Sarah Nazeer, profile picture
Uploaded bySarah Nazeer
PPTX, PDF16,328 views

Antibiotics

This document provides an overview of antibiotics, including their history, classification, mechanisms of action, and principles of administration. It discusses how antibiotics are classified based on their targets in bacteria and spectra of activity. Common antibiotics are also reviewed, along with how bacteria can develop resistance through modifications to antibiotic targets, altered uptake or efflux, and antibiotic inactivation through enzymes. Proper dosing, timing, route, and monitoring of patients are important to achieve the desired therapeutic effects of antibiotics.

Embed presentation

Downloaded 543 times
ANTIBIOTICS Presented by Department of Oral Medicine and radiology Dr Sarah Nazeer
CONTENTS  Introduction  History  Classification  Mechanism of action  Principles of antibiotic administration  Individual antibiotics  Clinical implications  Conclusion
Coined by Walksman in 1942 Ancient Greek ἀντί- Anti - against βίος -Biotic - Life Antibiotics are substances produced by microorganisms which suppress the growth of or kill other microorganisms at very low concentrations. Both synthetic +microbiologically produced drugs=ANTIMICROBIAL AGENT.
Antibiotics HISTORY
1877 Louis Pasteur Inhibition of some microbes by others; anthrax(Bacillus anthracis)
CLASSIFICATION
Classification of Antibiotics Inhibitors of Cell Wall Synthesis Protein Synthesis Inhibitors Inhibitors of Nucleic Acid Synthesis and Function Others: Vancomycine Bacitracin ß-lactam antibiotics Monobactams Chloramphenicole Carbapenems Cephalosporins Clindamycine Macrolides Penicillins Tetracyclines Antistaph: Methicillin Natural: Penicillin G Penicillin V Extended spectrum: Amoxicillin Ampicillin Erythromycine Azithromycine Clarithromycin e Quinolones Metronidazole Doxycycline Minocycline Tetracycline Ciproflaxicine Flagyl
Antibiotics A. CHEMICAL STRUCTURE Sulfonamides- Sulfadiazines, Sulfones, Dapsone, Paraaminosalicylic Acid(pas) Diaminopyrimidines- Trimethoprim -Lactam Antibiotics- Penicillins, Cephalosporins, Monobactums Tetracyclines- Oxytetracycline, Doxycycline
Antibiotics  Nitrobenzene Derivative- Chloramphenicol  Aminoglycosides- Streptomycin, Gentamycin, Neomycin  Macrolide Antibiotics- Erythromycin, Roxithromycin  Polypeptide Antibiotics- Polymixin-B , Colistin, Bacitracin
Antibiotics
 Interfere With D.N.A Synthesis- Acyclovir  Interfere With Intermediary Metabolism- Sulfonamides, Sulfones, Ethambutol C. TYPE OF ORGANISMS AGAINST WHICH PRIMARILY ACTIVE  Antibacterial- Pencillins, Aminoglycosides, Erythromycin  Antifungal- Griesofulvin, Ketoconazole  Antiviral- Acyclovir, Zidovudine  Antiprotozoal- Chloroquine, Metronidazole  Antihelminthic- Mebendazole
Antibiotics D. SPECTRUM OF ACTIVITY NARROW SPECTRUM BROAD SPECTRUM - Penicillin –G - Tetracyclines - Streptomycin -Chloramphenicol - Erythromycin E. TYPE OF ACTION PRIMARILY BACTERIOSTATIC - Sulphonamides - Tetracyclines - Chloramphenicol - Erythromycin
Antibiotics PRIMARILY BACTERIOCIDAL -Penicillin -Cephalosporins -Aminoglycosides -Polypeptides -Ciprofloxacin F. ANTIBIOTICS ARE OBTAINED FROM  Fungi - Penicillin -Cephalosporin -Griesofulvin
Antibiotics Bacteria -Polymyxin – B -Colistin -Bacitracin Actinomycetes -Aminoglycosides -Tetracyclines -Chloramphenicol G. RAPID KILLING ANTIBIOTICS -Penicillins -Cephalosporins -Metronidazole (Flagyl)
Bactericidal- the ability to kill the bacteria Bacteriostatic- the ability to inhibit or retard the growth of bacteria BACTERIOSTATIC V/S BACTERICIDAL Aminoglycosides Bacitracin Cephalosporins Metronidiazole vancomycin Penicillins ciprofloxacin streptomycin cotrimoxazole Chloramphenicol Clindamycin erythromycin Sulfonamides Tetracycline trimethoprim
ANTI - MICROBIAL DRUG TARGETS
 Erythromycin 250-500 Mg Qid  Clindamycin 150-300 Mg Qid Or 300-450 Mg Qid  Cephalosporins  Tetracyclines 250-500 Mg 2-4 Times Daily.  Doxycycline 100 Mg Every 12 Hours First Day Then 100 Mg Daily  Ciprofloxacin 250-500 Mg , 12th Hourly  Metronidazole ( Flagyl) Loading Dose - 1 Gram IV, maintainence Dose 500 Mg Qid, Oral Dose 500 Mg Qid.
MECHANISMS OF ANTIBACTERIAL RESISTANCE (1)  Structurally modified antibiotic target site, resulting in:  Reduced antibiotic binding  Formation of a new metabolic pathway preventing metabolism of the antibiotic
STRUCTURALLY MODIFIED ANTIBIOTIC TARGET SITE Interior of organism Cell wall Binding Target site Antibiotic Antibiotics normally bind to specific binding proteins on the bacterial cell surface
STRUCTURALLY MODIFIED ANTIBIOTIC TARGET SITE Antibiotics are no longer able to bind to modified binding proteins on the bacterial cell surface Interior of organism Cell wall Modified target site Antibiotic Changed site: blocked binding
MECHANISMS OF ANTIBACTERIAL RESISTANCE (2)  Altered uptake of antibiotics, resulting in:  Decreased permeability  Increased efflux
ALTERED UPTAKE OF ANTIBIOTICS: DECREASED PERMEABILITY Interior of organism Cell wall Porin channel into organism Antibiotic Antibiotics normally enter bacterial cells via porin channels in the cell wall
ALTERED UPTAKE OF ANTIBIOTICS: DECREASED PERMEABILITY Interior of organism Cell wall New porin channel into organism Antibiotic New porin channels in the bacterial cell wall do not allow antibiotics to enter the cells
ALTERED UPTAKE OF ANTIBIOTICS: INCREASED EFFLUX Antibiotics enter bacterial cells via porin Interior of organism Cell wall channels in the cell wall Porin channel through cell wall Antibiotic Entering Entering
ALTERED UPTAKE OF ANTIBIOTICS: INCREASED EFFLUX Once antibiotics enter bacterial cells, they are Interior of organism Cell wall immediately excluded from the cells via active pumps Porin channel through cell wall Antibiotic Entering Exiting Active pump
MECHANISMS OF ANTIBACTERIAL RESISTANCE (3)  Antibiotic inactivation  bacteria acquire genes encoding enzymes that inactivate antibiotics Examples include:  -lactamases  aminoglycoside-modifying enzymes  chloramphenicol acetyl transferase
ANTIBIOTIC INACTIVATION Interior of organism Antibiotic Cell wall Binding Target site Enzyme Inactivating enzymes target antibiotics
ANTIBIOTIC INACTIVATION Enzymes bind to antibiotic molecules Enzyme Binding Target site Interior of organism Antibiotic Cell wall Enzyme binding
ANTIBIOTIC INACTIVATION Enzymes destroy antibiotics or prevent binding to target sites Enzyme Target site Interior of organism Antibiotic Cell wall Antibiotic destroyed Antibiotic altered, binding prevented
PRINCIPLES OF ANTIBIOTIC ADMINISTRATION
PROPER DOSE  Prescribe or administer sufficient amounts to achieve the desired therapeutic effect, but not enough to cause injury to the host. o Relationship between antibiotic dose/ concentration. o Relationship between dose and body weight Individual dose = BW(kg)/70 x avg adult dose  Under-dosing – emergence of bacterial resistance.
AGE The dose of drug for children is often calculated from the adults dose Young’s formula Age Child dose = x adult dose Age +12 Dilling’s formula Age 20 Child dose = x adult dose
PROPER TIME-INTERVAL  The frequency of dosing is also important  Plasma half life (t 1/2)  The usual dosage interval for the therapeutic use of antibiotics is four times the t ½.
PROPER ROUTE OF ADMINISTRATION  Oral route - most common route  But some of the bacteria are not susceptible to the drug plasma concentrations produced by oral route and hence, parenteral routes are chosen.  Timing of administration
CONSISTENCY OF ROUTE OF ADMINISTRATION  Severity of the infection  After an initial response has been achieved immediate, discontinuation of parenteral therapy should not be done, since this can lead to a fall in therapeutic blood levels, causing recrudescence of the infection.  Bacteria are usually eradicated when the antibiotic is given for 5 to 7 days.
Antibiotic drug-combination therapy - Rationale • Minimize the emergence of antibiotic-resistant microorganisms. • To increase the certainty of a successful clinical outcome. • To treat mixed bacterial infections & severe infections of unknown etiology. • To prevent suprainfection. • To decrease toxicity without decreasing efficacy.
Indications :  In the patients with life threatening sepsis of unknown etiology.  When increased bactericidal effect against a specific organism is desired. e.g.: treatment of Enterococcus infection (penicillin & aminoglycoside)  Prevention of rapid emergence of resistant bacteria . e.g.: Tuberculosis  Treatment of odontogenic infections which could progress to more serious like retropharyngeal space infections. (penicillin and metronidazole)
Rules 1) 2 bactericidal drugs produce, supra-additive effects, but not antagonism i.e. (1+1>2) 2) The combination of a bacteriostatic and a bactericidal drug generally results in diminished effects i.e. (1+1<2) 3) 2 bacteriostatic drugs are never inhibitory i.e. (1+1=2)
PATIENT MONITORING  Adjunctive surgery  Fluid balance  Nutritional support CARE MUST BE TAKEN SPECIFICALLY ON 1. Response to treatment 2. Development of adverse drug reactions
RESPONSE TO TREATMENT  Most commonly, the response begins by the 2nd day and initially produces a subjective sense of feeling better.  There after, objective signs of improvement occur including a decrease in temperature, swelling, pain and lessening of trismus.  Duration of therapy (omfscna vol. 15 Feb 2003)
Antibiotics
 Penicillin was first antibiotic to be used clinically in 1941.  It was miracle that the least toxic drug of its kind was the first to be discovered.  It was originally obtained from the fungus Penicillium notatum, but the present source is a high yeilding mutant of P.chrysogenum.  Penicillinase is a beta lactamase developed by most staphylococci and many gram negative organisms, that is responsible for the breakdown of beta lactam ring
BASED ON THE SUSCEPTIBILITY TO PENICILLINASES AND SPECTRUM OF ACTION, PENICILLINS ARE CLASSIFIED AS:
DOSAGE PHENOXY METHYL PENICILLIN (OR) PENICILLIN (V)  Oral loading dose of 1000 mg followed by 500 mg every six hours for 6 – 10 days.  For severe infections antibiotics is taken every 4 hours to maintain more constant serum level CLOXACILLIN  250mg to 500 mg orally every 6 hours. AMOXICILLIN  500 mg every 8 hours for 6 – 10 days. CARBOXY PENICILLIN’S  125 to 250mg TID (or)  200 to 1000 mg IM /IV
TRADE NAMES AMOXICILLIN- 250/500mg EVERY 8 HOURS ACTIMOX AXL BLUEMOX MOX NOVAMOX WITH LACTOBACILLUS SPORES AMOLAC 500 NODIMOX LB NOVAMOX LB SWIMOX LB
BENZYL PENICILLIN (PENCILLIN G) •PnG is a narrow spectrum antibiotic; activity is limited primarily to gram positive bacteria •Is available in the form of water soluble sodium and potassium salts •This salts in a dry state are stable at room temperature for years. •The aqueous solution requires refrigeration and deteriorates considerably with in 72 hours. Antibacterial activity • Most potent, inhibits the growth of susceptible organism. • Mainly gram +ve, gram –ve cocci and some gram +ve bacilli with exception of enterococci. •Cocci – Highly sensitive – Streptococci, Pneumococci, Staph. aureus, N. gonorrhoeae, N. meningitis •Bacilli – B. anthracis, Corynebacterium diphtheriae, clostridium tetany and spirochetes . •Actinomyces israelii is moderately sensitive
Absorption fate and excretion : • About 1/3 of drug is activated on oral administration. • Absorbed from the duodenum. • Because of the inadequate absorption the oral dose should be 4/5 times larger than the intramuscular dose. • As food interferes with its absorption PnG should be given orally atleast 30 min after food or 2 to 3 hours before food. • B. Pencillin in aqueous solution is rapidly absorbed after SC or IM administration. • Peak plasma level of 8 to 10 units per ml is reached with in 15 to 30 min and drug disappears from plasma with in 3-6 hours.
• Widely distributed in the body and significant amounts appear in liver, bile, kidney, jointfluid and intestine. • PnG is excreted mainly by the kidney but in small part in the bile and other routes. • 50% drug is eliminated in urine with in first hour.
