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Mechanism of Protein synthesis
Formation of the Initiation Complex
Joining of 50S Ribosomal Subunit
Protein Elongation
Termination of Translation
Aminoglycoside
AminoglycosidesAminoglycosides
• Streptomycin – 1944
• Actinomycetes – Streptomyces griseus
• Bactericidal antibiotics
• Interfere with protein synthesis
• Used to treat aerobic Gram –ve bacteria
• Resemble each other in MOA, pharmacokinetic
therapeutic and toxic properties
• Relatively low margin of safety
• Exhibit ototoxicity and nephrotoxicity
Aminoglycosides
• Systemic
– Streptomycin
– Gentamicin
– Kanamycin
– Amikacin
– Sisomicin
– Tobramycin
– Netilimicin
• Topical
– Neomycin
– Framycetin
Mechanism of action
• Initially they penetrate
bacterial cell wall, to reach
periplasmic space through
porin channels (passive
diffusion)
• Further transport across
cytoplasmic membrane takes
place by active transport by
proton pump; an oxygen-
dependent process
Mechanism of Action
• Bind 30S ribosomal
subunits and interfere
the initiation complex
• Induce misreading of
genetic code on mRNA
• Breakup of polysomes
into monosomes
Post antibiotic effect
• Aminoglycosides exhibit concentration
dependent killing.
• They also possess significant Post-antibiotic
effect.
• Single daily dosing at least as effective as and
no more toxic than multiple dosing.
Mechanism of resistance
• Synthesis of plasmid mediated bacterial
transferase enzyme: Inactivate
aminoglycosides
• ↓ transport into bacterial cytosol
• Deletion/alteration of receptor protein on 30 S
ribosomal unit by mutation: prevents
attachment
Antibacterial spectrum
• Primarily against Gm –ve aerobic bacilli
– Proteus, pseudomonas
– E.Coli,enterobacter
– Klebsiella
– Shigella
• Only few Gm +ve cocci:
– staph aureus, strepto viridans
• Not effective against Gm +ve bacilli, Gm-ve
cocci and anaerobes
Pharmacokinetics
• Highly polar basic drugs: poor oral BA
• Administered parenterally or applied locally
• Poorly distributed and poorly protein bound
• Do not undergo any significant metabolism
• Nearly all IV dose is excreted unchanged in
urine
• Dose adjustment is needed in renal
insufficiency
Pharmacokinetics
Clinical uses
• Gram –ve bacillary infection
– Septicaemia, pelvic & abdominal sepsis
• Bacterial endocarditis –
– enterococcal, streptococcal or staphylococcal infection of
heart valves
• Pneumonias, Tuberculosis
• Tularemia
• Plague, Brucellosis
• Topical – Neomycin, Framycetin.
• Infections of conjunctiva or external ear
• To sterilize the bowel of patients who receive
immunosuppressive therapy, before surgery & in
hepatic coma
Shared toxicities
• Ototoxicity
– Vestibular damage
– Cochlear damage
• Nephrotoxicity
• Neuromuscular blockade
• Skin rash
Ototoxicity
• Impairment of VIII cranial nerve function
• May be irreversible
• Cochlear damage
– Hearing loss and tinnitus
– More with neomycin , amikacin and kanamycin
• Vestibular damage
– Vertigo, ataxia, loss of balance
– More with Streptomycin, gentamycin
• Tobramycin has both types of toxicity
• Netilimycin claimed to have low ototoxicity
Nephrotoxicity
• Gentamicin, amikacin and tobramycin are
more toxic than streptomycin
• Responsible for 10-15% of all renal failure
cases
• Reversible if drug promptly discontinued
• ↓ GFR, ↑ sr creatinine
• ↓clearance of antibiotic → ↑ ototoxicity
Neuromuscular blockade
• Cause N-M junction blockade by
– Displacing Ca2+
from NM junction
– By blocking post synaptic NM receptors
– Inhibiting Ach release from motor nerve
• Neomycin & streptomycin: more propensity
• Tobramycin least likely to produce it
• Myasthenic weakness ↑by these drugs
Streptomycin
• Ribosomal resistance develops fast
• Limited usefulness as single agent
• Plague, tularemia and brucellosis
– In combination with tetracycline
• SABE: due to Streptococcus Viridans & faecalis
– With penicillin but gentamicin preferred
• Reserve first line drug for tuberculosis used
only in combination
Chloramphenicol
• An antibiotic produced by Streptomyces
venezuelae, an organism first isolated in
1947 from a soil sample collected in
Venezuela.
Mechanism of Action
• Chloramphenicol inhibits protein synthesis in bacteria and,
to a lesser extent, in eukaryotic cells. The drug readily
penetrates bacterial cells, probably by facilitated diffusion.
• Chloramphenicol acts primarily by binding reversibly to the
50 S ribosomal subunit. Although binding of tRNA at the
codon recognition site on the 30 S ribosomal subunit is thus
undisturbed, the drug appears to prevent the binding of the
amino-acid-containing end of the aminoacyl tRNA to the
acceptor site on the 50 S ribosomal subunit. The interaction
between peptidyltransferase and its amino acid substrate
cannot occur, and peptide bond formation is inhibited
• Chloramphenicol also can inhibit mitochondrial protein
synthesis in mammalian cells, perhaps because
mitochondrial ribosomes resemble bacterial ribosomes
(both are 70 S) more than they do the 80 S cytoplasmic
ribosomes of mammalian cells.
