Penicillin, Streptomycin — Revision Notes

⚡ 30-Second Revision

Penicillin: — Beta-lactam antibiotic. Inhibits bacterial cell wall synthesis (peptidoglycan cross-linking) by binding to PBPs. Bactericidal. Natural: Penicillin G (acid-labile, parenteral), Penicillin V (acid-stable, oral). Resistance: Beta-lactamase enzymes. Side effect: Hypersensitivity.
Streptomycin: — Aminoglycoside antibiotic. Inhibits bacterial protein synthesis by binding to 30S ribosomal subunit. Bactericidal. Broad-spectrum. Used for TB. Side effects: Ototoxicity, Nephrotoxicity. Resistance: Ribosomal mutations, enzymatic inactivation.

2-Minute Revision

Penicillin, the first antibiotic, is a beta-lactam drug. Its defining feature is the beta-lactam ring, which is crucial for its action. It works by inhibiting the synthesis of the bacterial cell wall, specifically by blocking the cross-linking of peptidoglycan strands by penicillin-binding proteins (PBPs).

This makes it bactericidal. Natural penicillins like Penicillin G are acid-labile and given parenterally, while Penicillin V is acid-stable and can be taken orally. A major challenge is bacterial resistance, primarily through the production of beta-lactamase enzymes that destroy the beta-lactam ring.

Hypersensitivity reactions are a common side effect.

Streptomycin, an aminoglycoside, operates differently. It targets bacterial protein synthesis by binding irreversibly to the 30S ribosomal subunit. This binding causes misreading of mRNA and premature termination of protein production, leading to bacterial death.

It's a broad-spectrum, bactericidal antibiotic, notably effective against *Mycobacterium tuberculosis*. Its administration is parenteral due to poor oral absorption. Key side effects include ototoxicity (hearing/balance impairment) and nephrotoxicity (kidney damage), which necessitate careful monitoring.

Resistance can arise from ribosomal mutations or enzymatic inactivation.

5-Minute Revision

Let's consolidate our understanding of two pivotal antibiotics: Penicillin and Streptomycin. Penicillin, a member of the beta-lactam class, revolutionized medicine. Its core chemical feature is the strained beta-lactam ring.

This ring is the 'active site' that allows penicillin to irreversibly bind to and inhibit bacterial transpeptidase enzymes, also known as Penicillin-Binding Proteins (PBPs). These PBPs are vital for cross-linking peptidoglycan units, which form the rigid bacterial cell wall.

By blocking this process, penicillin weakens the cell wall, leading to osmotic lysis and bacterial death – hence, it's bactericidal. Natural penicillins like Penicillin G are acid-labile and must be injected, while Penicillin V is acid-stable and can be taken orally.

The Achilles' heel of penicillin is bacterial resistance, predominantly through the production of beta-lactamase enzymes that hydrolyze the beta-lactam ring, rendering the drug inactive. Allergic reactions, including potentially life-threatening anaphylaxis, are its most significant side effect.

Streptomycin, in contrast, belongs to the aminoglycoside class. Its structure features amino sugars linked to an aminocyclitol ring. Its mechanism of action is distinct: it targets the bacterial ribosome, specifically the 30S ribosomal subunit.

Streptomycin binds irreversibly to this subunit, disrupting the initiation of protein synthesis, causing misreading of mRNA codons, and leading to the production of non-functional proteins. This ultimately kills the bacterial cell, making it bactericidal.

Streptomycin is a broad-spectrum antibiotic, effective against many Gram-negative bacteria and, crucially, *Mycobacterium tuberculosis*. Due to poor oral absorption, it's administered parenterally. However, its use is limited by significant dose-related toxicities: ototoxicity (irreversible damage to hearing and balance) and nephrotoxicity (kidney damage).

Bacterial resistance to streptomycin can occur via ribosomal mutations or enzymatic modification of the drug. Understanding these distinct mechanisms and side effect profiles is key for NEET.

Prelims Revision Notes

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Antibiotics Definition: — Chemicals from microorganisms/synthetic, inhibit/kill other microbes, selectively toxic.
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Penicillin (Beta-Lactam):

* Discovery: Alexander Fleming (1928), mass production by Florey & Chain. * Structure: Contains a beta-lactam ring (four-membered cyclic amide) fused to a thiazolidine ring. R-group varies.

* Mechanism: Bactericidal. Inhibits bacterial cell wall synthesis. Binds to and inactivates Penicillin-Binding Proteins (PBPs), which are transpeptidases for peptidoglycan cross-linking. Leads to cell lysis.

* Types: * Natural: Penicillin G (benzylpenicillin) - acid-labile, parenteral. Penicillin V (phenoxymethylpenicillin) - acid-stable, oral. * Semi-synthetic: Methicillin (penicillinase-resistant), Ampicillin/Amoxicillin (extended spectrum).

* Spectrum: Natural penicillins are narrow-spectrum (mainly Gram-positive). * Resistance: Most common is production of beta-lactamase enzymes (penicillinase) that hydrolyze the beta-lactam ring.

* Side Effects: Hypersensitivity reactions (rash, anaphylaxis).

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Streptomycin (Aminoglycoside):

* Discovery: Selman Waksman (1943) from *Streptomyces griseus*. * Structure: Aminosugars linked by glycosidic bonds to an aminocyclitol (streptidine) ring. * Mechanism: Bactericidal. Inhibits bacterial protein synthesis.

Binds irreversibly to the 30S ribosomal subunit, causing mRNA misreading and premature termination of translation. * Spectrum: Broad-spectrum. Effective against many Gram-negative aerobes and *Mycobacterium tuberculosis*.

* Administration: Parenteral (poor oral absorption). * Resistance: Ribosomal mutations (altering 30S subunit), enzymatic inactivation (aminoglycoside-modifying enzymes), decreased uptake. * Side Effects: Ototoxicity (irreversible hearing loss/vestibular damage), Nephrotoxicity (reversible kidney damage), Neuromuscular blockade.

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Key Concepts: — Selective toxicity, bactericidal, bacteriostatic, narrow-spectrum, broad-spectrum.
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Comparison: — Penicillin (cell wall, beta-lactam) vs. Streptomycin (protein synthesis, aminoglycoside).

Vyyuha Quick Recall

Penicillin Cracks Walls, Streptomycin Prevents Proteins.

Penicillin: Cell Wall synthesis inhibitor.
Streptomycin: Protein Production inhibitor (30S ribosome).

Streptomycin's Outstanding Nuisances: Ototoxicity & Nephrotoxicity.