before clinical use. However, there are still some negative effects in using it. Side effects are generally less severe and include common side effects such as nausea, loose stools (faeces), and diarrhea.

Some side effects of antibiotics include:

Anorexia
Increased appetite
nosebleed
gout
Hepatotoxicity
hiccups
hyperkalemia
Arthralgia(joint pain)
Nephrolithiasis(kidney stones)
Decreased libido
Libido, increase
muscle pain (muscle pain)
nasal congestion

Frequently Asked Questions (FAQs)

1. How do antibiotics work?

There are many different types of antibiotics, but they work in two basic ways-

1. Some antibiotics, like penicillin, tend to dislodge bacteria when they kill them. They usually do this by interfering with the formation of the bacterial cell contents or cell wall.

2. Other types of antibiotics inhibit the growth of bacteria.

2. What are the Types of antibiotics based on the same structural class and similar properties?

The Types of antibiotics based on the same structural class and similar properties are-

Penicillin
macrolide
Sulfonamide
Cephalosporins
Tetracycline system
Fluoroquinolone
Aminoglycoside

3. Depending on the spectrum of antibiotics, how are they classified?

Depending on the spectrum of antibiotics, they are divided into two categories:

Wide range:

These are drugs that inhibit or destroy the growth of a wide range of Gram-positive and Gram-negative bacteria. For example amoxicillin

Narrow spectrum:

These types of antibiotics usually attack gram-positive or gram-negative bacteria. For example, penicillin G

Limited spectrum:

These antibiotics are also effective against certain types of organisms and diseases.

4. Write about the Side effects of antibiotics?

Some side effects of antibiotics include:

Anorexia
Increased appetite
nosebleed
gout
Hepatotoxicity
hiccups
hyperkalemia
Arthralgia(joint pain)
Nephrolithiasis(kidney stones)
Decreased libido
Libido, increase
muscle pain (muscle pain)
nasal congestion

5. What do you mean by Antibiotic Resistance?

The emergence of bacterial resistance to antibiotics is a very common phenomenon. The emergence of bacterial resistance reflects the evolutionary processes that occur during antibiotic treatment. Antibiotic therapy may tend to select bacterial strains that are genetically or physiologically enhanced to tolerate higher doses of antibiotic drugs. Under some conditions, the growth of resistant bacteria may be favorable, while the growth of sensitive bacteria is inhibited by antibiotics.

6. What is antibiotic resistance and why is it a growing concern?

Antibiotic resistance occurs when bacteria evolve to survive exposure to antibiotics. It's a growing concern because it makes infections harder to treat, potentially leading to more severe illnesses, increased healthcare costs, and higher mortality rates. Overuse and misuse of antibiotics accelerate this process.

7. How does antibiotic dosage and duration affect treatment efficacy and resistance development?

Proper dosage and duration are crucial for effective treatment and minimizing resistance. Underdosing or stopping treatment early can leave some bacteria alive, promoting resistance. Overdosing or unnecessarily long treatments can increase side effects and also promote resistance in the broader bacterial population.

8. What is antibiotic stewardship, and why is it important?

Antibiotic stewardship refers to coordinated programs and interventions designed to improve and measure the appropriate use of antibiotics. It's important because it helps preserve antibiotic effectiveness, reduce resistance, decrease healthcare costs, and improve patient outcomes by ensuring the right antibiotic is used at the right time, dose, and duration.

9. What is antibiotic prophylaxis and when is it appropriate?

Antibiotic prophylaxis is the preventive use of antibiotics before certain medical procedures or in high-risk situations. It's appropriate for procedures with a high risk of infection (like some surgeries) or in patients with compromised immune systems. However, overuse can contribute to antibiotic resistance.

10. What is antibiotic synergy, and how is it used in treatment?

Antibiotic synergy occurs when the combined effect of two antibiotics is greater than the sum of their individual effects. This is used in treatment to enhance efficacy, broaden the spectrum of activity, and potentially reduce the development of resistance. A classic example is the combination of trimethoprim and sulfamethoxazole.

11. Who discovered the first antibiotic and how did it revolutionize medicine?

Alexander Fleming discovered penicillin, the first antibiotic, in 1928. This discovery revolutionized medicine by providing a powerful tool to combat bacterial infections that were previously often fatal, dramatically reducing mortality rates and changing the course of medical history.