Pharmacokinetics:
• Chloramphenicol is available for oral administration
in two forms: the active drug itself and the inactive
prodrug, chloramphenicol palmitate (which is used to
prepare an oral suspension).
• Hydrolysis of the ester bond of chloramphenicol
palmitate is accomplished rapidly and almost
completely by pancreatic lipases in the duodenum
under normal physiologic conditions.
Absorption
• Chloramphenicol then is absorbed from the
gastrointestinal tract
• peak concentrations of 10 to 13 µg/ml occur within 2
to 3 hours after the administration of a 1-g dose.
• In patients with gastrointestinal disease or in
newborns, the bioavailability is greater for
chloramphenicol than for chloramphenicol palmitate,
probably because of the incomplete hydrolysis of the
latter
Absorption cont.
• The hydrolysis of chloramphenicol succinate
may be due to esterases of the liver, kidneys,
and lungs.
Absorption cont.
• Chloramphenicol succinate itself is rapidly cleared
from plasma by the kidneys.
• This renal clearance of the prodrug may affect the
overall bioavailability of chloramphenicol, because up
to 20% to 30% of the dose may be excreted prior to
hydrolysis.
• Poor renal function in the neonate and other states of
renal insufficiency result in increased plasma
concentrations of chloramphenicol succinate
Distribution
• Chloramphenicol is well distributed in all body fluids
and readily reaches therapeutic concentrations in
CSF, where values are approximately 60% of those in
plasma (range, 45% to 99%).
• Chloramphenicol is present in bile, is secreted into
milk, and readily traverses the placental barrier. It also
penetrates into the aqueous humor after
subconjunctival injection.
Fate and Excretion
• The half-life of chloramphenicol has been correlated
with plasma bilirubin concentrations.
• About 50% of chloramphenicol is bound to plasma
proteins.
• The half-life of the active drug (4 hours) is not
significantly changed in patients with renal failure
• The major route of elimination of chloramphenicol is
hepatic metabolism to the inactive glucuronide.
• Over a 24-hour period, 75% to 90% of an orally
administered dose is excreted; about 5% to 10% is in
the biologically active form.
Adverse effects cont.
Hematologic Toxicity
• The most important adverse effect of
chloramphenicol is on the bone marrow.
• Chloramphenicol affects the hematopoietic
system aplastic anemia, fatal pancytopenia,
• Leukopenia , thrombocytopenia.
Reversible bone marrow suppression
• A second, and dose-related, toxic hematologic
effect of chloramphenicol is a common and
predictable (but reversible) erythroid suppression
of the bone marrow.
• probably due to inhibitory action of the drug on
mitochondrial protein synthesis.
• It occurs regularly when plasma concentrations are
25 µg/ml or higher and is observed with the use of
large doses of chloramphenicol, prolonged
treatment, or both.
Gray baby syndrome
• Fatal chloramphenicol toxicity may develop in
neonates, especially premature babies, when they
are exposed to excessive doses of the drug.
• The manifestations in the first 24 hours are vomiting,
refusal to suck, irregular and rapid respiration,
abdominal distention, periods of cyanosis, and
passage of loose, green stools. Soon they become
flaccid, turn an ashen-gray color, and become
hypothermic
Hypersensitivity Reactions
• Although relatively uncommon, macular or vesicular
skin rashes occur as a result of hypersensitivity to
chloramphenicol.
• Angioedema is a rare complication. Jarisch-
Herxheimer reactions have been observed shortly
after institution of chloramphenicol therapy for
syphilis, brucellosis, and typhoid fever.
Therapeutic Uses
• Chloramphenicol has a wide range
activity that includes gram+, gram-,
aerobic and anaerobic bacteria
• Typhoid Fever
• Bacterial Meningitis
• Anaerobic Infections
• Rickettsial Diseases
• Brucellosis
Tetracycline
CONTENTS
• Introduction
• Classification and there structures
• Mechanism of action
• Structure Activity Relationship
• Spectrum of activity
• Toxicity and uses
INTRODUCTION
• Tetracyclines is a group of antibotic that include
tetracycline.
• Tetracyclines are obtained by fermentation from
Streptomyces spp. Or by chemical transformation of
natural products.
• They are derivatives of an octahydro- naphthacene,a
hydrocarbon system that comprises four annulated
six member rings.
CLASSIFICATION
TETRACYCLINES
SHORT ACTING:
•Tetracycline
•Oxytetracycline
INTERMEDIATE
ACTING:
•Demeclocycline
•Lymecycline
LONG ACTING:
•Doxycycline
•Minocycline
Mechanism of Action
• Tetracyclines are specific inhibitors of
bacterial protein synthesis. They bind to the
30S ribosomal subunit and thereby prevent
the binding of aminoacyl tRNA to the mRNA
ribosome complex.
• Tetracyclines also inhibit protein synthesis in the
host ,but are less likely to reach the concentration
required because eukaryotic cells do not have a
tetracycline uptake mechanism.
