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Anti infective agents antibiotics .

The document provides an overview of various antibiotic classes including aminoglycosides, carbapenems, monobactams, oxazolidinones, and fluoroquinolones, detailing their mechanisms of action and uses. It discusses the development and resistance issues associated with these antibiotics, emphasizing the importance of responsible usage to prevent resistance. Additionally, it outlines specific drugs within each class, their indications, side effects, and pharmacokinetic properties.

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Introduction to anti-infective drug classes: aminoglycosides, carbapenems, monobactams, oxazolidinones, fluoroquinolones.

Definition of antibiotics, their role in treating bacterial infections, and rising resistance due to misuse.

Introduction to anti-infective drug classes: aminoglycosides, carbapenems, monobactams, oxazolidinones, fluoroquinolones.

Definition and function of aminoglycosides, their usage against gram-negative bacteria and details on administration routes.

Examples of aminoglycosides, their mechanisms of action, and the specific clinical uses including combinations.

Examples of aminoglycosides, their mechanisms of action, and the specific clinical uses including combinations.

Examples of aminoglycosides, their mechanisms of action, and the specific clinical uses including combinations.

Details about neomycin, its spectrum of activity, forms of administration, and typical medical uses.

Introduction to carbapenems, their broad spectrum, mechanisms, contraindications, side effects, and common uses.

Explanation of monobactams, specifically aztreonam, its mechanism, uses, and advantages over other antibiotics.

Explanation of monobactams, specifically aztreonam, its mechanism, uses, and advantages over other antibiotics.

Explanation of monobactams, specifically aztreonam, its mechanism, uses, and advantages over other antibiotics.

Introduction to oxazolidinone antibiotics, specifically linezolid, their mechanism and resistance.

Introduction to oxazolidinone antibiotics, specifically linezolid, their mechanism and resistance.

Description of fluoroquinolones, their mechanism of action, and the evolution of this antibiotic class.

Classification of fluoroquinolones, their mechanisms of action, and resistance mechanisms in bacteria.

Classification of fluoroquinolones, their mechanisms of action, and resistance mechanisms in bacteria.

Classification of fluoroquinolones, their mechanisms of action, and resistance mechanisms in bacteria.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

Specific fluoroquinolones like norfloxacin, ciprofloxacin, and their pharmacokinetics, uses, and side effects.

List of references for the information provided throughout the presentation.