12. What is the concept of "selective pressure" in the context of antibiotic use and resistance?

Selective pressure refers to the evolutionary force exerted by antibiotics on bacterial populations. When exposed to antibiotics, susceptible bacteria die while resistant ones survive and reproduce. This process selects for resistant strains, especially when antibiotic concentrations are suboptimal. Understanding selective pressure is key to developing strategies to minimize resistance development.

13. What are antibiotics and how do they differ from other medications?

Antibiotics are medications specifically designed to fight bacterial infections. Unlike other drugs that may treat symptoms, antibiotics work by either killing bacteria or preventing their growth. They are ineffective against viruses, fungi, or other non-bacterial pathogens.

14. What is the mechanism of action for beta-lactam antibiotics like penicillin?

Beta-lactam antibiotics, including penicillin, work by interfering with bacterial cell wall synthesis. They bind to and inhibit enzymes called penicillin-binding proteins (PBPs) that are crucial for building the bacterial cell wall, leading to cell lysis and death.

15. How do antibiotics interact with the human immune system?

Antibiotics primarily work by directly affecting bacteria, but they can also interact with the immune system. Some antibiotics may have immunomodulatory effects, either enhancing or suppressing certain immune responses. Additionally, by reducing bacterial load, antibiotics allow the immune system to more effectively clear remaining pathogens.

16. How do aminoglycoside antibiotics work, and what are their major side effects?

Aminoglycosides work by binding to the 30S ribosomal subunit, causing misreading of the genetic code and inhibiting protein synthesis. They are bactericidal but can have serious side effects including kidney damage (nephrotoxicity) and hearing loss (ototoxicity), requiring careful monitoring during use.

17. How do glycopeptide antibiotics like vancomycin differ from other antibiotic classes?

Glycopeptide antibiotics like vancomycin work by inhibiting cell wall synthesis in a different way than beta-lactams. They bind to the D-alanyl-D-alanine terminus of peptidoglycan precursors, preventing cross-linking. They are often used as a "last resort" for resistant gram-positive infections, particularly methicillin-resistant Staphylococcus aureus (MRSA).

18. What role do probiotics play in mitigating antibiotic side effects?

Probiotics are beneficial bacteria that can help restore the balance of gut flora disrupted by antibiotics. They may reduce side effects like diarrhea and yeast infections by competing with harmful bacteria and supporting the immune system. However, timing is important as antibiotics can also kill probiotic bacteria.

19. How do antibiotics distinguish between harmful bacteria and beneficial bacteria in our bodies?

Antibiotics cannot distinguish between harmful and beneficial bacteria. They target specific bacterial structures or processes common to many bacteria types. This is why antibiotics can disrupt the normal gut flora, leading to side effects like diarrhea.

20. How do fluoroquinolone antibiotics work, and why are they sometimes restricted?

Fluoroquinolones work by inhibiting bacterial DNA gyrase and topoisomerase IV, enzymes essential for DNA replication. They are broad-spectrum and effective, but can have serious side effects including tendon damage and nervous system issues. This has led to restrictions on their use for less severe infections.

21. How do sulfonamide antibiotics work, and what are their unique side effects?

Sulfonamides work by inhibiting bacterial folate synthesis, which is essential for DNA production. They act as competitive inhibitors of the enzyme dihydropteroate synthetase. Unique side effects can include photosensitivity and, rarely, severe skin reactions like Stevens-Johnson syndrome.

22. How do tetracycline antibiotics work, and why are they not recommended for children?

Tetracyclines work by binding to the 30S ribosomal subunit, inhibiting protein synthesis in bacteria. They are not recommended for children under 8 years old or pregnant women because they can interfere with bone development and cause permanent tooth discoloration in developing teeth.

23. How do broad-spectrum antibiotics differ from narrow-spectrum antibiotics?

Broad-spectrum antibiotics are effective against a wide range of bacterial types, while narrow-spectrum antibiotics target specific bacterial species. Broad-spectrum antibiotics are often used when the exact pathogen is unknown, but they also have a higher risk of causing resistance and disrupting beneficial bacteria.

24. Why are some antibiotics bactericidal while others are bacteriostatic?

Bactericidal antibiotics (like penicillin) kill bacteria directly, often by disrupting essential cellular processes. Bacteriostatic antibiotics (like tetracycline) inhibit bacterial growth without necessarily killing them, allowing the body's immune system to clear the infection. The distinction is important for treating different types of infections and patients.

25. How do macrolide antibiotics like erythromycin work differently from beta-lactams?

Macrolide antibiotics, such as erythromycin, work by inhibiting bacterial protein synthesis. They bind to the 50S subunit of the bacterial ribosome, preventing the addition of new amino acids to growing peptide chains. This stops bacterial growth without directly killing the cells.

