This document provides information about a pharmacotherapeutics assignment on antibiotics submitted by a student. It includes an introduction to antibiotics that describes how they work and their different types. It then covers various topics related to antibiotics like their sources, classifications, mechanisms of action, specific drug classes like penicillins and cephalosporins, and adverse effects. The assignment appears to provide an overview of key concepts regarding antibiotics.

1. PHARMACOTHERAPEUTICS
ASSIGNMENT
ON
ANTIBIOTICS
SUBMITED BY:-
AAROMAL SATHEESH,
III-PHARMD,
ROLL NO:-8
JSS UNIVERSITY,MYSORE
SUBMITED TO:-
Mr.HIMANSHU J PATEL,
LECTURER,
DEP: OF PHARMACY PRACTISE,
JSS UNIVERSITY,MYSORE

2. INTRODUCTION
Antibiotics are a group of medicines that are used to treat infections caused by bacteria and certain parasites.
The Greek word anti means "against", and the Greek word bios means "life" (bacteria are life forms).They are
sometimes called antibacterials. Antibiotics can be taken by mouth as liquids, tablets, or capsules, or they can
be given by injection. Usually, people who need to have an antibiotic by injection are in hospital because they
have a severe infection. Antibiotics are also available as creams, ointments, or lotions to apply to the skin to
treat certain skin infections. It is important to remember that antibiotics only work against infections that are
caused by bacteria and certain parasites. They do not work against infections that are caused by viruses (for
example, the common cold or flu), or fungi (for example, thrush in the mouth or vagina), or fungal infect ions
of the skin. Before bacteria can multiply and cause symptoms, the body's immune system can usually destroy
them. We have special white blood cells that attack harmful bacteria. Even if symptoms do occur, our immune
system can usually cope and fight off the infection. There are occasions, however, when it is all too much and
some help is needed.....from antibiotics.
The first antibiotic was penicillin. Such penicillin-related antibiotics as ampicillin, amoxicillin and
benzylpenicilllin are widely used today to treat a variety of infections - these antibiotics have been around for
a long time. There are several different types of modern antibiotics and they are only available with a doctor's
prescription in most countries. Although there are a number of different types of antibiotic they all work in
one of two ways:
 A bactericidal antibiotic kills the bacteria. Penicillin is a bactericidal. A bactericidal usually either
interferes with the formation of the bacterium's cell wall or its cell contents.
 A bacteriostatic stops bacteria from multiplying.
If antibiotics are overused or used incorrectly there is a risk that the bacteria will become resistant - the
antibiotic becomes less effective against that type of bacterium. A broad-spectrum antibiotic can be used to
treat a wide range of infections. A narrow-spectrum antibiotic is only effective against a few types of bacteria.
There are antibiotics that attack aerobic bacteria, while others work against anaerobic bacteria. Aerobic
bacteria need oxygen, while anaerobic bacteria don’t. Antibiotics may be given beforehand, to prevent
infection, as might be the case before surgery. This is called 'prophylactic' use of antibiotics. They are
commonly used before bowel and orthopaedic surgery. It is not possible to list all the possible side-effects of
each antibiotic in this leaflet. However, as with all medicines, there are a number of side-effects that have been
reported with each of the different antibiotics.. Most side-effects of antibiotics are not serious. Common side-effects
include: soft stools, diarrhoea, or mild stomach upset such as nausea. Less commonly, some people
have an allergic reaction to an antibiotic, and some have died from a severe allergic reaction - this is very rare.
Antibiotics can kill off normal defence bacteria which live in the bowel and vagina. This may then allow
thrush or other bad bacteria to grow. Some patients may develop an allergic reaction to antibiotics - especially
penicillin. Side effects might include a rash, swelling of the tongue and face, and difficulty breathing. Allergic
reactions to antibiotics may be immediate or delayed hypersensitivity reactions2.If you have ever had an
allergic reaction to an antibiotic you must tell your doctor and/or pharmacist. Reactions to antibiotics can be
very serious, and sometimes fatal - they are called anaphylactic reactions. Antibiotics are usually taken by
mouth (orally); however, they can also be administered by injection, or applied directly to the affected part of
the body. Most antibiotics start having an effect on an infection within a few hours. It is important to remember
to complete the whole course of the medication to prevent the infection from coming back. If you do not
complete the course, there is a higher chance the bacteria may become resistant to future treatments - because
the ones that survive when you did not complete the course have had some exposure to the antibiotic and may
consequently have built up a resistance to it. Even if you are feeling better, you still need to complete the
course. It is crucial that you follow the instructions correctly if you want the medication to be effective.