ADVERSE REACTIONS : a) Miscellaneous reactions : • Nausea and vomiting on oral PnG • Sterile inflammatory reaction at the site of IM inj. • Prolonged IV administration may cause thrombophlebitis • Accidental IV administration of procaine PP cause anxiety, mental disturbances paraesthesia and convulsions b) Intolerance : • Major problem with PnG includes idiosyncratic, anaphylactic and allergic reactions
c) Other allergic reactions are • Skin rashes • Serum sickness • Renal disturbance • Hemolytic disturbance • Anaphylaxis • Jarisch herxheimer reaction • Super infection • Hyperkalemia
Uses : PnG is the drug of choice for infections 1. Streptococcal infections 2. Pneumococcal infections 3. Meningococcal infections 4. Gonorrhoea 5. Syphilis 6. Diphtheria 7. Tetanus and gas gangrene 8. Prophylactic uses
SEMI SYNTHETIC PENICILLINS The major drawbacks of benzyl penicillin are : 1. Inactivation by the gastric hydrochloric acid 2. Short duration of action 3. Poor penetration into CSF 4. Activity mainly against gram +ve organism 5. Possibility of anaphylaxis Attempts therefore have been made to synthesize pencillin free from such drawbacks. P.chrysogenum produces natural penicillins which produce the 6 amino-penicillanic acid (6-APA) nucleus. The attachment of side chains are inhibited and instead various organic radicals can be substituted. Thus a variety of semisynthetic resins are produced.
I) Acid resistant pencillins : 1. Potassium phenoxymethyl penicillin (penicillin V) • Similar antibacterial spectrum like benzylpenicillin. • More active against resistant staphylococci • Less inactivated by the gastric acid. • Plasma levels achieved is 2 to 5 times higher than benzylpenicillin. • 50-70% is bond to plasma proteins. • 25% of drug is eliminated in urine • Available as 60 & 125 mg tablets. • Administered in the dose of 250 –500 mg at 4-8 hours intervals, atleast 30 min before food. • This can be used in less serious infections (pneumocci and streptococci).
Dose : infants 60 mg, children 125-250 mg given 6 hourly CRYSTAPEN-V, KAYPEN, PENIVORAL 65, 130, 125, 250 mg tablets125 mg/5 ml dry ser 2. Potassium phenoxyethyl penicillin and 3. Azidocillin Both have similar properties to penicillin V and no difference in the antibacterial effect
II) Pencillinase resistant pencillins : 1. Methicillin 1. Effective in staphylococci 2. It is given IM or IV (slow) in the dose of 1 gm every 4-6 hours. 3. Haematuria, albuminuria and reversible interstitial nephritis are the special adverse effect of methicillin. 2. Cloxacillin 1. Weaker antibacterial activity. 2. Distrubuted thro out the body, but highest s concentration in kidney and liver. 30% excreted in urine. 3. Oral dose for adults 2-4 gm divided into 4 portions children 50-100mg/kg/day. 4. IM adults 2-12 gm/day, children 100-300 mg/kg/day every 4-6 hours. BIOCLOX, KLOX, CLOCILIN 0.25, 0.5 gm cap, 0.5 gm/vial.
Oxacillin, Dicloxacillin, Flucloxacillin are other isoxazolyl penicillins, similar to cloxacillin, but not marketed in India. Nafcillin : More active than methicillin and cloxacillin but less active than PnG 80% of drug bonds with plasma proteins excreted by liver in patients with renal failure. Dose is similar to cloxacillin.
III) Extended spectrum pencillins : 1. Amino pencillins 1. Ampicillin – • Antibacterial activity is similar to that of PnG that is more effective than PnG against a variety of gram-ve bacteria • Drug is effective against H.influenzae strep.viridans, N.gonorrhea, Salmonella, shigellae, Klebsilla and enterococci. Absorption, fate and excretion : • Oral absorption is incomplete but adequate • Food interferes with absorption • Partly excreted in bile and partly by kidney
Dose : 0.5-2 gm oral/IM or IV depending on severity of infection every 6 hours Children : 25-50 mg/kg/day AMPILIN, ROSCILLIAN, BIOCILIN – 250, 500 mg cap 100mg/ml ped drops, 250 mg/ml dry syr, 1 gm/vial inj. USES : • Urinary tract infections • Respiratory tract infections • Meningitis • Gonorrhoea • Typhoid fever • Bacillary dysentry • Septicaemias • SBE
Adverse effects : • Diarrhoea is frequent • Skin rashes is more common • Unabsorbed drug irritates lower intestines • Patient with history of hypersensitivity to PnG should not be given ampicillin.
AMOXYCILLIN : • This is a semisynthetic penicillin • (amino-p-hydroxy-benzylpencillin) • Antibacterial spectrum is similar to ampicillin but less effective than ampicillin for shigellosis. • Oral absorption is better; food does not interfere; higher and more sustained blood levels are produced. • It is less protein bond and urinary excretion is higher than that of ampicillin. • Incidence of diarrhoea is less
Dose : 0.25-1 g TDS oral; AMOXYLIN, NOVAMOX, SYNAMOX, MOX, AMOXIL 250, 500 mg cap, 125 mg/5ml dry syr, 500 mg/vial inj. USES : • Typhoid • Bronchitis • Urinary infection • SBE • Gonorrhoea
Carboxy penciillins : The Carboxypenicillins are extended spectrum penicillins, because they inhibit a wide variety of aerobic gram-ve bacilli They are ineffective against most strains of staph. Aureus They have following properties : 1. Highly active against anaerobes 2. Most useful in infections caused by other gram-ve rods 3. Act synergistically with amino glycoside antibiotics, particularly enterobacteriacea. 4. Much less active than penicillin G against gram+ve organisms 5. The CNS penetration is about 10% of their serum levels and hence not recommended for the treatment of meningeal infections.
CARBENICILLIN • Has similar spectrum as other penicillin • Weaker antibacterial activity than ampicillin • Active against –pseudomonas, proteus • < Salmonella , E coli Enterobacter • Inactive against – klebsiella and gram –ve cocci • Acid labile and has to be given by parenteral route only • Peak plasma level is 2hours and excreted in urine
Dose : 1-2g im/iv 4-6hours Adverse effects : • Cause congestive heart failure • Bleeding disorders-impaired platelet function Uses : • Pseudomonas ,burns, UTI and septicemia • PYOPEN,CARBELIN 1g,5g per vial
UREIDOPENICILLINS – PIPERACILLIN ( PIPRIL)- antipseudomonal pencillin Has similar indications of carbenicillin
WHAT IF…. PATIENT IS ALLERGIC TO PNC? patient allergic to penicilln early infection late infection periodontal infection clindamycin erythromycin metrinidazole doxycyclin
CEPHALOSPORINS  Group of semi-synthetic antibiotics derived from cephalosporin, “C” obtained from fungus Cephalosporium.  Chemically related to penicillins (contain β-lactum ring)  Have been classified as first, second, third and fourth generation. Based on: When the were introduced Bacterial susceptibility patterns Resistance to -lactamase Pharmacokinetics
FIRST GENERATION These are active against gram-positive bacteria but weaker against gram-negative bacteria. e.g.Cephalothin, cephalexin. SECOND GENERATION More active against gram-negative organisms with some members active against anaerobes. e.gCefuroxime, Cefaclor THIRD GENERATION Very active against gram–negative and gram-positive, but not effective against anaerobes. e.gCefotaxime, Cefixime FOURTH GENERATION Very effective against anaerobes and resistant to beta lactamase .e.g.Cefipime
TRADE NAMES CEFADROXIL-500mg Every 12 hrs ACTIDROX ACUDROX CEDROX CEFOXID CEFUROXIME 125 mg Every 12 hrs ACTUM CEFTAZ CEFEXL MAXIM
CEFIXIME -200-400 mg in a single or two divided doses AFIXIM CEFI CEFEXY NOVAFEX CEFEPIME- 1-2 g 8-12 hourly BIOPIME CEPIME NOVAPIME
TETRACYCLINES  Obtained from soil actinomycetes.  The first to be introduced was chlortetracycline in 1948 under the name “Aureomycin’.  These bind to 30S ribosomal subunit and inhibit the binding of aminoacyl-tRNA to the A site.  On the basis of chronology of development they may be divided in to 3 groups Group – I Group – II Group – III Chlortetracycline Domeclocycline Doxycycline Oxytetracycline Methacycline Minocycline Tetracycline
PRECAUTIONS  Not used during pregnancy, lactation ,childhood.  Avoided in patients on diuretics- blood urea levels rise in such cases  Used cautiously in renal and hepatic patients.  Not used with penicillins
TRADE NAMES TETRACYCLINE- 500mg every 8 hrs ACHROMYCIN HOSTACYCLINE TETLIN DOXYCYCLINE-100 mg every 12 hrs APIDOX DOXYN SWIDOX TETRADOX Antibiotics
MACROLIDES  These are antibiotics having a macrocyclic lactone ring with attached sugars.  Erythromycin is the first member discovered in 1950s.  For the past 40 years erythromycin has been the only macrolide antibiotic.  Roxythromycin, Clarithromycin, Azithromycin are the next additions in macrolides.
ERYTHROMYCIN  It was Isolated from Streptomyces erythreus in 1952.  Water solubility of erythromycin is limited and the solution remains stable only when kept in cold.  It acts by inhibiting bacterial protein synthesis. It combines with 50S ribosomes subunits and interferes with translocation. ANTIMICROBIAL SPECTRUM It is narrow, includes mostly gram positive organisms and few gram negative bacteria and overlaps considerably with that of Penicillin G.
DOSAGE Erythromycin estolate- 250-500mg qid. ALTHROCIN, E-MYCIN Erythromycin stearate- 250-500mg qid ERYTHROCIN, ERYSTER Erythromycin base - 250-500mg qid. ERYSAFE, EROMED
DRUG INTERACTIONS 1) Interaction with warfarin leads to serious bleeding in patients undergoing anticoagulation therapy. 2) Interaction with lovastatin, drug given for cholesterol reduction leads to severe muscle weakness. 3) Interaction with Theophylline, a bronchodilator used for asthmatic patients leads to toxic concentrations of the same resulting in cardiac arrhythmias
Newer macrolides were made Azithromycin –loading dose;500mg 1st day Followed by 250mg daily. AZID AZEE AZIPAR AZIWIN Clarithromycin – 250-500mg every 12 hrs for 6-10 days. CLAR CLARIWIN MACLAR
METRONIDAZOLE  Introduced in 1959 for the treatment of “Trichomonas Vulgaris”.  Used especially for serous anaerobic infections, including those of the orofacial region.  Distributed well in to bone, saliva, mucosa, and even brain abscess.  Bactericidal
TRADE NAMES METRONIDAZOLE-200-400mg every 8 hrs FLAGYL METROGYL MET METRONIDAZOLE AND AMOXYCILLIN 200mg + 250 mg every 8 hrs STEDMOX -M
PREVENTING RESISTANCE TO DRUGS  Limit the use of antimicrobial agents to the treatment of specific pathogens sensitive to the drug being used.  Notorious-Make sure doses are high enough, and the duration of drug therapy long enough , combination therapy.  To be cautious about the indiscriminate, inadequate or unduly prolonged use of anti-infectives
SUPERINFECTIONS:  During treatment normal host bacteria that are susceptible to the drugs are eliminated.  In the normal state, these bacteria live in peaceful coexistence with the host and by their physical presence prevent bacteria capable of producing disease from growing in large numbers.  The normal flora acts as a defense mechanisms, but when the indigenous flora is altered, the pathogenic bacteria resistant to an antibiotic may cause a secondary infection, or superinfection.  Example is of candidiasis with the use of penicillin, which eliminates the gram-positive cocci (seen after long term high dose penicillin therapy).
 The use of antibiotics has been standard practice for patients identified as being at risk of developing endocarditis.  The link between dental procedures and IE remains a controversial subject. In 1984, Guntheroth reported a low incidence of bacteremia associated with dental procedures and suggested that meticulous oral hygiene was more important in the prevention of IE than any antibiotic regimen.
Antibiotics should only be prescribed on the basis of a defined need otherwise their use may present more of a risk to the patient than the infection being treated or prevented. Antibiotics can be responsible for various adverse effects, including drug interactions, nausea, gastrointestinal upsets, potentially fatal allergic reactions and antibiotic associated colitis The indiscriminate prescribing of antibiotics can also cause drug resistance which is an emerging and significant problem
CONCLUSION  Although antibiotics do not prevent all post-operative infections, they can reduce their incidence significantly when administered correctly.  We should prescribe effective, short-course therapies, directed at improving the outcome of our patients.  Future treatment strategies will not only include the aggressive use of traditional management methods but also the understanding of normal immune system-associated defects and newer antimicrobials.
THANK YOU

