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broad spectrum antibiotics - Dr Sanjana Ravindra

This document discusses broad spectrum antibiotics. It begins with definitions of key terms like antibiotic, pharmacokinetics, and pharmacodynamics. It then covers the history of antibiotics from traditional empirical uses to the modern era including the discoveries of penicillin and other drugs. The document categorizes antibiotics based on their spectrum of activity, mechanism of action, source, and susceptible organisms. It also addresses principles of antibiotic therapy such as selection, combinations, prophylaxis, resistance, and misuse.

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ANTIBIOTICS BROAD SPECTRUM ANTIBIOTICS Dr Sanjana Ravindra 1st year PG Dept. of OMR
CONTENT DEFINITION INTRODUCTION HISTORY PRINCIPLES OF ANTIBACTERIAL THERAPY CLASSIFICATION AND MECHANISM OF ACTION USES OF ANTIBIOTICS ADVERSE EFFECTS OF ANTIBIOTICS BROAD SPECTRUM ANTIBIOTIC DRUGS LOCAL DRUG DELIVERY SYSTEM ANTIBIOTICS IN DENTISTRY REFERENCES
DEFINITION S 1) DRUG is any substance or product that is used or intended to be used to modify or explore physiological systems or pathological states for the benefit of the reciepient 2) PHARMACOKINETICS is the study of absorption, distribution, metabolism and excretion of drugs ie what the body does to the drug 3) PHARMACODYNAMICS is the study of effects of the drugs on the body and their mechanism of action ie what the drug does to the body 4) THERAPEUTICS deals with the use of drugs in prevention and treatment of diseases
5) ANTIBIOTIC AGENT Against life (Greek-anti means against and biosis means life). Chemical substances produced by microorganisms that have the capacity in dilute solutions, to produce antimicrobial action 6) ANTIMICROBIAL AGENT Substances that will suppress the growth / multiplication of microorganisms. antimicrobial agents may be antibacterial, antiviral / antifungal 7) ANTIBACTERIAL AGENT substances that destroy or suppress the growth / multiplication of bacteria. They are classified as antibiotic or synthetic agents DEFINITION S
INTRODUCTIO N Chemical substances produced by microorganisms that supress the growth of other microorganisms and may eventually destroy them. • K.D. TRIPATHI Chemical substance produced by microorganisms, which at a high dilution can inhibit the growth and/or multiplication or kill another microorganism. • - WAKSMAN AND WOODRUFF(1942)
The term 'antibiosis', meaning "against life", was introduced by the french bacteriologist Jean Paul Vuillemin  Antibiosis was first described in 1877 in bacteria when Louis Pasteur and Robert Koch observed that an airborne bacillus could inhibit the growth of bacillus anthracis INTRODUCTIO N https://www.google.co.in/search?q=antib-hist
The term antibiotic was first used in 1942 by Selman Waksman and his collaborators in journal articles to describe “any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.” The term "antibiotic" derives from anti + βιωτικός (biōtikos), "fit for life, lively“, which comes from βίωσις (biōsis), "way of life“,and that from βίος (bios), "life“ https://www.google.co.in/search?q=Waksman-antib
HISTORY History of chemotherapy is divided into two phases. (A) the period of empirical use (B) modern era.
Chinese  ‘mouldy curd’ on boils Hindus  ‘chaulmoogra oil” in leprosy Aztecs  ‘chenopodium’ for intestinal worms Paracelsus  mercury for syphilis and cinchona bark for fever PERIOD OF EMPIRICAL USE: https://www.google.co.in/search?q=plantshist6orical
 1871 Joseph Lister experimented with the antibacterial action on human tissue on what he called penicillium glaucium  1877 Louis Pasteur postulated that bacteria could kill other bacteria ( anthrax bacilli)  1928 Sir Alexander Fleming discovered enzyme lysozyme and the antibiotic substance penicillin from the fungus Penicillium notatum  During 1940 and 50s streptomycin, chloramphenicol and tetracyclin were discovered  1942 Selman Waksman used the term antibiotics MODERN HISTORY https://www.google.co.in/search?q=anti-pioneers
https://www.google.co.in/search?q=fleming-alexander
BROAD SPECTRUM 1. Tetracycline 2. Chloramphenicol 3. Sulfonamides 4. Trimethoprim NARROW SPECTRUM 1. Bacitracin 2. Clindamycin 3. Macrolides 4. Metronidazole 5. Penicillin G,V 6. Penicillinase resistant penicillin 7. Polymixin 8. Vancomycin BASED ON SPECTRUM OF ACTIVITY Neidle E A, Pharmacology and therapeutics for Dentistry, 4th edition. Pg 48 EXTENDED SPECTRUM 1. Aminoglycosides 2. Carbacephems 3. Cephalosporins 4. Extended spectrum of penicillins 5. Fluoroquinolones 6. Monobactams CLASSIFICATI ON
BASED ON TYPE OF ACTION Bacteriostatic • Sulfonamides • Tetracyclines • Chloramphenicol • Erythromycin • Ethambutol Bactericidal • Penicillins • Aminoglycosides • Rifampin • Cotrimoxazole • Cephalosporins • Vancomycin • Nalidixic acid • Ciprofloxacin Neidle E A, Pharmacology and therapeutics for Dentistry, 4th edition. Pg 48
ANTIBIOTICS ARE OBTAINED FROM ACTINOMYCETES Penicillin Cephalosporin Griseofulvin Polymyxin B Colistin Bacitracin Tyrothricin Aminoglycosides Tetracyclines Chloramphenicol Macrolides Polyenes BACTERIA FUNGI Neidle E A, Pharmacology and therapeutics
BASED ON ORGANISMS SUSCEPTIBLE EFFECTIVE AGAINST GRAM +VE BACTERIA PENICILLINS MACROLIDS BACITRACIN EFFECTIVE AGAINST GRAM –VE BACTERIA STREPTOMYCIN EFFECTIVE AGAINST BOTH GRAM +VE AND –VE BACTERIA AMPICILLIN TETRACYCLIN CHLORAMPHENICOL AMOXICILLIN CEPHALOSPORIN NEOMYCIN EFFECTIVE AGAINST ACID-FAST BACILLI STREPTOMYCIN RIFAMPIN KANAMYCIN AGAINST PROTOZOA TETRACYCLIN EFFECTIVE AGAINST FUNGI NYSTATIN AMPHOTERICIN B ANTIMALIGNANCY ANTIBIOTICS ACTINOMYCIN D MITOMYCIN
PRINICIPLES OF ANTIBIOTIC THERAPY Selection of antibacterial agent Antibacterial combinations Antibacterial prophylaxis Microbial drug resistance Dangers of antibacterial therapy Misuse of antibacterial agents
SELECTION OF ANTIBIOTIC AGENT 1)HOST RELATED FACTORS Age of the patient Pregnancy and neonatal period Immunocompetency status of the patient Severity of the infection Allergic reaction and intolerance Genetic factors Renal and hepatic function
2)PATHOGEN RELATED FACTORS Evaluation of the probable microbial etiology and expected clinical course of the infection Identification of the causative microorganism and its sensitivity to antibiotic drugs Possibility of drug resistance 3)DRUG RELATED FACTORS Nature of the drug Risk of drug toxicity The cost of therapy Pharmacokinetic properties of the drug Probability of drug compliance by the patient
ANTIBACTERIAL COMBINATIONS 1) SIMULTANEOUS USE OF TWO OR MORE ANTIBIOTICS IS NOT ROUTINELY RECOMMMENDED. THESE DRUGS CAN BE COMBINED UNDER FOLLOWING REASONS To achieve an additive or synergistic effect against a single organism In mixed infections with bacteria sensitive to different drugs To delay the development of or to overcome the drug resistance To decrease the adverse reactions to an individual drug When etiological diagnosis is difficult, the infection is severe and body defense is poor For reducing chances of superinfections
2) IF A BACTERIOSTATIC DRUG IS COMBINED WITH BACTERIOCIDAL AGENT FOLLOWING THINGS MAY BE HAPPEN Drug antagonism Additive effect oftenly synergestic rarely 3) COMBINED ANTIBIOTIC THERAPY INVOLVES CERTAIN RISKS Emergence of organism resistant to the multiple drugs used Increased risk of adverse reactions Increased risk of superinfection by resistant organisms Sense of false security Increase in cost of therapy
ANTIBACTERIAL PROPHYLAXIS For prevention of meningococcal infections in healthy children during an epidemic, for prevention of diseases like syphilis, gonorrhea, malaria. For preventing endocarditis following minor surgical procedures like tonsillectomy or tooth extraction in patients with cardiac lesions. For preventing invasion of blood stream by pathogens during certain surgical manipulations. In patients with compound musculoskeletal injury, penetrating wounds and skull injuries.
For those puncture wounds that are at high risk of infection. Animal bite as they are at high risk of infection by oral flora. To prevent microbial complications like bronchopnemonia e.g. Cases of measles and tetanus. In paralytic states to prevent aspiration bronchopnemonia
DANGERS OF ANTIBACTERIAL THERAPY  Development of allergic and anaphylactic reactions e.g. Pennicillin  Selective toxicity  Development of superinfection  Development of multiple drug resistant organisms  Deficiency of certain vitamins  Fetal damage  A false sense of security in the patient as well as in physician  Failure to respond to antibiotic therapy
MISUSE OF ANTIBIOTIC THERAPY Antibiotic misuse, sometimes called antibiotic abuse or antibiotic overuse.  Produce serious effects on health. From antibiotics now available , one needs to know the important representatives of each class and know them well e.g. Action , dosage . It is a contributing factor to the creation of multidrug-resistant bacteria, informally called "super bugs" relatively harmless bacteria can develop resistance to multiple antibiotics and cause life-threatening infections.
MICROBIAL DRUG RESISTANCE The recent emergence of antibiotic resistance in bacterial pathogens, both nosocomialy and in the community, is a very serious development that threatens the end of the antibiotic era. Drug resistance is not a characteristic of all bacteria and many strains responsible for common infections have largely remained susceptible to antibiotics e.G. Pneumococci, streptococcus pyogenes, meningococci, and treponema pallidum.
Bacterial resistance is often quantitative and not qualitative. Thus an antibacterial substance which is not effective in small doses may inhibit the bacteria in vitro in large concentrations. For an antibiotic to be effective, it must reach its target in an active form, bind to the target, and interfere with its function. Accordingly, bacterial resistance to an antimicrobial agent is attributable to three general mechanisms: (1) the drug does not reach its target, (2) the drug is not active, or (3) the target is altered .
Natural resistance In organisms which are naturally resistant, the drug sensitive enzyme reactions may be absent .  some naturally resistant organisms may elaborate a substance which destroys the antibiotic e.G. E coli produce pencillinase which destroys penicillin . Following the use of an antibiotic agent which destroys the sensitive strain , these naturally resistant variants multiply and become dominant.