3. SOURCES OF ANTIBACTERIAL AGENT
NATURAL
Mainly fungal
sources
NATURAL ANTIBIOTICS
SYNTHETIC
Chemically
designed in the lab
The original antibiotics which were derived from fungal source can be referred to as “natural” antibiot ics.
Organisms develop resistance faster to the natural antimicrobials because they have been pre-exposed to these
compounds in nature. Natural antibiotics are often more toxic than synthetic antibiotics.
e.g.:- Benzyl penicillin and Gentamicin are natural antibiotics
SYNTHETIC ANTIBIOTICS
These are drugs having an advantage that the bacteria are not exposed to the compounds until they are released.
They are also designed to have even greater effectiveness and less toxicity. There is an inverse relationship
between toxicity and effectiveness as you move from natural to synthetic antibiotics
e.g.:-Moxifloxacin and Norfloxacin are synthetic antibiotics
SEMI-SYNTHETIC ANTIBIOTICS
These are drugs developed to decrease toxicity and increase effectiveness
e.g.:- Ampicillin and Amikacin are semi-synthetic antibiotics
SEMI-SYNTHETIC
Chemically altered
natural compound

4. CLASSIFICATION OF ANTIBIOTICS
ANTIBIOTIC
S
Although there are several classification schemes for antibiotics, based on bacterial spectrum (broad versus
narrow) or route of administration (injectable versus oral versus topical), or type of activity (bactericidal vs.
bacteriostatic), the most useful is based on chemical structure. Antibiotics within a structural class will
generally show similar patterns of effectiveness, toxicity, and allergic potential. Antibiotics are usually
classified based on their structure and function. Five functional groups cover most antibiotics
INHIBITOR OF CELL WALL SYNTHESIS
INHIBITOR OF PROTEIN SYNTHESIS
INHIBITOR OF MEMBRANE FUNCTION
INHIBITOR OF NUCLEIC ACID SYNTHESIS
ANTI-METABOLITES
BACTERIAL SPECTRUM
 Broad
 Narrow
TYPES OF ACTIVITY
 Bactericidal
 Bacteriostatic
ROUTE OF
ADMINISTRATION
 Injectable
 Oral

5. MECHANISM ANTIBIOTICS
CELLWALL SYNTHESIS INHIBITOR Beta-lactamase Inhibitors
Penicillin
Cephalosporin
Carbapenems
Monobactam
Glycopeptide
Vancomycin
PROTEIN SYNTHESIS INHIBITOR Inhibit 30s Subunit
Aminoglycosides (Gentamicin)
Tetracycline
Inhibit 50s Subunit
Macrolides
Chloramphenicol
Clindamycin
Linezolid
Streptogramins
MEMBRANE FUNCTION INHIBITOR Lipopeptides
Polypeptide
Colistin
Polymyxins
Cyclic Lipopeptides
NUCLEIC ACID SYNTHESIS INHIBITOR Quinolone
Ciprofloxacin
Furanes
ANTI-METABOLITES
Sulfonamides
Trimethoprim/Sulfamethoxazole