More Related Content

PPTX
Antibiotics
byDr Revathy Mohan
 
PPTX
Antibiotics
byAman Ullah
 
PPTX
Antibiotics
byMr. Mata Deen
 
PPTX
Antibiotics: classification and spectrum of action
byBashar Mudallal
 
PPTX
Spectrum of commonly used antibiotics
byMahen Kothalawala
 
PPT
Antibiotics ppt
byCrystal Rose
 
PDF
Antimicrobial drugs 2017
byDr Md Abdullah Yusuf Sohel
 
PPTX
Basics of Antimicrobial Drugs
byASSOCHAM
 
Antibiotics
byDr Revathy Mohan
 
Antibiotics
byAman Ullah
 
Antibiotics
byMr. Mata Deen
 
Antibiotics: classification and spectrum of action
byBashar Mudallal
 
Spectrum of commonly used antibiotics
byMahen Kothalawala
 
Antibiotics ppt
byCrystal Rose
 
Antimicrobial drugs 2017
byDr Md Abdullah Yusuf Sohel
 
Basics of Antimicrobial Drugs
byASSOCHAM
 

What's hot

PPT
2. cephalosporins.ppt
byNEHA BHARTI
 
PDF
ANTIMICROBIAL DRUGS (Part 2)
bySurya Amal
 
PPTX
Beta lactam antibiotics
byMangeshBansod2
 
PPTX
Cephalosporins
byVIJAI KUMAR
 
PPTX
Antiviral drugs
byRahul Bhati
 
PPTX
Quinolones.pptx
bySubramani Parasuraman
 
PPTX
Monobactams and carbapenems
byANUSHA SHAJI
 
PPT
Antimicrobials
byDr. Majid Mohiuddin (Hashmi)
 
PPT
Pharmacology of Antibiotics
byGanapathy Tamilselvan
 
PPTX
Quinolones
byJagirPatel3
 
PPTX
Quinolones
byRahul Kunkulol
 
PPT
Tetracyclin and chloramphenicol: Pharmacology, Mechanism of Action & Uses
byDr. Arun Sharma, MD
 
PPT
PHARMACOLOGY - ANTIBIOTICS
byNurse ReviewDotOrg
 
PDF
Introduction to antimicrobials
byZainab&Sons
 
PPTX
Cell wall inhibitors
byZainab&Sons
 
PPTX
Beta Lactam Antibiotics
bySaurav Ch. Sarma
 
PPT
Aminoglycosides
byDrSahilKumar
 
PPT
Fluoroquinolones
byDrSahilKumar
 
PPT
Chloramphenicol & Tetracyclines
byDrSahilKumar
 
PPTX
Aminoglycosides
byIqraMalik83
 
2. cephalosporins.ppt
byNEHA BHARTI
 
ANTIMICROBIAL DRUGS (Part 2)
bySurya Amal
 
Beta lactam antibiotics
byMangeshBansod2
 
Cephalosporins
byVIJAI KUMAR
 
Antiviral drugs
byRahul Bhati
 
Quinolones.pptx
bySubramani Parasuraman
 
Monobactams and carbapenems
byANUSHA SHAJI
 
Antimicrobials
byDr. Majid Mohiuddin (Hashmi)
 
Pharmacology of Antibiotics
byGanapathy Tamilselvan
 
Quinolones
byJagirPatel3
 
Quinolones
byRahul Kunkulol
 
Tetracyclin and chloramphenicol: Pharmacology, Mechanism of Action & Uses
byDr. Arun Sharma, MD
 
PHARMACOLOGY - ANTIBIOTICS
byNurse ReviewDotOrg
 
Introduction to antimicrobials
byZainab&Sons
 
Cell wall inhibitors
byZainab&Sons
 
Beta Lactam Antibiotics
bySaurav Ch. Sarma
 
Aminoglycosides
byDrSahilKumar
 
Fluoroquinolones
byDrSahilKumar
 
Chloramphenicol & Tetracyclines
byDrSahilKumar
 
Aminoglycosides
byIqraMalik83
 

Viewers also liked

PPTX
Antibiotics
byAhmed Galal Mohamed
 
PPT
Antibiotics
bysatyawankumar
 
PPTX
Lecture 02
byDr. Geoffrey K. K. Maiyoh
 
PDF
Antibiotic classification
byAparna Rajeevi
 
PPTX
bassem julphar antibiotic classification
byBassem attia
 
PDF
Antibiotics
bySurya Prajapat
 
PPT
Antibiotics: Introduction to classification
byBhoj Raj Singh
 
PPTX
Classification of antibiotics
byLuis George Lopez Cadenaz
 
PPTX
Presentation1
byJackline Lado
 
PPT
Guidelines For Antibiotic Use by doctor Saleem
byMuhammad Saleem
 
PPTX
Antibiotics
byHammad Tariq
 
PPT
Antibiotics
byMD Specialclass
 
PPTX
Presentation on antibiotics.
byphmosarrof
 
Antibiotics
byAhmed Galal Mohamed
 
Antibiotics
bysatyawankumar
 
Lecture 02
byDr. Geoffrey K. K. Maiyoh
 
Antibiotic classification
byAparna Rajeevi
 
bassem julphar antibiotic classification
byBassem attia
 
Antibiotics
bySurya Prajapat
 
Antibiotics: Introduction to classification
byBhoj Raj Singh
 
Classification of antibiotics
byLuis George Lopez Cadenaz
 
Presentation1
byJackline Lado
 
Guidelines For Antibiotic Use by doctor Saleem
byMuhammad Saleem
 
Antibiotics
byHammad Tariq
 
Antibiotics
byMD Specialclass
 
Presentation on antibiotics.
byphmosarrof
 

Similar to Antibiotics

PPTX
ANTIBIOTICS.pptx
byAmeerasalahudheen1
 
PPTX
6.antibiotics in oral and maxillofacial surgery
byTejaswini498924
 
PPTX
Anti-Microbials.pptx
byPATNIHUSAINIBLOODBAN
 
PDF
Principles of antimicrobial therapy - Pharmacology
byAreej Abu Hanieh
 
PPTX
ANTIBIOTICS IN ORAL & MAXILLOFACIAL SURGERY
byankitaraj63
 
PDF
Antibacterial drugs medical.pdf
byTharushiCiriatthage
 
PPTX
ANTIBIOTICS SEMINAR.pptx department of prosthodotics
byAnjaliPrasannan2
 
PPTX
penicillin in dentistry (ANTIBIOTICS) - by shefali jain
bypradeepjain24
 
PPT
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
PPT
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
PPT
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
PDF
L P 1 Antimicrobial Therapy - 2024_٠٨٠٣٢٧.pdf
byArfatAlmuallad
 
PDF
3-Antimicrobialfggggggg Chemotherapy.pdf
byht549sqbpt
 
PPT
Antibiotics and antibacterial drugs
byvasanramkumar
 
PPTX
Antibiotics 150406092448-conversion-gate01
byMostafa Abd El Fattah
 
PPTX
Antibiotics
byMohammed Ezz El-din
 
PDF
Antibiotics
byWalahassan4
 
PPTX
Antibiotics & analgesics dentistry
byHema Latha
 
PPTX
Antibiotics in pediatric dentistry
byShubham Gupta
 
PPTX
Antibiotics, analgesics and emergency drugs
byAbhishek Roy
 
ANTIBIOTICS.pptx
byAmeerasalahudheen1
 
6.antibiotics in oral and maxillofacial surgery
byTejaswini498924
 
Anti-Microbials.pptx
byPATNIHUSAINIBLOODBAN
 
Principles of antimicrobial therapy - Pharmacology
byAreej Abu Hanieh
 
ANTIBIOTICS IN ORAL & MAXILLOFACIAL SURGERY
byankitaraj63
 
Antibacterial drugs medical.pdf
byTharushiCiriatthage
 
ANTIBIOTICS SEMINAR.pptx department of prosthodotics
byAnjaliPrasannan2
 
penicillin in dentistry (ANTIBIOTICS) - by shefali jain
bypradeepjain24
 
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
Antimicrobial chemotherapy &amp; bacterial resistance dr. ihsan alsaimary
bydr.Ihsan alsaimary
 