Spectrum of activity
• Tetracyclines are broad spectrum antibiotics,
active against wide range of Gram-positive
and Gram-negative bacteria, spirochetes,
mycoplasm, rickettsiae, and chalmydiae.
Toxicity of tetracycline
• Use of this medication for prolonged or repeated
periods may result in oral thrush or a new yeast
infection (oral or vaginal fungal infection).
• Nausea, vomiting, diarrhea, loss of appetite, mouth
sores, black hairy tongue, sore
throat, dizziness, headache, or rectal discomfort may
occur.
• This antibiotic treats only bacterial infections. It will
not work for viral infections (e.g.,common cold, flu).
Unnecessary use or overuse of any antibiotic can
lead to its decreased effectiveness.
Uses of tetracycline
• Tetracycline is used to treat a wide variety of
infections, including acne. It is an antibiotic
that works by stopping the growth of bacteria.
– Used in treatment of infections like septicemia,
endocarditis , meningitis.
Macrolides
• Belong to the Polypetide class of naturalBelong to the Polypetide class of natural
products.products.
• A group of antibiotics consisting of aA group of antibiotics consisting of a
macrolide ringmacrolide ring
• A large lactone ring to which one or more deoxy sugars,A large lactone ring to which one or more deoxy sugars,
are attached.are attached.
• The lactone ring can be either 14, 15 or 16 memberedThe lactone ring can be either 14, 15 or 16 membered.
• Naturally-occurring macrolide derived fromNaturally-occurring macrolide derived from
Streptomyces erythreusStreptomyces erythreus
• Problems with erythromycinProblems with erythromycin
• Acid labileAcid labile
• Narrow spectrumNarrow spectrum
• Poor GI tolerancePoor GI tolerance
• Short elimination half-lifeShort elimination half-life
Structural derivatives
Clarithromycin and AzithromycinClarithromycin and Azithromycin
• Broader spectrum of activityBroader spectrum of activity
• Improved PK properties –Improved PK properties –
» Better bioavailabilityBetter bioavailability
» Better tissue penetrationBetter tissue penetration
» Prolonged half-livesProlonged half-lives
• Improved tolerabilityImproved tolerability
• Inhibits protein synthesis by reversibly binding toInhibits protein synthesis by reversibly binding to
thethe 50S50S ribosomal subunitribosomal subunit
– Suppression of RNA-dependent protein synthesisSuppression of RNA-dependent protein synthesis
byby inhibition of translocation of mRNAinhibition of translocation of mRNA
• TypicallyTypically bacteriostaticbacteriostatic activityactivity
• BactericidalBactericidal at high concentrations against veryat high concentrations against very
susceptible organismssusceptible organisms
Gram-Positive AerobesGram-Positive Aerobes ::
Erythromycin & clarithromycin display the best activityErythromycin & clarithromycin display the best activity
(Clarithro>Erythro>Azithro)(Clarithro>Erythro>Azithro)
• Methicillin-susceptibleMethicillin-susceptible Staphylococcus aureusStaphylococcus aureus
• Streptococcus pneumoniaeStreptococcus pneumoniae –resistance is developing–resistance is developing
• Group and viridans streptococciGroup and viridans streptococci
• Bacillus spBacillus sp..
• Corynebacterium sp.Corynebacterium sp.
Gram-Negative AerobesGram-Negative Aerobes – Newer macrolides with– Newer macrolides with
enhanced activityenhanced activity
(Azithro>Clarithro>Erythro)(Azithro>Clarithro>Erythro)
• H. influenzae (not erythro),H. influenzae (not erythro),
• M. catarrhalis,M. catarrhalis,
• Neisseria sp.Neisseria sp.
• Do NOT have activity against anyDo NOT have activity against any EnterobacteriaceaeEnterobacteriaceae
Macrolide Spectrum of Activity
AnaerobesAnaerobes – Upper airway anaerobes– Upper airway anaerobes
Atypical BacteriaAtypical Bacteria – All have excellent activity– All have excellent activity
• Legionella pneumophila - DOCLegionella pneumophila - DOC
• Chlamydia sp.Chlamydia sp.
• Mycoplasma sp.Mycoplasma sp.
