The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
This document discusses aminoglycoside antibiotics, including their mechanism of action, spectrum of activity, pharmacokinetics, therapeutic uses, and adverse effects. Aminoglycosides inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit and are effective against many gram-negative and some gram-positive bacteria. They have concentration-dependent bactericidal activity but can cause ototoxicity and nephrotoxicity. Common aminoglycosides include gentamicin, tobramycin, and amikacin, which are used to treat serious infections like sepsis, pneumonia, and endocarditis.
1) Aminoglycosides are a class of antibiotics that are used to treat infections caused by aerobic gram-negative bacteria by inhibiting protein synthesis.
2) They are derived from actinomycetes bacteria and have an aminosugar component joined by an aminocyclitol component.
3) Common side effects include ototoxicity (hearing loss and dizziness) and nephrotoxicity (kidney damage). Dosing must be monitored based on a patient's kidney function.
This document summarizes key information about aminoglycoside antibiotics. It describes their origin from soil actinomycetes, common agents like streptomycin, gentamicin and tobramycin. It outlines their mechanism of action inhibiting protein synthesis, broad-spectrum activity against gram-negative bacteria and some protozoa. Resistance development via modifying enzymes is discussed. Important aspects of pharmacokinetics like renal excretion and dosing/monitoring are covered. The document also reviews the individual pharmacological properties and therapeutic uses of different aminoglycosides and their potential adverse effects like ototoxicity and nephrotoxicity.
This document provides an overview of aminoglycoside antibiotics, including their classification, mechanism of action, antibacterial spectrum, pharmacokinetics, resistance, and adverse effects. Aminoglycosides are obtained from Streptomyces and Micromonospora bacteria and interfere with bacterial protein synthesis. They are effective against many gram-negative bacteria but not gram-positive or anaerobic species. Due to poor absorption, aminoglycosides must be administered parenterally. They have concentration-dependent bacterial killing and a post-antibiotic effect. Adverse effects include ototoxicity, nephrotoxicity, and neuromuscular blockade. Common aminoglycosides discussed are streptomycin, gent
The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
The document discusses various protein synthesis inhibitors including aminoglycosides, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and oxazolidinones. It describes the stages of protein synthesis, mechanisms of action, antimicrobial spectra, resistance mechanisms, pharmacokinetics, clinical uses, and toxicities of each class of inhibitors.
This document discusses aminoglycoside antibiotics, including their mechanism of action, spectrum of activity, pharmacokinetics, therapeutic uses, and adverse effects. Aminoglycosides inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit and are effective against many gram-negative and some gram-positive bacteria. They have concentration-dependent bactericidal activity but can cause ototoxicity and nephrotoxicity. Common aminoglycosides include gentamicin, tobramycin, and amikacin, which are used to treat serious infections like sepsis, pneumonia, and endocarditis.
1) Aminoglycosides are a class of antibiotics that are used to treat infections caused by aerobic gram-negative bacteria by inhibiting protein synthesis.
2) They are derived from actinomycetes bacteria and have an aminosugar component joined by an aminocyclitol component.
3) Common side effects include ototoxicity (hearing loss and dizziness) and nephrotoxicity (kidney damage). Dosing must be monitored based on a patient's kidney function.
This document summarizes key information about aminoglycoside antibiotics. It describes their origin from soil actinomycetes, common agents like streptomycin, gentamicin and tobramycin. It outlines their mechanism of action inhibiting protein synthesis, broad-spectrum activity against gram-negative bacteria and some protozoa. Resistance development via modifying enzymes is discussed. Important aspects of pharmacokinetics like renal excretion and dosing/monitoring are covered. The document also reviews the individual pharmacological properties and therapeutic uses of different aminoglycosides and their potential adverse effects like ototoxicity and nephrotoxicity.
This document provides an overview of aminoglycoside antibiotics, including their classification, mechanism of action, antibacterial spectrum, pharmacokinetics, resistance, and adverse effects. Aminoglycosides are obtained from Streptomyces and Micromonospora bacteria and interfere with bacterial protein synthesis. They are effective against many gram-negative bacteria but not gram-positive or anaerobic species. Due to poor absorption, aminoglycosides must be administered parenterally. They have concentration-dependent bacterial killing and a post-antibiotic effect. Adverse effects include ototoxicity, nephrotoxicity, and neuromuscular blockade. Common aminoglycosides discussed are streptomycin, gent
This document discusses aminoglycoside antibiotics. It begins by defining aminoglycosides as a group of antibiotics used to treat aerobic gram-negative bacterial infections. It notes their structure consists of amino sugars linked to a hexose nucleus. While effective, their use is limited by serious toxicity risks like nephrotoxicity and ototoxicity. Streptomycin was the first discovered in 1943. The document then provides detailed information on various aminoglycosides including their structures, sources, uses, mechanisms of action, resistance, pharmacokinetics, spectrum of activity, dosing and administration routes, toxicity, and drug interactions.