Some microbes have always been resistant to certain antibacterial agents. They lack the metabolic process or the target site which is affected by the particular drug. This is generally a group or species charateristic e .G. Gm-ive bacilli are normally unaffected by penicillin G or M. Tuberculosis is insensitive to tetracyclines.
Acquired microbial resistance It is the development of resistance by an organism (which was sensitive before) due to the use of an AMA over a period of time. This can happen with any microbe and is a major clinical problem. However, development of resistance is dependent on the microorganism as well as the drug. Some bacteria are notorious for rapid acquisition of resistance, e.G. Staphylococci, coliforms, tubercle bacilli. .
Others like strep. Pyogenes and spirochetes have not developed significant resistance to penicillin despite its Widespread use for > 50 years. It can arise in bacteria in several ways. Microbes acquire resistance after a change in their DNA. Such change may occur in A) genetic mutation B) genetic exchange - conjugation - Transduction - Transformation
Mutation It is a stable and heritable genetic change that occurs spontaneously and randomly among microorganisms.  Any sensitive population of a microbe contains a few mutant cells which require higher concentration of the ama for inhibition. Mutation and resistance may be: (I ) single step.- A single gene mutation may confer higher degree of resistance; emerges rapidly, e.G. Enterococci to streptomycin, E. Coli and staphylococci to rifampin (Ii ) multistep.· A number of gene modifications are involved, sensitivity decreases gradually in a stepwise manner. Resistance to erythromycin, tetracyclines and chloramphenicol is developed by many organisms in this manner.
Conjugation : This may involve chromosomal or extrachromosomal (plasmid) dna.  The gene carrying the 'resistance' or 'r' factor is transferred only if another 'resistance transfer factor' (rtf) is also present. Chloramphenicol resistance of typhoid bacilli, streptomycin resistance of e. Coli, penicillin resistance of haemophilus. Concomitant acquisition of multidrug resistance has occurred by conjugation. Thus, this is a very important mechanism of horizontal transmission of resistance. GENE TRANSFER
TRANSDUCTION: It is the transfer of gene carrying resistance through the agency of a bacteriophage. The r factor is taken up by the phage and delivered to another bacterium which it infects. Certain instances of penicillin, erythromycin and chloramphenicol resistance have been found to be phage mediated.
TRANSFORMATION :  A resistant bacterium may release the resistance carrying DNA into the medium and this may be imbibed by another sensitive organism-becoming unresponsive to the drug.  This mechanism is probably not clinically significant except isolated instances of pneumococcal resistance to penicillin g due to altered penicillin binding protein
CROSS RESISTANCE : Acquisition of resistance to one AMA conferring resistance to another AMA, to which the organism has not been exposed, is called cross resistance. This is more commonly seen between chemically or mechanistically related drugs, e.G. Resistance to one sulfonamide means resistance to all others, and resistance to one tetracycline means insensitivity to all others. Sometimes unrelated drugs show partial cross resistance, e.G. Between tetracyclines and chloramphenicol, between erythromycin and lincomycin.
PREVENTION OF DRUG RESISTANCE No indiscriminate and inadequate or unduly prolonged use of amas should be made. This would minimize the selection pressure and resistant strains will get less chance to preferentially propagate. Prefer rapidly acting and selective (narrow spectrum) amas whenever possible; broad-spectrum drugs should be used only specifically. Use combination of amas whenever prolonged therapy is undertaken, e.G. Tuberculosis, SABE. Infection by organisms notorious for developing Resistance, e.G. Staph. Aureus, E. Coli, M. Tuberculosis, Proteus, etc. Must be treated intensively.
INDICATIONS OF ANTIBIOTICS * Diabetics mellitus, immunoglobulin deficiency, malnutrition and alcoholism. * Acute severe rapidly spreading infection * Pericoronitis, osteomyelitis, fracture, soft tissue wound and odontogenic infection * Post operative wound infection * Prevention of endocarditis in high risk patients undergoing any dental procedures that is likely to cause gingival bleeding THERAPEUTIC PROPHYLACTIC
USES OF ANTIBIOTICS Infections of all systems  Pus formation Sepsis Quinsy Skin infections Mucous membrane infections Septicaemia Empirical therapy Prophylactic therapy
CONTROL AND ERADICATION OF INFECTIONS OF ORAL CAVITY. • Local factors; 1) Swelling, 2) Lymphadenitis, 3) Trismus, 4) Dyshagia 5) Chronic draining sinus tract. • Systemic factors; 1) Cellulitis. 2) Osteomyelitis. 3) Infections of salivary gland. 4) Compound fractures. 5) Infected cysts. 6) Infected oro-antral fistula. 7) Pericoronitis
SIDE EFFECTS OF ANTIBIOTICS Diarrhoea Bloating and indigestion Abdominal pain Loss of appetite Being sick Feeling sick Itchy skin rash Coughing Life-threatening allergic reaction
BROAD SPECTRUM ANTIBIOTICS 1. TETRACYCLINE 2. CHLORAMPHENICOL 3. SULFONAMIDES 4. TRIMETHOPRIM
TETRACYCLIN E Defination : They are octahydro napthacene derivatives which are bacteriostatic and broad spectrum antibiotics that kills certain infection causing microorganisms and are used to treat wide variety of infections.  Tetracyclines are napthacene derivatives.  The napthacene nucleus is made up by fusion of 4 partially unsaturated cyclohexane radicals and hence the name tetracyclines.  Tetracyclines are bacteriostatic & effective against rapidly multiplying bacteria https://www.google.co.in/search?q=tetracycline+structure
According to duration of action: • Short-acting (Half-life is 6-8 hrs) • Tetracycline • Chlortetracycline • Oxytetracycline • Intermediate-acting (Half-life is ~12 hrs) • Demeclocycline • Methacycline • Long-acting (Half-life is 16 hrs or more) • Doxycycline • Minocycline • Tigecycline CLASSIFICATI ON
 Primarily bacteriostatic.  Inhibit protein synthesis by binding to 30s ribosomes in susceptible organism. Thus, attachment of aminoacyl-t-rna to the mrna-ribosome complex is interfered with. As a result, peptide chains fail to grow.  It is effective against gram –ve and gram +ve bacteria, rickettsial, spirochetees, protozoa and mycoplasma. MECHANISM OF ACTION tripathi
 Orally- saliva- liver- bile  They cross placental barrier  Tetracyclines have chelating property-form insoluble & unabsorbable complexes with calcium and other metals.  Doxycycline & minocycline are completely absorbed irrespective of food.  Milk, iron preparations, nonsystemic antacids & sucralfate reduce their absorption . administration of these substances & tetracyclines should be staggered, if the cannot be avoided altogether. PHARMACOKINETICS
(A) IRRITATIVE EFFECTS: - Epigastric pain, nausea, vomiting, diarrhoea. - Doxycycline is known to cause esophageal ulcerations. (B) DOSE RELATED TOXICITY: 1.) LIVER DAMAGE: - Fatty infiltration of liver, jaundice, in pregnancy, Can cause acute hepatic necrosis. ADVERSE EFFECTS
2.) KIDNEY DAMAGE: - Fancony syndrome – like condition 3.) PHOTOTOXICITY: - Sunburn, severe skin reactions 4.) ANTIANABOLIC EFFECT : - Reduce protein synthesis & have an overall catabolic effect. - They induce negative nitrogen balance & can increase blood urea.
5.) LNCREASED INTRACRANIAL PRESSURE In some infants. 6.) DIABETES INSIPIDUS - Demeclocycline antagonizes ADH action & reduces urine concentrating ability of the kidney. 7.) VESTIBULAR TOXICITY - Minocycline has produced vertigo which subside when the drug is discontinued.
(C) HYPERSENSITIVITY - This is infrequent with tetracyclines. - Skin rashes, urticaria, glossitis, pruritus, even exfoliative dermatitis have been reported. - Angioedema & anaphylaxis are extremely rare. (D) SUPERINFECTION: - Marked suppression of the resident flora. - Intestinal superinfection by candida albicans can occur. - Oral manifestations are very rare.
https://www.google.co.in/search?q=tetracycline+staining  Hypoplasia and brown discolouration of teeth  Not used in 3rd trimester  Deposits in bones and teeth- yellow discolouration  Not recoomended- children below 8 yrs and pregnant women – permanently discolour developing teeth and alter bone growth (E) TOOTH DISCOLOURATION
PRECAUTIONS 1.) Tetracyclines should not be used during pregnancy, lactation and in children. 2.) They shouldbe avoided in patients on diuretics: blood urea may rise in such patients. 3.) They should be used cautiously in renal or hepatic insufficiency. 4.) Preparations should never be used beyond their expiry date. 5.) Do not mix injectable tetracyclines with penicillin-inactivation occurs. 6.) Do not inject tetracyclines intrathecally.
(A) MEDICINAL USES - Clinical use has declined due to the introduction of Fluoroquinolones and other agents. - DRUG OF 1ST CHOICE: (A) venereal diseases (B) atypical pneumonia (C) cholera  limit the diarrhoea duration. (D) brucellosis  combined with gentamicin. (E) plague (F) relapsing fever. (G) rickettsial infections. USES
- DRUG OF 2ND CHOICE: (A) to penicillin / ampicillin for tetanus , anthrax , actinomycosis infections. (B) to ciprofloxacin / ceftriazone for gonorrhea in patients allergic to penicillin. (C) to ceftriaxone for syphilis in patients allergic to penicillin. (D) to azithromycin for chlamydial infections. - Also can be used for UTI , pneumonia, amoebiasis, acne, lung disease.
(B) dental uses : • of limited use in treating acute infections , but are of importance in periodontal disease. • Suppress the activity of collagenases derived from the neutrophils and fibroblasts, that contribute to gingival inflammation. • Collagenases are calcium dependent & tetracyclines chelate the calcium. • May benefit periodontal inflammation by releasing free radicals of oxygen.
ADMINISTRATION  oral capsule is the dosage form in which tetracyclines are most commonly administered.  The capsule should be taken 1/2 hr before or 2 hr after food.  Not recommended by i.M. Route because it is painful & absorption from the injection site is poor.  Slow i.V. Injection may be given in severe cases, but is rarely require now.  A variety of topical preparations are available , but should not be use because there is high risk of sensitization .