6. GENERAL MECHANISM OF ACTION
Antibiotics are very commonly used substances to eradicate bacterial infections by bacteriostatic or even
bactericide effect. They act at a very specific stage (target), although other less important or secondary
interactions can occur The study of the action mechanism of these antibiotics enables us to show the action
specificity of these products in the bacteria. This specificity is more accurate when the target is not to be found
in the eukaryotic cells: in this case the antibiotic may be considered as entirely atoxic. If the study of the action
mechanism of antibiotics gives a better understanding of the use of these drugs, their action at a definite stage
in bacterial metabolism is a valuable tool for scientists in their approach to cell functioning. Antibacteria l
action generally falls within one of four mechanisms, three of which involve the inhibition or regulation of
enzymes involved in cell wall biosynthesis, nucleic acid metabolism and repair, or protein synthes is,
respectively. The fourth mechanism involves the disruption of membrane structure. Many of these cellula r
functions targeted by antibiotics are most active in multiplying cells. Since there is often overlap in these
functions between prokaryotic bacterial cells and eukaryotic mammalian cells, it is not surprising that some
antibiotics have also been found to be useful as anticancer agents.

7. CELLWALL SYNTHESIS INHIBITOR
β- LACTAMS
Similar in structure, as well as, function All have a common structural ß-lactam ring. Antibiotics vary by side
chains attached All beta-lactams are subject to inactivation by bacterial-produced enzymes called beta-lactamases
There are about 50 different Beta (ß)-lactams currently on the market They are all bactericida l
,non-toxic (i.e., they can be administered at high doses) and are relatively inexpensive. Beta-lactams are
organic acids and most are soluble in water.
E.g:- PENICILLINS, CEPHALOSPORINS, MONOBACTAMS
Mechanism of Action
These are structural analogues of the natural D-Ala-D-Ala.They covalently bind to the PBPs (transpeptidase)
leading to the inhibition of tranpeptidation reaction essential for peptidoglycan synthesis. They are bactericida l
against susceptible organism. The β-lactam nucleus of the molecule irreversibly binds to (acylates) the Ser403
residue of the PBP active site. This irreversible inhibition of the PBPs prevents the final crosslinking
(transpeptidation) of the nascent peptidoglycan layer, disrupting cell wall synthesis. Specific antibacteria ls
interfere with the synthesis of the cell wall, weakening the peptidoglycan scaffold within the bacterial wall so
that the structural integrity eventually fails. Since mammalian cells have a plasma membrane but lack the
peptidoglycan wall structure, this class of antibacterials selectively targets the bacteria with no significant
negative effect on the cells of the mammalian host.
PENICILLIN ANTIBIOTICS
Penicillin (sometimes abbreviated PCN or pen) is a group of antibiotics derived from Penicillium fungi,
including penicillin G (intravenous use), penicillin V (oral use), procaine penicillin, and benzathine penicilli n
(intramuscular use).Penicillin antibiotics were among the first drugs to be effective against many previously
serious diseases, such as bacterial infections caused by staphylococci and streptococci. Penicillin are still
widely used today, though misuse has now made many types of bacteria resistant. All penicillins are β-lactam
antibiotics and are used in the treatment of bacterial infections caused by susceptible, usually Gram-positive,
organisms.
Pharmacokinetics
They gets widely distributed through out the body and reaches high concentration in the urine. It also reaches
significant level in bile, liver, skeletal muscle, brain and plasma. Its level gets raised in the presence of
inflammation Only a small amount of the total drug in serum is present as free drug, the concentration of
which is determined by protein binding. Penicillin is also excreted into sputum and milk to levels 3-15% of
those present in the serum
Resistance
Resistance to penicillins and other b-lactams is due to one of four general mechanisms: (1) inactivation of
antibiotic by β -lactamase, (2) modification of target PBPs, (3) impaired penetration of drug to target PBPs,
and (4) efflux. β -Lactamase production is the most common mechanism of resistance. Resistance due to
impaired penetration of antibiotic to target PBPs occurs only in gram-negative species because of their
impermeable outer cell wall membrane, which is absent in gram-positive bacteria. β-Lactam antibiotics cross
the outer membrane and enter gram-negative organisms via outer membrane protein channels (porins).
Absence of the proper channel or down-regulation of its production can greatly impair drug entry to cell