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ANTI INFECTIVE AGENTS ā AMINOGLYCOSIDES ā CARBAPENEMS ā MONOBACTAMS ā OXAZOLIDINONE ā FLUOROQUINOLONES Guided by - Prof. Gayatri Sapkale Department of Pharmaceutical Chemistry YTIP, University Of Mumbai Prepared by - Rohan Jagdale T. Y. B. Pharm 2020-21
What are antibiotics ā— Antibiotics, also known as antibacterials, are medications that destroy or slow down the growth of bacteria. ā— They include a range of powerful drugs and are used to treat diseases caused by bacteria. ā— Antibiotics cannot treat viral infections, such as cold, ļ¬‚u, and most coughs. ā— The ļ¬rst antibiotic was penicillin. Penicillin-based antibiotics, such as ampicillin, amoxicillin, and penicillin G, are still available to treat a variety of infections and have been around for a long time. ā— Several types of modern antibiotics are available, and they are usually only available with a prescription in most countries. Topical antibiotics are available in over-the-counter (OTC) creams and ointments.
Resistance ā— Some medical professionals have concerns that people are overusing antibiotics. They also believe that this overuse contributes toward the growing number of bacterial infections that are becoming resistant to antibacterial medications. ā— Alexander Fleming, speaking in his Nobel Prize acceptance speech in 1945, said::-ā€œThen there is the danger that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug, make them resistant.ā€ ā— As the man who discovered the ļ¬rst antibiotic almost 70 years ago predicted, drug resistance is starting to become commonplace.
CONTENTS ā AMINOGLYCOSIDES - Gentamicin & Neomycin ā CARBAPENEMS - Imipenem & Meropenem ā MONOBACTAMS - Aztreonam & Tigemonam ā OXAZOLIDINONES - Linezolid ā FLUOROQUINOLONES - ā– Norfloxacin ā– Ciprofloxacin ā– Sparfloxacin ā– Gatifloxacin ā– Levofloxacin ā– Lomefloxacin
AMINOGLYCOSIDES
Defination & Introduction ā— Aminoglycosides are a group of natural and semisynthetic antibiotics having polybasic amino groups linked glycosidically with two or more aminosugars. ā— Aminoglycosides are used to treat various bacterial infections caused by gram negative bacteria. ā— Aminoglycosides can be combined with penicillins or cephalosporins to show prolonged attack on gram-ve bacterial infections. ā— They shows antibiotic action by inhibiting the bacterial protein synthesis. ā— The drug will break down in the stomach without showing antibiotic activity through oral route but it shows better activity through parentral route.
ā–ŖExamples of aminoglycosides are:- Streptomycin, Amikacin Neomycin, Kanamycin,Gentamycin, Netilmycin ā–Ŗ Topical aminoglycosides - Neomycin & Framycetin ā–ŖThe above drugs are various aminoglycosides used to treat gram-ve bacterial infections. ā–ŖWidely in combination with B-lactum antibiotic. _ serious infections with gram - ve bacteria _ Combination with vancomycin gram +ve endocarditis. ā–ŖTreatment of Tuberculosis
Mechanism of action ā— Aminoglycosides inhibit protein synthesis in bacteria by binding irreversibly to the 30S ribosomal subunit. ā— This inhibits transfer of aminoacyl-tRNA to the peptidyl site, causing premature termination of the peptide chain; it also increases the frequency of misreading of mRNA. ā— Aminoglycosides may also damage bacterial cell membranes, causing leakage of intracellular contents. They are bactericidal. ā— Aminoglycosides are potent bactericidal antibiotics that act by creating fissures in the outer membrane of the bacterial cell. They are particularly active against aerobic, gram-negative bacteria and act synergistically against certain gram-positive organisms.
Mechanism of resistance ā–ŖSynthesis of plasmid mediated bacterial transferase enzyme: Inactivate aminoglycosides ā–Ŗ transport into bacterial cytosol ā–ŖDeletion/alteration of receptor protein on 30 S ribosomal unit by mutation: prevents attachment
Gentamicin ā— Drug class: Aminoglycoside antibiotic ā— Protein binding: 0ā€“10% ā— Formula: C21H43N5O7 ā— Bioavailability: limited bioavailability by mouth ā— Elimination half-life: 2 h
Gentamicin ā–ŖObtained from Micromonospora purpurea ā–ŖMost commonly used aminoglycoside - More potent than Streptomycin - Broader spectrum: pseudomonas, proteus, E.coli, klebsiella, enterobacter, serratia - Low cost, reliability of use, long experience - Acts synergistically with ampicillin, penicillin G,Ticarcillin, ceftriaxone, Vancomycin ā–ŖIneffective against M.tuberculosis ā–ŖRelatively more nephrotoxicc
Gentamicin uses ā–ŖUse restricted to serious Gm-ve bacillary infections ā–ŖSepticaemia, sepsis, fever in immunocompromised patients - Used with penicillins ā–ŖPelvic infections :with metronidazole ā–ŖSABE: with Penicillin G or ampicillin or vancomycin ā–ŖColiform infection: with ampicillin or ceftriaxone ā–ŖPseudomonal infections: with ticarcillin ā–ŖMeningitis by Gm-ve bacilli: Il generation cephalosporin alone or with gentamicin
Neomycin
Neomycin ā–Ŗwide spectrum active against Gram-ve bacilli and some gram+ve cocci ā–ŖPseudomonas and strep.pyogenes not sensitive ā–ŖToo toxic for parenteral use, limited to topical use ā–ŖFormula: C23H46N6O13 ā–ŖTrade name: Neo-rx ā–ŖElimination half-life: 2 to 3 hours
Neomycin uses ā–ŖTopically used in skin, eye and external ear infections combined with bacitracin or polymyxin-B to widen antibacterial spectrum and to prevent emergence of resistant strains ā–ŖOrally - Preparation of bowel before surgery 1gm TDS -Hepatic coma: Supresses ammonia forming -coliforms prevents encephalopathy (Lactulose more preferred) ā–ŖBladder irrigation along with polymyxin B
CARBAPENEMS
What are carbapenems Carbapenems are a class of beta-lactam antibiotics with a broad spectrum of antibacterial activity. They have a structure that renders them highly res istant to beta-lactamases. Carbapenem antibiotics were originally developed from thienamycin,a naturally-derived product of Streptomyces cattleya.
ā— Mechanism of action :Inhibits bacterial cell wall synthesis , bind to penicillin binding protein and inhibit transpeptidation of peptidoglycan. ā— Examples :-Imipenem, Meropenem, Ertapenem and Doripenem ā— Converge: ā— _Aerobic gram negatives (including ESBLs), aerobic gram positives (MSSA, Streptococcus),anaerobes except MRSA, VRE and Atypical ā— _Ertapenem do Not cover Enterococcus, Acinetobacter, Pseudomonas, and MRSA ā— It is a bactericidal, time dependent ā— Mechanism of resistance: poor binding affinity for PBP 2a (found on MRSA) and PBP 5 (found on E faecium). ā— Alteration of targets, decreased accumulation due to decreased permeability, and enzymatic inactivation.
