ANTIBIOTICS

ANTIBIOTICS
JAI NARAIN VYAS UNIVERSITY, JODHPUR
ASSISTANT PROFESSOR:- ASHWIN SINGH
CHOUHAN
DEPARTMENT:- PHARMACOLOGY
E-mail:- ashwinsingh26061992@gmail.com

JNVU PHARMACY, JODHPUR
ANTIBIOTICS
Antibiotics are chemical compounds used to kill
or inhibit the growth of bacteria. Strictly speaking,
antibiotics are a subgroup of organic anti-infective agents
that are derived from bacteria or moulds that are toxic to
other bacteria. However, the term antibiotic is now used
loosely to include anti-infectives produced from synthetic
and semisynthetic compounds.
The term antibiotic may be used interchangeably with
the term antibacterial. However, it is incorrect to use the
term antibiotic when referring to antiviral, antiprotozoal
and antifungal agents.

HISTORY OF ANTIBIOTICS
Penicillin was the first antibiotic used
successfully in treating bacterial infections.
Sir Alexander Fleming first discovered it in
1928, but its potential for treatment against
infections wasn’t recognised until over a
decade later when Ernst B Chain, Sir Howard
Florey and Norman Heatley produced enough
purified penicillin to treat patients with. By
the 1950s, a large number of antibiotics
were being discovered and manufactured for
the treatment of diseases caused by
infecting bacteria. Over the last 50 years,
antibiotics have transformed the patterns of
disease and death.

CLASSIFICATION OF ANTIBIOTICS
Antibiotics can be classified in several ways.
The most common method classifies them according to
their chemical structure as antibiotics sharing the same
or similar chemical structure will generally show similar
patterns of antibacterial activity,
effectiveness, toxicity and allergic potential.
B-lactam antibiotics inhibit bacterial cell wall
synthesis. They include:
Penicillins
Cephalosporins
Carbapenems
Penicillins
Penicillin G
Amoxicillin
Flucloxacillin
Cephalosporins
Cefoxitin

Cefotaxime
Ceftriaxone
Carbapenem
Imipenem
Macrolides inhibit bacterial protein synthesis.
Erythromycin
Azithromycin
Clarithromycin
Tetracyclines inhibit bacterial protein synthesis.
 Tetracycline
 Minocycline
 Doxycycline
 Lymecycline
Fluoroquinolones inhibit bacterial DNA synthesis.
Norfloxacin
Ciprofloxacin
Enoxacin
Ofloxacin JNVU PHARMACY, JODHPUR

Sulphonamides block bacterial cell metabolism by
inhibiting enzymes.
Trimethoprim + sulphamethoxazole
Aminoglycosides inhibit bacterial protein
synthesis.
Gentamicin
Amikacin
Imidazole antibiotics inhibit bacterial DNA
synthesis.
Metronidazole
Peptides inhibit bacterial cell wall synthesis.
Bacitracin
Lincosamides inhibit bacterial protein synthesis.
Clindamycin
Lincomycin
The following drugs inhibit bacterial protein
synthesis.
Fusidic acid
Mupirocin

USES OF ANTIBIOTICS
Antibiotics only work against infections caused by
bacteria. Bacterial infections are much less common
than viral infections. Most coughs and colds are of viral
origin so antibiotics should not be prescribed for these.
Antibiotics should only used when absolutely necessary,
because:
There is increasing resistance of bacteria to treatment
Resistant bacteria are selected out by the use of
antibiotics.
Antibiotics may have serious adverse effects in some
people Some common bacterial infections that do require
antibiotic therapy include:
Staphyloccal skin infections, eg, impetigo (school sores)
Streptococcal skin infections, eg, cellulitis
Some ear and sinus infections

'Strep throat' — sore throat caused by Streptococcus
If these infections remain untreated, the resulting disease
may be serious and even fatal.
In severe bacterial infections where patients may be
hospitalized, often an intravenous broad-spectrum
antibiotic (one that is active against many different
bacteria) is given to start treatment. As soon as
laboratory tests confirm the infecting bacteria, the
antibiotic should be changed to one that is active against
specific bacteria. After 48 hours of intravenous treatment,
if there is clinical improvement, the patient may be
switched to an oral form of the antibiotic.