8. Clinical Use
Except for oral amoxicillin, penicillins should be given 1-2 hours before or after a meal; they should not be
given with food to minimize binding to food proteins and acid inactivation. Blood levels of all penicillins can
be raised by simultaneous administration of probenecid, 0.5 g (10 mg/kg in children) every 6 hours orally,
which impairs renal tubular secretion of weak acids such as b-lactam compounds.
Adverse Drug Reactions
The penicillins are remarkably nontoxic. Most of the serious adverse effects are due to hypersensitivit y.
Allergic reactions include anaphylactic shock (very rare¾0.05% of recipients); serum sickness-type reactions
(now rare¾urticaria, fever, joint swelling, angioneurotic edema, intense pruritus, and respiratory
embarrassment occurring 7-12 days after exposure); and a variety of skin rashes. Oral lesions, fever, interstit ia l
nephritis (an autoimmune reaction to a penicillin-protein complex), eosinophilia, haemolytic anaemia and
other hematologic disturbances, and vasculitis may also occur
CEPHALOSPORIN ANTIBIOTICS
Cephalosporins are similar to penicillins, but more stable to many bacterial b-lactamases and therefore have
a broader spectrum of activity. However, strains of E coli and Klebsiella species expressing extended-spectrum
b-lactamases that can hydrolyse most cephalosporins are becoming a problem. Cephalosporins are
not active against enterococci and L monocytogenes .They are mainly classified into
1) First Generation Cephalosporin
E.g.:- Cefadroxil, Cefazolin, Cephalexin, Cephalothin e.t.c
2) Second Generation Cephalosporins
E.g.:- Cefaclor, Cefamandole, Cefonicid, Cefuroxime, Cefprozil, e.t.c
3) Third Generation Cephalosporins
E.g.:- Cefoperazone, Cefotaxime, Ceftazidime, Ceftizoxime, Ceftriaxone, e.t.c
4) Fourth Generation Cephalosporins
E.g.:- Cefepime (Maxipime), Cefluprenam, Cefoselis, Cefozopran, e.t.c
Adverse Drug Reactions
Common adverse drug reactions (ADRs) (≥ 1% of patients) associated with the cephalosporin therapy include :
diarrhea, nausea, rash, electrolyte disturbances, and pain and inflammation at injection site. Infrequent ADRs
(0.1–1% of patients) include vomiting, headache, dizziness, oral and vaginal candidiasis, pseudomembranous
colitis, superinfection, eosinophilia, nephrotoxicity, neutropenia, thrombocytopenia,and fever.
Resistance
Resistance to cephalosporin antibiotics can involve either reduced affinity of existing PBP components or the
acquisition of a supplementary β-lactam-insensitive PBP. Currently, some Citrobacter freundii, Enterobacter
cloacae, Neisseria gonorrhoeae, and Escherichia coli strains are resistant to cephalosporin. Some Morganella
morganii, Proteus vulgaris, Providencia rettgeri, Pseudomonas aeruginosa and Serratia marcescens strains
have also developed resistance to cephalosporin to varying degree
Clinical Use
Cephalosporins are indicated for the prophylaxis and treatment of infections caused by bacteria susceptible
to this particular form of antibiotic. First-generation cephalosporins are active predominantly against Gram-positive
bacteria, and successive generations have increased activity against Gram-negative bacteria (albeit
often with reduced activity against Gram-positive organisms)