ā— Contraindications: Hypersensitivity ,ertapenerm(Infants less than 3 months), ā— Side effects: Nausea, vomiting, diarrhea ,seizures(imipenem) ā— Pregnancy category: B ā— Dosage Form: IV, IM
ā–ŖEFFECTIVE AGAINST: Aerobic and anaerobic, Gram positive and gram negative bacteria ā–ŖCHARACTERISTICS: Broad Spectrum Intravenous Resistant to beta-lactamase enzymes ā–ŖSIDE-EFFECT: Seizuregenic at high doses Imipenem
Meropenem ā–ŖEFFECTIVE AGAINST: Aerobic and anaerobic, Gram positive and gram negative bacteria ā–ŖCHARACTERISTICS: Ultra Broad Spectrum Intravenous Resistant to beta-lactamase enzymes ā–ŖSIDE-EFFECT: Diarrhoea Vomiting headache
Carbapenems common uses ā–ŖImipenem Broad spectrum, covers Gram-positive, Gram-negative (including ESBL-producing strains), Pseudomonas and anaerobes ā–ŖMeropenem Less seizure-inducing potential, can be used to treat CNS infections ā–ŖErtapenem - Lacks activity vs. Acinetobacter and Pseudomonas -Has limited activity against penicillin-resistant pneumococci
MONOBACTAMS
ā— Monobactams are monocyclic and bacterially-produced Ī²-lactam antibiotics. The Ī²-lactam ring is not fused to another ring, in contrast to most other Ī²-lactams. ā— The main monobactum is aztreonam, which is resistant to most B-lactamases ā— Plasma half life is 2 hours. ā— Aztreonam has an unusual spectrum of activity & is effective only against Gram-ve Aerobic bacilli such as pseudomonas species, Neisseria meningitidis and Haemophilus influenzae. ā— It has no action against Gram positive organisms or anaerobes.
Aztreonam ā–ŖIt is a monocyclic B- Lactam compound (monobactam) ā–ŖMechanism: -Interacts with penicillin-binding proteins of susceptible micro-organisms and induces the formation of long filamentous bacterial structures ā–ŖIt is resistant to many of the B- Lactamases that are elaborated by most gram-negative bacteria
ā–Ŗ Adverse effects :- - Usually well tolerated - Patients with penicillins or cephalosporins allergy not to react to aztreonam ā–Ŗ Uses :- - Active against Gram-ve - aerobes only - Alternative for penicillins and cephalosporins. - Safe alternative to aminoglycosides, esp. in elderly and patients with renal impairments.
ā–ŖTigemonam is a monobactam antibiotic . ā–ŖIt has Gram-positive activity, and is stable against Ī²-lactamases, but has no activity against Psedomonas. ā–ŖSQ-30836 (tigemonam dicholate) is an orally absorbed salt of tigemonam
OXAZOLIDINONES
What are Oxazolidinone antibiotics? Oxazolidinone antibiotics are a class of synthetic antibacterial agents that act as a protein synthesis inhibitor on the ribosomal 50S subunit of the bacteria. This prevents the formation of the 70S initiation complex which is a prerequisite for bacterial reproduction. Oxazolidinones are used for gram-positive infections and can be bacteriostatic or bactericidal depending on bacteria being treated. ā–ŖEffective against Organisms - gram-positive bacteria including MRSA, VRE and Streptococcus pneumoniae.Mycobacterium tuberculosis and Nocardia. ā–ŖIn clinical use :- Linezolid. ā–ŖIn clinical trials - Radezolid, Torezolid
Linezolid-1st to be approved ā–ŖIndicated _VRE infection _nosocomial and com munity-acquired pneumonia _skin and soft tissue infections.(SSTIs) ā–Ŗbacteriostatic against drug-resistant organisms like MRSA and VRE. Inhibits bacterial protein synthes is at an early stage and inhibits the formation of a function al initiation complex. ā–ŖResistance- Mutations in the peptidyl transferase centre of the rRNA ā–ŖSerious adverse effects bone marrow suppression, peripheral and optic neuropathy, lactic acidos is, and serotonin syndrome.
Structure - activity relationship leading to development of linezolid
FLOUROQUINOLONES
Quinolones ā–ŖThe quinolones are a family of synthetic broad-spectrum antibiotics. The term quinolone(s) refers to potent synthetic chemotherapeutic antibacterial agent. ā–ŖThe first generation of the quinolones begins with the introduction of nalidixic acid in 1962 for treatment of urinary tract infections in humans. Nalidixic acid was discovered by George Lesher and co-workers in a distillate during an attempt at chloroquine synthesis. ā–ŖThey prevent bacterial DNA from unwinding and duplicating
Fluoroquinolones The Fluoroquinolones are a relatively new group of antibiotics. first Fluroquinolones were introduced in 1986, but they are really modified quinolones, a class of antibiotics, whose accidental discovery occurred in the early 1960.
ā–ŖThe fluoroquinolones are a family of synthetic, broad-spectrum antibacterial agents with bactericidal activity. The first fluoroquinolones were widely used because they were the only orally administered agents available for the treatment of serious infections caused by gram-negative organisms, including Pseudomonas species.
Classification
Fourth generation ā— Fourth generation fluoroquinolones act at DNA gyrase and topoisomerase IV. This dual action slows development of resistance. ā— clinafloxacin ā— gatifloxacin ā— gemifloxacin ā— moxifloxacin ā— sitafloxacin ā— trovafloxacin ā— Prulifloxacin In development ā— garenoxacin (Geninax) (application withdrawn due to toxicity) ā— delafloxacin
Mechanism of action ā–ŖIt blocks bacterial DNA synthesis by - Inhibition of bacterial Topoisomerase lI (DNAGyrase) - Inhibition of Topoisomerase IV ā–ŖInhibition of ATP dependent DNA gyrase; which nicks doule stranded DNA, introduces negative supercoils and then reseals the nicked ends. This is required to prevent excessive positive supercoiling of DNA strands when they seperate to permit replication or transcription.
ā–ŖInhibition of DNA gyrase also prevents the relaxation of positively supercoiled DNA. ā–ŖInhibition of DNA nicking-closing enzyme responsible for DNA elongation, which leads to break in double stranded DNA. ā–ŖInhibition of topoisomerase IV interferes with the separation of replicated chromosomal DNA into respective daughter cells during cell division. ā–ŖThe critical imbalance in cellular metabolism resulting from the inhibition of enzymes precipitates a sequence of cellular events which may lead to: - Premature cell division. - Delayed cell division. - Total failure of cell division leading to lysis of the cell