26. What is the difference between empiric and definitive antibiotic therapy?

Empiric therapy involves starting antibiotics based on the most likely pathogens before identifying the specific cause of infection. Definitive therapy is initiated after the causative organism and its antibiotic susceptibility are known. Empiric therapy is broader and may be adjusted to definitive therapy once test results are available.

27. What is the "post-antibiotic effect" and why is it important in dosing strategies?

The post-antibiotic effect refers to the continued suppression of bacterial growth after antibiotic concentrations have fallen below inhibitory levels. This effect varies among antibiotics and bacteria, and is important in determining dosing intervals. Antibiotics with a longer post-antibiotic effect may be administered less frequently.

28. What is the role of combination antibiotic therapy, and when is it typically used?

Combination antibiotic therapy involves using two or more antibiotics simultaneously. It's typically used to broaden the spectrum of coverage for empiric therapy, treat polymicrobial infections, prevent the emergence of resistance, or achieve synergistic effects. Common examples include treatment for tuberculosis or severe hospital-acquired infections.

29. How do antibiotics affect the human microbiome, and what are the long-term consequences?

Antibiotics can significantly disrupt the human microbiome by killing both harmful and beneficial bacteria. This disruption can lead to short-term side effects like diarrhea and yeast infections. Long-term consequences may include increased susceptibility to certain infections, altered metabolism, and potential links to conditions like obesity and autoimmune disorders.

30. What is the mechanism of action for polymyxin antibiotics, and why are they considered "last-resort" drugs?

Polymyxins work by disrupting the bacterial cell membrane, leading to cell death. They bind to lipopolysaccharides in the outer membrane of gram-negative bacteria, causing membrane instability. They're considered "last-resort" due to their potential for serious side effects, particularly kidney damage, and are typically reserved for multidrug-resistant gram-negative infections.

31. How do antibiotics cross the blood-brain barrier, and why is this important for treating central nervous system infections?

Not all antibiotics can cross the blood-brain barrier effectively. Those that do typically have high lipid solubility, low protein binding, or utilize specific transport mechanisms. This ability is crucial for treating central nervous system infections like meningitis. Examples of antibiotics that cross well include fluoroquinolones, metronidazole, and some beta-lactams like ceftriaxone.

32. What is the difference between time-dependent and concentration-dependent antibiotics?

Time-dependent antibiotics (like beta-lactams) are most effective when the concentration is maintained above the minimum inhibitory concentration (MIC) for an extended period. Concentration-dependent antibiotics (like aminoglycosides) are most effective when high peak concentrations are achieved. This distinction affects dosing strategies and administration frequencies.

33. How do antibiotics affect bacterial biofilms, and why are biofilm-associated infections challenging to treat?

Bacterial biofilms are communities of bacteria encased in a self-produced extracellular matrix. Many antibiotics struggle to penetrate biofilms effectively, and bacteria within biofilms often enter a slow-growing state that makes them less susceptible to antibiotics. This makes biofilm-associated infections, such as those on medical implants, particularly challenging to treat.

34. What is the role of efflux pumps in antibiotic resistance, and how do they work?

Efflux pumps are protein structures in bacterial cell membranes that can actively expel antibiotics from the cell. This mechanism contributes to antibiotic resistance by reducing the intracellular concentration of the drug below effective levels. Some bacteria can upregulate or acquire genes for efflux pumps, enhancing their resistance to multiple antibiotics.

35. How do antibiotics interact with other medications, and why is this important to consider in treatment?

Antibiotics can interact with other medications in various ways, including altering drug metabolism, affecting absorption, or competing for elimination pathways. For example, some antibiotics can reduce the effectiveness of oral contraceptives or increase the risk of bleeding with anticoagulants. Understanding these interactions is crucial for safe and effective treatment.

36. How do antimetabolite antibiotics like trimethoprim work, and why are they often combined with other drugs?

Antimetabolite antibiotics like trimethoprim work by interfering with bacterial metabolism, specifically by inhibiting enzymes involved in folate synthesis. Trimethoprim is often combined with sulfamethoxazole (a sulfonamide) because they act on different steps of the same metabolic pathway, creating a synergistic effect that enhances efficacy and reduces the likelihood of resistance development.