OXYTETRACYCLINE: (TERRAMYCIN) 250 – 500 MG EVERY 6 HRS TETRACYCLINE: (ACHROMYCIN, RESTECLIN) 250 MG – 4 G EVERY 6 HRS DOSAGES https://www.google.co.in/search?q=tetracycline+tablet
DEMECLOCYCLINE: (LEDERMYCIN) ADULT: 150 MG 4 X DAILY 300 MG BID. CHILD: 7 – 13 MG/KG DIVIDED EVERY 6 – 12 HRS. MINOCYCLINE: (CYANOMYCIN) ADULT: 200 MG FOLLOWED BY 100 MG EVERY 12 HRS. CHILD: 4 MG/KGhttps://www.google.co.in/search?q=tetracycline+tablet
DOXYCYCLINE: (TETRADOX, BIODOXI, DOXT, NOVADOX) ADULT: 200 MG ON DAY 1 FOLLOWED BY 100 MG OD CHILD: 4 MG/KG IN 2 DIVIDED DOSES, FOLLOWED BY 2 MG/KG DAILY. https://www.google.co.in/search?q=tetracycline+tablet
TETRACYCLINE EFFECTIVE IN TREATING PERIODONTAL DISEASE BECAUSE • Adjuvant role in Chronic Periodontitis - control gingival inflammation - normalize the periodontal microflora from a mixture of anerobic G- bacilli and spirochetes. • Highly active against Actinobacillus actinomycetum comitans in Aggressive Periodontitis - prevents gingival destruction and bone loss.
TERATOGENIC EFFECTS OF TETRACYCLINES PERIOD STRUCTURE AFFECTED DEFORMITY mid pregnancy to 5 months of postnatal life Deciduous teeth Brownish discolouration, ill formed and are more susceptible to caries 2 months to 5 years of age Permanent teeth Pigmentation, discolouration Pregnancy and childhood up to 8 years of age Skeleton Depressed bone growth
CHLORAMPHENICO L • Broad spectrum antibiotic first obtained from streptomyces venezuelae. MECHANISM OF ACTION  It is bacteriostatic but for some organisms it is bacteriocidal. It binds to 50s ribosomal subunit and inhibits protein synthesis  It is unique among natural compounds because it contains a NITROBENZENE moiety and is a derivative of DICHLOROCETIC ACID.  It acts by inhibiting protein synthesis (by binding reversibly to the 50s ribosomal subunit). https://www.google.co.in/search?q=chloramphenicol+structure
64 USES :  Typhoid fever(S.typhi)  Bacterial meningitis (H.influenzae)  Anaerobic infections  Rickettsial disease (eg.Rocky mountain spotted fever)  Brucellosis  UTI Adult 250 -500mg 6hrly Children 25 – 50mg /kg/day
65 ADVERSE EFFECTS :  Bone marrow depression  Hypersensitivity reactions  Irritative effects  Superinfections  Gray baby syndrome
GRAY BABY SYNDROME / ASHEN GRAY CYANOSIS Newborn babies given high doses of chloramphenicol – develop vomiting, refusal of feeds, hypotonia, hypothermia, abdominal distension, metabolic acidosis https://www.google.co.in/search?q=gray+baby
It is the fixed dose combination of trimethoprim and sulfamethoxazole. Trimethoprim it is diaminopyrimidine and related to antimalarial drug pyrimethamine.  Sulfamethoxazole selected for the combination because it has nearly the same T ½ as trimethoprim. COTRIMOXAZOL E
ANTIBACTERIAL SPECTRUM : Individually, both sulfonamide and trimethoprim are bacteriostatic. Combination becomes cidal against many organisms. Organisms covered by the combination are-salmonella typhi, serratia, klebsiella, enterobacter, pneumocystis jiroveci.  Many sulfonamide resistant strains of staph. Aureus, strep. Pyogenes, shigella, enteropathogenic E. Coli, influenzae , gonococci and meningococci.
Why sulfamethoxazole + trimethoprim ? Both have nearly the same t1/2 (- 10 hr). Optimal synergy is exhibited at a concentration ratio of Sulfamethoxazole 20 : trimethoprim 1. MIC of each component may be reduced by 3-6 times. This ratio is obtained in the plasma when the two are given in a dose ratio of 5 : 1, because trimethoprim enters many tissues, has a larger volume of distribution than sulfamethoxazole and attains lower plasma concentration
PHARMOKINETICS : Trimethoprim crosses blood-brain barrier and placenta, while sulfamethoxazole has a poorer entry. Trimethoprim is more rapidly absorbed than sulfamethoxazole.  Trimethoprim is 40% plasma protein bound, while sulfamethoxazole is 65% bound. Trimethoprim is partly metabolized in liver and excreted in urine.
ADVERSE EFFECTS:  Nausea, vomiting, stomatitis, headache, rashes.  Rarely, folate deficiency (megaloblastic anemia)  Blood dyscrasias.
CONTRAINDICATIONS:  Pregnancy: - teratogenic effects may occur due to trimethoprim. - Neonatal haemolysis, methaemoglobinaemia.  Renal disease: - patient may develop uraemia.  Aids patients: - fever, rash, bone marrow hypoplasia.  Elderly patients: - bone marrow toxicity.  Diuretics + cotrimoxazole = thrombocytopenia.
USES:  Tonsilitis, pharyngitis, sinusitis, otitis media, chronic bronchitis.  Orodental uses very rare  only if allergies to β – lactam antibiotics are present.  Major indications include uti, bacterial dysentery.  Effective alternative to chloramphenicol in the case of typhoid fever, but strains are known to be resistant.  Alternative for chancroid, granuloma inguanale, neutropenic patients. BRAND NAME SEPTRAN, SEPMAX, BACTRIM, CIPLIN, ORIPRIM, SUPRISTOL, FORTRIM.
 First anti-microbial agents effective against pyogenic bacterial infections. Sulfonamido-chrysoidine (prontosil red)  used by Domagk to treat streptococcal infection in mice. SULPHONAMID E
A LARGE NUMBER OF SULFONAMIDES WERE PRODUCED AND USED EXTENSIVELY, BUT BECAUSE OF RAPID EMERGENCE OF BACTERIAL RESISTANCE AND AVAILABILITY OF MANY SAFER AND MORE EFFECTIVE ANTIBIOTICS CURRENT UTILITY IS LIMITED EXCEPT IN COMBINATION WITH TRIMETHOPRIM (COTRIMAXOZOLE) AND PYRIMETHAMINE.
CLASSIFICATION: (A) short acting (4-8 hrs): - Sulfadiazine. (B) intermediate acting (8-12 hrs): - sulfamethoxazole, sulfamoxole. (C) long acting (approx. 7 days): - Sulfadoxine, sulfamethopyrazine. (D) special purpose sulfonamides: - Sulfacetamide sodium, sulfasalazine mafenide, silver sulfadiazine.
ANTIBACTERIAL SPECTRUM : They are primarily bacteristatic against gm +ve and gm –ive bacteria. However , bacteriocidal action can be attained in urine. Sensitive to strepto. Pyogenes , haemophilus influenzae , vibrio cholerae , meningococci , gonococci , E coli and shigella.
RESISTANCE: Some bacteria are capable of developing resistance to sulfonamides like pneumococci, gonococci, staph. Aureus, meningococci, some strep. Pyogenes. It is due to (a) produce increased amounts of PABA. (B) folate synthetase enzyme has low affinity. (C) adopt an alternative pathway for folate metabolism.
Pharmacokinetics: Rapidly absorbed by the g.I.T. Extent of plasma binding differs in different members ( 10 – 90 % ). Highly protein bound members are longer acting .  attains the same concentration in the csf as in plasma.  Excreted mainly by the kidney through glomerular filtration. The more lipid soluble members are highly reabsorbed in the tubule hence longer acting . Crosses placenta freely.
THE PRIMARY PATHWAY FOR THE METABOLISM OF SULFONAMIDES IS ACETYLATION AT N 4 BY NON MICROSOMAL ENZYME IN LIVER THE ACETYLATED DERIVATIVE IS INACTIVE AND GENERALLY LESS SOLUBLE IN URINE THAN PARENT DRUG MAY PRECIPITATE
Sulfadiazine : Rapidly absorbed orally Rapidly excreted in urine  50% plasma protein bound 20-40% acetylated Aderivative is less soluble in urine = crystalluria Good penetrabilityi n brain and CSF Preferred compound for meningitis Dose: 0 5 g qid to 2 g tds; sulfadiazine 0.5 g tab
Sulfamethoxazole : Slower oral absorption Slower urinary excretion  T 1/2 in adults is 10 hours Preferred compound for combining with trimethoprim because the t1/2 of both is similar A high fraction is acetylated – crystalluria dose: 1 g BD for 2 days, then 0.5 g BD. Gantanol 0.5 g tab.
Sliver sulfadiazine : Active against a large number of bacteria and fungi, It slowly releases silver ions which appear to be largely responsible for the antimicrobial action Most effective drugs for preventing infection of burnt surfaces and chronic ulcers and is well tolerated. It is not good for treating established infection. Local side effects are-burning sensation on application and itch. Sil vlrin 1% cream, argenex 1% cream With chlorhexidine 0.2%.
ADVERSE EFFECTS :  Crystalluria is dose related Hypersensitivity reactions occur in 2-5 % patients. These are mostly in the form of rashes, urticaria and drug fever. Photosensitization is reported. Stevens-johnson syndrome and exfoliative dermatitis are more common with long-acting agents. Hepatitis, unrelated to dose, occurs in 0.1 % patients.•
Topical use of sulfonamides is not recommended because of risk of contact sensitization. • Sulfonamides cause haemolysis in a dose dependent manner in individuals with g-6-pd deficiency. Neutropenia and other blood dyscrasias are rare. • Kernicterus may be precipitated in the newborn, especially premature, by displacement of bilirubin from plasma protein binding sites and more permeable blood-brain barrier
Interactions :  sulfonamides inhibit the metabolism (possibly displace from protein binding also ) of phenytoin, tolbutamide and warfarin enhance their action. They displace methotrexate from binding and decrease its renal excretion = toxicity can occur. Fixed dose combinations of sulfonamides with penicillins are banned in india.
Uses : Systemic use of sulfonamides alone is rare now. Though they can be employed for suppressive therapy of chronic uti, for streptococcal pharyngitis and gum infection. Combined with trimethoprim (as cotrimoxazole) sulfamethoxazole is used for many bacterial infections and nocardiasis .
Along with pyrimethamine, certain sulfonamides are used for malaria and toxoplasmosis. Ocular sulfacetamide sod. (10-30%) is a cheap alternative in trachoma/ inclusion conjunctivitis. Topical silver sulfadiazine or mafenide are used for preventing infection on burn surfaces.