ANTIBIOTIC RESISTANCE
The overuse and inappropriate use of antibiotics has led
to antibiotic resistance.
Bacteria that were once susceptible to antibiotics have
developed ways to survive the drugs that were meant to
kill or weaken them. This is also known as antibacterial
resistance or drug resistance. Some diseases such as
tuberculosis, gonorrhoea and childhood bacterial ear
infections, that were once easily treated with antibiotics
are now again becoming difficult to treat as bacteria have
become resistant to these drugs. About 70% of bacteria
that cause infections in hospitals are resistant to at least
one of the antibiotics most commonly used to treat
infections. Methicillin (meticillin) resistant Staphylococcus
aureus (MRSA) is a particular problem for patients with
skin diseases, ulcers and surgical wounds.

Doctor responsibility
Only prescribe antibiotics if bacterial infection present
Prescribe the approved dose and duration or as
recommended by experts
Educate patient about the importance of completing
their course of antibiotics as instructed
Patient responsibility
Understand that not all infections are bacterial and that
not all bacterial infections will clear on antibiotics
(eg, folliculitis)
Take antibiotics exactly as instructed (ie, with or without
food etc)
Ensure you finish the course of antibiotics

SIDE EFFECTS OF ANTIBIOTICS
Antibiotics are associated with many side effects,
including cutaneous adverse reactions. Some side effects
are class-related but most reactions are specific to the
agent in that individual.
Some common problems with antibiotics are listed below:
Allergy to certain antibiotics or classes of antibiotics (eg,
penicillin allergy)
Many antibiotics cause gastrointestinal problems (eg,
diarrhoea, vomiting, nausea)
Antibiotics kill not only their targets but other useful
micro-organisms that live in and on our body (flora) to
prevent other diseases (eg, oral and/or vaginal thrush).
A variety of skin rashes can occur, which may be
mild(eg,hives)or
devastating (eg, toxic epidermal necrolysis).

Beta- Lactam antibiotics
Beta- Lactam antibiotics: Antibiotics Containing the
beta lactam (alpa- 4 membraned cyclic amide) ring
structure constitute the dominant class of agent currently
employed for the chemotherapy of bacterial infections.
beta lactam antibiotics are broad class of antibiotics,
structure having a lactam group with a heteroatom
structure consisting cyclic amide with 3 carbon atom and
one nitrogen atom. Beta lactam antibiotics inhibit the
growth of many gram positive and gram Negative
bacteria by interfering with the bacteria cell wall
biosynthesis.
beta lactam compound classification
Saturated five membered ring
Unsaturated five membered ring
Unsaturated 6 membered ring
beta lactam not fused with any other ring

STRUCTURE OF PENICILLIN
Penicillins are a group of β-lactam antibiotics consisting of natural
penicillins and semisynthetic penicillins. The basic structure of all
penicillins, natural and semisynthetic, is 6-aminopenicillanic acid
composed of a four membered heterocyclic β-lactam ring fused with
a five membered (benzylpenicillin), penicillin V (Phenoxymethyl
penicillin), thiazolidine ring.
This basic structure combines with N-acyl group which is variable
and shows structural differences in different type of penicillins. The
N-acyl group is the side chain attached to the amino group of 6-
aminopenicillanic acid. However, there are three natural penicillins
that are produced directly and can be obtained from the fermentation
Iiquours of Pencillium.
6-aminopenicillanic acid
N-acyl group

MECHANISM ACTION OF ANTIBIOTICS

TABLE 1. COMMON ANTIBACTERIAL DRUGS BY MODE OF ACTION
MODE OF ACTION TARGET DRUG CLASS
INHIBIT CELL WALL BIOSYNTHESIS
Penicillin-binding proteins
β-lactams: penicillins, cephalosporins,
monobactams, carbapenems
Peptidoglycan subunits Glycopeptides
Peptidoglycan subunit transport Bacitracin
INHIBIT BIOSYNTHESIS OF PROTEINS
30S ribosomal subunit Aminoglycosides, tetracyclines
50S ribosomal subunit
Macrolides, lincosamides, chloramphenicol,
oxazolidinones
DISRUPT MEMBRANES
Lipopolysaccharide, inner and outer
membranes
Polymyxin B, colistin, daptomycin
INHIBIT NUCLEIC ACID SYNTHESIS
RNA Rifamycin
DNA Fluoroquinolones
ANTIMETABOLITES
Folic acid synthesis enzyme Sulfonamides, trimethoprim
Mycolic acid synthesis enzyme Isonicotinic acid hydrazide
MYCOBACTERIAL ADENOSINE
TRIPHOSPHATE (ATP) SYNTHASE
INHIBITOR
Mycobacterial ATP synthase Diarylquinolin