L P 1 Antimicrobial Therapy - 2024_٠٨٠٣٢٧.pdf
byArfatAlmuallad
 
3-Antimicrobialfggggggg Chemotherapy.pdf
byht549sqbpt
 
Antibiotics and antibacterial drugs
byvasanramkumar
 
Antibiotics 150406092448-conversion-gate01
byMostafa Abd El Fattah
 
Antibiotics
byMohammed Ezz El-din
 
Antibiotics
byWalahassan4
 
Antibiotics & analgesics dentistry
byHema Latha
 
Antibiotics in pediatric dentistry
byShubham Gupta
 
Antibiotics, analgesics and emergency drugs
byAbhishek Roy
 

Recently uploaded

PDF
Application of ICT Lecture 3 ICT in Education.pdf
byKhalil Khan Marwat
 
PPTX
How to Create a Search Panel in Odoo 18
byCeline George
 
PPTX
CARDIOTONIC CHAPTER NO. 5 PHARMACOGNOSY DIGITALIS AND ARJUNA BARK
byGanu Gavade
 
PDF
First Semester BCA Exam 2025 – Constitution Values – 1 Solved Answers.pdf
byKuvempu University
 
PPTX
CHAPTER NO.6 PLANT FIBRES USED AS SURGICAL DRESSINGS.pptx
byGanu Gavade
 
PDF
Pharmaceutical Biotechnology unitI Notes
byBhagyashree Prakash Gajbhare
 
PPTX
GRADE-1-Q3-MATH-WEEK-6.pptx_202633333333
byKennethGraceAngeles1
 
PDF
BỘ 20 ĐỀ THI GIẢ LẬP MỨC ĐỘ 9+ KỲ THI TỐT NGHIỆP TRUNG HỌC PHỔ THÔNG NĂM 2026...
byNguyen Thanh Tu Collection
 
PPTX
English 8 Q3 Wk6.pptx prewriting opinion editorial article
byjacquelyncastre03
 
PDF
Application of Information and Communication Technology Content.pdf
byKhalil Khan Marwat
 
PPTX
English 8 Q3 Wk8.pptx opinion editorial article( Writing , Revising, Editing...
byjacquelyncastre03
 
PPTX
Capacity Building Programme for Teachers on Equitable and Inclusive Education
byMUKHTAR133762
 
PPTX
Mixing Pharmaceutical Engineering .pptxx
byShraddha Bandgar
 
PPTX
How to Manage Credit Limits in Odoo 18 Accounting
byCeline George
 
PPTX
How to use sorted() method in Odoo 18
byCeline George
 
PPTX
Road Safety as a shared responsibility, 2026
bySougata Pal
 
PDF
PROBLEM SLOVING AND PYTHON PROGRAMMING Unit 1.pdf
byA R SIVANESH M.E., (Ph.D)
 
PDF
how to write your (written) research instruments
byThelma Villaflores
 
PPTX
Prepositions of Place : English Grammar Presentation
byPintoo Dhillon
 
PPTX
Prenatal Development of Cranium, Jaw and Face
byHarshita Dhanrajani
 
Application of ICT Lecture 3 ICT in Education.pdf
byKhalil Khan Marwat
 
How to Create a Search Panel in Odoo 18
byCeline George
 
CARDIOTONIC CHAPTER NO. 5 PHARMACOGNOSY DIGITALIS AND ARJUNA BARK
byGanu Gavade
 
First Semester BCA Exam 2025 – Constitution Values – 1 Solved Answers.pdf
byKuvempu University
 
CHAPTER NO.6 PLANT FIBRES USED AS SURGICAL DRESSINGS.pptx
byGanu Gavade
 
Pharmaceutical Biotechnology unitI Notes
byBhagyashree Prakash Gajbhare
 
GRADE-1-Q3-MATH-WEEK-6.pptx_202633333333
byKennethGraceAngeles1
 
BỘ 20 ĐỀ THI GIẢ LẬP MỨC ĐỘ 9+ KỲ THI TỐT NGHIỆP TRUNG HỌC PHỔ THÔNG NĂM 2026...
byNguyen Thanh Tu Collection
 
English 8 Q3 Wk6.pptx prewriting opinion editorial article
byjacquelyncastre03
 
Application of Information and Communication Technology Content.pdf
byKhalil Khan Marwat
 
English 8 Q3 Wk8.pptx opinion editorial article( Writing , Revising, Editing...
byjacquelyncastre03
 
Capacity Building Programme for Teachers on Equitable and Inclusive Education
byMUKHTAR133762
 
Mixing Pharmaceutical Engineering .pptxx
byShraddha Bandgar
 
How to Manage Credit Limits in Odoo 18 Accounting
byCeline George
 
How to use sorted() method in Odoo 18
byCeline George
 
Road Safety as a shared responsibility, 2026
bySougata Pal
 
PROBLEM SLOVING AND PYTHON PROGRAMMING Unit 1.pdf
byA R SIVANESH M.E., (Ph.D)
 