This document discusses aminoglycoside antibiotics, which consist of amino sugars and a hexose nucleus. They are used to treat aerobic gram-negative bacterial infections. Streptomycin was the first discovered in 1943. Aminoglycosides act by interfering with bacterial protein synthesis and binding to the 30S ribosomal subunit. They are effective against many gram-negative bacteria but have serious toxicity risks like nephrotoxicity and ototoxicity. Therapeutic drug monitoring is important when using these antibiotics due to their narrow therapeutic index.
1. Aminoglycoside antibiotics like streptomycin, gentamicin, and tobramycin act by interfering with bacterial protein synthesis, making them effective against many aerobic gram-negative bacteria.
2. They work by binding to the bacterial ribosome and inhibiting protein translation, which disrupts the integrity of the bacterial cell membrane and leads to cell death.
3. While highly effective antibiotics, aminoglycosides have the potential for ototoxicity and nephrotoxicity, so monitoring of hearing, balance, and kidney function is important during treatment.
This document provides information on various aminoglycoside antibiotics, including their classification, mechanisms of action, resistance, and side effects. It discusses several specific aminoglycosides - streptomycin, gentamicin, amikacin, neomycin, kanamycin, and framycetin. All aminoglycosides are bactericidal, acting by binding to bacterial ribosomes and inhibiting protein synthesis. Resistance can occur via enzymatic modification or decreased drug accumulation in bacteria. Adverse effects include ototoxicity and nephrotoxicity.
This document provides information on various aminoglycoside antibiotics, including their classification, mechanisms of action, resistance, and side effects. It discusses several specific aminoglycosides - streptomycin, gentamicin, amikacin, neomycin, kanamycin, and framycetin. It describes how these antibiotics are produced by soil microbes and are bactericidal by binding to bacterial ribosomes. Resistance can occur through enzymatic modification or impaired drug entry into cells. Adverse effects include ototoxicity and nephrotoxicity.
This document provides an overview of aminoglycoside antibiotics. It discusses that aminoglycosides are a group of bactericidal antibiotics used to treat aerobic Gram-negative bacteria by preventing bacterial protein synthesis. Some key points covered include:
- Aminoglycosides like streptomycin were first discovered in the 1940s from soil bacteria. Common systemic aminoglycosides include gentamicin, tobramycin, and amikacin.
- Their mechanism of action involves binding to the 30S ribosomal subunit of bacteria to prevent proper initiation complex formation and protein synthesis.
- They have concentration-dependent bacterial killing and a post-antibiotic effect. Resistance can develop via enzymatic modification or
The document provides information about aminoglycosides, a class of antibiotics. It discusses the discovery of the first aminoglycoside streptomycin in 1944. It then summarizes that aminoglycosides are first-line therapies for infections like plague, tularemia, and tuberculosis caused by aerobic gram-negative bacteria. The document also lists some common aminoglycosides and provides brief sections on their mechanisms of action, microbial resistance, absorption, uses, and adverse effects.
This document provides information on aminoglycoside and macrolide antibiotics. It discusses the mechanism of action, toxicity, and examples of various aminoglycoside antibiotics like streptomycin, gentamicin, tobramycin, and erythromycin. The key points are that aminoglycosides inhibit bacterial protein synthesis by binding to bacterial ribosomes, but can cause ototoxicity and nephrotoxicity as side effects. Erythromycin was the first macrolide antibiotic discovered and works by binding to bacterial ribosomes to inhibit protein synthesis.
This document provides information on aminoglycoside antibiotics including their definition, classification, history, properties, mechanisms of action, resistance, pharmacokinetics, toxicities, and details on specific aminoglycosides such as streptomycin, gentamicin, kanamycin, and tobramycin. Aminoglycosides are a group of natural and semisynthetic antibiotics with polybasic amino groups linked to aminosugars that are active against aerobic gram-negative bacteria and some gram-positive bacteria. They work by interfering with bacterial protein synthesis and exhibit concentration-dependent bactericidal effects and post-antibiotic effects. However, they can also cause ototoxicity and nephrotoxicity.
Aminoglycosides are a group of natural or semi-synthetic antibiotics containing an amino sugar component and are used systemically or topically. They are derived from soil actinomycetes, not absorbed orally, and primarily target aerobic gram-negative bacteria through binding to bacterial ribosomes and inhibiting protein synthesis. Common examples include streptomycin, gentamicin, and tobramycin. While effective treatments, aminoglycosides can cause ototoxicity and nephrotoxicity.