TABLE 2. DRUGS THAT INHIBIT BACTERIAL CELL WALL SYNTHESIS
MECHANISM OF ACTION DRUG CLASS SPECIFIC DRUGS
NATURAL OR
SEMISYNTHETIC
SPECTRUM OF ACTIVITY
INTERACT DIRECTLY WITH
PBPS AND INHIBIT
TRANSPEPTIDASE ACTIVITY
Penicillins
Penicillin G, penicillin V Natural
Narrow-spectrum against gram-
positive and a few gram-negative
bacteria
Ampicillin, amoxicillin Semisynthetic
positive bacteria but with
increased gram-negative
spectrum
Methicillin Semisynthetic
positive bacteria only, including
strains producing penicillinase
Cephalosporins
Cephalosporin C Natural
Narrow-spectrum similar to
penicillin but with increased
gram-negative spectrum
First-generation cephalosporins Semisynthetic
Narrow-spectrum similar to
cephalosporin C
Second-generation cephalosporins Semisynthetic
Narrow-spectrum but with
increased gram-negative
spectrum compared with first
generation
Third- and fourth-generation
cephalosporins
Semisynthetic
Broad-spectrum against gram-
positive and gram-negative
bacteria, including some β-
lactamase producers
Fifth-generation cephalosporins Semisynthetic
bacteria, including MRSA
Monobactams Aztreonam Semisynthetic
negative bacteria, including some
β-lactamase producers
Carbapenems
Imipenem, meropenem,
doripenem
Semisynthetic
Broadest spectrum of the β-
lactams against gram-positive and
gram-negative bacteria, including
many β-lactamase producers
LARGE MOLECULES THAT BIND
TO THE PEPTIDE CHAIN OF
PEPTIDOGLYCAN SUBUNITS,
BLOCKING
TRANSGLYCOSYLATION AND
TRANSPEPTIDATION
Glycopeptides Vancomycin Natural
Narrow spectrum against gram-
positive bacteria only, including
multidrug-resistant strains
BLOCK TRANSPORT OF
PEPTIDOGLYCAN SUBUNITS
ACROSS CYTOPLASMIC
MEMBRANE
Bacitracin Bacitracin Natural
bacteria

TABLE 3. DRUGS THAT INHIBIT BACTERIAL PROTEIN SYNTHESIS
MOLECULAR
TARGET
MECHANISM OF
ACTION
DRUG CLASS SPECIFIC DRUGS
BACTERIOSTATIC
OR BACTERICIDAL
SPECTRUM OF
ACTIVITY
30S SUBUNIT
Causes mismatches
between codons and
anticodons, leading to
faulty proteins that
insert into and disrupt
cytoplasmic
membrane
Aminoglycosides
Streptomycin,
gentamicin,
neomycin, kanamycin
Bactericidal Broad spectrum
Blocks association of
tRNAs with ribosome
Tetracyclines
Tetracycline,
doxycycline,
tigecycline
Bacteriostatic Broad spectrum
50S SUBUNIT
Blocks peptide bond
formation between
amino acids
Macrolides
Erythromycin,
azithromycin,
telithromycin
Bacteriostatic Broad spectrum
Lincosamides
Lincomycin,
clindamycin
Bacteriostatic Narrow spectrum
Not applicable Chloramphenicol Bacteriostatic Broad spectrum
Interferes with the
formation of the
initiation complex
between 50S and 30S
subunits and other
factors.
Oxazolidinones Linezolid Bacteriostatic Broad spectrum

TABLE 4. DRUGS THAT INHIBIT BACTERIAL MEMBRANE FUNCTION
MECHANISM OF ACTION DRUG CLASS SPECIFIC DRUGS SPECTRUM OF ACTIVITY CLINICAL USE
INTERACTS WITH
LIPOPOLYSACCHARIDE
IN THE OUTER
MEMBRANE OF GRAM-
NEGATIVE BACTERIA,
KILLING THE CELL
THROUGH THE
EVENTUAL DISRUPTION
OF THE OUTER
MEMBRANE AND
CYTOPLASMIC
MEMBRANE
Polymyxins
Polymyxin B
Narrow spectrum against
gram-negative bacteria,
including multidrug-
resistant strains
Topical preparations to
prevent infections in
wounds
Polymyxin E (colistin)
gram-negative bacteria,
resistant strains
Oral dosing to
decontaminate bowels to
prevent infections in
immunocompromised
patients or patients
undergoing invasive
surgery/procedures.
Intravenous dosing to
treat serious systemic
infections caused by
multidrug-resistant
pathogens
INSERTS INTO THE
CYTOPLASMIC
MEMBRANE OF GRAM-
POSITIVE BACTERIA,
DISRUPTING THE
MEMBRANE AND
KILLING THE CELL
Lipopeptide Daptomycin
gram-positive bacteria,
resistant strains
Complicated skin and skin-
structure infections and
bacteremia caused by
gram-positive pathogens,
including MRSA