89 LOCAL DRUG DELIVERY OF ANTIBIOTICS • Limitation of systemic therapy, mouth rinse & irrigation have, promoted for research for development of alternative delivery system • Requirement of treating periodontal disease include 1. Controlled release of drug 2. Maintained localized concentration of drug at infection site for optimum time 3. Minimal side effect
90 VARIOUS LOCAL DRUG DELIVEREY OF ANTIBIOTICS • ACTISITE (TETRACYCLINES) • ARESTIN (MINOCYCLINE) • ATRIDIOX (METRONIDAZOLE ) • PERIO CHIP (CHLOR HEXIDINE) • ELYZOL (METRONIDAZOLE )
91 TETRACYCLINE – CONTAINING FIBER (ACTISITE ) First local delivery product for antibiotic Feature 1. Ethylene or vinyl acetate copolymer fiber 2. Diameter 0.5 mm 3. Containing Tetracycline 12.7 mg/ 9 inch 4. When packed into periodontal pocket, it is well tolerated by oral tissue 5. For 10 day it sustains tetracycline concentration exceeding 1300 ug/ ml https://www.google.co.in/search?q=LDD+actisite
92 ACTISITE....... Effect Reduction in probing depth Reduction in Bleeding on probing Increase in clinical attachment level Normally no staining on teeth Reduction in plaque micro organism
93 SUB GINGIVAL DELIVERY OF DOXYCLINE ATRIDIOX • Atridox is gel system that incorporate the antibiotic Doxycycline (10%) in syringeable gel system • It is a Biodegradable mixture • Drug introduced Subgingivally • Applied with or without Scaling or Root planning Effect Increase in clinical attachment level Reduction in plaque micro organism Probing depth reduction https://www.google.co.in/search?q=LDD+ATRIDIOX
94 SUB GINGIVAL DELIVERY FOR MINOCYCLINE (ARESTIN) 1. Sub Gingival Delivery system contain 2% (w/w) Minocycline hydrochloride 2. Use as a adjuvant to Sub Gingival debridement 3. Biodegradable mixture in syringe Effect are Reduction in Pocket depth Reduction in gingival bleeding Reduction in plaque microorganism
95 SUB GINGIVAL DELIVERY OF METRONIDAZOLE ELYZOL • ELYZOL Containing an oil based Metronidazole 25% dental gel • Applied in viscous consistency to the pocket where is liquidized by body heat and hard again contact with water • Preparation contain Metronidazole benzoate, which is converted into active substance by esterase in GCF • Effective after scaling & Root planning
ANTIBIOTIC PROPHYLAXIS FOR DENTAL PROCEDURES  Definition: “The administration of antibiotics to patients who have no known infection in order to prevent microbial colonization and reduce the potential of post – operative complications.” - Michael g. Newman  Principles: (A) benefits > risks. (B) antibiotic loading dose should be used (C) should be selected based on the most likely organism to cause an infection. (D) should be present in the blood and target tissues before the spread of micro – organisms. (E) should be continued as long as contamination persists
 American Heart Association: (Infective Endocarditis) SITUATION DRUG DOSAGE (30 – 60 min. before procedure single dose) Oral Administration Amoxicillin Adults: 2 g Children: 50 mg/kg Inability to take Oral medication a.) Ampicillin b.) Cefazolin/Ceftriaxone Adults: 2 g I.M/I.V. Children: 50 mg/kg I.M/I.V Adults: 1 g I.M/I.V Children: 50 mg/kg I.M/I.V Allergy to Penicillin and Ampicillin a.) Clindamycin b.) Azithromycin/Clarithromycin c.) Cephalexin Adults: 600 mg Children: 20 mg/kg Adults: 500 mg Children: 15 mg/kg Adults: 2 g Children: 50 mg/kg Allergy to Penicillin and Ampicillin + Inability to take oral medication a.) Cefazolin/Ceftriaxone b.) Clindamycin Phosphate Adults: 1 g I.M./I.V. Children: 50 mg/kg I.M./I.V. Adults: 600 mg I.M/I.V Children: 20 mg/kg I.M/I.V.
ANTIBIOTICS IN VARIOUS DENTAL CONDITIONS WHEN ARE ANTIBIOTICS USED?  Useful as treatment adjuncts to conventional periodontal therapy.  Successful when the micro-organism has reached the connective tissue of the diseased gingiva.  They should never be used if treatment is removal of plaque. Agent is most effective when the dominant micro – organism is determined.
CONDITION DRUG DOSAGE Acute Ulcerative Necrotizing Gingivitis a) Amoxicillin b) Metronidazole a.) 500 mg QID x 5 days b.) 400 mg TID x 7 days. Periodontal Abscess a) Amoxicillin b.) Clindamycin ( Penicillin allergy) c.) Azithromycin a.) 1 g loading dose, then 500 mg TID x 3 days b.) 600 mg loading dose, then 300 mg QID x 3 days. c.) 1 g loading dose, then 500 mg QID x 3 days. Localized Aggressive Periodontitis a.) Tetracycline b.) Doxycycline c.) Augmentin ( If resistant to the Tetracyclines) a.) 250 mg x 14 days, every 8 weeks. b.) 100 mg/day c.) 325 mg TID x 14 days.
Endodontic Infections: - Acute Periapical Abcess: Amoxicillin 500 mg TID x 5 days - Adjunctive Treatment: Penicillin 1 g loading dose, then 500 mg every 6 hrs x 7 – 10 days. Penicillin Allergy: Erythromycin 1 g loading dose, then 500 mg every 6 hrs x 7 days. Doxycycline 200 mg loading dose, the 100 mg every 6 hrs x 7 days.
 Cellulitis: Adult: Amoxicillin 500 mg TID x 5 days Child: 20 – 50 mg/kg/day in 2 – 3 divided doses.  Osteomyelitis: 1.) Aqueous Penicillin 2 MU I.V. every 4 hrs + Metronidazole 400 mg every 6 hrs. If condition improves after 48 – 72 hrs, then switch to Penicillin V 500 mg every 4 hrs + Metronidazole 400 mg every 6 hrs x 4 – 6 weeks. 2.) Ampicillin 1.5 -3 g x 6hrs. If condition improves after 48-72hrs switch to Augmentin 1 g BID x 4 – 6 weeks
3.) Penicillin V 2g + Metronidazole 400 mg every 8 hrs. x 2 - 4weeks after last the seqestrum was removed and the patient was without symptoms 4.) Clindamycin 600 - 900mg every 6 hrs. I.V. then Clindamycin 400 - 600mg every 6 hours or 2-4 weeks 5.) Cefoxitin 1 g every 8 hours I.V. / 2 g every 4 hrs I.M. until no symptoms, then switch to Cephalexin 500 mg every 6 hrs for 2-6 weeks.
 Dento – Alveolar Abscesses/Space Infections: - Amoxicillin 500 mg TID x 5 days. Metronidazole 400 mg TID x 5 days. - Penicillin Allergy: Clindamycin 600 mg  Pediatric Doses: (a) Amoxicillin: 250 mg TID x 5 days. 20 – 40 mg/kg oral susp. (b) Ampicillin: 50 – 100 mg/kg in 4 divided doses (c) Cephalexin: 25 – 50 mg/kg in 4 – 6 divided doses. (d) Clindamycin: 8 – 25 mg/kg in 3 – 4 divided doses. (e) Erythromycin: 30 – 40 mg/kg in 4 divided doses (f) Penicillin V: 25 – 50 mg/kg in 4 divided doses.
CULTURE SENSITIVITY AND TESTING  Many oral infections are treated without identification of the specific etiologic agent.  This leads to unsuspected resistance and therefore the treatment can become unsuccessful or inadequate.  Quantitative Tests: - Determines how much the minimum inhibitory concentration inhibits the growth of the organism.
- Minimum Inhibitory Concentration: (MIC) - Lowest concentration of the agent that inhibits the growth of the organism. - Minimum Bactericidal Concentration: (MBC) - Lowest concentration of antimicrobial agent that allows less that 0.1 % of the original inoculum to survive.  METHODS OF SUSCEPTIBILITY TESTING: (a) Chromogenic Cephalosporin Test: - Used to detect the β – Lactamase enzyme. - Colour of the disc changes from yellow to red.
(b) Disc Diffusion Method: - Incorporates the measurement of zone diameters, representing the ability of a particular agent to exert its effect.
(c) Dilution Methods: - Recommended for slow growing facultative anaerobic bacteria found in oral infections. - Also determines the bactericidal activity of synergism or antagonism between agents. (e.g Microdilution test, Agar dilution test)  Interpretation of Results: - An organism is considered to be susceptible if the Minimal Inhibitory Concentration is lower than the peak concentration in blood.
LIST OF REFERENCES 1. www.Merriam-webster.Com 2. Essentials of general pharmacology, K D Tripati : Jaypee Publications,5th edition 2003 3. Goodman and Gilman. The pharmacological basis of therapeutics, 9th edition. 4. Michael G Newman, “Antibiotic/Antimicrobial Use in Dental Practice” 5. CIMS India (www.mims.com) 6. Dental pulse for entrance examination 7. Maureen K Bolon, “The Newer Fluoroquinolones,” 2011 8. www.medical.theclinics.com
9. Foundation in microbiology: basic principle by Kathleen park, 2nd edition 10.Lippincott’s illustrated reviews pharnacology., 2nd edition 2000 11.Satoskar, bhandarkar , Nirmala rege . pharmacology and therapeutics, 20th edition. 12.Burket's textbook of oral medicine, lester william burket, martin s. Greenberg, michael glick, jonathan A. Ship 11th edition, 13.Carranza's clinical periodontology, michael G. Newman, henry takei, perry R. Klokkevold, fermin A. Carranza LIST OF REFERENCES

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broad spectrum antibiotics - Dr Sanjana Ravindra

  • 1.
    ANTIBIOTICS BROAD SPECTRUM ANTIBIOTICS DrSanjana Ravindra 1st year PG Dept. of OMR
  • 2.
    CONTENT DEFINITION INTRODUCTION HISTORY PRINCIPLES OF ANTIBACTERIALTHERAPY CLASSIFICATION AND MECHANISM OF ACTION USES OF ANTIBIOTICS ADVERSE EFFECTS OF ANTIBIOTICS BROAD SPECTRUM ANTIBIOTIC DRUGS LOCAL DRUG DELIVERY SYSTEM ANTIBIOTICS IN DENTISTRY REFERENCES
  • 3.
    DEFINITION S 1) DRUG isany substance or product that is used or intended to be used to modify or explore physiological systems or pathological states for the benefit of the reciepient 2) PHARMACOKINETICS is the study of absorption, distribution, metabolism and excretion of drugs ie what the body does to the drug 3) PHARMACODYNAMICS is the study of effects of the drugs on the body and their mechanism of action ie what the drug does to the body 4) THERAPEUTICS deals with the use of drugs in prevention and treatment of diseases
  • 4.
    5) ANTIBIOTIC AGENTAgainst life (Greek-anti means against and biosis means life). Chemical substances produced by microorganisms that have the capacity in dilute solutions, to produce antimicrobial action 6) ANTIMICROBIAL AGENT Substances that will suppress the growth / multiplication of microorganisms. antimicrobial agents may be antibacterial, antiviral / antifungal 7) ANTIBACTERIAL AGENT substances that destroy or suppress the growth / multiplication of bacteria. They are classified as antibiotic or synthetic agents DEFINITION S
  • 5.