how to write your (written) research instruments
byThelma Villaflores
 
Prepositions of Place : English Grammar Presentation
byPintoo Dhillon
 
Prenatal Development of Cranium, Jaw and Face
byHarshita Dhanrajani
 

Antibiotics

  • 1.
    ANTIBIOTICS Presented by Department of Oral Medicine and radiology Dr Sarah Nazeer
  • 2.
    CONTENTS  Introduction  History  Classification  Mechanism of action  Principles of antibiotic administration  Individual antibiotics  Clinical implications  Conclusion
  • 3.
    Coined by Walksmanin 1942 Ancient Greek ἀντί- Anti - against βίος -Biotic - Life Antibiotics are substances produced by microorganisms which suppress the growth of or kill other microorganisms at very low concentrations. Both synthetic +microbiologically produced drugs=ANTIMICROBIAL AGENT.
  • 4.
  • 5.
    1877 Louis PasteurInhibition of some microbes by others; anthrax(Bacillus anthracis)
  • 8.
  • 9.
    Classification of Antibiotics Inhibitors of Cell Wall Synthesis Protein Synthesis Inhibitors Inhibitors of Nucleic Acid Synthesis and Function Others: Vancomycine Bacitracin ß-lactam antibiotics Monobactams Chloramphenicole Carbapenems Cephalosporins Clindamycine Macrolides Penicillins Tetracyclines Antistaph: Methicillin Natural: Penicillin G Penicillin V Extended spectrum: Amoxicillin Ampicillin Erythromycine Azithromycine Clarithromycin e Quinolones Metronidazole Doxycycline Minocycline Tetracycline Ciproflaxicine Flagyl
  • 10.
    Antibiotics A. CHEMICALSTRUCTURE Sulfonamides- Sulfadiazines, Sulfones, Dapsone, Paraaminosalicylic Acid(pas) Diaminopyrimidines- Trimethoprim -Lactam Antibiotics- Penicillins, Cephalosporins, Monobactums Tetracyclines- Oxytetracycline, Doxycycline
  • 11.
    Antibiotics  NitrobenzeneDerivative- Chloramphenicol  Aminoglycosides- Streptomycin, Gentamycin, Neomycin  Macrolide Antibiotics- Erythromycin, Roxithromycin  Polypeptide Antibiotics- Polymixin-B , Colistin, Bacitracin
  • 13.
  • 14.
     Interfere WithD.N.A Synthesis- Acyclovir  Interfere With Intermediary Metabolism- Sulfonamides, Sulfones, Ethambutol C. TYPE OF ORGANISMS AGAINST WHICH PRIMARILY ACTIVE  Antibacterial- Pencillins, Aminoglycosides, Erythromycin  Antifungal- Griesofulvin, Ketoconazole  Antiviral- Acyclovir, Zidovudine  Antiprotozoal- Chloroquine, Metronidazole  Antihelminthic- Mebendazole
  • 15.
    Antibiotics D. SPECTRUMOF ACTIVITY NARROW SPECTRUM BROAD SPECTRUM - Penicillin –G - Tetracyclines - Streptomycin -Chloramphenicol - Erythromycin E. TYPE OF ACTION PRIMARILY BACTERIOSTATIC - Sulphonamides - Tetracyclines - Chloramphenicol - Erythromycin
  • 16.
    Antibiotics PRIMARILY BACTERIOCIDAL -Penicillin -Cephalosporins -Aminoglycosides -Polypeptides -Ciprofloxacin F. ANTIBIOTICS ARE OBTAINED FROM  Fungi - Penicillin -Cephalosporin -Griesofulvin
  • 17.
    Antibiotics Bacteria -Polymyxin– B -Colistin -Bacitracin Actinomycetes -Aminoglycosides -Tetracyclines -Chloramphenicol G. RAPID KILLING ANTIBIOTICS -Penicillins -Cephalosporins -Metronidazole (Flagyl)
  • 18.
    Bactericidal- the abilityto kill the bacteria Bacteriostatic- the ability to inhibit or retard the growth of bacteria BACTERIOSTATIC V/S BACTERICIDAL Aminoglycosides Bacitracin Cephalosporins Metronidiazole vancomycin Penicillins ciprofloxacin streptomycin cotrimoxazole Chloramphenicol Clindamycin erythromycin Sulfonamides Tetracycline trimethoprim
  • 19.
    ANTI - MICROBIALDRUG TARGETS
  • 20.
     Erythromycin 250-500Mg Qid  Clindamycin 150-300 Mg Qid Or 300-450 Mg Qid  Cephalosporins  Tetracyclines 250-500 Mg 2-4 Times Daily.  Doxycycline 100 Mg Every 12 Hours First Day Then 100 Mg Daily  Ciprofloxacin 250-500 Mg , 12th Hourly  Metronidazole ( Flagyl) Loading Dose - 1 Gram IV, maintainence Dose 500 Mg Qid, Oral Dose 500 Mg Qid.
  • 21.
    MECHANISMS OF ANTIBACTERIAL RESISTANCE (1)  Structurally modified antibiotic target site, resulting in:  Reduced antibiotic binding  Formation of a new metabolic pathway preventing metabolism of the antibiotic
  • 22.
    STRUCTURALLY MODIFIED ANTIBIOTICTARGET SITE Interior of organism Cell wall Binding Target site Antibiotic Antibiotics normally bind to specific binding proteins on the bacterial cell surface
  • 23.
    STRUCTURALLY MODIFIED ANTIBIOTICTARGET SITE Antibiotics are no longer able to bind to modified binding proteins on the bacterial cell surface Interior of organism Cell wall Modified target site Antibiotic Changed site: blocked binding
  • 24.
    MECHANISMS OF ANTIBACTERIAL RESISTANCE (2)  Altered uptake of antibiotics, resulting in:  Decreased permeability  Increased efflux
  • 25.
    ALTERED UPTAKE OFANTIBIOTICS: DECREASED PERMEABILITY Interior of organism Cell wall Porin channel into organism Antibiotic Antibiotics normally enter bacterial cells via porin channels in the cell wall
  • 26.
    ALTERED UPTAKE OFANTIBIOTICS: DECREASED PERMEABILITY Interior of organism Cell wall New porin channel into organism Antibiotic New porin channels in the bacterial cell wall do not allow antibiotics to enter the cells
  • 27.
    ALTERED UPTAKE OFANTIBIOTICS: INCREASED EFFLUX Antibiotics enter bacterial cells via porin Interior of organism Cell wall channels in the cell wall Porin channel through cell wall Antibiotic Entering Entering
  • 28.
    ALTERED UPTAKE OFANTIBIOTICS: INCREASED EFFLUX Once antibiotics enter bacterial cells, they are Interior of organism Cell wall immediately excluded from the cells via active pumps Porin channel through cell wall Antibiotic Entering Exiting Active pump
  • 29.
    MECHANISMS OF ANTIBACTERIAL RESISTANCE (3)  Antibiotic inactivation  bacteria acquire genes encoding enzymes that inactivate antibiotics Examples include:  -lactamases  aminoglycoside-modifying enzymes  chloramphenicol acetyl transferase
  • 30.
    ANTIBIOTIC INACTIVATION Interiorof organism Antibiotic Cell wall Binding Target site Enzyme Inactivating enzymes target antibiotics
  • 31.
    ANTIBIOTIC INACTIVATION Enzymesbind to antibiotic molecules Enzyme Binding Target site Interior of organism Antibiotic Cell wall Enzyme binding
  • 32.
    ANTIBIOTIC INACTIVATION Enzymesdestroy antibiotics or prevent binding to target sites Enzyme Target site Interior of organism Antibiotic Cell wall Antibiotic destroyed Antibiotic altered, binding prevented
  • 33.
    PRINCIPLES OF ANTIBIOTIC ADMINISTRATION
  • 34.
    PROPER DOSE Prescribe or administer sufficient amounts to achieve the desired therapeutic effect, but not enough to cause injury to the host. o Relationship between antibiotic dose/ concentration. o Relationship between dose and body weight Individual dose = BW(kg)/70 x avg adult dose  Under-dosing – emergence of bacterial resistance.
  • 35.
    AGE The doseof drug for children is often calculated from the adults dose Young’s formula Age Child dose = x adult dose Age +12 Dilling’s formula Age 20 Child dose = x adult dose
  • 36.
    PROPER TIME-INTERVAL The frequency of dosing is also important  Plasma half life (t 1/2)  The usual dosage interval for the therapeutic use of antibiotics is four times the t ½.
  • 37.
    PROPER ROUTE OFADMINISTRATION  Oral route - most common route  But some of the bacteria are not susceptible to the drug plasma concentrations produced by oral route and hence, parenteral routes are chosen.  Timing of administration
  • 38.
    CONSISTENCY OF ROUTEOF ADMINISTRATION  Severity of the infection  After an initial response has been achieved immediate, discontinuation of parenteral therapy should not be done, since this can lead to a fall in therapeutic blood levels, causing recrudescence of the infection.  Bacteria are usually eradicated when the antibiotic is given for 5 to 7 days.
  • 39.
    Antibiotic drug-combination therapy- Rationale • Minimize the emergence of antibiotic-resistant microorganisms. • To increase the certainty of a successful clinical outcome. • To treat mixed bacterial infections & severe infections of unknown etiology. • To prevent suprainfection. • To decrease toxicity without decreasing efficacy.
  • 40.
    Indications : In the patients with life threatening sepsis of unknown etiology.  When increased bactericidal effect against a specific organism is desired. e.g.: treatment of Enterococcus infection (penicillin & aminoglycoside)  Prevention of rapid emergence of resistant bacteria . e.g.: Tuberculosis  Treatment of odontogenic infections which could progress to more serious like retropharyngeal space infections. (penicillin and metronidazole)