This document provides information on various classes of antibiotics used in chemotherapy. It discusses aminoglycosides, their mechanism of action as inhibiting protein synthesis, indications such as gram negative infections, and important nursing responsibilities like monitoring for ototoxicity and nephrotoxicity. Macrolides and broad spectrum antibiotics like tetracycline and chloramphenicol are also summarized. Their mechanisms, uses, adverse effects and nursing care are highlighted. Sulphonamides are described as inhibiting folic acid synthesis, with uses for UTIs and dosing examples provided.
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This document discusses aminoglycoside antibiotics. It defines aminoglycosides as having polybasic amino groups linked glycosidically to amino sugars. It then classifies some common aminoglycosides as streptomycin, gentamicin, kanamycin, and amikacin. The document discusses the properties, mechanisms of action, resistance, pharmacokinetics, toxicities and interactions of aminoglycosides. It provides more detailed information about specific aminoglycosides including streptomycin, gentamicin, kanamycin, tobramycin, and neomycin.
systemic anti-microbials in periodontal therapyMehul Shinde
This document discusses the use of systemic antimicrobials in periodontal therapy. It provides an overview of the rationale for using antibiotics to treat periodontal diseases, commonly prescribed antibiotics like amoxicillin, metronidazole, tetracyclines, and their mechanisms of action, side effects, and clinical usage. Guidelines for antibiotic use recommend they be used as an adjunct to scaling and root planing based on microbial analysis and not as monotherapy. The ideal antibiotic would be pathogen-specific, non-toxic, substantive, and inexpensive.
This document discusses various classes of antibiotics including aminoglycosides, carbapenems, cephalosporins, erythromycins, and penicillins. It provides details on the mechanism of action, spectrum of activity, therapeutic uses, and precautions for each class. The main classes of antibiotics covered are defined by their chemical structure and each class generally has a different range of antibacterial activity. Common examples of drugs within each class are also listed along with their dosages and routes of administration.
This document discusses aminoglycoside and spectinomycin antibiotics. It describes that aminoglycosides like streptomycin are produced by Streptomyces bacteria and inhibit protein synthesis in bacteria. Their mechanism of action involves binding to the bacterial ribosome. Common adverse effects are nephrotoxicity and ototoxicity. Spectinomycin also inhibits bacterial protein synthesis and is used as an alternative treatment for drug-resistant gonorrhea.
Pyramidal, bony cavity facial skeleton
Base anterior, apex posterior
Contains and protects eyeball, muscles, nerves, vessels & most of the lacrimal apparatus
Bones forming orbit lined with periorbita
Forms Fascial sheath of the eyeball
By the end of the lecture, students should be able to:
Describe briefly development of the thyroid & parathyroid glands.
Describe the shape, position, relations and structure of the thyroid gland.
Describe the shape, position, blood supply & lymphatic drainage of the parathyroid glands.
List the blood supply & lymphatic drainage of the thyroid gland.
Describe the most common congenital anomalies of the thyroid gland.
List the nerves endanger with thyroidectomy operation.
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This document discusses aminoglycoside antibiotics. It begins by defining aminoglycosides as a group of antibiotics used to treat aerobic gram-negative bacterial infections. It notes their structure consists of amino sugars linked to a hexose nucleus. While effective, their use is limited by serious toxicity risks like nephrotoxicity and ototoxicity. Streptomycin was the first discovered in 1943. The document then provides detailed information on various aminoglycosides including their structures, sources, uses, mechanisms of action, resistance, pharmacokinetics, spectrum of activity, dosing and administration routes, toxicity, and drug interactions.
This document discusses aminoglycoside antibiotics, which consist of amino sugars and a hexose nucleus. They are used to treat aerobic gram-negative bacterial infections. Streptomycin was the first discovered in 1943. Aminoglycosides act by interfering with bacterial protein synthesis and binding to the 30S ribosomal subunit. They are effective against many gram-negative bacteria but have serious toxicity risks like nephrotoxicity and ototoxicity. Therapeutic drug monitoring is important when using these antibiotics due to their narrow therapeutic index.
1. Aminoglycoside antibiotics like streptomycin, gentamicin, and tobramycin act by interfering with bacterial protein synthesis, making them effective against many aerobic gram-negative bacteria.
2. They work by binding to the bacterial ribosome and inhibiting protein translation, which disrupts the integrity of the bacterial cell membrane and leads to cell death.