9. PROTEIN SYNTHESIS INHIBITOR
Protein synthesis is a complex, multi-step process involving many enzymes as well as conformational
alignment. However, the majority of antibiotics that block bacterial protein synthesis interfere with the
processes at the 30S subunit or 50S subunit of the 70S bacterial ribosome. The aminoacyltRNA synthet ises
that activate each amino acid required for peptide synthesis are not antibiotic targets. Instead, the primary
steps in the process that are attacked are (1) the formation of the 30S initiation complex (made up of mRNA,
the 30S ribosomal subunit, and formyl-methionyl-transfer RNA), (2) the formation of the 70S ribosome by
the 30S initiation complex and the 50S ribosome, and (3) the elongation process of assembling amino acids
into a polypeptide..
AMINOGLYCOSIDES
These are group of natural and semisynthetic antibiotics having polybasic amino group linked glycosidica ll y
to two or more aminosugar residue. Aminoglycosides are bactericidal and are more active at alkaline Ph. They
act by interfering with bacterial protein synthesis. All of them exhibit ototoxicity and nephrotoxicity. They
are excreted unchanged in urine by glomerular filtration.
Mechanism of Action
Aminoglycosides bind to the RNA of the 30S ribosomal sub-unit. The resulting change in ribosome
structure affects all stages of normal protein synthesis.
 Initiation step of translation
 Blocks elongation of peptide bond formation
 Release of incomplete, toxic proteins
Translational errors are frequent and many non-functional or toxic proteins are produced. Theincorpora t ion
of such abnormal proteins into the cytoplasmic membrane compromises its function.The bactericidal activit y
of aminoglycosides ultimately stops protein synthesis and dramatically damage the cytoplasmic membrane.
Pharmacokinetics
Aminoglycosides are not well absorbed when given orally, so need to be given intravenously for systemic
infections. Absorption by I.M route is rapid and complete, however in critically ill patients I.M absorption can
vary considerably. Peak serum concentrations of aminoglycosides are reached within 30-120 minutes after
I.M injection. Distribution is mainly restricted to extracellular fluids. Protein binding of these antibiotics is
less than 10%. Aminoglycosides distribute well in synovial, peritoneal, ascetic and pleural fluids.
Aminoglycosides are primarily excreted unchanged through the kidney by glomerular filtration. The 80-90%
of the administered dose is excreted in the urine resulting in high urinary concentrations. A small amount of
aminoglycoside is excreted by bile
Adverse Effects
Nephrotoxicity: A wide variation in the incidence. Usually reversible. Increase in serum creatinine and BUN.
Otoxicity: Cochlear and vestibular. Bilateral and permanent. Other adverse effects: Hypersensitivity reactions,
superinfection, CNS effects and GI disturbances.

10. MEMBRANE FUNCTION INHIBITOR
POLYPEPTIDE ANTIBIOTICS
These are low molecular weight cationic polypeptide antibiotics, which are powerful bactericidal agents, but
not used systematically due to toxicity. All produced by bacteria. Clinically used ones are:-
POLIMYXIN B AND COLISTIN
These were obtained in the late 1940s Bacillus Polymyxa and B Colistimus respectively. They are active
against gram-ve bacteria only. Both are similar in activity, but Colistin is more potent on Pseudomonas,
Salmonella etc.
Mechanism of Action
They are rapid acting bactericidal agents having a detergent like action on the cell membrane. The have high
affinity for phospholipids: the peptide molecules orient between the phospholipid and protein film in gram
negative bacterial cell membrane causing membrane distortion or pseudopore formation. As a result ions,
amino acids, leak out. Sensitive bacteria take up more of the antibiotic and inactivate the bacterial endotoxin.
They exhibit bacterial synergism with many other AMAs by improving their penetration inyo the bacterial
cell.
Resistance
Resistance to these antibiotics has never been a problem.There is no cross resistance with any other AMA
Dosage
Polymyxin B :- ( 1mg = 10,000 U)
Colistine Sulfate: - 25- 100 mg TDS oral
Adverse Effects
When given orally, the side effects are limited to g.i.t- occasional nausea, vomiting, diarrhoea. Systemic
toxicity of these drugs are high, Flushing and parenthesis (due to liberation of histamine from mast cells),
marked kidney damage, neurological disturbances, neuromuscular blockade.
Clinical Uses
Topically:- Usually in combination with other antimicrobials for skin infection , burns , otitis external ,
conjunctivitis , corneal ulcer- caused by gram negative bacteria including Pseudomonas
Orally:-Gram negative bacillary diarrhoeas, especially in infants and children, Pseudomonas superinfec t ion
entities