  • 41.
    Rules 1) 2bactericidal drugs produce, supra-additive effects, but not antagonism i.e. (1+1>2) 2) The combination of a bacteriostatic and a bactericidal drug generally results in diminished effects i.e. (1+1<2) 3) 2 bacteriostatic drugs are never inhibitory i.e. (1+1=2)
  • 42.
    PATIENT MONITORING Adjunctive surgery  Fluid balance  Nutritional support CARE MUST BE TAKEN SPECIFICALLY ON 1. Response to treatment 2. Development of adverse drug reactions
  • 43.
    RESPONSE TO TREATMENT  Most commonly, the response begins by the 2nd day and initially produces a subjective sense of feeling better.  There after, objective signs of improvement occur including a decrease in temperature, swelling, pain and lessening of trismus.  Duration of therapy (omfscna vol. 15 Feb 2003)
  • 44.
  • 46.
     Penicillin wasfirst antibiotic to be used clinically in 1941.  It was miracle that the least toxic drug of its kind was the first to be discovered.  It was originally obtained from the fungus Penicillium notatum, but the present source is a high yeilding mutant of P.chrysogenum.  Penicillinase is a beta lactamase developed by most staphylococci and many gram negative organisms, that is responsible for the breakdown of beta lactam ring
  • 47.
    BASED ON THESUSCEPTIBILITY TO PENICILLINASES AND SPECTRUM OF ACTION, PENICILLINS ARE CLASSIFIED AS:
  • 48.
    DOSAGE PHENOXY METHYLPENICILLIN (OR) PENICILLIN (V)  Oral loading dose of 1000 mg followed by 500 mg every six hours for 6 – 10 days.  For severe infections antibiotics is taken every 4 hours to maintain more constant serum level CLOXACILLIN  250mg to 500 mg orally every 6 hours. AMOXICILLIN  500 mg every 8 hours for 6 – 10 days. CARBOXY PENICILLIN’S  125 to 250mg TID (or)  200 to 1000 mg IM /IV
  • 49.
    TRADE NAMES AMOXICILLIN-250/500mg EVERY 8 HOURS ACTIMOX AXL BLUEMOX MOX NOVAMOX WITH LACTOBACILLUS SPORES AMOLAC 500 NODIMOX LB NOVAMOX LB SWIMOX LB
  • 51.
    BENZYL PENICILLIN (PENCILLING) •PnG is a narrow spectrum antibiotic; activity is limited primarily to gram positive bacteria •Is available in the form of water soluble sodium and potassium salts •This salts in a dry state are stable at room temperature for years. •The aqueous solution requires refrigeration and deteriorates considerably with in 72 hours. Antibacterial activity • Most potent, inhibits the growth of susceptible organism. • Mainly gram +ve, gram –ve cocci and some gram +ve bacilli with exception of enterococci. •Cocci – Highly sensitive – Streptococci, Pneumococci, Staph. aureus, N. gonorrhoeae, N. meningitis •Bacilli – B. anthracis, Corynebacterium diphtheriae, clostridium tetany and spirochetes . •Actinomyces israelii is moderately sensitive
  • 52.
    Absorption fate andexcretion : • About 1/3 of drug is activated on oral administration. • Absorbed from the duodenum. • Because of the inadequate absorption the oral dose should be 4/5 times larger than the intramuscular dose. • As food interferes with its absorption PnG should be given orally atleast 30 min after food or 2 to 3 hours before food. • B. Pencillin in aqueous solution is rapidly absorbed after SC or IM administration. • Peak plasma level of 8 to 10 units per ml is reached with in 15 to 30 min and drug disappears from plasma with in 3-6 hours.
  • 53.
    • Widely distributedin the body and significant amounts appear in liver, bile, kidney, jointfluid and intestine. • PnG is excreted mainly by the kidney but in small part in the bile and other routes. • 50% drug is eliminated in urine with in first hour.
  • 54.
    ADVERSE REACTIONS : a) Miscellaneous reactions : • Nausea and vomiting on oral PnG • Sterile inflammatory reaction at the site of IM inj. • Prolonged IV administration may cause thrombophlebitis • Accidental IV administration of procaine PP cause anxiety, mental disturbances paraesthesia and convulsions b) Intolerance : • Major problem with PnG includes idiosyncratic, anaphylactic and allergic reactions
  • 55.
    c) Other allergicreactions are • Skin rashes • Serum sickness • Renal disturbance • Hemolytic disturbance • Anaphylaxis • Jarisch herxheimer reaction • Super infection • Hyperkalemia
  • 56.
    Uses : PnGis the drug of choice for infections 1. Streptococcal infections 2. Pneumococcal infections 3. Meningococcal infections 4. Gonorrhoea 5. Syphilis 6. Diphtheria 7. Tetanus and gas gangrene 8. Prophylactic uses
  • 57.
    SEMI SYNTHETIC PENICILLINS The major drawbacks of benzyl penicillin are : 1. Inactivation by the gastric hydrochloric acid 2. Short duration of action 3. Poor penetration into CSF 4. Activity mainly against gram +ve organism 5. Possibility of anaphylaxis Attempts therefore have been made to synthesize pencillin free from such drawbacks. P.chrysogenum produces natural penicillins which produce the 6 amino-penicillanic acid (6-APA) nucleus. The attachment of side chains are inhibited and instead various organic radicals can be substituted. Thus a variety of semisynthetic resins are produced.
  • 58.
    I) Acid resistantpencillins : 1. Potassium phenoxymethyl penicillin (penicillin V) • Similar antibacterial spectrum like benzylpenicillin. • More active against resistant staphylococci • Less inactivated by the gastric acid. • Plasma levels achieved is 2 to 5 times higher than benzylpenicillin. • 50-70% is bond to plasma proteins. • 25% of drug is eliminated in urine • Available as 60 & 125 mg tablets. • Administered in the dose of 250 –500 mg at 4-8 hours intervals, atleast 30 min before food. • This can be used in less serious infections (pneumocci and streptococci).
  • 59.
    Dose : infants60 mg, children 125-250 mg given 6 hourly CRYSTAPEN-V, KAYPEN, PENIVORAL 65, 130, 125, 250 mg tablets125 mg/5 ml dry ser 2. Potassium phenoxyethyl penicillin and 3. Azidocillin Both have similar properties to penicillin V and no difference in the antibacterial effect
  • 60.
    II) Pencillinase resistantpencillins : 1. Methicillin 1. Effective in staphylococci 2. It is given IM or IV (slow) in the dose of 1 gm every 4-6 hours. 3. Haematuria, albuminuria and reversible interstitial nephritis are the special adverse effect of methicillin. 2. Cloxacillin 1. Weaker antibacterial activity. 2. Distrubuted thro out the body, but highest s concentration in kidney and liver. 30% excreted in urine. 3. Oral dose for adults 2-4 gm divided into 4 portions children 50-100mg/kg/day. 4. IM adults 2-12 gm/day, children 100-300 mg/kg/day every 4-6 hours. BIOCLOX, KLOX, CLOCILIN 0.25, 0.5 gm cap, 0.5 gm/vial.
  • 61.
    Oxacillin, Dicloxacillin, Flucloxacillinare other isoxazolyl penicillins, similar to cloxacillin, but not marketed in India. Nafcillin : More active than methicillin and cloxacillin but less active than PnG 80% of drug bonds with plasma proteins excreted by liver in patients with renal failure. Dose is similar to cloxacillin.
  • 62.
    III) Extended spectrumpencillins : 1. Amino pencillins 1. Ampicillin – • Antibacterial activity is similar to that of PnG that is more effective than PnG against a variety of gram-ve bacteria • Drug is effective against H.influenzae strep.viridans, N.gonorrhea, Salmonella, shigellae, Klebsilla and enterococci. Absorption, fate and excretion : • Oral absorption is incomplete but adequate • Food interferes with absorption • Partly excreted in bile and partly by kidney
  • 63.
    Dose : 0.5-2gm oral/IM or IV depending on severity of infection every 6 hours Children : 25-50 mg/kg/day AMPILIN, ROSCILLIAN, BIOCILIN – 250, 500 mg cap 100mg/ml ped drops, 250 mg/ml dry syr, 1 gm/vial inj. USES : • Urinary tract infections • Respiratory tract infections • Meningitis • Gonorrhoea • Typhoid fever • Bacillary dysentry • Septicaemias • SBE
  • 64.
    Adverse effects : • Diarrhoea is frequent • Skin rashes is more common • Unabsorbed drug irritates lower intestines • Patient with history of hypersensitivity to PnG should not be given ampicillin.
  • 65.