Schematic representation of mechanism of action of fluoroquinolones
Complex formed between DNA, topoisomerase and fluoroquinolones
Mechanism of resistance
Mechanism of resistance Resistance to fluoroquinolones mostly occurs by two mechanisms that are mutations in the both target enzymes DNA gyrase in Gram-negative bacteria and topoisomerase IV in Gram-positive bacteria. The second way that reduced accumulation of the fluoroquinolones can occur is through an efflux system. Resistance is due to increased expression of chromosomal gene leading to increased efflux of the fluoroquinolones
Norļ¬‚oxacin
Medical use ā— It was patended in 1977 and approved in 1983. ā— Trade names - Noroxin, Chibroxin, Trizolin ā— Route of administration - Oral, opthalmic. ā— Bioavailability - 30 to 40% ā— Elimination half-life - 3 to 4 hours. ā–Ŗ Complicated urinary tract infections. ā–ŖUncomplicated urethral and cervical gonorrhea ā–ŖProstatitis due to E. coli ā–ŖSyphilis treatment
Contraindication- Norfloxacin is contraindicated in those with history of tendonitis, tendon rupture and those with hypersensitivity of flouroquinolones. Adverse effects - Common side effects include gastrointestinal effects, such as nausea, vomiting and diarrhea as well as headache and insomnia
Ciproļ¬‚oxacin
ā–Ŗ2nd generation fluoroquinolone. ā–ŖMost potent fluoroquinolone against P. aeruginosaNot effective against Gram +ve and anaerobes. ā–ŖMainly effective against Gram -ve bacteria :- H. Influenzae Enterobacteriacae Campylobacter. M. Catarrhalis Pseudomonas. N. Gonorrhea ā–ŖIntracellular Pathogen :- M. Tuberculosis. Mycoplasma Legionella Chlamydia Brucella
Pharmacokinetics ā— Well absorbed orally ( available i.v. ) ā— Di&tri-valent cations interfere with its absorption (milk, Mg, Al, Ca, antacid) ā— Concentrates in many tissues, esp. kidney, prostate,lung & bones/ joints ā— Do not cross Blood brain barrier ā— Excreted mainly through the kidney (tubular & glomerular) (probencid interferes with tubular secretion) ā— Accumulate in renal insufficiency ā— Up to 20% metabolized by liver ā— Half life - 3.3 hours
Clinical uses ā— Urinary tract infections (Paeruginosae,E.coli,Klebsiella) ā— Osteomyelitis due to Paeruginosa ā— Gonorrhea ā— Travellers' diarrhea- ciprofloxacin commonly used (if there's a bloody diarrhea) ā— Prostatitis ā— Legionnaires' disease ā— Brucellosis ā— Diabetic foot infections ā— Anthrax ā— Eradication of menengiococci from carriers
ā–ŖSide effects - Nausea, vomiting & diarrheaa - CNS effects :confusion, insomnia, headache, dizziness & anxiety.(indirectly by modifying GAPA transmitter in the CNS) - May damage growing cartilage - Tendinitis ( rare but more serious) (irreversible) (may lead to tendon rupture)
ā–ŖContraindications :- Children/ adolescents (under 18), pregnancy and lactation (secreted in milk) It's not contraindicated in adolescents it's not preferred so you have to measure benfits vs. risks ā–ŖDrug interaction :- Iron or antacids containing Mg, Ca, or Al> reduce oral absorption Elevates serum levels of theophylline, warfarin & glibenclamide
Sparļ¬‚oxacin ā— It was patended in 1985 & approved for medical use in 1993 ā— Trade names - Spacin, Zagam ā— Route of administration - mouth ā— Bioavailability - 92 % ā— Elimination half-life - 16 to 30 hours
, ā–ŖPharmacological properties ā— Sparfloxacin is about 37-45% bound to proteins in the blood. ā— Sparfloxacin achieves a high degree of penetration into most tissues, except for the central nervous system. ā–ŖMechanism of action Sparfloxacin, like other quinolones and fluoroquinolones, are bactericidal drugs, actively killing bacteria. ā–ŖMedical uses The compound is indicated for treating community-acquired lower respiratory tract infections (acute sinusitis, exacerbations of chronic bronchitis caused by susceptible bacteria, community-acquired pneumonia)
Gatiļ¬‚oxacin ā— It was patented in 1986 and approved for medical use in 1999. ā— Fourth generation antibiotic ā— Route of administration - Oral (Discontinued), Intravenous (discontinued), now Opthalmic only. ā— Elimination half-life - 7 to 14 hours
Clinical use Gatifloxacin ophthalmic solution is used to treat bacterial conjunctivitis (pinkeye; infection of the membrane that covers the outside of the eyeballs and the inside of the eyelids) in adults and children 1 year of age and older.This medication treats only bacterial eye infections. It will not work for other types of eye infections. Side effects Blurred vision, watery eyes, headache, eye irritation/pain/dryness/redness, bad taste in mouth may occur. Use of this medication for prolonged or repeated periods may result in a new fungal eye infection.
Availability Gatifloxacin is currently available in the US and Canada only as an ophthalmic solution. In 2011, the Union Health and Family Welfare Ministry of India banned the manufacture, sale, and distribution of gatifloxacin because of its adverse side effects. In China, gatifloxacin is sold in tablet as well as in eye drop formulations.
Levoļ¬‚oxacin
ā–ŖBrand name - leflox, 1-cyn, qumic ā–Ŗ3rd generation fluoroquinolone ā–ŖSpectrum: Gram-ve, Gram+ve (S. aureus including MRSA & S. pneumoniae) and Legionella pneumophila, atypical resp. pathogens, Mycobacterium tuberculosis ā–ŖIndications: - Chronic bronchitis and CAP - Nosocomial pneumonia - Intra-abdominal infections
ā–ŖAdverse reaction. - Blood glucose disturbances in DM patients - QTC prolongation, torsades de pointes, arrhythmias - Nausea, Gl upset - Interstitial nephritis Oral Parentral Opthalmic 100mg 5mg/ml iv 5mg/ml solution 250 mg 25mg/ml iv 500 mg ā–ŖAvailable forms
Lomeļ¬‚oxacin ā— 2nd generation. ā— Equal in activity to Ciprofloxacin. ā— Single daily administration. ā— High incidence of Phototoxicity and QT prolongation. ā— Brand name - Maxaquin
ā— used to treat chronic bronchitis, as well as complicated and uncomplicated urinary tract infections. Also used in- ā— Escherichia coli Infections ā— Klebsiella Infections ā— Proteus Infections ā— Pseudomonas Infections ā— Staphylococcal Infections ā–ŖClinical uses ā–ŖLomefloxacin is available in the following forms: - Ophthalmic Solution - Oral Tablet (Lomefloxacin 400 Mg Oral Tablet)
References https://www.drugs.com https://www.medindia.net https://drugs.ncats.io/ https://www.researchgate.net https://en.wikipedia.org https://go.drugbank.com/drugs
Anti infective agents antibiotics .

