Penicillin, Streptomycin — Core Principles

Core Principles

Antibiotics are chemical agents that selectively kill or inhibit the growth of bacteria. Penicillin, discovered by Alexander Fleming, was the first antibiotic, belonging to the beta-lactam class. Its core structure features a beta-lactam ring, which is crucial for its action.

Penicillin works by inhibiting bacterial cell wall synthesis, specifically by inactivating transpeptidase enzymes (penicillin-binding proteins) that cross-link peptidoglycan. It is primarily bactericidal and effective against Gram-positive bacteria.

Bacterial resistance often arises from beta-lactamase enzymes that hydrolyze the beta-lactam ring.

Streptomycin, discovered by Selman Waksman, is an aminoglycoside antibiotic. Its structure contains amino sugars linked to an aminocyclitol ring. Streptomycin is bactericidal and inhibits bacterial protein synthesis by binding irreversibly to the 30S ribosomal subunit, causing mRNA misreading and production of non-functional proteins.

It has a broad spectrum, notably effective against Gram-negative bacteria and *Mycobacterium tuberculosis*. Key side effects include ototoxicity (hearing/balance loss) and nephrotoxicity (kidney damage).

Both antibiotics exemplify selective toxicity, targeting bacterial processes absent or different in human cells.

Important Differences

vs Streptomycin

Aspect	This Topic	Streptomycin
Class of Antibiotic	Penicillin (Beta-Lactam)	Streptomycin (Aminoglycoside)
Chemical Structure Key Feature	Contains a beta-lactam ring fused to a thiazolidine ring.	Composed of amino sugars linked by glycosidic bonds to an aminocyclitol (streptidine) ring.
Mechanism of Action	Inhibits bacterial cell wall synthesis by inactivating transpeptidase enzymes (PBPs).	Inhibits bacterial protein synthesis by binding irreversibly to the 30S ribosomal subunit.
Primary Target in Bacteria	Bacterial cell wall (peptidoglycan synthesis).	Bacterial 30S ribosomal subunit.
Spectrum of Activity (Natural Forms)	Narrow-spectrum, primarily Gram-positive bacteria and some Gram-negative cocci.	Broad-spectrum, effective against many Gram-negative aerobic bacteria and *Mycobacterium tuberculosis*.
Mode of Administration (Natural Forms)	Penicillin G: Parenteral (acid-labile); Penicillin V: Oral (acid-stable).	Parenteral (intramuscular/intravenous) due to poor oral absorption.
Key Resistance Mechanism	Production of beta-lactamase enzymes that hydrolyze the beta-lactam ring.	Ribosomal mutations, enzymatic inactivation by aminoglycoside-modifying enzymes, decreased uptake.
Major Side Effects	Hypersensitivity reactions (rashes, anaphylaxis), gastrointestinal disturbances.	Ototoxicity (hearing/balance loss), nephrotoxicity (kidney damage), neuromuscular blockade.

Penicillin and streptomycin, while both bactericidal antibiotics, differ fundamentally in their chemical structures, cellular targets, and mechanisms of action. Penicillin, a beta-lactam, disrupts bacterial cell wall synthesis, primarily targeting Gram-positive bacteria. Its efficacy is often compromised by beta-lactamase enzymes. Streptomycin, an aminoglycoside, inhibits bacterial protein synthesis by binding to the 30S ribosome, effective against a broader range including Gram-negative bacteria and *Mycobacterium tuberculosis*. However, it carries risks of ototoxicity and nephrotoxicity. Understanding these distinctions is crucial for appropriate therapeutic selection and for NEET aspirants to grasp the diverse strategies of antimicrobial drugs.