• UreaplasmaUreaplasma
Macrolide Spectrum of Activity
Other Bacteria –
• Mycobacterium aviumMycobacterium avium complexcomplex
(MAC – only A and C),(MAC – only A and C),
• Treponema pallidum,Treponema pallidum,
• CampylobacterCampylobacter
• Borrelia, BordetellaBorrelia, Bordetella
• BrucellaBrucella
• PasteurellaPasteurella
AbsorptionAbsorption
ErythromycinErythromycin – variable absorption, food may– variable absorption, food may
decrease the absorptiondecrease the absorption
– Base: destroyed by gastric acid; enteric coatedBase: destroyed by gastric acid; enteric coated
– Esters and ester salts: more acid stableEsters and ester salts: more acid stable
ClarithromycinClarithromycin – acid stable and well-absorbed– acid stable and well-absorbed
regardless of presence of foodregardless of presence of food
AzithromycinAzithromycin –acid stable; food decreases absorption–acid stable; food decreases absorption
of capsulesof capsules
DistributionDistribution
 Extensive tissue and cellular distributionExtensive tissue and cellular distribution
 clarithromycin and azithromycin withclarithromycin and azithromycin with
extensiveextensive penetrationpenetration
 Minimal CSF penetrationMinimal CSF penetration
– Gastrointestinal – up to 33 %
Nausea, vomiting, diarrhea, dyspepsia
Gastic pain, cramps
Most common with erythro; less with new agents
– Cholestatic hepatitis - rare
 > 1 to 2 weeks of erythromycin estolate
– Thrombophlebitis – IV Erythro and Azithro
Dilution of dose; slow administration
– Other: Ototoxicity (high dose erythro );
QTc prolongation;
Allergy
Erythromycin and Clarithromycin ONLY– are
inhibitors of cytochrome p450 system in the
liver; may increase concentrations of:
Theophylline Digoxin, Disopyramide
Carbamazepine Valproic acid
Cyclosporine Terfenadine, Astemizole
Phenytoin Cisapride
Warfarin Ergot alkaloids
• ENT infections , Tonsillitis, URTIENT infections , Tonsillitis, URTI
• Mycoplasma pneumonie infectionsMycoplasma pneumonie infections
• Legionnaires DiseaseLegionnaires Disease
• Chlamydial infections (any macrolides)Chlamydial infections (any macrolides)
• Diphtheria (erythromycin)Diphtheria (erythromycin)
• Pertussis (erythromycin)Pertussis (erythromycin)
• Strep/Staph Infections; alternatives in patientsStrep/Staph Infections; alternatives in patients
allergic to Penicillinallergic to Penicillin
• Prophylaxis against endocarditis in dentalProphylaxis against endocarditis in dental
proceduresprocedures
• Campylobacter/ Helicobacter Infections :Campylobacter/ Helicobacter Infections :clarithroclarithro
• Tetanus: in patients allergic to PenicillinTetanus: in patients allergic to Penicillin
• Mycobacterial Infections:Mycobacterial Infections: Clathri / AzithroClathri / Azithro Ist choiceIst choice
“Drug of Choice” for
 Mycoplasma pneumoniae
Legionella pneumophila
 Chlamydia pneumoniae, C. trachomatis
Bordetella pertussis (whooping cough)
C. diphtheriae
Esters of erythromycinEsters of erythromycin -sterate/estolate/ethylsuccinate are
resistant to inactivation.

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Protein synthesis inhibitors

  • 2. Formation of the Initiation Complex
  • 3. Joining of 50S Ribosomal Subunit
  • 7. AminoglycosidesAminoglycosides • Streptomycin – 1944 • Actinomycetes – Streptomyces griseus • Bactericidal antibiotics • Interfere with protein synthesis • Used to treat aerobic Gram –ve bacteria • Resemble each other in MOA, pharmacokinetic therapeutic and toxic properties • Relatively low margin of safety • Exhibit ototoxicity and nephrotoxicity
  • 8. Aminoglycosides • Systemic – Streptomycin – Gentamicin – Kanamycin – Amikacin – Sisomicin – Tobramycin – Netilimicin • Topical – Neomycin – Framycetin
  • 9. Mechanism of action • Initially they penetrate bacterial cell wall, to reach periplasmic space through porin channels (passive diffusion) • Further transport across cytoplasmic membrane takes place by active transport by proton pump; an oxygen- dependent process
  • 10. Mechanism of Action • Bind 30S ribosomal subunits and interfere the initiation complex • Induce misreading of genetic code on mRNA • Breakup of polysomes into monosomes
  • 11. Post antibiotic effect • Aminoglycosides exhibit concentration dependent killing. • They also possess significant Post-antibiotic effect. • Single daily dosing at least as effective as and no more toxic than multiple dosing.
  • 12. Mechanism of resistance • Synthesis of plasmid mediated bacterial transferase enzyme: Inactivate aminoglycosides • ↓ transport into bacterial cytosol • Deletion/alteration of receptor protein on 30 S ribosomal unit by mutation: prevents attachment
  • 13. Antibacterial spectrum • Primarily against Gm –ve aerobic bacilli – Proteus, pseudomonas – E.Coli,enterobacter – Klebsiella – Shigella • Only few Gm +ve cocci: – staph aureus, strepto viridans • Not effective against Gm +ve bacilli, Gm-ve cocci and anaerobes
  • 14. Pharmacokinetics • Highly polar basic drugs: poor oral BA • Administered parenterally or applied locally • Poorly distributed and poorly protein bound • Do not undergo any significant metabolism • Nearly all IV dose is excreted unchanged in urine • Dose adjustment is needed in renal insufficiency
  • 16. Clinical uses • Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis • Bacterial endocarditis – – enterococcal, streptococcal or staphylococcal infection of heart valves • Pneumonias, Tuberculosis • Tularemia • Plague, Brucellosis • Topical – Neomycin, Framycetin. • Infections of conjunctiva or external ear • To sterilize the bowel of patients who receive immunosuppressive therapy, before surgery & in hepatic coma
  • 17. Shared toxicities • Ototoxicity – Vestibular damage – Cochlear damage • Nephrotoxicity • Neuromuscular blockade • Skin rash
  • 18. Ototoxicity • Impairment of VIII cranial nerve function • May be irreversible • Cochlear damage – Hearing loss and tinnitus – More with neomycin , amikacin and kanamycin • Vestibular damage – Vertigo, ataxia, loss of balance – More with Streptomycin, gentamycin • Tobramycin has both types of toxicity • Netilimycin claimed to have low ototoxicity
  • 19. Nephrotoxicity • Gentamicin, amikacin and tobramycin are more toxic than streptomycin • Responsible for 10-15% of all renal failure cases • Reversible if drug promptly discontinued • ↓ GFR, ↑ sr creatinine • ↓clearance of antibiotic → ↑ ototoxicity
  • 20. Neuromuscular blockade • Cause N-M junction blockade by – Displacing Ca2+ from NM junction – By blocking post synaptic NM receptors – Inhibiting Ach release from motor nerve • Neomycin & streptomycin: more propensity • Tobramycin least likely to produce it • Myasthenic weakness ↑by these drugs
  • 21. Streptomycin • Ribosomal resistance develops fast • Limited usefulness as single agent • Plague, tularemia and brucellosis – In combination with tetracycline • SABE: due to Streptococcus Viridans & faecalis – With penicillin but gentamicin preferred • Reserve first line drug for tuberculosis used only in combination
  • 22. Chloramphenicol • An antibiotic produced by Streptomyces venezuelae, an organism first isolated in 1947 from a soil sample collected in Venezuela.