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This document provides information on various aminoglycoside antibiotics, including their classification, mechanisms of action, resistance, and side effects. It discusses several specific aminoglycosides - streptomycin, gentamicin, amikacin, neomycin, kanamycin, and framycetin. All aminoglycosides are bactericidal, acting by binding to bacterial ribosomes and inhibiting protein synthesis. Resistance can occur via enzymatic modification or decreased drug accumulation in bacteria. Adverse effects include ototoxicity and nephrotoxicity.
This document provides information on various aminoglycoside antibiotics, including their classification, mechanisms of action, resistance, and side effects. It discusses several specific aminoglycosides - streptomycin, gentamicin, amikacin, neomycin, kanamycin, and framycetin. It describes how these antibiotics are produced by soil microbes and are bactericidal by binding to bacterial ribosomes. Resistance can occur through enzymatic modification or impaired drug entry into cells. Adverse effects include ototoxicity and nephrotoxicity.
This document provides an overview of aminoglycoside antibiotics. It discusses that aminoglycosides are a group of bactericidal antibiotics used to treat aerobic Gram-negative bacteria by preventing bacterial protein synthesis. Some key points covered include:
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The document provides information about aminoglycosides, a class of antibiotics. It discusses the discovery of the first aminoglycoside streptomycin in 1944. It then summarizes that aminoglycosides are first-line therapies for infections like plague, tularemia, and tuberculosis caused by aerobic gram-negative bacteria. The document also lists some common aminoglycosides and provides brief sections on their mechanisms of action, microbial resistance, absorption, uses, and adverse effects.
This document provides information on aminoglycoside and macrolide antibiotics. It discusses the mechanism of action, toxicity, and examples of various aminoglycoside antibiotics like streptomycin, gentamicin, tobramycin, and erythromycin. The key points are that aminoglycosides inhibit bacterial protein synthesis by binding to bacterial ribosomes, but can cause ototoxicity and nephrotoxicity as side effects. Erythromycin was the first macrolide antibiotic discovered and works by binding to bacterial ribosomes to inhibit protein synthesis.
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1. Dr. NDAYISABA CORNEILLE
CEO of CHG
MBChB,DCM,BCSIT,CCNA
Supported BY
INHIBITORS OF
BACTERIAL PROTEIN
SYNTHESIS
2. There are 2 subgroups of antibiotics
which inhibit bacterial protein
synthesis
a) Inhibitors of bacterial protein
synthesis by binding to 30s
ribosomal subunit
1. Aminoglycosides
2. Tetracyclines
3. Aminoglycosides
— Are bactericidal
— Inhibit protein synthesis by interfering with
ribosomal function
— Are very useful against aerobic gram-ve
microorganisms
5. 8. Netilmicin
9. Paramomycin etc
Antibacterial activity of aminoglycosides
Mainly kill gram negative organisms
Kill some gram positive bacteria
Streptomycin is active against mycobacterium
tuberculosis & its currently reserved for tx of
TB
7. Mechanism of action of aminoglycosides
— All aminoglycosides irreversibly inhibit bacterial
protein synthesis
— This eventually lead to bacterial cell death
— These drugs act by binding to the 30s ribosomal
subunit
— This leads to interference with the formation of
initiation complex of the peptide chain
8. Events that occur before drug action
1. Initial event is passive diffusion via porin channels
across the outer membrane.
2. Drug is then actively tpted across cell membrane into
cytoplasm by an oxygen-dependent process.
3. The transmembrane electrochemical gradient supplies
energy for this process & tpt is coupled to a proton
pump.
9. Protein synthesis is inhibited by in at least 3 ways;
Interference with the initiation complex of peptide formation
Misreading of mRNA, which causes incorporation of
incorrect amino acids into the peptide, resulting in a
nonfunctional or toxic protein;
Breakup of polysomes into nonfunctional monosomes.
o Activities occur more or less simultaneously & overall
effect is irreversible & lethal for the cell.
10. Mechanisms of resistance
a) Production of transferase enzyme or enzymes
inactivates the aminoglycoside by;
adenylylation,
acetylation, or
phosphorylation.
o This is the principal type of resistance
encountered clinically.
11. b) Impaired entry of aminoglycoside into the cell.
o May be genotypic, ie, resulting frm mutation or deletion
of a porin protein or proteins involved in tpt a
maintenance of electrochemical gradient
o May phenotypic e.g. resulting frm growth conditions
under which oxygen-dependent tpt process described
above is not functional.