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Anti infective agents antibiotics .

  • 1.
    ANTI INFECTIVE AGENTS āAMINOGLYCOSIDES ā CARBAPENEMS ā MONOBACTAMS ā OXAZOLIDINONE ā FLUOROQUINOLONES Guided by - Prof. Gayatri Sapkale Department of Pharmaceutical Chemistry YTIP, University Of Mumbai Prepared by - Rohan Jagdale T. Y. B. Pharm 2020-21
  • 2.
    What are antibiotics ā—Antibiotics, also known as antibacterials, are medications that destroy or slow down the growth of bacteria. ā— They include a range of powerful drugs and are used to treat diseases caused by bacteria. ā— Antibiotics cannot treat viral infections, such as cold, ļ¬‚u, and most coughs. ā— The ļ¬rst antibiotic was penicillin. Penicillin-based antibiotics, such as ampicillin, amoxicillin, and penicillin G, are still available to treat a variety of infections and have been around for a long time. ā— Several types of modern antibiotics are available, and they are usually only available with a prescription in most countries. Topical antibiotics are available in over-the-counter (OTC) creams and ointments.
  • 3.
    Resistance ā— Some medicalprofessionals have concerns that people are overusing antibiotics. They also believe that this overuse contributes toward the growing number of bacterial infections that are becoming resistant to antibacterial medications. ā— Alexander Fleming, speaking in his Nobel Prize acceptance speech in 1945, said::-ā€œThen there is the danger that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug, make them resistant.ā€ ā— As the man who discovered the ļ¬rst antibiotic almost 70 years ago predicted, drug resistance is starting to become commonplace.
  • 4.
    CONTENTS ā AMINOGLYCOSIDES -Gentamicin & Neomycin ā CARBAPENEMS - Imipenem & Meropenem ā MONOBACTAMS - Aztreonam & Tigemonam ā OXAZOLIDINONES - Linezolid ā FLUOROQUINOLONES - ā– Norfloxacin ā– Ciprofloxacin ā– Sparfloxacin ā– Gatifloxacin ā– Levofloxacin ā– Lomefloxacin
  • 5.
  • 6.
    Defination & Introduction ā—Aminoglycosides are a group of natural and semisynthetic antibiotics having polybasic amino groups linked glycosidically with two or more aminosugars. ā— Aminoglycosides are used to treat various bacterial infections caused by gram negative bacteria. ā— Aminoglycosides can be combined with penicillins or cephalosporins to show prolonged attack on gram-ve bacterial infections. ā— They shows antibiotic action by inhibiting the bacterial protein synthesis. ā— The drug will break down in the stomach without showing antibiotic activity through oral route but it shows better activity through parentral route.
  • 7.
    ā–ŖExamples of aminoglycosidesare:- Streptomycin, Amikacin Neomycin, Kanamycin,Gentamycin, Netilmycin ā–Ŗ Topical aminoglycosides - Neomycin & Framycetin ā–ŖThe above drugs are various aminoglycosides used to treat gram-ve bacterial infections. ā–ŖWidely in combination with B-lactum antibiotic. _ serious infections with gram - ve bacteria _ Combination with vancomycin gram +ve endocarditis. ā–ŖTreatment of Tuberculosis
  • 8.
    Mechanism of action ā—Aminoglycosides inhibit protein synthesis in bacteria by binding irreversibly to the 30S ribosomal subunit. ā— This inhibits transfer of aminoacyl-tRNA to the peptidyl site, causing premature termination of the peptide chain; it also increases the frequency of misreading of mRNA. ā— Aminoglycosides may also damage bacterial cell membranes, causing leakage of intracellular contents. They are bactericidal. ā— Aminoglycosides are potent bactericidal antibiotics that act by creating fissures in the outer membrane of the bacterial cell. They are particularly active against aerobic, gram-negative bacteria and act synergistically against certain gram-positive organisms.
  • 10.
    Mechanism of resistance ā–ŖSynthesisof plasmid mediated bacterial transferase enzyme: Inactivate aminoglycosides ā–Ŗ transport into bacterial cytosol ā–ŖDeletion/alteration of receptor protein on 30 S ribosomal unit by mutation: prevents attachment
  • 12.
    Gentamicin ā— Drug class:Aminoglycoside antibiotic ā— Protein binding: 0ā€“10% ā— Formula: C21H43N5O7 ā— Bioavailability: limited bioavailability by mouth ā— Elimination half-life: 2 h
  • 13.
    Gentamicin ā–ŖObtained from Micromonosporapurpurea ā–ŖMost commonly used aminoglycoside - More potent than Streptomycin - Broader spectrum: pseudomonas, proteus, E.coli, klebsiella, enterobacter, serratia - Low cost, reliability of use, long experience - Acts synergistically with ampicillin, penicillin G,Ticarcillin, ceftriaxone, Vancomycin ā–ŖIneffective against M.tuberculosis ā–ŖRelatively more nephrotoxicc
  • 14.
    Gentamicin uses ā–ŖUse restrictedto serious Gm-ve bacillary infections ā–ŖSepticaemia, sepsis, fever in immunocompromised patients - Used with penicillins ā–ŖPelvic infections :with metronidazole ā–ŖSABE: with Penicillin G or ampicillin or vancomycin ā–ŖColiform infection: with ampicillin or ceftriaxone ā–ŖPseudomonal infections: with ticarcillin ā–ŖMeningitis by Gm-ve bacilli: Il generation cephalosporin alone or with gentamicin