TABLE 5. DRUGS THAT INHIBIT BACTERIAL NUCLEIC ACID SYNTHESIS
MECHANISMS OF
ACTION
SPECTRUM OF
ACTIVITY
CLINICAL USE
INHIBITS BACTERIAL
RNA POLYMERASE
ACTIVITY AND BLOCKS
TRANSCRIPTION,
KILLING THE CELL
Rifamycin Rifampin
Narrow spectrum with
activity against gram-
positive and limited
numbers of gram-
negative bacteria. Also
active
against Mycobacterium
tuberculosis.
Combination therapy for
treatment of tuberculosis
INHIBITS THE
ACTIVITY OF DNA
GYRASE AND BLOCKS
DNA REPLICATION,
KILLING THE CELL
Fluoroquinolones
Ciprofloxacin, ofloxacin,
moxifloxacin
Broad spectrum against
gram-positive and gram-
negative bacteria
Wide variety of skin and
systemic infections

TABLE 6. ANTIMETABOLITE DRUGS
METABOLIC PATHWAY
TARGET
MECHANISM OF
ACTION
SPECTRUM OF
ACTIVITY
FOLIC ACID
SYNTHESIS
Inhibits the enzyme
involved in production of
dihydrofolic acid
Sulfonamides Sulfamethoxazole
negative bacteria
Sulfones Dapsone
Inhibits the enzyme
involved in the production
of tetrahydrofolic acid
Not applicable Trimethoprim
negative bacteria
MYCOLIC ACID
SYNTHESIS
Interferes with the
synthesis of mycolic acid
Not applicable Isoniazid
Narrow spectrum
against Mycobacterium sp
p., including M.
tuberculosis

Sulfonamides are composed of a sulfur atom that has two sets of
double bonds to two oxygen atoms, a carbon-based side group, and a
nitrogen atom bonded to the sulfur itself. In organic chemistry, an
amide contains a carbonyl group bonded to a nitrogen atom.
Sulfonamides are similar but the carbonyl group is replaced with a
sulfone (a sulfur with two oxygen atoms). That's why the term
'amide' appears in the name!
The 'R' groups in the figure simply represent any generic carbon-
based side chain and could be virtually anything. For example, R
could be a methyl group, a benzene ring, an alkane ring, or some
other group. If the nitrogen atom contains two hydrogens, the
sulfonamide is classified primary, if there is one hydrogen it's
secondary, and if no hydrogens are present on the nitrogen, it's a
tertiary sulfonamide.
SULFONAMIDES
Structure of Sulfonamides

AMINOGLYCOSIDES
DESCRIPTION
Aminoglycosides are a group of antibiotics that inhibit
bacterial protein synthesis and are particularly active
against Gram-negative bacteria. This group of antibiotics
includes several drugs, sharing the same basic chemical
structure:
Amikacin,arbekacin,gentamicin,kanamycin,neomycin,neti
lmicin,paromomycin, streptomycin, tobramycin
CHEMICAL STRUCTURE
The aminoglycosides consist of two or more amino
sugars joined in glycosidic linkage to an hexose nucleus.
Different aminoglycosides are distinguished by the amino
sugars attached to the aminocyclitol. Streptomycin differs
from the other aminoglycoside antibiotics in that it
contains streptidine rather than 2-deoxystreptamine, and
the aminocyclitol is not in a central position.

TETRACYCLINES
Tetracyclines are composed of a rigid skeleton of 4 fused rings. The
rings structure of tetracyclines is divided into an upper modifiable
region and a lower non modifiable region. An active tetracycline
requires a C10 phenol as well as a C11-C12 keto-enol substructure in
conjugation with a 12a-OH group and a C1-C3 diketo substructure.
Removal of the dimethylamine group at C4 reduces antibacterial
activity. Replacement of the carboxylamine group at C2 results in
reduced antibacterial activity but it is possible to add substituents to
the amide nitrogen to get more soluble analogs like the
prodrug lymecycline.
The simplest tetracycline with measurable antibacterial activity is 6-
deoxy-6-demethyltetracycline and its structure is often considered to
be the minimum pharmacophore for the tetracycle class of
antibiotics. C5-C9 can be modified to make derivatives with varying
antibacterial activity.

MACROLIDES

CEPHALOSPORINS

ANTIBIOTICS

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