    INTRODUCTIO N Chemical substances producedby microorganisms that supress the growth of other microorganisms and may eventually destroy them. • K.D. TRIPATHI Chemical substance produced by microorganisms, which at a high dilution can inhibit the growth and/or multiplication or kill another microorganism. • - WAKSMAN AND WOODRUFF(1942)
  • 6.
    The term 'antibiosis',meaning "against life", was introduced by the french bacteriologist Jean Paul Vuillemin  Antibiosis was first described in 1877 in bacteria when Louis Pasteur and Robert Koch observed that an airborne bacillus could inhibit the growth of bacillus anthracis INTRODUCTIO N https://www.google.co.in/search?q=antib-hist
  • 7.
    The term antibioticwas first used in 1942 by Selman Waksman and his collaborators in journal articles to describe “any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.” The term "antibiotic" derives from anti + βιωτικός (biōtikos), "fit for life, lively“, which comes from βίωσις (biōsis), "way of life“,and that from βίος (bios), "life“ https://www.google.co.in/search?q=Waksman-antib
  • 8.
    HISTORY History of chemotherapyis divided into two phases. (A) the period of empirical use (B) modern era.
  • 9.
    Chinese  ‘mouldycurd’ on boils Hindus  ‘chaulmoogra oil” in leprosy Aztecs  ‘chenopodium’ for intestinal worms Paracelsus  mercury for syphilis and cinchona bark for fever PERIOD OF EMPIRICAL USE: https://www.google.co.in/search?q=plantshist6orical
  • 10.
     1871 JosephLister experimented with the antibacterial action on human tissue on what he called penicillium glaucium  1877 Louis Pasteur postulated that bacteria could kill other bacteria ( anthrax bacilli)  1928 Sir Alexander Fleming discovered enzyme lysozyme and the antibiotic substance penicillin from the fungus Penicillium notatum  During 1940 and 50s streptomycin, chloramphenicol and tetracyclin were discovered  1942 Selman Waksman used the term antibiotics MODERN HISTORY https://www.google.co.in/search?q=anti-pioneers
  • 11.
  • 12.
    BROAD SPECTRUM 1. Tetracycline 2.Chloramphenicol 3. Sulfonamides 4. Trimethoprim NARROW SPECTRUM 1. Bacitracin 2. Clindamycin 3. Macrolides 4. Metronidazole 5. Penicillin G,V 6. Penicillinase resistant penicillin 7. Polymixin 8. Vancomycin BASED ON SPECTRUM OF ACTIVITY Neidle E A, Pharmacology and therapeutics for Dentistry, 4th edition. Pg 48 EXTENDED SPECTRUM 1. Aminoglycosides 2. Carbacephems 3. Cephalosporins 4. Extended spectrum of penicillins 5. Fluoroquinolones 6. Monobactams CLASSIFICATI ON
  • 13.
    BASED ON TYPEOF ACTION Bacteriostatic • Sulfonamides • Tetracyclines • Chloramphenicol • Erythromycin • Ethambutol Bactericidal • Penicillins • Aminoglycosides • Rifampin • Cotrimoxazole • Cephalosporins • Vancomycin • Nalidixic acid • Ciprofloxacin Neidle E A, Pharmacology and therapeutics for Dentistry, 4th edition. Pg 48
  • 14.
    ANTIBIOTICS ARE OBTAINED FROM ACTINOMYCETES Penicillin Cephalosporin Griseofulvin PolymyxinB Colistin Bacitracin Tyrothricin Aminoglycosides Tetracyclines Chloramphenicol Macrolides Polyenes BACTERIA FUNGI Neidle E A, Pharmacology and therapeutics
  • 15.
    BASED ON ORGANISMSSUSCEPTIBLE EFFECTIVE AGAINST GRAM +VE BACTERIA PENICILLINS MACROLIDS BACITRACIN EFFECTIVE AGAINST GRAM –VE BACTERIA STREPTOMYCIN EFFECTIVE AGAINST BOTH GRAM +VE AND –VE BACTERIA AMPICILLIN TETRACYCLIN CHLORAMPHENICOL AMOXICILLIN CEPHALOSPORIN NEOMYCIN EFFECTIVE AGAINST ACID-FAST BACILLI STREPTOMYCIN RIFAMPIN KANAMYCIN AGAINST PROTOZOA TETRACYCLIN EFFECTIVE AGAINST FUNGI NYSTATIN AMPHOTERICIN B ANTIMALIGNANCY ANTIBIOTICS ACTINOMYCIN D MITOMYCIN
  • 16.
    PRINICIPLES OF ANTIBIOTIC THERAPY Selectionof antibacterial agent Antibacterial combinations Antibacterial prophylaxis Microbial drug resistance Dangers of antibacterial therapy Misuse of antibacterial agents
  • 17.
    SELECTION OF ANTIBIOTICAGENT 1)HOST RELATED FACTORS Age of the patient Pregnancy and neonatal period Immunocompetency status of the patient Severity of the infection Allergic reaction and intolerance Genetic factors Renal and hepatic function
  • 18.
    2)PATHOGEN RELATED FACTORS Evaluationof the probable microbial etiology and expected clinical course of the infection Identification of the causative microorganism and its sensitivity to antibiotic drugs Possibility of drug resistance 3)DRUG RELATED FACTORS Nature of the drug Risk of drug toxicity The cost of therapy Pharmacokinetic properties of the drug Probability of drug compliance by the patient
  • 19.
    ANTIBACTERIAL COMBINATIONS 1) SIMULTANEOUS USEOF TWO OR MORE ANTIBIOTICS IS NOT ROUTINELY RECOMMMENDED. THESE DRUGS CAN BE COMBINED UNDER FOLLOWING REASONS To achieve an additive or synergistic effect against a single organism In mixed infections with bacteria sensitive to different drugs To delay the development of or to overcome the drug resistance To decrease the adverse reactions to an individual drug When etiological diagnosis is difficult, the infection is severe and body defense is poor For reducing chances of superinfections
  • 20.
    2) IF ABACTERIOSTATIC DRUG IS COMBINED WITH BACTERIOCIDAL AGENT FOLLOWING THINGS MAY BE HAPPEN Drug antagonism Additive effect oftenly synergestic rarely 3) COMBINED ANTIBIOTIC THERAPY INVOLVES CERTAIN RISKS Emergence of organism resistant to the multiple drugs used Increased risk of adverse reactions Increased risk of superinfection by resistant organisms Sense of false security Increase in cost of therapy
  • 21.
    ANTIBACTERIAL PROPHYLAXIS For prevention ofmeningococcal infections in healthy children during an epidemic, for prevention of diseases like syphilis, gonorrhea, malaria. For preventing endocarditis following minor surgical procedures like tonsillectomy or tooth extraction in patients with cardiac lesions. For preventing invasion of blood stream by pathogens during certain surgical manipulations. In patients with compound musculoskeletal injury, penetrating wounds and skull injuries.
  • 22.
    For those puncturewounds that are at high risk of infection. Animal bite as they are at high risk of infection by oral flora. To prevent microbial complications like bronchopnemonia e.g. Cases of measles and tetanus. In paralytic states to prevent aspiration bronchopnemonia
  • 23.
    DANGERS OF ANTIBACTERIAL THERAPY Development of allergic and anaphylactic reactions e.g. Pennicillin  Selective toxicity  Development of superinfection  Development of multiple drug resistant organisms  Deficiency of certain vitamins  Fetal damage  A false sense of security in the patient as well as in physician  Failure to respond to antibiotic therapy
  • 24.
    MISUSE OF ANTIBIOTIC THERAPY Antibioticmisuse, sometimes called antibiotic abuse or antibiotic overuse.  Produce serious effects on health. From antibiotics now available , one needs to know the important representatives of each class and know them well e.g. Action , dosage . It is a contributing factor to the creation of multidrug-resistant bacteria, informally called "super bugs" relatively harmless bacteria can develop resistance to multiple antibiotics and cause life-threatening infections.
  • 25.
    MICROBIAL DRUG RESISTANCE Therecent emergence of antibiotic resistance in bacterial pathogens, both nosocomialy and in the community, is a very serious development that threatens the end of the antibiotic era. Drug resistance is not a characteristic of all bacteria and many strains responsible for common infections have largely remained susceptible to antibiotics e.G. Pneumococci, streptococcus pyogenes, meningococci, and treponema pallidum.
  • 26.
    Bacterial resistance isoften quantitative and not qualitative. Thus an antibacterial substance which is not effective in small doses may inhibit the bacteria in vitro in large concentrations. For an antibiotic to be effective, it must reach its target in an active form, bind to the target, and interfere with its function. Accordingly, bacterial resistance to an antimicrobial agent is attributable to three general mechanisms: (1) the drug does not reach its target, (2) the drug is not active, or (3) the target is altered .
  • 27.
    Natural resistance In organismswhich are naturally resistant, the drug sensitive enzyme reactions may be absent .  some naturally resistant organisms may elaborate a substance which destroys the antibiotic e.G. E coli produce pencillinase which destroys penicillin . Following the use of an antibiotic agent which destroys the sensitive strain , these naturally resistant variants multiply and become dominant.
  • 28.
    Some microbes havealways been resistant to certain antibacterial agents. They lack the metabolic process or the target site which is affected by the particular drug. This is generally a group or species charateristic e .G. Gm-ive bacilli are normally unaffected by penicillin G or M. Tuberculosis is insensitive to tetracyclines.
  • 29.
    Acquired microbial resistance Itis the development of resistance by an organism (which was sensitive before) due to the use of an AMA over a period of time. This can happen with any microbe and is a major clinical problem. However, development of resistance is dependent on the microorganism as well as the drug. Some bacteria are notorious for rapid acquisition of resistance, e.G. Staphylococci, coliforms, tubercle bacilli. .
  • 30.
    Others like strep.Pyogenes and spirochetes have not developed significant resistance to penicillin despite its Widespread use for > 50 years. It can arise in bacteria in several ways. Microbes acquire resistance after a change in their DNA. Such change may occur in A) genetic mutation B) genetic exchange - conjugation - Transduction - Transformation
  • 31.
    Mutation It is astable and heritable genetic change that occurs spontaneously and randomly among microorganisms.  Any sensitive population of a microbe contains a few mutant cells which require higher concentration of the ama for inhibition. Mutation and resistance may be: (I ) single step.- A single gene mutation may confer higher degree of resistance; emerges rapidly, e.G. Enterococci to streptomycin, E. Coli and staphylococci to rifampin (Ii ) multistep.· A number of gene modifications are involved, sensitivity decreases gradually in a stepwise manner. Resistance to erythromycin, tetracyclines and chloramphenicol is developed by many organisms in this manner.