  • 15.
  • 16.
    Neomycin ā–Ŗwide spectrum activeagainst Gram-ve bacilli and some gram+ve cocci ā–ŖPseudomonas and strep.pyogenes not sensitive ā–ŖToo toxic for parenteral use, limited to topical use ā–ŖFormula: C23H46N6O13 ā–ŖTrade name: Neo-rx ā–ŖElimination half-life: 2 to 3 hours
  • 17.
    Neomycin uses ā–ŖTopically usedin skin, eye and external ear infections combined with bacitracin or polymyxin-B to widen antibacterial spectrum and to prevent emergence of resistant strains ā–ŖOrally - Preparation of bowel before surgery 1gm TDS -Hepatic coma: Supresses ammonia forming -coliforms prevents encephalopathy (Lactulose more preferred) ā–ŖBladder irrigation along with polymyxin B
  • 18.
  • 19.
    What are carbapenems Carbapenemsare a class of beta-lactam antibiotics with a broad spectrum of antibacterial activity. They have a structure that renders them highly res istant to beta-lactamases. Carbapenem antibiotics were originally developed from thienamycin,a naturally-derived product of Streptomyces cattleya.
  • 20.
    ā— Mechanism ofaction :Inhibits bacterial cell wall synthesis , bind to penicillin binding protein and inhibit transpeptidation of peptidoglycan. ā— Examples :-Imipenem, Meropenem, Ertapenem and Doripenem ā— Converge: ā— _Aerobic gram negatives (including ESBLs), aerobic gram positives (MSSA, Streptococcus),anaerobes except MRSA, VRE and Atypical ā— _Ertapenem do Not cover Enterococcus, Acinetobacter, Pseudomonas, and MRSA ā— It is a bactericidal, time dependent ā— Mechanism of resistance: poor binding affinity for PBP 2a (found on MRSA) and PBP 5 (found on E faecium). ā— Alteration of targets, decreased accumulation due to decreased permeability, and enzymatic inactivation.
  • 21.
    ā— Contraindications: Hypersensitivity,ertapenerm(Infants less than 3 months), ā— Side effects: Nausea, vomiting, diarrhea ,seizures(imipenem) ā— Pregnancy category: B ā— Dosage Form: IV, IM
  • 22.
    ā–ŖEFFECTIVE AGAINST: Aerobic andanaerobic, Gram positive and gram negative bacteria ā–ŖCHARACTERISTICS: Broad Spectrum Intravenous Resistant to beta-lactamase enzymes ā–ŖSIDE-EFFECT: Seizuregenic at high doses Imipenem
  • 23.
    Meropenem ā–ŖEFFECTIVE AGAINST: Aerobic andanaerobic, Gram positive and gram negative bacteria ā–ŖCHARACTERISTICS: Ultra Broad Spectrum Intravenous Resistant to beta-lactamase enzymes ā–ŖSIDE-EFFECT: Diarrhoea Vomiting headache
  • 24.
    Carbapenems common uses ā–ŖImipenem Broadspectrum, covers Gram-positive, Gram-negative (including ESBL-producing strains), Pseudomonas and anaerobes ā–ŖMeropenem Less seizure-inducing potential, can be used to treat CNS infections ā–ŖErtapenem - Lacks activity vs. Acinetobacter and Pseudomonas -Has limited activity against penicillin-resistant pneumococci
  • 25.
  • 26.
    ā— Monobactams aremonocyclic and bacterially-produced Ī²-lactam antibiotics. The Ī²-lactam ring is not fused to another ring, in contrast to most other Ī²-lactams. ā— The main monobactum is aztreonam, which is resistant to most B-lactamases ā— Plasma half life is 2 hours. ā— Aztreonam has an unusual spectrum of activity & is effective only against Gram-ve Aerobic bacilli such as pseudomonas species, Neisseria meningitidis and Haemophilus influenzae. ā— It has no action against Gram positive organisms or anaerobes.
  • 28.
    Aztreonam ā–ŖIt is amonocyclic B- Lactam compound (monobactam) ā–ŖMechanism: -Interacts with penicillin-binding proteins of susceptible micro-organisms and induces the formation of long filamentous bacterial structures ā–ŖIt is resistant to many of the B- Lactamases that are elaborated by most gram-negative bacteria
  • 29.
    ā–Ŗ Adverse effects:- - Usually well tolerated - Patients with penicillins or cephalosporins allergy not to react to aztreonam ā–Ŗ Uses :- - Active against Gram-ve - aerobes only - Alternative for penicillins and cephalosporins. - Safe alternative to aminoglycosides, esp. in elderly and patients with renal impairments.
  • 31.
    ā–ŖTigemonam is a monobactamantibiotic . ā–ŖIt has Gram-positive activity, and is stable against Ī²-lactamases, but has no activity against Psedomonas. ā–ŖSQ-30836 (tigemonam dicholate) is an orally absorbed salt of tigemonam
  • 32.
  • 33.
    What are Oxazolidinoneantibiotics? Oxazolidinone antibiotics are a class of synthetic antibacterial agents that act as a protein synthesis inhibitor on the ribosomal 50S subunit of the bacteria. This prevents the formation of the 70S initiation complex which is a prerequisite for bacterial reproduction. Oxazolidinones are used for gram-positive infections and can be bacteriostatic or bactericidal depending on bacteria being treated. ā–ŖEffective against Organisms - gram-positive bacteria including MRSA, VRE and Streptococcus pneumoniae.Mycobacterium tuberculosis and Nocardia. ā–ŖIn clinical use :- Linezolid. ā–ŖIn clinical trials - Radezolid, Torezolid
