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

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.

SOURCES OF ANTIBACTERIAL AGENT

NATURAL ANTIBIOTICS

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

NATURAL

Mainly fungal

sources

SYNTHETIC

Chemically

designed in the lab

SEMI-SYNTHETIC

Chemically altered

natural compound

CLASSIFICATION OF ANTIBIOTICS

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

ANTIBIOTICS

BACTERIAL SPECTRUM

Broad

Narrow

TYPES OF ACTIVITY

Bactericidal

Bacteriostatic

ROUTE OF

ADMINISTRATION

Injectable

Oral

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

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.

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 crosslink ing

(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 penicillin

(intramuscular use).Penicillin antibiotics were among the first drugs to be effective against many previous ly

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

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 hypersensitivity.

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)

PROTEIN SYNTHESIS INHIBITOR

Protein synthesis is a complex, multi-step process involving many enzymes as well as conformationa l

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 lly

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 activity

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.

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

NUCLEIC ACID SYNTHESIS INHIBITOR

QUINOLONES

These are synthetic antimicrobials having a quinolone structure that are active primarily against gram-negative

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.

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

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 lly

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.

SULFONAMIDES TRIMETHOPRIM / SULFAMETHOXAZOLE

Bacteriostatic

Introduced in 1930’s – first effective systemic antimicrobial agent

Used for treatment of acute, uncomplicated UTI’s

TMP/SXT is bactericidal

Broad spectrum

Synergistic action

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)

REFERENCE

Article of SA Waksman (1947). "What Is an Antibiotic or an Antibiotic Substance?". Mycologia 39

(5): 565–56,ncbi mediline (www.mediline.com)

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 inhibitory 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