  • 32.
    Conjugation : Thismay involve chromosomal or extrachromosomal (plasmid) dna.  The gene carrying the 'resistance' or 'r' factor is transferred only if another 'resistance transfer factor' (rtf) is also present. Chloramphenicol resistance of typhoid bacilli, streptomycin resistance of e. Coli, penicillin resistance of haemophilus. Concomitant acquisition of multidrug resistance has occurred by conjugation. Thus, this is a very important mechanism of horizontal transmission of resistance. GENE TRANSFER
  • 33.
    TRANSDUCTION: It is thetransfer of gene carrying resistance through the agency of a bacteriophage. The r factor is taken up by the phage and delivered to another bacterium which it infects. Certain instances of penicillin, erythromycin and chloramphenicol resistance have been found to be phage mediated.
  • 34.
    TRANSFORMATION :  Aresistant bacterium may release the resistance carrying DNA into the medium and this may be imbibed by another sensitive organism-becoming unresponsive to the drug.  This mechanism is probably not clinically significant except isolated instances of pneumococcal resistance to penicillin g due to altered penicillin binding protein
  • 35.
    CROSS RESISTANCE : Acquisitionof resistance to one AMA conferring resistance to another AMA, to which the organism has not been exposed, is called cross resistance. This is more commonly seen between chemically or mechanistically related drugs, e.G. Resistance to one sulfonamide means resistance to all others, and resistance to one tetracycline means insensitivity to all others. Sometimes unrelated drugs show partial cross resistance, e.G. Between tetracyclines and chloramphenicol, between erythromycin and lincomycin.
  • 36.
    PREVENTION OF DRUGRESISTANCE No indiscriminate and inadequate or unduly prolonged use of amas should be made. This would minimize the selection pressure and resistant strains will get less chance to preferentially propagate. Prefer rapidly acting and selective (narrow spectrum) amas whenever possible; broad-spectrum drugs should be used only specifically. Use combination of amas whenever prolonged therapy is undertaken, e.G. Tuberculosis, SABE. Infection by organisms notorious for developing Resistance, e.G. Staph. Aureus, E. Coli, M. Tuberculosis, Proteus, etc. Must be treated intensively.
  • 38.
    INDICATIONS OF ANTIBIOTICS *Diabetics mellitus, immunoglobulin deficiency, malnutrition and alcoholism. * Acute severe rapidly spreading infection * Pericoronitis, osteomyelitis, fracture, soft tissue wound and odontogenic infection * Post operative wound infection * Prevention of endocarditis in high risk patients undergoing any dental procedures that is likely to cause gingival bleeding THERAPEUTIC PROPHYLACTIC
  • 39.
    USES OF ANTIBIOTICS Infections ofall systems  Pus formation Sepsis Quinsy Skin infections Mucous membrane infections Septicaemia Empirical therapy Prophylactic therapy
  • 40.
    CONTROL AND ERADICATIONOF INFECTIONS OF ORAL CAVITY. • Local factors; 1) Swelling, 2) Lymphadenitis, 3) Trismus, 4) Dyshagia 5) Chronic draining sinus tract. • Systemic factors; 1) Cellulitis. 2) Osteomyelitis. 3) Infections of salivary gland. 4) Compound fractures. 5) Infected cysts. 6) Infected oro-antral fistula. 7) Pericoronitis
  • 41.
    SIDE EFFECTS OF ANTIBIOTICS Diarrhoea Bloatingand indigestion Abdominal pain Loss of appetite Being sick Feeling sick Itchy skin rash Coughing Life-threatening allergic reaction
  • 42.
    BROAD SPECTRUM ANTIBIOTICS 1. TETRACYCLINE 2.CHLORAMPHENICOL 3. SULFONAMIDES 4. TRIMETHOPRIM
  • 43.
    TETRACYCLIN E Defination : Theyare octahydro napthacene derivatives which are bacteriostatic and broad spectrum antibiotics that kills certain infection causing microorganisms and are used to treat wide variety of infections.  Tetracyclines are napthacene derivatives.  The napthacene nucleus is made up by fusion of 4 partially unsaturated cyclohexane radicals and hence the name tetracyclines.  Tetracyclines are bacteriostatic & effective against rapidly multiplying bacteria https://www.google.co.in/search?q=tetracycline+structure
  • 44.
    According to durationof action: • Short-acting (Half-life is 6-8 hrs) • Tetracycline • Chlortetracycline • Oxytetracycline • Intermediate-acting (Half-life is ~12 hrs) • Demeclocycline • Methacycline • Long-acting (Half-life is 16 hrs or more) • Doxycycline • Minocycline • Tigecycline CLASSIFICATI ON
  • 45.
     Primarily bacteriostatic. Inhibit protein synthesis by binding to 30s ribosomes in susceptible organism. Thus, attachment of aminoacyl-t-rna to the mrna-ribosome complex is interfered with. As a result, peptide chains fail to grow.  It is effective against gram –ve and gram +ve bacteria, rickettsial, spirochetees, protozoa and mycoplasma. MECHANISM OF ACTION tripathi
  • 46.
     Orally- saliva-liver- bile  They cross placental barrier  Tetracyclines have chelating property-form insoluble & unabsorbable complexes with calcium and other metals.  Doxycycline & minocycline are completely absorbed irrespective of food.  Milk, iron preparations, nonsystemic antacids & sucralfate reduce their absorption . administration of these substances & tetracyclines should be staggered, if the cannot be avoided altogether. PHARMACOKINETICS
  • 47.
    (A) IRRITATIVE EFFECTS: -Epigastric pain, nausea, vomiting, diarrhoea. - Doxycycline is known to cause esophageal ulcerations. (B) DOSE RELATED TOXICITY: 1.) LIVER DAMAGE: - Fatty infiltration of liver, jaundice, in pregnancy, Can cause acute hepatic necrosis. ADVERSE EFFECTS
  • 48.
    2.) KIDNEY DAMAGE: -Fancony syndrome – like condition 3.) PHOTOTOXICITY: - Sunburn, severe skin reactions 4.) ANTIANABOLIC EFFECT : - Reduce protein synthesis & have an overall catabolic effect. - They induce negative nitrogen balance & can increase blood urea.
  • 49.
    5.) LNCREASED INTRACRANIALPRESSURE In some infants. 6.) DIABETES INSIPIDUS - Demeclocycline antagonizes ADH action & reduces urine concentrating ability of the kidney. 7.) VESTIBULAR TOXICITY - Minocycline has produced vertigo which subside when the drug is discontinued.
  • 50.
    (C) HYPERSENSITIVITY - Thisis infrequent with tetracyclines. - Skin rashes, urticaria, glossitis, pruritus, even exfoliative dermatitis have been reported. - Angioedema & anaphylaxis are extremely rare. (D) SUPERINFECTION: - Marked suppression of the resident flora. - Intestinal superinfection by candida albicans can occur. - Oral manifestations are very rare.
  • 51.
    https://www.google.co.in/search?q=tetracycline+staining  Hypoplasia andbrown discolouration of teeth  Not used in 3rd trimester  Deposits in bones and teeth- yellow discolouration  Not recoomended- children below 8 yrs and pregnant women – permanently discolour developing teeth and alter bone growth (E) TOOTH DISCOLOURATION
  • 52.
    PRECAUTIONS 1.) Tetracyclines shouldnot be used during pregnancy, lactation and in children. 2.) They shouldbe avoided in patients on diuretics: blood urea may rise in such patients. 3.) They should be used cautiously in renal or hepatic insufficiency. 4.) Preparations should never be used beyond their expiry date. 5.) Do not mix injectable tetracyclines with penicillin-inactivation occurs. 6.) Do not inject tetracyclines intrathecally.
  • 53.
    (A) MEDICINAL USES -Clinical use has declined due to the introduction of Fluoroquinolones and other agents. - DRUG OF 1ST CHOICE: (A) venereal diseases (B) atypical pneumonia (C) cholera  limit the diarrhoea duration. (D) brucellosis  combined with gentamicin. (E) plague (F) relapsing fever. (G) rickettsial infections. USES
  • 54.
    - DRUG OF2ND CHOICE: (A) to penicillin / ampicillin for tetanus , anthrax , actinomycosis infections. (B) to ciprofloxacin / ceftriazone for gonorrhea in patients allergic to penicillin. (C) to ceftriaxone for syphilis in patients allergic to penicillin. (D) to azithromycin for chlamydial infections. - Also can be used for UTI , pneumonia, amoebiasis, acne, lung disease.
  • 55.
    (B) dental uses: • of limited use in treating acute infections , but are of importance in periodontal disease. • Suppress the activity of collagenases derived from the neutrophils and fibroblasts, that contribute to gingival inflammation. • Collagenases are calcium dependent & tetracyclines chelate the calcium. • May benefit periodontal inflammation by releasing free radicals of oxygen.
  • 56.
    ADMINISTRATION  oral capsuleis the dosage form in which tetracyclines are most commonly administered.  The capsule should be taken 1/2 hr before or 2 hr after food.  Not recommended by i.M. Route because it is painful & absorption from the injection site is poor.  Slow i.V. Injection may be given in severe cases, but is rarely require now.  A variety of topical preparations are available , but should not be use because there is high risk of sensitization .
  • 57.
    OXYTETRACYCLINE: (TERRAMYCIN) 250 – 500MG EVERY 6 HRS TETRACYCLINE: (ACHROMYCIN, RESTECLIN) 250 MG – 4 G EVERY 6 HRS DOSAGES https://www.google.co.in/search?q=tetracycline+tablet
  • 58.
    DEMECLOCYCLINE: (LEDERMYCIN) ADULT: 150 MG4 X DAILY 300 MG BID. CHILD: 7 – 13 MG/KG DIVIDED EVERY 6 – 12 HRS. MINOCYCLINE: (CYANOMYCIN) ADULT: 200 MG FOLLOWED BY 100 MG EVERY 12 HRS. CHILD: 4 MG/KGhttps://www.google.co.in/search?q=tetracycline+tablet
  • 59.
    DOXYCYCLINE: (TETRADOX, BIODOXI, DOXT,NOVADOX) ADULT: 200 MG ON DAY 1 FOLLOWED BY 100 MG OD CHILD: 4 MG/KG IN 2 DIVIDED DOSES, FOLLOWED BY 2 MG/KG DAILY. https://www.google.co.in/search?q=tetracycline+tablet
  • 60.
    TETRACYCLINE EFFECTIVE INTREATING PERIODONTAL DISEASE BECAUSE • Adjuvant role in Chronic Periodontitis - control gingival inflammation - normalize the periodontal microflora from a mixture of anerobic G- bacilli and spirochetes. • Highly active against Actinobacillus actinomycetum comitans in Aggressive Periodontitis - prevents gingival destruction and bone loss.