  • 34.
    Linezolid-1st to beapproved ā–ŖIndicated _VRE infection _nosocomial and com munity-acquired pneumonia _skin and soft tissue infections.(SSTIs) ā–Ŗbacteriostatic against drug-resistant organisms like MRSA and VRE. Inhibits bacterial protein synthes is at an early stage and inhibits the formation of a function al initiation complex. ā–ŖResistance- Mutations in the peptidyl transferase centre of the rRNA ā–ŖSerious adverse effects bone marrow suppression, peripheral and optic neuropathy, lactic acidos is, and serotonin syndrome.
  • 36.
    Structure - activityrelationship leading to development of linezolid
  • 37.
  • 38.
    Quinolones ā–ŖThe quinolones area family of synthetic broad-spectrum antibiotics. The term quinolone(s) refers to potent synthetic chemotherapeutic antibacterial agent. ā–ŖThe first generation of the quinolones begins with the introduction of nalidixic acid in 1962 for treatment of urinary tract infections in humans. Nalidixic acid was discovered by George Lesher and co-workers in a distillate during an attempt at chloroquine synthesis. ā–ŖThey prevent bacterial DNA from unwinding and duplicating
  • 39.
    Fluoroquinolones The Fluoroquinolones area relatively new group of antibiotics. first Fluroquinolones were introduced in 1986, but they are really modified quinolones, a class of antibiotics, whose accidental discovery occurred in the early 1960.
  • 40.
    ā–ŖThe fluoroquinolones area family of synthetic, broad-spectrum antibacterial agents with bactericidal activity. The first fluoroquinolones were widely used because they were the only orally administered agents available for the treatment of serious infections caused by gram-negative organisms, including Pseudomonas species.
  • 41.
  • 42.
    Fourth generation ā— Fourthgeneration fluoroquinolones act at DNA gyrase and topoisomerase IV. This dual action slows development of resistance. ā— clinafloxacin ā— gatifloxacin ā— gemifloxacin ā— moxifloxacin ā— sitafloxacin ā— trovafloxacin ā— Prulifloxacin In development ā— garenoxacin (Geninax) (application withdrawn due to toxicity) ā— delafloxacin
  • 43.
    Mechanism of action ā–ŖItblocks bacterial DNA synthesis by - Inhibition of bacterial Topoisomerase lI (DNAGyrase) - Inhibition of Topoisomerase IV ā–ŖInhibition of ATP dependent DNA gyrase; which nicks doule stranded DNA, introduces negative supercoils and then reseals the nicked ends. This is required to prevent excessive positive supercoiling of DNA strands when they seperate to permit replication or transcription.
  • 44.
    ā–ŖInhibition of DNAgyrase also prevents the relaxation of positively supercoiled DNA. ā–ŖInhibition of DNA nicking-closing enzyme responsible for DNA elongation, which leads to break in double stranded DNA. ā–ŖInhibition of topoisomerase IV interferes with the separation of replicated chromosomal DNA into respective daughter cells during cell division. ā–ŖThe critical imbalance in cellular metabolism resulting from the inhibition of enzymes precipitates a sequence of cellular events which may lead to: - Premature cell division. - Delayed cell division. - Total failure of cell division leading to lysis of the cell
  • 46.
    Schematic representation ofmechanism of action of fluoroquinolones
  • 47.
    Complex formed betweenDNA, topoisomerase and fluoroquinolones
  • 48.
  • 49.
    Mechanism of resistance Resistanceto fluoroquinolones mostly occurs by two mechanisms that are mutations in the both target enzymes DNA gyrase in Gram-negative bacteria and topoisomerase IV in Gram-positive bacteria. The second way that reduced accumulation of the fluoroquinolones can occur is through an efflux system. Resistance is due to increased expression of chromosomal gene leading to increased efflux of the fluoroquinolones
  • 51.
  • 52.
    Medical use ā— Itwas patended in 1977 and approved in 1983. ā— Trade names - Noroxin, Chibroxin, Trizolin ā— Route of administration - Oral, opthalmic. ā— Bioavailability - 30 to 40% ā— Elimination half-life - 3 to 4 hours. ā–Ŗ Complicated urinary tract infections. ā–ŖUncomplicated urethral and cervical gonorrhea ā–ŖProstatitis due to E. coli ā–ŖSyphilis treatment
  • 53.
    Contraindication- Norfloxacin is contraindicatedin those with history of tendonitis, tendon rupture and those with hypersensitivity of flouroquinolones. Adverse effects - Common side effects include gastrointestinal effects, such as nausea, vomiting and diarrhea as well as headache and insomnia
  • 55.
  • 56.