c) The receptor protein on 30S ribosomal subunit may be
deleted or altered as a result of a mutation
12. Pharmacokinetics
These drugs are given;
— Intravenously
— Intramuscular
— Topical application on mucous membranes
These drugs are not absorbed from the GIT thus
they are not given orally
13. — O.D dosing of aminoglycosides currently preferred
Why OD dosing is preferred
— Its more convenient to administer
— It provides large doses at once which results into
rapid killing of bacteria
— Aminoglycosides are excreted by kidneys
— These drugs accumulate in pts with renal failure
14. Distribution of aminoglycosides
— They are poorly distributed to most body
tissues bcoz they are highly polar thus do
not enter cells readily
— These drugs can reach brain cells in
presence of active inflammation of the
meninges
15. Clinical uses of aminoglycosides
— Given in combination with ampicillin or ceftriaxone
in tx of gram negative septicemia
— Given in combination with penicillin during tx of
bacterial endocarditis cozed by enterococci,
viridans streptococci & staph
— Given post-operatively after surgical operations
— Tx of septic wounds
— Tx of TB
17. Streptomycin
o Isolated from a strain of Streptomyces griseus.
o Ribosomal resistance develops readily, limiting its role as a single
agent.
Clinical Uses
1. Mycobacterial infections
o Used as a 2nd -line agent for tx of other forms of TB except TBM.
o Used as 1st line agent in tx of TB Meningitis
o Dosage is 0.5–1 g/d (7.5–15 mg/kg/d for children)
o Given IM or IV .
18. 2. Nontuberculous infections
a) Plague
b) Tularemia
c) Sometimes brucellosis,
Dosage 1 g/d (15 mg/kg/d for children)
Given IM in combination with an oral tetracycline.
d) Enterococcal endocarditis
— For tx endocarditis due to viridans streptococci
19. e) Viridans streptococcal endocarditis
Penicillin plus streptomycin is effective for and 2-week therapy of
Viridans streptococcal endocarditis
Gentamicin has largely replaced streptomycin for these indications.
o Streptomycin remains a useful agent for treating
enterococcal infections
Contraindications
o Pregnancy, can cause deafness in the newborn
o Renal failure
o Vestibular disorders
20. Gentamicin
o Isolated from Micromonospora purpurea.
o Effective against both gram-positives & gram-negative
o Many of its properties resemble those of other
aminoglycosides.
o Sisomicin is very similar to the C1a component of
gentamicin.
21. Clinical Uses
IM or IV administration
Used mainly in severe infections e.g.
1. Gram negative Septicemia
2. Pneumonia
o Such infections are usually caused by gram-negative bacteria that are
likely to be resistant to other drugs, esp
Pseudomonas, - Enterobacter,
Serratia - Proteus,
Acinetobacter -Klebsiella.
o It usually is used in combination with 2nd agent, as alone may not be
effective for infections outside urinary tract.
22. o Gentamicin shld not be used as a single agent to Rx
staphylococcal infections bcoz resistance develops
rapidly.
o Agents shld not be used for single-agent therapy of
pneumonia becoz penetration of infected lung tissue is
poor & local conditions of low pH + low oxygen
tension contribute to poor activity.
o Gentamicin 5–6 mg/kg/d traditionally is given IV TID,
but OD administration is just as effective
23. o Serum [gentamicin] & renal function shld be monitored
if given for more than a few days or if renal function is
changing (eg, in sepsis complicated by acute renal
failure).
Topical administration
o Creams, ointments & solutions containing 0.1–
0.3% gentamicin sulfate are used.
24. Indications include
I. Ocular infections
II. Infected burns
III. Infected wounds
IV. Infected skin lesions
V. Prevention of IV catheter infections.
o Topical gentamicin is partly inactivated by purulent
exudates.
25. Intrathecal administration
o Meningitis cozed by gram-negative bacteria .
o Dose is 1–10 mg/d.
o Neither intrathecal nor intraventricular gentamicin was
beneficial in neonates with meningitis.
o Intraventricular gentamicin was toxic.
o 3RD generation cephalosporins for gram-negative
meningitis is currently preferred
26. TOBRAMYCIN.
Clinical uses
o Rx of Pseudomonas aeruginosa LRTIs complicating cystic fibrosis. A
300-mg dose regardless of the pt's age or weight by inhalation thus
less adverse effects
o Gentamicin & tobramycin are otherwise interchangeable clinically.
Caution shld be used when administering tobramycin to pts with;
I. Preexisting renal diseases
II. Vestibular
III. Hearing disorders
27. Amikacin
o Semisynthetic derivative of kanamycin;
o It is less toxic than the parent molecule.
o It is resistant to many enzymes that inactivate gentamicin &
tobramycin.
o Its therefore used against some microorganisms resistant to
the latter drugs.
Pharmacokinetics
o Dose is 500 mg BD (15 mg/kg/d)
o IM route
28. Clinical uses
1. Multidrug-resistant Mycobacterium tuberculosis.
Effective even to streptomycin-resistant strains.