  • 61.
    TERATOGENIC EFFECTS OF TETRACYCLINES PERIODSTRUCTURE AFFECTED DEFORMITY mid pregnancy to 5 months of postnatal life Deciduous teeth Brownish discolouration, ill formed and are more susceptible to caries 2 months to 5 years of age Permanent teeth Pigmentation, discolouration Pregnancy and childhood up to 8 years of age Skeleton Depressed bone growth
  • 63.
    CHLORAMPHENICO L • Broad spectrumantibiotic first obtained from streptomyces venezuelae. MECHANISM OF ACTION  It is bacteriostatic but for some organisms it is bacteriocidal. It binds to 50s ribosomal subunit and inhibits protein synthesis  It is unique among natural compounds because it contains a NITROBENZENE moiety and is a derivative of DICHLOROCETIC ACID.  It acts by inhibiting protein synthesis (by binding reversibly to the 50s ribosomal subunit). https://www.google.co.in/search?q=chloramphenicol+structure
  • 64.
    64 USES :  Typhoidfever(S.typhi)  Bacterial meningitis (H.influenzae)  Anaerobic infections  Rickettsial disease (eg.Rocky mountain spotted fever)  Brucellosis  UTI Adult 250 -500mg 6hrly Children 25 – 50mg /kg/day
  • 65.
    65 ADVERSE EFFECTS : Bone marrow depression  Hypersensitivity reactions  Irritative effects  Superinfections  Gray baby syndrome
  • 66.
    GRAY BABY SYNDROME/ ASHEN GRAY CYANOSIS Newborn babies given high doses of chloramphenicol – develop vomiting, refusal of feeds, hypotonia, hypothermia, abdominal distension, metabolic acidosis https://www.google.co.in/search?q=gray+baby
  • 67.
    It is thefixed dose combination of trimethoprim and sulfamethoxazole. Trimethoprim it is diaminopyrimidine and related to antimalarial drug pyrimethamine.  Sulfamethoxazole selected for the combination because it has nearly the same T ½ as trimethoprim. COTRIMOXAZOL E
  • 68.
    ANTIBACTERIAL SPECTRUM : Individually,both sulfonamide and trimethoprim are bacteriostatic. Combination becomes cidal against many organisms. Organisms covered by the combination are-salmonella typhi, serratia, klebsiella, enterobacter, pneumocystis jiroveci.  Many sulfonamide resistant strains of staph. Aureus, strep. Pyogenes, shigella, enteropathogenic E. Coli, influenzae , gonococci and meningococci.
  • 69.
    Why sulfamethoxazole +trimethoprim ? Both have nearly the same t1/2 (- 10 hr). Optimal synergy is exhibited at a concentration ratio of Sulfamethoxazole 20 : trimethoprim 1. MIC of each component may be reduced by 3-6 times. This ratio is obtained in the plasma when the two are given in a dose ratio of 5 : 1, because trimethoprim enters many tissues, has a larger volume of distribution than sulfamethoxazole and attains lower plasma concentration
  • 70.
    PHARMOKINETICS : Trimethoprim crossesblood-brain barrier and placenta, while sulfamethoxazole has a poorer entry. Trimethoprim is more rapidly absorbed than sulfamethoxazole.  Trimethoprim is 40% plasma protein bound, while sulfamethoxazole is 65% bound. Trimethoprim is partly metabolized in liver and excreted in urine.
  • 71.
    ADVERSE EFFECTS:  Nausea,vomiting, stomatitis, headache, rashes.  Rarely, folate deficiency (megaloblastic anemia)  Blood dyscrasias.
  • 72.
    CONTRAINDICATIONS:  Pregnancy: -teratogenic effects may occur due to trimethoprim. - Neonatal haemolysis, methaemoglobinaemia.  Renal disease: - patient may develop uraemia.  Aids patients: - fever, rash, bone marrow hypoplasia.  Elderly patients: - bone marrow toxicity.  Diuretics + cotrimoxazole = thrombocytopenia.
  • 73.
    USES:  Tonsilitis, pharyngitis,sinusitis, otitis media, chronic bronchitis.  Orodental uses very rare  only if allergies to β – lactam antibiotics are present.  Major indications include uti, bacterial dysentery.  Effective alternative to chloramphenicol in the case of typhoid fever, but strains are known to be resistant.  Alternative for chancroid, granuloma inguanale, neutropenic patients. BRAND NAME SEPTRAN, SEPMAX, BACTRIM, CIPLIN, ORIPRIM, SUPRISTOL, FORTRIM.
  • 74.
     First anti-microbialagents effective against pyogenic bacterial infections. Sulfonamido-chrysoidine (prontosil red)  used by Domagk to treat streptococcal infection in mice. SULPHONAMID E
  • 75.
    A LARGE NUMBEROF SULFONAMIDES WERE PRODUCED AND USED EXTENSIVELY, BUT BECAUSE OF RAPID EMERGENCE OF BACTERIAL RESISTANCE AND AVAILABILITY OF MANY SAFER AND MORE EFFECTIVE ANTIBIOTICS CURRENT UTILITY IS LIMITED EXCEPT IN COMBINATION WITH TRIMETHOPRIM (COTRIMAXOZOLE) AND PYRIMETHAMINE.
  • 76.
    CLASSIFICATION: (A) short acting(4-8 hrs): - Sulfadiazine. (B) intermediate acting (8-12 hrs): - sulfamethoxazole, sulfamoxole. (C) long acting (approx. 7 days): - Sulfadoxine, sulfamethopyrazine. (D) special purpose sulfonamides: - Sulfacetamide sodium, sulfasalazine mafenide, silver sulfadiazine.
  • 77.
    ANTIBACTERIAL SPECTRUM : Theyare primarily bacteristatic against gm +ve and gm –ive bacteria. However , bacteriocidal action can be attained in urine. Sensitive to strepto. Pyogenes , haemophilus influenzae , vibrio cholerae , meningococci , gonococci , E coli and shigella.
  • 78.
    RESISTANCE: Some bacteria arecapable of developing resistance to sulfonamides like pneumococci, gonococci, staph. Aureus, meningococci, some strep. Pyogenes. It is due to (a) produce increased amounts of PABA. (B) folate synthetase enzyme has low affinity. (C) adopt an alternative pathway for folate metabolism.
  • 79.
    Pharmacokinetics: Rapidly absorbed bythe g.I.T. Extent of plasma binding differs in different members ( 10 – 90 % ). Highly protein bound members are longer acting .  attains the same concentration in the csf as in plasma.  Excreted mainly by the kidney through glomerular filtration. The more lipid soluble members are highly reabsorbed in the tubule hence longer acting . Crosses placenta freely.
  • 80.
    THE PRIMARY PATHWAYFOR THE METABOLISM OF SULFONAMIDES IS ACETYLATION AT N 4 BY NON MICROSOMAL ENZYME IN LIVER THE ACETYLATED DERIVATIVE IS INACTIVE AND GENERALLY LESS SOLUBLE IN URINE THAN PARENT DRUG MAY PRECIPITATE
  • 81.
    Sulfadiazine : Rapidly absorbedorally Rapidly excreted in urine  50% plasma protein bound 20-40% acetylated Aderivative is less soluble in urine = crystalluria Good penetrabilityi n brain and CSF Preferred compound for meningitis Dose: 0 5 g qid to 2 g tds; sulfadiazine 0.5 g tab
  • 82.
    Sulfamethoxazole : Slower oralabsorption Slower urinary excretion  T 1/2 in adults is 10 hours Preferred compound for combining with trimethoprim because the t1/2 of both is similar A high fraction is acetylated – crystalluria dose: 1 g BD for 2 days, then 0.5 g BD. Gantanol 0.5 g tab.
  • 83.
    Sliver sulfadiazine : Activeagainst a large number of bacteria and fungi, It slowly releases silver ions which appear to be largely responsible for the antimicrobial action Most effective drugs for preventing infection of burnt surfaces and chronic ulcers and is well tolerated. It is not good for treating established infection. Local side effects are-burning sensation on application and itch. Sil vlrin 1% cream, argenex 1% cream With chlorhexidine 0.2%.
  • 84.
    ADVERSE EFFECTS : Crystalluria is dose related Hypersensitivity reactions occur in 2-5 % patients. These are mostly in the form of rashes, urticaria and drug fever. Photosensitization is reported. Stevens-johnson syndrome and exfoliative dermatitis are more common with long-acting agents. Hepatitis, unrelated to dose, occurs in 0.1 % patients.•
  • 85.
    Topical use ofsulfonamides is not recommended because of risk of contact sensitization. • Sulfonamides cause haemolysis in a dose dependent manner in individuals with g-6-pd deficiency. Neutropenia and other blood dyscrasias are rare. • Kernicterus may be precipitated in the newborn, especially premature, by displacement of bilirubin from plasma protein binding sites and more permeable blood-brain barrier
  • 86.
    Interactions :  sulfonamidesinhibit the metabolism (possibly displace from protein binding also ) of phenytoin, tolbutamide and warfarin enhance their action. They displace methotrexate from binding and decrease its renal excretion = toxicity can occur. Fixed dose combinations of sulfonamides with penicillins are banned in india.
  • 87.
    Uses : Systemic useof sulfonamides alone is rare now. Though they can be employed for suppressive therapy of chronic uti, for streptococcal pharyngitis and gum infection. Combined with trimethoprim (as cotrimoxazole) sulfamethoxazole is used for many bacterial infections and nocardiasis .
  • 88.
    Along with pyrimethamine,certain sulfonamides are used for malaria and toxoplasmosis. Ocular sulfacetamide sod. (10-30%) is a cheap alternative in trachoma/ inclusion conjunctivitis. Topical silver sulfadiazine or mafenide are used for preventing infection on burn surfaces.
  • 89.
    89 LOCAL DRUG DELIVERYOF ANTIBIOTICS • Limitation of systemic therapy, mouth rinse & irrigation have, promoted for research for development of alternative delivery system • Requirement of treating periodontal disease include 1. Controlled release of drug 2. Maintained localized concentration of drug at infection site for optimum time 3. Minimal side effect
  • 90.
    90 VARIOUS LOCAL DRUGDELIVEREY OF ANTIBIOTICS • ACTISITE (TETRACYCLINES) • ARESTIN (MINOCYCLINE) • ATRIDIOX (METRONIDAZOLE ) • PERIO CHIP (CHLOR HEXIDINE) • ELYZOL (METRONIDAZOLE )
  • 91.
    91 TETRACYCLINE – CONTAINING FIBER(ACTISITE ) First local delivery product for antibiotic Feature 1. Ethylene or vinyl acetate copolymer fiber 2. Diameter 0.5 mm 3. Containing Tetracycline 12.7 mg/ 9 inch 4. When packed into periodontal pocket, it is well tolerated by oral tissue 5. For 10 day it sustains tetracycline concentration exceeding 1300 ug/ ml https://www.google.co.in/search?q=LDD+actisite
  • 92.