    ā–Ŗ2nd generation fluoroquinolone.ā–ŖMost potent fluoroquinolone against P. aeruginosaNot effective against Gram +ve and anaerobes. ā–ŖMainly effective against Gram -ve bacteria :- H. Influenzae Enterobacteriacae Campylobacter. M. Catarrhalis Pseudomonas. N. Gonorrhea ā–ŖIntracellular Pathogen :- M. Tuberculosis. Mycoplasma Legionella Chlamydia Brucella
  • 57.
    Pharmacokinetics ā— Well absorbedorally ( available i.v. ) ā— Di&tri-valent cations interfere with its absorption (milk, Mg, Al, Ca, antacid) ā— Concentrates in many tissues, esp. kidney, prostate,lung & bones/ joints ā— Do not cross Blood brain barrier ā— Excreted mainly through the kidney (tubular & glomerular) (probencid interferes with tubular secretion) ā— Accumulate in renal insufficiency ā— Up to 20% metabolized by liver ā— Half life - 3.3 hours
  • 58.
    Clinical uses ā— Urinarytract infections (Paeruginosae,E.coli,Klebsiella) ā— Osteomyelitis due to Paeruginosa ā— Gonorrhea ā— Travellers' diarrhea- ciprofloxacin commonly used (if there's a bloody diarrhea) ā— Prostatitis ā— Legionnaires' disease ā— Brucellosis ā— Diabetic foot infections ā— Anthrax ā— Eradication of menengiococci from carriers
  • 59.
    ā–ŖSide effects - Nausea,vomiting & diarrheaa - CNS effects :confusion, insomnia, headache, dizziness & anxiety.(indirectly by modifying GAPA transmitter in the CNS) - May damage growing cartilage - Tendinitis ( rare but more serious) (irreversible) (may lead to tendon rupture)
  • 60.
    ā–ŖContraindications :- Children/ adolescents(under 18), pregnancy and lactation (secreted in milk) It's not contraindicated in adolescents it's not preferred so you have to measure benfits vs. risks ā–ŖDrug interaction :- Iron or antacids containing Mg, Ca, or Al> reduce oral absorption Elevates serum levels of theophylline, warfarin & glibenclamide
  • 62.
    Sparļ¬‚oxacin ā— It waspatended in 1985 & approved for medical use in 1993 ā— Trade names - Spacin, Zagam ā— Route of administration - mouth ā— Bioavailability - 92 % ā— Elimination half-life - 16 to 30 hours
  • 63.
    , ā–ŖPharmacological properties ā—Sparfloxacin is about 37-45% bound to proteins in the blood. ā— Sparfloxacin achieves a high degree of penetration into most tissues, except for the central nervous system. ā–ŖMechanism of action Sparfloxacin, like other quinolones and fluoroquinolones, are bactericidal drugs, actively killing bacteria. ā–ŖMedical uses The compound is indicated for treating community-acquired lower respiratory tract infections (acute sinusitis, exacerbations of chronic bronchitis caused by susceptible bacteria, community-acquired pneumonia)
  • 65.
    Gatiļ¬‚oxacin ā— It waspatented in 1986 and approved for medical use in 1999. ā— Fourth generation antibiotic ā— Route of administration - Oral (Discontinued), Intravenous (discontinued), now Opthalmic only. ā— Elimination half-life - 7 to 14 hours
  • 66.
    Clinical use Gatifloxacin ophthalmicsolution is used to treat bacterial conjunctivitis (pinkeye; infection of the membrane that covers the outside of the eyeballs and the inside of the eyelids) in adults and children 1 year of age and older.This medication treats only bacterial eye infections. It will not work for other types of eye infections. Side effects Blurred vision, watery eyes, headache, eye irritation/pain/dryness/redness, bad taste in mouth may occur. Use of this medication for prolonged or repeated periods may result in a new fungal eye infection.
  • 67.
    Availability Gatifloxacin is currentlyavailable in the US and Canada only as an ophthalmic solution. In 2011, the Union Health and Family Welfare Ministry of India banned the manufacture, sale, and distribution of gatifloxacin because of its adverse side effects. In China, gatifloxacin is sold in tablet as well as in eye drop formulations.
  • 68.
  • 69.
    ā–ŖBrand name -leflox, 1-cyn, qumic ā–Ŗ3rd generation fluoroquinolone ā–ŖSpectrum: Gram-ve, Gram+ve (S. aureus including MRSA & S. pneumoniae) and Legionella pneumophila, atypical resp. pathogens, Mycobacterium tuberculosis ā–ŖIndications: - Chronic bronchitis and CAP - Nosocomial pneumonia - Intra-abdominal infections
  • 70.
    ā–ŖAdverse reaction. - Bloodglucose disturbances in DM patients - QTC prolongation, torsades de pointes, arrhythmias - Nausea, Gl upset - Interstitial nephritis Oral Parentral Opthalmic 100mg 5mg/ml iv 5mg/ml solution 250 mg 25mg/ml iv 500 mg ā–ŖAvailable forms
  • 72.
    Lomeļ¬‚oxacin ā— 2nd generation. ā—Equal in activity to Ciprofloxacin. ā— Single daily administration. ā— High incidence of Phototoxicity and QT prolongation. ā— Brand name - Maxaquin
  • 73.
    ā— used totreat chronic bronchitis, as well as complicated and uncomplicated urinary tract infections. Also used in- ā— Escherichia coli Infections ā— Klebsiella Infections ā— Proteus Infections ā— Pseudomonas Infections ā— Staphylococcal Infections ā–ŖClinical uses ā–ŖLomefloxacin is available in the following forms: - Ophthalmic Solution - Oral Tablet (Lomefloxacin 400 Mg Oral Tablet)
  • 75.