  • 23. Mechanism of Action • Chloramphenicol inhibits protein synthesis in bacteria and, to a lesser extent, in eukaryotic cells. The drug readily penetrates bacterial cells, probably by facilitated diffusion. • Chloramphenicol acts primarily by binding reversibly to the 50 S ribosomal subunit. Although binding of tRNA at the codon recognition site on the 30 S ribosomal subunit is thus undisturbed, the drug appears to prevent the binding of the amino-acid-containing end of the aminoacyl tRNA to the acceptor site on the 50 S ribosomal subunit. The interaction between peptidyltransferase and its amino acid substrate cannot occur, and peptide bond formation is inhibited
  • 24.
  • 25. • Chloramphenicol also can inhibit mitochondrial protein synthesis in mammalian cells, perhaps because mitochondrial ribosomes resemble bacterial ribosomes (both are 70 S) more than they do the 80 S cytoplasmic ribosomes of mammalian cells.
  • 26. Pharmacokinetics: • Chloramphenicol is available for oral administration in two forms: the active drug itself and the inactive prodrug, chloramphenicol palmitate (which is used to prepare an oral suspension). • Hydrolysis of the ester bond of chloramphenicol palmitate is accomplished rapidly and almost completely by pancreatic lipases in the duodenum under normal physiologic conditions.
  • 27. Absorption • Chloramphenicol then is absorbed from the gastrointestinal tract • peak concentrations of 10 to 13 µg/ml occur within 2 to 3 hours after the administration of a 1-g dose. • In patients with gastrointestinal disease or in newborns, the bioavailability is greater for chloramphenicol than for chloramphenicol palmitate, probably because of the incomplete hydrolysis of the latter
  • 28. Absorption cont. • The hydrolysis of chloramphenicol succinate may be due to esterases of the liver, kidneys, and lungs.
  • 29. Absorption cont. • Chloramphenicol succinate itself is rapidly cleared from plasma by the kidneys. • This renal clearance of the prodrug may affect the overall bioavailability of chloramphenicol, because up to 20% to 30% of the dose may be excreted prior to hydrolysis. • Poor renal function in the neonate and other states of renal insufficiency result in increased plasma concentrations of chloramphenicol succinate
  • 30. Distribution • Chloramphenicol is well distributed in all body fluids and readily reaches therapeutic concentrations in CSF, where values are approximately 60% of those in plasma (range, 45% to 99%). • Chloramphenicol is present in bile, is secreted into milk, and readily traverses the placental barrier. It also penetrates into the aqueous humor after subconjunctival injection.
  • 31. Fate and Excretion • The half-life of chloramphenicol has been correlated with plasma bilirubin concentrations. • About 50% of chloramphenicol is bound to plasma proteins. • The half-life of the active drug (4 hours) is not significantly changed in patients with renal failure • The major route of elimination of chloramphenicol is hepatic metabolism to the inactive glucuronide. • Over a 24-hour period, 75% to 90% of an orally administered dose is excreted; about 5% to 10% is in the biologically active form.
  • 32. Adverse effects cont. Hematologic Toxicity • The most important adverse effect of chloramphenicol is on the bone marrow. • Chloramphenicol affects the hematopoietic system aplastic anemia, fatal pancytopenia, • Leukopenia , thrombocytopenia.
  • 33. Reversible bone marrow suppression • A second, and dose-related, toxic hematologic effect of chloramphenicol is a common and predictable (but reversible) erythroid suppression of the bone marrow. • probably due to inhibitory action of the drug on mitochondrial protein synthesis. • It occurs regularly when plasma concentrations are 25 µg/ml or higher and is observed with the use of large doses of chloramphenicol, prolonged treatment, or both.