    92 ACTISITE....... Effect Reduction in probingdepth Reduction in Bleeding on probing Increase in clinical attachment level Normally no staining on teeth Reduction in plaque micro organism
  • 93.
    93 SUB GINGIVAL DELIVERYOF DOXYCLINE ATRIDIOX • Atridox is gel system that incorporate the antibiotic Doxycycline (10%) in syringeable gel system • It is a Biodegradable mixture • Drug introduced Subgingivally • Applied with or without Scaling or Root planning Effect Increase in clinical attachment level Reduction in plaque micro organism Probing depth reduction https://www.google.co.in/search?q=LDD+ATRIDIOX
  • 94.
    94 SUB GINGIVAL DELIVERYFOR MINOCYCLINE (ARESTIN) 1. Sub Gingival Delivery system contain 2% (w/w) Minocycline hydrochloride 2. Use as a adjuvant to Sub Gingival debridement 3. Biodegradable mixture in syringe Effect are Reduction in Pocket depth Reduction in gingival bleeding Reduction in plaque microorganism
  • 95.
    95 SUB GINGIVAL DELIVERYOF METRONIDAZOLE ELYZOL • ELYZOL Containing an oil based Metronidazole 25% dental gel • Applied in viscous consistency to the pocket where is liquidized by body heat and hard again contact with water • Preparation contain Metronidazole benzoate, which is converted into active substance by esterase in GCF • Effective after scaling & Root planning
  • 96.
    ANTIBIOTIC PROPHYLAXIS FORDENTAL PROCEDURES  Definition: “The administration of antibiotics to patients who have no known infection in order to prevent microbial colonization and reduce the potential of post – operative complications.” - Michael g. Newman  Principles: (A) benefits > risks. (B) antibiotic loading dose should be used (C) should be selected based on the most likely organism to cause an infection. (D) should be present in the blood and target tissues before the spread of micro – organisms. (E) should be continued as long as contamination persists
  • 97.
     American HeartAssociation: (Infective Endocarditis) SITUATION DRUG DOSAGE (30 – 60 min. before procedure single dose) Oral Administration Amoxicillin Adults: 2 g Children: 50 mg/kg Inability to take Oral medication a.) Ampicillin b.) Cefazolin/Ceftriaxone Adults: 2 g I.M/I.V. Children: 50 mg/kg I.M/I.V Adults: 1 g I.M/I.V Children: 50 mg/kg I.M/I.V Allergy to Penicillin and Ampicillin a.) Clindamycin b.) Azithromycin/Clarithromycin c.) Cephalexin Adults: 600 mg Children: 20 mg/kg Adults: 500 mg Children: 15 mg/kg Adults: 2 g Children: 50 mg/kg Allergy to Penicillin and Ampicillin + Inability to take oral medication a.) Cefazolin/Ceftriaxone b.) Clindamycin Phosphate Adults: 1 g I.M./I.V. Children: 50 mg/kg I.M./I.V. Adults: 600 mg I.M/I.V Children: 20 mg/kg I.M/I.V.
  • 98.
    ANTIBIOTICS IN VARIOUSDENTAL CONDITIONS WHEN ARE ANTIBIOTICS USED?  Useful as treatment adjuncts to conventional periodontal therapy.  Successful when the micro-organism has reached the connective tissue of the diseased gingiva.  They should never be used if treatment is removal of plaque. Agent is most effective when the dominant micro – organism is determined.
  • 99.
    CONDITION DRUG DOSAGE AcuteUlcerative Necrotizing Gingivitis a) Amoxicillin b) Metronidazole a.) 500 mg QID x 5 days b.) 400 mg TID x 7 days. Periodontal Abscess a) Amoxicillin b.) Clindamycin ( Penicillin allergy) c.) Azithromycin a.) 1 g loading dose, then 500 mg TID x 3 days b.) 600 mg loading dose, then 300 mg QID x 3 days. c.) 1 g loading dose, then 500 mg QID x 3 days. Localized Aggressive Periodontitis a.) Tetracycline b.) Doxycycline c.) Augmentin ( If resistant to the Tetracyclines) a.) 250 mg x 14 days, every 8 weeks. b.) 100 mg/day c.) 325 mg TID x 14 days.
  • 100.
    Endodontic Infections: - AcutePeriapical Abcess: Amoxicillin 500 mg TID x 5 days - Adjunctive Treatment: Penicillin 1 g loading dose, then 500 mg every 6 hrs x 7 – 10 days. Penicillin Allergy: Erythromycin 1 g loading dose, then 500 mg every 6 hrs x 7 days. Doxycycline 200 mg loading dose, the 100 mg every 6 hrs x 7 days.
  • 101.
     Cellulitis: Adult: Amoxicillin500 mg TID x 5 days Child: 20 – 50 mg/kg/day in 2 – 3 divided doses.  Osteomyelitis: 1.) Aqueous Penicillin 2 MU I.V. every 4 hrs + Metronidazole 400 mg every 6 hrs. If condition improves after 48 – 72 hrs, then switch to Penicillin V 500 mg every 4 hrs + Metronidazole 400 mg every 6 hrs x 4 – 6 weeks. 2.) Ampicillin 1.5 -3 g x 6hrs. If condition improves after 48-72hrs switch to Augmentin 1 g BID x 4 – 6 weeks
  • 102.
    3.) Penicillin V2g + Metronidazole 400 mg every 8 hrs. x 2 - 4weeks after last the seqestrum was removed and the patient was without symptoms 4.) Clindamycin 600 - 900mg every 6 hrs. I.V. then Clindamycin 400 - 600mg every 6 hours or 2-4 weeks 5.) Cefoxitin 1 g every 8 hours I.V. / 2 g every 4 hrs I.M. until no symptoms, then switch to Cephalexin 500 mg every 6 hrs for 2-6 weeks.
  • 103.
     Dento –Alveolar Abscesses/Space Infections: - Amoxicillin 500 mg TID x 5 days. Metronidazole 400 mg TID x 5 days. - Penicillin Allergy: Clindamycin 600 mg  Pediatric Doses: (a) Amoxicillin: 250 mg TID x 5 days. 20 – 40 mg/kg oral susp. (b) Ampicillin: 50 – 100 mg/kg in 4 divided doses (c) Cephalexin: 25 – 50 mg/kg in 4 – 6 divided doses. (d) Clindamycin: 8 – 25 mg/kg in 3 – 4 divided doses. (e) Erythromycin: 30 – 40 mg/kg in 4 divided doses (f) Penicillin V: 25 – 50 mg/kg in 4 divided doses.
  • 104.
    CULTURE SENSITIVITY AND TESTING Many oral infections are treated without identification of the specific etiologic agent.  This leads to unsuspected resistance and therefore the treatment can become unsuccessful or inadequate.  Quantitative Tests: - Determines how much the minimum inhibitory concentration inhibits the growth of the organism.
  • 105.
    - Minimum InhibitoryConcentration: (MIC) - Lowest concentration of the agent that inhibits the growth of the organism. - Minimum Bactericidal Concentration: (MBC) - Lowest concentration of antimicrobial agent that allows less that 0.1 % of the original inoculum to survive.  METHODS OF SUSCEPTIBILITY TESTING: (a) Chromogenic Cephalosporin Test: - Used to detect the β – Lactamase enzyme. - Colour of the disc changes from yellow to red.
  • 106.
    (b) Disc DiffusionMethod: - Incorporates the measurement of zone diameters, representing the ability of a particular agent to exert its effect.
  • 107.
    (c) Dilution Methods: -Recommended for slow growing facultative anaerobic bacteria found in oral infections. - Also determines the bactericidal activity of synergism or antagonism between agents. (e.g Microdilution test, Agar dilution test)  Interpretation of Results: - An organism is considered to be susceptible if the Minimal Inhibitory Concentration is lower than the peak concentration in blood.
  • 108.
    LIST OF REFERENCES 1. www.Merriam-webster.Com 2.Essentials of general pharmacology, K D Tripati : Jaypee Publications,5th edition 2003 3. Goodman and Gilman. The pharmacological basis of therapeutics, 9th edition. 4. Michael G Newman, “Antibiotic/Antimicrobial Use in Dental Practice” 5. CIMS India (www.mims.com) 6. Dental pulse for entrance examination 7. Maureen K Bolon, “The Newer Fluoroquinolones,” 2011 8. www.medical.theclinics.com
  • 109.
    9. Foundation inmicrobiology: basic principle by Kathleen park, 2nd edition 10.Lippincott’s illustrated reviews pharnacology., 2nd edition 2000 11.Satoskar, bhandarkar , Nirmala rege . pharmacology and therapeutics, 20th edition. 12.Burket's textbook of oral medicine, lester william burket, martin s. Greenberg, michael glick, jonathan A. Ship 11th edition, 13.Carranza's clinical periodontology, michael G. Newman, henry takei, perry R. Klokkevold, fermin A. Carranza LIST OF REFERENCES

Editor's Notes

  • #14  Bactericidal agents should be selected over bacteriostatic ones in circumstances in which local or systemic host defenses are impaired.
  • #39 IN PATIENTS WHERE THE HOST RESPONSE IS DECREASED BY DISEASES LIKE MORE THAN 1/3 RD ARE USED FOR THIS PURPOSE. May be used to protect healthy persons from acquisition of or invasion of specific micro-organisms to which they are exposed.
  • #41 While prescribing antibiotics clinician should consider both systemic and local factors.
  • #47 GIVEN ORALLY, SECRETED IN SALIVA, CONCENTRATED IN LIVER, EXCRETED IN BILE
  • #61  Have an important adjuvant role in Chronic Periodontitis, to help control gingival inflammation & helps to normalize the periodontal microflora from a mixture of anerobic G- bacilli and spirochetes. Highly active against Actinobacillus actinomycetum comitans in Aggressive Periodontitis . And hence prevents gingival destruction and bone loss.
  • #64 It is broad and includes gram – organisms, some gram + organisms, anaerobic bacteria, rickettsiae, chlamydia, mycoplasma. Chloramphenical is rapidly absorbed fro the gut, penetration in tissues is excellent, attains high conc. In C.S.F. It is metabolised in liver by conjugation.
  • #65 Because of the risk of bone marrow toxicity and availability of safer drugs, It is not generally preferred.
  • #67 It may be fatal. As newborn cannot metabolize( due to inadequate hepatic glucuronidation) and excrete chloramphenicol adequately, toxicity resullts
  • #99 Periodontal Diseases: - The most common are Gingivitis and Periodontitis. - Occurs due to the presence of specific bacteria adjacent to or associated with the periodontal structures.