37. What is the role of pharmacokinetics and pharmacodynamics in antibiotic dosing and efficacy?

Pharmacokinetics describes how the body processes a drug (absorption, distribution, metabolism, excretion), while pharmacodynamics describes the drug's effects on the body. For antibiotics, understanding these principles is crucial for determining optimal dosing regimens. For example, maintaining drug concentrations above the MIC (pharmacodynamics) depends on how quickly the body eliminates the drug (pharmacokinetics).

38. How do antibiotics affect bacterial gene expression, and how does this relate to resistance development?

Antibiotics can induce changes in bacterial gene expression beyond their primary targets. This can include upregulation of stress response genes, efflux pumps, or alternative metabolic pathways. Some of these changes can contribute to short-term survival and potentially lead to the development of resistance mechanisms over time.

39. What is the significance of the minimum inhibitory concentration (MIC) in antibiotic therapy?

The minimum inhibitory concentration (MIC) is the lowest concentration of an antibiotic that prevents visible growth of a bacterium. It's a key measure of antibiotic susceptibility used to guide treatment decisions. Achieving concentrations above the MIC at the infection site is crucial for effective therapy, while staying below toxic levels to minimize side effects.

40. How do carbapenems differ from other beta-lactam antibiotics, and why are they considered "last-line" agents?

Carbapenems are a class of beta-lactam antibiotics with a broader spectrum of activity and greater resistance to beta-lactamase enzymes compared to other beta-lactams. They're considered "last-line" agents because they're effective against many multidrug-resistant bacteria. However, their use is restricted to prevent the development of resistance, preserving their efficacy for the most serious infections.

41. What is the role of antibiotic adjuvants, and how might they help combat resistance?

Antibiotic adjuvants are compounds that enhance the effectiveness of antibiotics without having direct antibacterial activity themselves. They can work by inhibiting resistance mechanisms, improving antibiotic penetration, or modulating the host immune response. Adjuvants offer a promising strategy to extend the useful life of existing antibiotics and combat resistance.

42. How do antibiotics affect bacterial communication systems like quorum sensing?

Some antibiotics can interfere with bacterial quorum sensing, a communication system that allows bacteria to coordinate their behavior based on population density. Disrupting quorum sensing can affect biofilm formation, virulence factor production, and potentially antibiotic tolerance. Understanding these effects could lead to new strategies for combating bacterial infections.

43. What is the concept of "collateral sensitivity" in antibiotic resistance, and how might it be exploited?

Collateral sensitivity occurs when bacteria that develop resistance to one antibiotic become more susceptible to another. This phenomenon arises from trade-offs in bacterial fitness associated with resistance mechanisms. Exploiting collateral sensitivity, for example through carefully designed antibiotic cycling strategies, could potentially help manage and reduce antibiotic resistance.

44. How do antibiotics interact with the human gut microbiome, and what are the potential long-term health implications?

Antibiotics can cause significant disruptions to the gut microbiome, potentially leading to long-term alterations in its composition and function. This disruption has been associated with various health issues, including increased susceptibility to infections, metabolic disorders, and potential links to conditions like inflammatory bowel disease and allergies. Understanding these interactions is crucial for developing more targeted antibiotic therapies and mitigating negative health impacts.

45. What is the role of horizontal gene transfer in spreading antibiotic resistance, and how does this affect treatment strategies?

Horizontal gene transfer is a process by which bacteria can acquire genetic material, including antibiotic resistance genes, from other bacteria. This can occur through mechanisms like conjugation, transformation, and transduction. It allows for rapid spread of resistance traits between different bacterial species and even genera. Understanding this process is crucial for developing strategies to limit the spread of resistance and informs approaches like combination therapies and antibiotic stewardship programs.

46. How do antibiotics affect bacterial persistence, and why is this important in recurrent infections?

Bacterial persistence refers to a phenomenon where a small subpopulation of bacteria enters a dormant state, becoming tolerant to antibiotics without genetic changes. Antibiotics can induce this state in some bacteria. Persisters can survive antibiotic treatment and later revert to an active state, potentially causing recurrent infections. Understanding persistence is crucial for developing strategies to prevent chronic and relapsing infections.

47. What is the concept of the "mutant selection window" in antibiotic therapy, and how does it relate to resistance development?

The mutant selection window is the range of antibiotic concentrations between the minimum inhibitory concentration (MIC) and the mutant prevention concentration (MPC). Within this window, resistant mutants can be selectively amplified. Maintaining antibiotic concentrations above the MPC can prevent the selection of resistant mutants. Understanding this concept is crucial for designing dosing regimens that minimize the risk of resistance development.