Kanamycin-resistant strains may be cross-resistant to
amikacin.
o Dosage of amikacin for TB is 7.5–15 mg/kg/d as OD or
2-3 times weekly injection
o Always used in combination with other drugs to which
the isolate is susceptible.
29. Netilmicin
o Shares many x-tics with gentamicin & tobramycin.
o However its resistant to enzymatic degradation due to
addition of an ethyl group to the 1-amino position of the
2-deoxystreptamine ring.
o Thus Netilmicin may be active against some
gentamicin & tobramycin-resistant bacteria.
30. Neomycin & Kanamycin
o Closely related.
o Paromomycin is also a member of this group.
o All have similar properties.
Antimicrobial Activity & Resistance
Drugs of neomycin group are active against;
I. Gram-positive & gram-negative bacteria
II. Some mycobacteria.
31. Pseudomonas & streptococci are generally resistant.
Mechanisms of antibacterial action & resistance
o The same as with other aminoglycosides.
o Their in bowel preparation for elective surgery has
resulted in selection of resistant organisms & some
outbreaks of enterocolitis in hospitals.
o Cross-resistance btn kanamycin & neomycin is
complete.
32. Pharmacokinetics
o Drugs of the neomycin group are poorly absorbed frm
GIT.
o After oral dose, intestinal flora is suppressed or
modified & the drug is excreted in the feces.
o Excretion of any absorbed drug is mainly thru
glomerular filtration into the urine.
33. Clinical Uses for Neomycin &kanamycin
o Clinical uses are now limited;
1. Topical
2. Oral use.
o Neomycin is too toxic for parenteral use.
A)Topical administration
o Solutions containing 1–5 mg/mL are used on;
1. Infected surfaces
2. Injected into joints, pleural cavity, tissue spaces, or
abscess cavities with infection .
34. o Total amount of drug given in this fashion must be
limited to 15 mg/kg/d bcoz at higher doses enough drug
may be absorbed to coz systemic toxicity.
B. Oral administration
1. Preparation for elective bowel surgery,
o 1 g of neomycin is given orally 6–8 hourly for 1–2 days
& often combined with 1 g of erythromycin base.
35. o This reduces aerobic bowel flora with little effect
on anaerobes.
2. In hepatic coma,
o Coliform flora can be suppressed
o Neomycin 1 g every 6–8 hours together with
reduced protein intake, thus reducing ammonia
intoxication.
o Use of neomycin for hepatic coma has been almost
entirely supplanted by lactulose, which is less
toxic.
36. 3. Intestinal amebiasis
o Paromomycin, 1 g every 6 hours orally for 2 weeks,
o Has been effective.
Adverse reactions
1. Nephrotoxicity
2. Ototoxicity.
3. Hypersensitivity is not common
4. Neuromuscular blockade & respiratory arrest
37. Ototoxicity
o Auditory function is affected more than vestibular.
o Deafness has occurred, esp in adults with impaired
renal function & prolonged elevation of drug levels.
Neuromuscular blockade & respiratory arrest.
o Due to sudden absorption of postoperatively instilled
kanamycin frm peritoneal cavity (3–5 g).
o Ca gluconate & neostigmine can act as antidotes.
38. Hypersensitivity is uncommon,
o Prolonged application of neomycin-containing
ointments to skin & eyes has resulted in severe allergic
reactions.
Spectinomycin
o Aminocyclitol antibiotic that is structurally related to
aminoglycosides.
o It lacks amino sugars & glycosidic bonds.
39. Mechanism of action
o Inhibits protein synthesis
Antibacterial spectrum
o Active in vitro against many gram-positives & gram-negatives,
o Some strains of gonococci may be resistant
Clinical uses
o Almost solely as alternative Rx for drug-resistant gonorrhea
o Gonorrhea in penicillin-allergic patients
Pharmacokinetics
o Rapidly absorbed after IM.
o A single dose of 40 mg/kg up to a max of 2 g.