  • 34. Gray baby syndrome • Fatal chloramphenicol toxicity may develop in neonates, especially premature babies, when they are exposed to excessive doses of the drug. • The manifestations in the first 24 hours are vomiting, refusal to suck, irregular and rapid respiration, abdominal distention, periods of cyanosis, and passage of loose, green stools. Soon they become flaccid, turn an ashen-gray color, and become hypothermic
  • 35. Hypersensitivity Reactions • Although relatively uncommon, macular or vesicular skin rashes occur as a result of hypersensitivity to chloramphenicol. • Angioedema is a rare complication. Jarisch- Herxheimer reactions have been observed shortly after institution of chloramphenicol therapy for syphilis, brucellosis, and typhoid fever.
  • 36. Therapeutic Uses • Chloramphenicol has a wide range activity that includes gram+, gram-, aerobic and anaerobic bacteria • Typhoid Fever • Bacterial Meningitis • Anaerobic Infections • Rickettsial Diseases • Brucellosis
  • 38. CONTENTS • Introduction • Classification and there structures • Mechanism of action • Structure Activity Relationship • Spectrum of activity • Toxicity and uses
  • 39. INTRODUCTION • Tetracyclines is a group of antibotic that include tetracycline. • Tetracyclines are obtained by fermentation from Streptomyces spp. Or by chemical transformation of natural products. • They are derivatives of an octahydro- naphthacene,a hydrocarbon system that comprises four annulated six member rings.
  • 41. Mechanism of Action • Tetracyclines are specific inhibitors of bacterial protein synthesis. They bind to the 30S ribosomal subunit and thereby prevent the binding of aminoacyl tRNA to the mRNA ribosome complex. • Tetracyclines also inhibit protein synthesis in the host ,but are less likely to reach the concentration required because eukaryotic cells do not have a tetracycline uptake mechanism.
  • 42.
  • 43. Spectrum of activity • Tetracyclines are broad spectrum antibiotics, active against wide range of Gram-positive and Gram-negative bacteria, spirochetes, mycoplasm, rickettsiae, and chalmydiae.
  • 44. Toxicity of tetracycline • Use of this medication for prolonged or repeated periods may result in oral thrush or a new yeast infection (oral or vaginal fungal infection). • Nausea, vomiting, diarrhea, loss of appetite, mouth sores, black hairy tongue, sore throat, dizziness, headache, or rectal discomfort may occur. • This antibiotic treats only bacterial infections. It will not work for viral infections (e.g.,common cold, flu). Unnecessary use or overuse of any antibiotic can lead to its decreased effectiveness.
  • 45. Uses of tetracycline • Tetracycline is used to treat a wide variety of infections, including acne. It is an antibiotic that works by stopping the growth of bacteria. – Used in treatment of infections like septicemia, endocarditis , meningitis.
  • 47.
  • 48. • Belong to the Polypetide class of naturalBelong to the Polypetide class of natural products.products. • A group of antibiotics consisting of aA group of antibiotics consisting of a macrolide ringmacrolide ring • A large lactone ring to which one or more deoxy sugars,A large lactone ring to which one or more deoxy sugars, are attached.are attached. • The lactone ring can be either 14, 15 or 16 memberedThe lactone ring can be either 14, 15 or 16 membered.
  • 49. • Naturally-occurring macrolide derived fromNaturally-occurring macrolide derived from Streptomyces erythreusStreptomyces erythreus • Problems with erythromycinProblems with erythromycin • Acid labileAcid labile • Narrow spectrumNarrow spectrum • Poor GI tolerancePoor GI tolerance • Short elimination half-lifeShort elimination half-life
  • 50. Structural derivatives Clarithromycin and AzithromycinClarithromycin and Azithromycin • Broader spectrum of activityBroader spectrum of activity • Improved PK properties –Improved PK properties – » Better bioavailabilityBetter bioavailability » Better tissue penetrationBetter tissue penetration » Prolonged half-livesProlonged half-lives • Improved tolerabilityImproved tolerability
  • 51. • Inhibits protein synthesis by reversibly binding toInhibits protein synthesis by reversibly binding to thethe 50S50S ribosomal subunitribosomal subunit – Suppression of RNA-dependent protein synthesisSuppression of RNA-dependent protein synthesis byby inhibition of translocation of mRNAinhibition of translocation of mRNA • TypicallyTypically bacteriostaticbacteriostatic activityactivity • BactericidalBactericidal at high concentrations against veryat high concentrations against very susceptible organismssusceptible organisms
  • 52.
  • 53. Gram-Positive AerobesGram-Positive Aerobes :: Erythromycin & clarithromycin display the best activityErythromycin & clarithromycin display the best activity (Clarithro>Erythro>Azithro)(Clarithro>Erythro>Azithro) • Methicillin-susceptibleMethicillin-susceptible Staphylococcus aureusStaphylococcus aureus • Streptococcus pneumoniaeStreptococcus pneumoniae –resistance is developing–resistance is developing • Group and viridans streptococciGroup and viridans streptococci • Bacillus spBacillus sp.. • Corynebacterium sp.Corynebacterium sp.