    AMOXYCILLIN : •This is a semisynthetic penicillin • (amino-p-hydroxy-benzylpencillin) • Antibacterial spectrum is similar to ampicillin but less effective than ampicillin for shigellosis. • Oral absorption is better; food does not interfere; higher and more sustained blood levels are produced. • It is less protein bond and urinary excretion is higher than that of ampicillin. • Incidence of diarrhoea is less
  • 66.
    Dose : 0.25-1g TDS oral; AMOXYLIN, NOVAMOX, SYNAMOX, MOX, AMOXIL 250, 500 mg cap, 125 mg/5ml dry syr, 500 mg/vial inj. USES : • Typhoid • Bronchitis • Urinary infection • SBE • Gonorrhoea
  • 67.
    Carboxy penciillins : The Carboxypenicillins are extended spectrum penicillins, because they inhibit a wide variety of aerobic gram-ve bacilli They are ineffective against most strains of staph. Aureus They have following properties : 1. Highly active against anaerobes 2. Most useful in infections caused by other gram-ve rods 3. Act synergistically with amino glycoside antibiotics, particularly enterobacteriacea. 4. Much less active than penicillin G against gram+ve organisms 5. The CNS penetration is about 10% of their serum levels and hence not recommended for the treatment of meningeal infections.
  • 68.
    CARBENICILLIN • Hassimilar spectrum as other penicillin • Weaker antibacterial activity than ampicillin • Active against –pseudomonas, proteus • < Salmonella , E coli Enterobacter • Inactive against – klebsiella and gram –ve cocci • Acid labile and has to be given by parenteral route only • Peak plasma level is 2hours and excreted in urine
  • 69.
    Dose : 1-2gim/iv 4-6hours Adverse effects : • Cause congestive heart failure • Bleeding disorders-impaired platelet function Uses : • Pseudomonas ,burns, UTI and septicemia • PYOPEN,CARBELIN 1g,5g per vial
  • 70.
    UREIDOPENICILLINS – PIPERACILLIN( PIPRIL)- antipseudomonal pencillin Has similar indications of carbenicillin
  • 71.
    WHAT IF…. PATIENTIS ALLERGIC TO PNC? patient allergic to penicilln early infection late infection periodontal infection clindamycin erythromycin metrinidazole doxycyclin
  • 72.
    CEPHALOSPORINS  Groupof semi-synthetic antibiotics derived from cephalosporin, “C” obtained from fungus Cephalosporium.  Chemically related to penicillins (contain β-lactum ring)  Have been classified as first, second, third and fourth generation. Based on: When the were introduced Bacterial susceptibility patterns Resistance to -lactamase Pharmacokinetics
  • 73.
    FIRST GENERATION Theseare active against gram-positive bacteria but weaker against gram-negative bacteria. e.g.Cephalothin, cephalexin. SECOND GENERATION More active against gram-negative organisms with some members active against anaerobes. e.gCefuroxime, Cefaclor THIRD GENERATION Very active against gram–negative and gram-positive, but not effective against anaerobes. e.gCefotaxime, Cefixime FOURTH GENERATION Very effective against anaerobes and resistant to beta lactamase .e.g.Cefipime
  • 74.
    TRADE NAMES CEFADROXIL-500mgEvery 12 hrs ACTIDROX ACUDROX CEDROX CEFOXID CEFUROXIME 125 mg Every 12 hrs ACTUM CEFTAZ CEFEXL MAXIM
  • 75.
    CEFIXIME -200-400 mgin a single or two divided doses AFIXIM CEFI CEFEXY NOVAFEX CEFEPIME- 1-2 g 8-12 hourly BIOPIME CEPIME NOVAPIME
  • 76.
    TETRACYCLINES  Obtainedfrom soil actinomycetes.  The first to be introduced was chlortetracycline in 1948 under the name “Aureomycin’.  These bind to 30S ribosomal subunit and inhibit the binding of aminoacyl-tRNA to the A site.  On the basis of chronology of development they may be divided in to 3 groups Group – I Group – II Group – III Chlortetracycline Domeclocycline Doxycycline Oxytetracycline Methacycline Minocycline Tetracycline
  • 77.
    PRECAUTIONS  Notused during pregnancy, lactation ,childhood.  Avoided in patients on diuretics- blood urea levels rise in such cases  Used cautiously in renal and hepatic patients.  Not used with penicillins
  • 78.
    TRADE NAMES TETRACYCLINE-500mg every 8 hrs ACHROMYCIN HOSTACYCLINE TETLIN DOXYCYCLINE-100 mg every 12 hrs APIDOX DOXYN SWIDOX TETRADOX Antibiotics
  • 79.
    MACROLIDES  Theseare antibiotics having a macrocyclic lactone ring with attached sugars.  Erythromycin is the first member discovered in 1950s.  For the past 40 years erythromycin has been the only macrolide antibiotic.  Roxythromycin, Clarithromycin, Azithromycin are the next additions in macrolides.
  • 80.
    ERYTHROMYCIN  Itwas Isolated from Streptomyces erythreus in 1952.  Water solubility of erythromycin is limited and the solution remains stable only when kept in cold.  It acts by inhibiting bacterial protein synthesis. It combines with 50S ribosomes subunits and interferes with translocation. ANTIMICROBIAL SPECTRUM It is narrow, includes mostly gram positive organisms and few gram negative bacteria and overlaps considerably with that of Penicillin G.
  • 81.
    DOSAGE Erythromycin estolate-250-500mg qid. ALTHROCIN, E-MYCIN Erythromycin stearate- 250-500mg qid ERYTHROCIN, ERYSTER Erythromycin base - 250-500mg qid. ERYSAFE, EROMED
  • 82.
    DRUG INTERACTIONS 1)Interaction with warfarin leads to serious bleeding in patients undergoing anticoagulation therapy. 2) Interaction with lovastatin, drug given for cholesterol reduction leads to severe muscle weakness. 3) Interaction with Theophylline, a bronchodilator used for asthmatic patients leads to toxic concentrations of the same resulting in cardiac arrhythmias
  • 83.
    Newer macrolides weremade Azithromycin –loading dose;500mg 1st day Followed by 250mg daily. AZID AZEE AZIPAR AZIWIN Clarithromycin – 250-500mg every 12 hrs for 6-10 days. CLAR CLARIWIN MACLAR
  • 84.
    METRONIDAZOLE  Introducedin 1959 for the treatment of “Trichomonas Vulgaris”.  Used especially for serous anaerobic infections, including those of the orofacial region.  Distributed well in to bone, saliva, mucosa, and even brain abscess.  Bactericidal
  • 85.
    TRADE NAMES METRONIDAZOLE-200-400mgevery 8 hrs FLAGYL METROGYL MET METRONIDAZOLE AND AMOXYCILLIN 200mg + 250 mg every 8 hrs STEDMOX -M
  • 86.
    PREVENTING RESISTANCE TODRUGS  Limit the use of antimicrobial agents to the treatment of specific pathogens sensitive to the drug being used.  Notorious-Make sure doses are high enough, and the duration of drug therapy long enough , combination therapy.  To be cautious about the indiscriminate, inadequate or unduly prolonged use of anti-infectives
  • 87.
    SUPERINFECTIONS:  Duringtreatment normal host bacteria that are susceptible to the drugs are eliminated.  In the normal state, these bacteria live in peaceful coexistence with the host and by their physical presence prevent bacteria capable of producing disease from growing in large numbers.  The normal flora acts as a defense mechanisms, but when the indigenous flora is altered, the pathogenic bacteria resistant to an antibiotic may cause a secondary infection, or superinfection.  Example is of candidiasis with the use of penicillin, which eliminates the gram-positive cocci (seen after long term high dose penicillin therapy).
  • 89.
     The useof antibiotics has been standard practice for patients identified as being at risk of developing endocarditis.  The link between dental procedures and IE remains a controversial subject. In 1984, Guntheroth reported a low incidence of bacteremia associated with dental procedures and suggested that meticulous oral hygiene was more important in the prevention of IE than any antibiotic regimen.
  • 93.
    Antibiotics should onlybe prescribed on the basis of a defined need otherwise their use may present more of a risk to the patient than the infection being treated or prevented. Antibiotics can be responsible for various adverse effects, including drug interactions, nausea, gastrointestinal upsets, potentially fatal allergic reactions and antibiotic associated colitis The indiscriminate prescribing of antibiotics can also cause drug resistance which is an emerging and significant problem
  • 94.
    CONCLUSION  Althoughantibiotics do not prevent all post-operative infections, they can reduce their incidence significantly when administered correctly.  We should prescribe effective, short-course therapies, directed at improving the outcome of our patients.  Future treatment strategies will not only include the aggressive use of traditional management methods but also the understanding of normal immune system-associated defects and newer antimicrobials.
  • 95.