40. Commonest S/E of aminoglycosides
1. Ototoxicity with features of vestibular & auditory
damage
Features auditory damage
– Tinnitus
– Hearing loss
Features vestibular damage
– Vertigo
41. Ataxia
Loss of balance
2.Nephrotoxicity with acute tubular necrosis
Other S/Es
— Hypersensitivity reactions like body rash
— Paralysis of respiratory muscles due to
neuromuscular junction blockade
— Hypomagnesaemia after prolonged use
42. Risk factors for S/Es of aminoglycosides
Prolonged tx therapy with
aminoglycosides for > 5 days
Giving large doses of aminoglycosides
Old age
Renal failure
Concurrent use of loop diuretics with
aminoglycosides
43. – Concurrent use of nephrotoxic drugs
like vancomycin, amphotericin B with
aminoglycosides
Contraindications
1. Pts with renal failure
2. Pts with vestibular damage
3. Pts with h/o hypersensitivity to
aminoglycosides
44. b) Inhibitors of protein synthesis by
binding to 50s ribosomal subunit
1. Amphenicols
– Chloramphenicol
2. Macrolides
– Erythromycin
– Azithromycin
47. Azithromycin
This is a semi synthetic derivative of erythromycin
o Its ½ life is 2–4 days thus its given O.D
o Its available inform of capsules ,tablets & syrups
for paediatrics
It shld be administered 1 hour before or 2 hours
after meals
Al & Mg antacids delay absorption of azithromycin
from the gut but they do not affect the drug
bioavailability
48. Dosage
Adults;
— 500mgs od for 3 days
— 500mgs start then 250mgs od for 4 days
— 1g start
Paediatrics
— 10mg/kg od for 3 days
49. Antibacterial activity ;
Its active against
o Mycobacterium avium complex
o Toxoplasma gondii
o Chlamydia
o Haemophilus influenzae
o Slightly less active than erythromycin &
clarithromycin against staph & streptococci
50. Indications
1. Chlamydial cervicitis
2. Chlamydial Urethritis (non gonococcal
urethritis)
3. CNS toxoplasmosis
4. Bacterial community acquired pneumonia
5. Treatment of streptococcal pharyngitis
6. Otitis media
51. 7. Mild to moderate typhoid fever due to
resistant s. typhi
8. Skin & soft tissue infections like cellulitis
,boils
9. Prophylaxis against group A streptococcal
pharyngitis
10. Eradication of mycobacterium avium
complex which cozes severe wasting in ISS
pts
11. Uncomplicated genital chlamydia infections
52. This is a semi synthetic derivative of
erythromycin
It has similar indications to those of
erythromycin
It has lower incidence of GI intolerance
Clarithromycin is more stable in gastric acid &
its well absorbed from the gut compared with
erythromycin
CLARITHROMYCIN
53. Antibacterial activity
Almost identical with erythromycin
But clarithromycin is more active against
a. Mycobacterium avium complex
b. Mycobacterium leprae
c. Toxoplasma gondii
Erythromycin-resistant streptococci & staph
are also resistant to clarithromycin
54. Its ½ life is 6 hrs thus its given BD
Its well distributed to most body tissues
Dosage
Adults
250–500 mg bid
Paediatrics
7.5 mgs/kg BD
55. Indications
1. Otitis media
2. Respiratory tract infections
3. Used in triple therapy mgt of PUD by
eradicating helicobacter pylori
4. Tx of brain toxoplasmosis in ISS pts
5. Boils (Furunculosis);deep seated infection
of hair follicles
56. 6. Carbuncles; a cluster of boils with spread of
bacterial infection to subcutaneous tissues
7. Chronic prostatitis
8. Septic wounds in combination with fragyl
9. Non Gonococcal urethritis due to
mycoplasma & chlamydia spp
10. Mastitis & breast abscesses
58. This is an antibiotic obtained from
a micro-organism known as Streptomyces
erythreus
It can be safely given to;
1. Pregnant mothers
2. Breastfeeding women
3. Children
Erythromycin
59. Antimicrobial activity of erythromycin
It kills;
1. Gram +ve organisms like
Streptococci e.g s. pneumoniae
Staphylococci
Corynebacteria
60. 2. Gram -ve organisms such as;