11. NUCLEIC ACID SYNTHESIS INHIBITOR
QUINOLONES
These are synthetic antimicrobials having a quinolone structure that are active primarily against gram-negat ive
bacteria, though the newer fluorinated compound also inhibit gram-positive ones. The first member NALIDIXIC
ACID introduced in mid-1960s had usefulness limited to urinary and g.i.t tract infection because of low
potency, modest blood and tissue level restricted spectrum and high frequency of bacterial resistance. In 1980s,
fluorination of quinolone structure at position 6 and introduction of a piperazine substitution at position 7
resulted in derivatives called FLUROQUINOLONES, which is more potent, expanded spectrum, better tissue
penetration and good tolerability.
CIPROFLOXACIN
They are the most potent first generation FQ active against a broad range of bacteria, the most susceptible
ones are the aerobic gram-negative bacilli, especially Enterobacteriaceae and Neisseria. They are active
against many beta-lactam and amino-glycoside resistant bacteria.
Mechanism of Action
They inhibit the enzyme bacterial DNA gyrace, which nicks double-stranded DNA, introduce negative
supercoils and the reseal the nicked ends. The DNA gyrace consist of two A and two B subunits. The A subunit
carries out nicking of DNA, B subunits introduces negative supercoils and then A subunits reseals the strand.
FQ binds to A subunit with high affinity and interfere with its strand cutting and releasing function.
Resistance
Resistance noted was because of chromosomal mutation producing a DNA gyrace or topoisomerase IV with
reduced affinity for FQs, or due to reduced permeability/increased efflux of these drugs across bacterial
membranes. FQ resistant mutants are not easily selected, therefore resistance to FQs is slow to develop
Pharmacokinetics
They are rapidly absorbed orally, but food delays absorption and first pass metabolism occurs. The plasma
protein binding is about 20-30%.It is excreted primarily in urine both by glomerular filteration and tubular
secretion. Urinary and biliary concentration are 10-50 fold higher than plasma concentration.
Adverse Effects
They have good safety records, side effects occurs only in ~10% patient, but generally mild. Common adverse
effects occurs at g.i.t including nausea, vomiting, anorexia, in CNS:- dizziness, headache, restlessness,
insomnia, and rarely tremor. It causes hypersensitivity reaction like rashes, photo sensitivity, swelling of lips
etc. It also causes tendon rupture.
Clinical Uses:-It is having bactericidal property. It is used in urinary tract infection, Gonorrhoea, Chancroid -
where it is used as a 2nd line agent. It is widely used in the treatment of typhoid-1st line agent. They can reduce
the stool volume in Cholera. It is used in osteomyelitis and Tuberculosis, Conjunctivitis, Meningitis and
Prophylaxis.