Editor's Notes

  • #35 The dosage prescribed must be capable of establishing a concentration of antibiotic that is 3 to 4 times the MIC . Therapeutic levels greater than 3 to 4 times the MIC generally do not improve the therapeutic results. But increases the toxicity and is wasteful MIC-min inhibitory concentration:-It is the lowest concentration of an antibiotic which prevents visible growth of a bacterium determined in microwell culture plates. DRUG DOSAGE: ‘Dose’ is the appropriate amount of a drug needed to produce a certain degree of response in a patient.
  • #37 Plasma half-life is the time with in which one half of the absorbed dose of drug is excreted. The time interval has been established for various antibiotics. Because most antibiotics are eliminated by the kidneys, the patients with preexisting renal disease and subsequent decreased clearance may require longer intervals between the doses to avoid overdosing.
  • #38 Comfortable to both clinician and the patient. Most of the oral antibiotics should be taken in fasting state (30min before or 2hrs after the meal) for maximum absorption.
  • #39 If the infection is mild enough oral administrations are sufficient. When treating a serious, established infections, parenteral antibiotic therapy is frequently the method of choice. So after 5th day of parenteral administration , the blood levels achievable with oral administrations are sufficient
  • #40 In routine infections, the combination therapy should be avoided to prevent the opportunity for resistant bacteria to emerge.
  • #41 A. when it is necessary to increase the antibacterial spectrum
  • #44 Usually eradication of infection generally is reached by the 3rd day, and the patient becomes relatively asymptomatic. An additional 2 day-course will complete 5 days which will be safer.