Neisseria spp
Chlamydia spp like C. trachomatis ,
C. psittaci, C. pneumoniae
Legionella spp
Helicobacter
Listeria spp
Campylobacter spp
61. Bordetella pertussis
Bartonella henselae & Bartonella
quintana etiologic agents of cat-scratch
disease + bacillary angiomatosis
Haemophilus influenzae are less
susceptible
62. 3. Mycoplasma spp
4. Some mycobacteria like M. kansasii& M.
scrofulaceum
5. Some rickettsia spp
6. Treponema pallidum
Dosage
Adults
250–500 mg every QID
Paediatrics
10-15 MG QID OR TDS
63. It should be administered on an empty
stomach bcoz food interferes with its
absorption
½ life of erythromycin is about 1.5 hours
thus is given QID
Distribution
Distributed widely to various body tissues
except to brain & CSF
Its taken up by polymorphonuclear
leukocytes & macrophages
It crosses the placenta & reaches fetus but
it has no teratogenic effects
64. Indications; its indicated in treatment of
conditions like;
1. Vaginal d/c syndrome in pregnancy
2. Urethral discharge syndrome in pregnancy
3. Acute glomerulonephritis
4. Genital ulcer disease in pregnancy
5. Amnionitis
65. 6. Mastitis
7. Breast abscess
8. Puerperal sepsis
9. Obstructed labour in combination with
metronidazole
10. Ophthalmia neonatoram; pus d/c from eyes
of a neonate
11. Streptococcal pharyngitis
66. 12. Moderate to severe pneumonia
13. Whooping cough
14. Chronic prostatitis
15. Septic wounds in combination with fragyl
16. Non Gonococcal urethritis due to
mycoplasma & chlamydia spp
67. 12. Boils (Furunculosis);deep seated infection
of hair follicles
13. Carbuncles; a cluster of boils with spread of
bacterial infection to subcutaneous tissues
Other indications
Impetigo; acute inflammation of outer layer
of skin
68. Pemphigus; a rare potentially fatal skin
disease characterised by intra-epidermal
skin bullae on apparently healthy skin or
mucous membranes
Cellulitis & erysipelas; acute inflammation of
skin & subcutaneous tissues
Campylobacter enteritis
Treatment of trachoma
69. Acne vulgaris
Rosacea
Prophylaxis against diphtheria
Prophylaxis against endocarditis during
dental procedures in individuals with
valvular heart disease
70. Adverse reactions
GI S/Es
1. Anorexia
2. Nausea
3. Vomiting
4. Diarrhea
5. GI intolerance due to direct stimulation of
gut motility
71. 6. Hypersensitivity reactions like;
Hepatitis with Jaundice & impaired liver
function
Fever
Urticaria
Rashes
Steven Johnson's syndrome
Toxic epidermal necrosis
72. Drug interactions
• It inhibits cytochrome P450 enzymes
thus ↑ serum levels of drugs like;
– Aminophylline
– Oral anticoagulants
– Cyclosporine
– Methylprednisolone
– Digoxin
73. Chloramphenicol is the only example of
amphenicol antibiotics
Chloramphenicol
A broad-spectrum antibiotic alongside the
tetracyclines
This is a bacteriostatic antimicrobial
Its no longer a 1st line antibiotic in most
developed countries due to its S/Es &
microbial resistance to the drug
AMPHENICOLS
74. Mechanism of action
o Potent inhibitor of microbial protein synthesis
o It binds reversibly to 50S subunit of bacterial ribosome
o This inhibits peptidyl transferase step of protein synthesis
Antimicrobial Activity;
o Its effective against a variety of;
Gram +ve like H influenzae, N meningitidis
Gram-ve bacteria
Most anaerobic organisms like bacteroides to which CAF
isbactericidal
75. Distribution
Widely distributed to virtually all tissues & body
fluids including CNS & CSF
This drug penetrates cell membranes readily
Metabolism
Occurs in liver
Excretion
Mainly by are kidneys
Small amount of active drug is excreted into bile &
76. Dosage;
Adults; 500-1000mg every 6 hours
PO & IV;
50mg/kg in 4 divided doses/d
100mg/kg 4 divided doses in conditions like;
Septicaemia
Meningitis
Children;
50-100mg/kg/d in 4 divided doses
Neonates < 2 wks;
25mg/kg/d in 4 divided doses
77. Indications of chloramphenicol
1. Septicaemia esp due N. meningitidis
2. Pyogenic meningitis due strep pneumoniae,
N.meningitidis , H. influenzae
3. Epiglottitis due to H. influenzae
4. Septic wounds
5. Tx of bacterial conjunctivitis & keratitis
6. Tx of enteric fever /typhoid fever
78. 7. Tx of bacillary dysentery in pregnancy as cipro &
cotrimoxazole are contraindicated
8. First choice drug tx for staphylococcal brain
abscesses
9. 2nd line drug in tx of tetracycline-resistant cholrea
10. Tx of typhus fever; an infection cozed by
rickettsiae which are transmitted by lice, rat fleas,
rodent mites
79. 11. Tx of plague ;an acute severe bacterial infection
with high fatality rate cozed by yersinia pestis
which is transmitted by infected ground rodent
fleas
12. Rocky Mountain spotted fever due to rickettsia
80. Why CAF is rarely used now days
Due to its potential toxicity
Wide occurrence of bacterial resistance to
CAF
Availability of many other effective antibiotics
81. Drug interactions of CAF
1. Inhibits cytochrome p450 enzymes that metabolize
several drugs thus leads to ↑ [serum] of;
– CCBs
– Antidepressants
– Anti-epileptic drugs
– Oral hypoglycemics
– PPIs
82. 2. Like other bacteriostatic inhibitors of
microbial protein synthesis, CAF
antagonizes bactericidal drugs like;
Penicillins
Aminoglycosides
Contraindications
1. Acute porphyria
2. Breast feeding mothers