12. ANTI-METABOLITES
These are analogues related to the normal components of DNA or of tco-enzymes involved in the nucleic acid
synthesis. They are so called folate pathway inhibitors or anti-metabolites. Folic acid is essential for the
synthesis of adenine and thymine, two of the four nucleic acids that make up our genes, DNA and
chromosomes. Humans do not synthesize folic acid.
SULFONAMIDES TRIMETHOPRIM / SULFAMETHOXAZOLE
 Bacteriostatic
 Introduced in 1930’s – first effective
systemic antimicrobial agent
 Used for treatment of acute,
uncomplicated UTI’s
SULFONAMIDES
 TMP/SXT is bactericidal
 Broad spectrum
 Synergistic action
They are the first antimicrobial agents effective against pyogenic bacterial infection. Primarily they are
bacteriostatic against gram-positive and gram negative bacteria. Because of rapid emergence of bacterial
resistance and the availability of safer and more effective antibiotics their current utility is limited, except in
combination with trimethoprim or pyrimethamine.
Mechanism of Action
Sulphonamides being structural analogues of PABA (P- Aminobenzoic Acid), inhibits bacterial folate
synthase and so folic acid is not formed and a number of essential metabolic reaction suffer. Sulfonamides
competitively inhibits the union of PABA with pteridine residue to form dihydropteroic acid which conjugates
with glutamic acid to produce dihydrofolic acid. They may also form an altered folate which is metabolica ll y
injurious
Resistance to Sulfonamides
Most bacteria are capable of developing resistance to sulphonamides (mainly, gonococci, pneumococci,
meningococci). The resistance mutants either will produce increased amount of PABA or, their folate synthase
enzyme has low affinity for sulfonamides or else they will adopt an alternative pathway in folate metabolism.
Development of resistance has markedly limited the clinical usefulness of this class of compounds.
Pharmacokinetics
They are rapidly and completely absorbed from the g.i.t. Extend of plasma protein binding differs considerably
(10-95%) among different members. Metabolism takes place in the liver by acetylation at N4 by
nonmicrosomal acetyl transferase.They are excreted by kidney through glomerular filtration.
Medicinal Uses
They are usually employed for the suppressive therapy of chronic urinary tract infection, for the streptococcal
pharyngitis and gum infection: such uses are outmoded. They are given in combination with trimethoprim (as
cortimoxazole), sulfamethaxazole is used for many bacterial infection. It is a cheap alternative in the treatment
of conjunctivitis, trachoma etc.
Adverse Effect
Common adverse effects includes nausea, vomiting, epigastric pain, hepatitis (in 0.1% patient),
Hypersensitivity reaction (2-5% patient) which is mostly in form of rashes, urticarial and drug fever.
Haemolysis can occur in G-6 PD deficient patient with high dose of sulfonamides. Crystalluria even though
dose related, is frequent now.

13. CONCLUSION
Antibiotics are very commonly used substances to eradicate bacterial infections by bacteriostatic or even
bactericide effect. They act at a very specific stage (target), although other less important or secondary
interactions can occur .The study of the action mechanism of these antibiotics enables us to show the action
specificity of these products in the bacteria. This specificity is more accurate when the target is not to be found
in the eukaryotic cells: in this case the antibiotic may be considered as entirely atoxic .Itis important to
remember that antibiotics only work against infections that are caused by bacteria and certain parasites. They
do not work against infections that are caused by viruses (for example, the common cold or flu), or fungi (for
example, thrush in the mouth or vagina), or fungal infections of the skin. It is important to take antibiotics in
the correct way. If you do not, this may reduce how well they work. For example, some antibiotics need to be
taken with food and others should be taken on an empty stomach.
If you do not take your antibiotics in the right way it will affect their absorption (how much gets into the
body), and therefore they may not work as well. So, follow the instructions as given by your doctor and on
the leaflet that comes with the antibiotic you are prescribed. They are only available from your chemist, with
a doctor's prescription. The length of treatment varies a lot. It depends on what kind of infection you have,
how severe it is and how quickly you get better after starting treatment It is very rare for anyone not to be able
to take some type of antibiotic. The main reason why you may not be able to take an antibiotic is if you have
had an allergic reaction to an antibiotic in the past. If you think you have had a side-effect to one of your
medicines you can report this on the Yellow Card Scheme. You can do this online at the following web
address:www.mhra.gov.uk/yellowcard. (The Yellow Card Scheme is used to make pharmacists, doctors and
nurses aware of any new side-effects that medicines may have caused)

14. REFERENCE
 Article of SA Waksman (1947). "What Is an Antibiotic or an Antibiotic Substance?". Mycologia 39
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 Baker-Austin C, Wright MS, Stepanauskas R, McArthur JV (April 2006). "Co-selection of antibiot ic
and metal resistance". Trends Microbiol.
 Maack C, Cremers B, Flesch M, Hoper A, Sudkamp M, Bohm M “ Antibiotics –Cell wall inhibitor y
Action “Webmd 568-598
 K D Tripati, Seventh edition , Polypeptides:: Sulfonamides , Pg: 768-72, 823-25, KATZUNG
Pharmacology Tenth Ed,
 Lippincott_-_Modern_Pharmacology_With_Clinical_Applications_
 GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed.
(2006) by kaball