  • 54. Gram-Negative AerobesGram-Negative Aerobes – Newer macrolides with– Newer macrolides with enhanced activityenhanced activity (Azithro>Clarithro>Erythro)(Azithro>Clarithro>Erythro) • H. influenzae (not erythro),H. influenzae (not erythro), • M. catarrhalis,M. catarrhalis, • Neisseria sp.Neisseria sp. • Do NOT have activity against anyDo NOT have activity against any EnterobacteriaceaeEnterobacteriaceae
  • 55. Macrolide Spectrum of Activity AnaerobesAnaerobes – Upper airway anaerobes– Upper airway anaerobes Atypical BacteriaAtypical Bacteria – All have excellent activity– All have excellent activity • Legionella pneumophila - DOCLegionella pneumophila - DOC • Chlamydia sp.Chlamydia sp. • Mycoplasma sp.Mycoplasma sp. • UreaplasmaUreaplasma
  • 56. Macrolide Spectrum of Activity Other Bacteria – • Mycobacterium aviumMycobacterium avium complexcomplex (MAC – only A and C),(MAC – only A and C), • Treponema pallidum,Treponema pallidum, • CampylobacterCampylobacter • Borrelia, BordetellaBorrelia, Bordetella • BrucellaBrucella • PasteurellaPasteurella
  • 57. AbsorptionAbsorption ErythromycinErythromycin – variable absorption, food may– variable absorption, food may decrease the absorptiondecrease the absorption – Base: destroyed by gastric acid; enteric coatedBase: destroyed by gastric acid; enteric coated – Esters and ester salts: more acid stableEsters and ester salts: more acid stable ClarithromycinClarithromycin – acid stable and well-absorbed– acid stable and well-absorbed regardless of presence of foodregardless of presence of food AzithromycinAzithromycin –acid stable; food decreases absorption–acid stable; food decreases absorption of capsulesof capsules
  • 58. DistributionDistribution  Extensive tissue and cellular distributionExtensive tissue and cellular distribution  clarithromycin and azithromycin withclarithromycin and azithromycin with extensiveextensive penetrationpenetration  Minimal CSF penetrationMinimal CSF penetration
  • 59.
  • 60. – Gastrointestinal – up to 33 % Nausea, vomiting, diarrhea, dyspepsia Gastic pain, cramps Most common with erythro; less with new agents – Cholestatic hepatitis - rare  > 1 to 2 weeks of erythromycin estolate – Thrombophlebitis – IV Erythro and Azithro Dilution of dose; slow administration – Other: Ototoxicity (high dose erythro ); QTc prolongation; Allergy
  • 61. Erythromycin and Clarithromycin ONLY– are inhibitors of cytochrome p450 system in the liver; may increase concentrations of: Theophylline Digoxin, Disopyramide Carbamazepine Valproic acid Cyclosporine Terfenadine, Astemizole Phenytoin Cisapride Warfarin Ergot alkaloids
  • 62. • ENT infections , Tonsillitis, URTIENT infections , Tonsillitis, URTI • Mycoplasma pneumonie infectionsMycoplasma pneumonie infections • Legionnaires DiseaseLegionnaires Disease • Chlamydial infections (any macrolides)Chlamydial infections (any macrolides) • Diphtheria (erythromycin)Diphtheria (erythromycin) • Pertussis (erythromycin)Pertussis (erythromycin)
  • 63. • Strep/Staph Infections; alternatives in patientsStrep/Staph Infections; alternatives in patients allergic to Penicillinallergic to Penicillin • Prophylaxis against endocarditis in dentalProphylaxis against endocarditis in dental proceduresprocedures • Campylobacter/ Helicobacter Infections :Campylobacter/ Helicobacter Infections :clarithroclarithro • Tetanus: in patients allergic to PenicillinTetanus: in patients allergic to Penicillin • Mycobacterial Infections:Mycobacterial Infections: Clathri / AzithroClathri / Azithro Ist choiceIst choice
  • 64. “Drug of Choice” for  Mycoplasma pneumoniae Legionella pneumophila  Chlamydia pneumoniae, C. trachomatis Bordetella pertussis (whooping cough) C. diphtheriae Esters of erythromycinEsters of erythromycin -sterate/estolate/ethylsuccinate are resistant to inactivation.

Notas do Editor

  1. Ribosomes are involved in protein synthesis by bacteria
  2. This complex moves along mrna so that sucessive codons of mRNA pass along ribosome from a site to p site Codon is triplet of 3 nucleotides which codes for specific amino acid needed for protein synthesis
  3. All are sulfate salts which are highly water soluble; solutions are stable for months They ionize in solution are not absorbed orally, distribute only extracellularly, do not penetrate brain or csf. More active in alkaliner ph. There is only partial cross resistance among them. Streptomycin – 1944 Actinomycetes – Streptomyces griseus
  4. Streptomycin and all other aminoglycosides whose name end with suffix mycin are obtained from genus streptomyces. Gentamicin other micins they are obtained from micromonospora or semisynthetically e.g netilimycin
  5. That is why beta lactum antibiotics which weaken or inhibit bacterial cell wall synthesis facilitate passive diffusion of aminoglycosides if given together- synergistic action. Subsequently further transport of aminoglycosides across the cytoplasmic membrane takes place by energy dependent and oxygen dependent active transport . As such transport cannot take place in anaerobic conditions, aminoglycosides are inactive against anaerobic bacteria.
  6. These drugs then bind to 30 S ribosomal units of bacteria and prevent formation of initiation complex. Which is prerequisite for peptide synthesis. Lack of formation of initiation complex causes 30 S subunit to misread genetic code on mRNA. Incorrect aminoacids are thus incorporated into growing peptide chain which are of no use for bacterial growth. The formation of improper initiation complex also blocks the movement of ribosomes, resulting in mRNA chain attached with single ribosomes (Monosomes). Thus aminoglycosides also interfere with in the assembly of polysomes which result in accumulation of nonfunctional ribosomes. Penetration is favoured by high pH. Aminoglycosides are 20 times more active in alkaline than acidic pH. Cidal action: secondary changes in integrity of bacterial cell membrane, because other antibiotics which inhibit protein synthesis are bacteriostatic. After exposure to aminoglycosides , sensitive bacteria become more permeable ; ions aminoacids and even protein leak out followed by cell death. This probably results from incorporation of faulty proteins into cell membrane.one of the consequences of aminoglycoside induced alteration of cell membrane is augmentation of carrier mediated entry of the antibiotic. This reinforces the lethal action. The cidal action of aminoglycosides is concentration dependentand they also exert prolonged post antibiotic effect.
  7. Antibacterial activity of aminoglycosides, fluoroquinolones and metronidazole is conc dependent. While that of beta lactums and vancomycin is time dependent. Conc dependent killing: more effective if higher blood conc are reached periodically. Time dependent killing: more effective if blood levels are maintained above the MIC for as long duration as possible. Post antibiotic effect: A persistant supression of bacterial growth. After brief a brief exposure of an antimicrobial agent. Inhibiton of bacterial growth is even seen when Conc of drug falls below MIC. REFLECTS time required by bacteria to return to normal growth. PAE is most significant with drugs that act by inhibiting bacterial protein synthesis or DNA synthesis. (Amino, Fluro, tetracycline, chloramphenicol, rifampicin. Post antibiotioc effect explains why these drugs can be given in a single daily dose even though they have a short half life (1-3) Hrs.
  8. Bacterial transferase enzymes are: phosphotransferases, acetyl tranferases and adenyl transferases. Which inactivate aminoglycosides by acetylatuion, adennylkation and phosphorylation. Decreased transport may result from mutation or deletion of porin channels or protein involved in transportor by makink o2+ energy dependent transport system non functional.
  9. Except salmonella
  10. Highly polar basic drugs: do not permit their membrane permeability, as a result they have very poor oral bioavailabilty entire oral dose excreted in faeces. When given parenterally they fail to reach intraoccular fluid or csf as they do not penetrate most cellular compartments. They do not undergo any significant metabolism Nearly all of IV dose is excreted unchanged in urine. Cleared by kidneys through glomerular filtration resulting in fairly high urinary conc. Which makes them useful in UTI. Use of urinary alkalinzer makes these drugs more effective. Excretion is directly proportional to renal clearance. nOrmal half life= 1.5 -3 hrs in renal insufficiency it may increase to 24 -48 hrs. these are only removed partly by hemodialysis and peritoneal dialysis. Hence dose adjustment is needed to avoid toxicity.
  11. Concentrated in labyrinthine fluid endolymph and perilymph and slowly removed from it. Conc dependent destructive changes are observed. Coclear damage:Initailly is asymptomatic can only be detected by audiometry. Tinnitus then appears follwed by hearing loss. Tinnitus disappears in 4 -10 days but frequency loss persists. Hearing loss affects high frequency sound first then to low frequency sounds. Hearing loss is permanent because no regeneration of sensory cells occurs. Older pt and those with prexixting hearing defect are mosre susceptible. Vestibular damage: headache is usually first to appear, followed by nausea, vomiting, diziness, nystagmus, vertigo. When drug is stopped in this phase, it passes into chronic phase lasting for 6-10 weeks in which patient is asymptomatic while in bed and only difficulty during walking. Compensation by visual and proprioceptive positioning and recovery occurs in often occurs over 1-2 years. Aminoglycoside induced ototoxicity is worsened by coadministration of vancomycin, furosemide, ethacrynic acid. While lessened by Calcium. EARLY DISCONTINUATION OF DRUG PREVENTS DAMAGE AND PERMIT RECOVERY
  12. Larger the number of constituent Amino group on aminoglycoside molecule more are the chances for its inherent nephrotoxic potential. Neomycin, gentamicin, amikacin and tobramycin are more toxic than More in elderly and prexisting kidney disease. Caused by inhibition of an intracellular lysosomal Phospholipase A2 in renal brush border. This leads to lysosomal distension, rupture and release of acid hydrolases and free aminoglycoside into cytosol. Which binds to other cellular organelles like mitochondria, displaces calcium and leads to mitochondrial degeneration and necrosis. Necrotic cellular debris are then sloughed off and passes into urine, leaving denuded basement mebrane. It manifests as tubular dammage resulting in loss of urinary conc power, low GFR, nitrogen retention, albuminuria and casts . Aminoglycosides attain high conc in renal cortex toxicity is related to total amount of drug received by patient . Interfere with pg production related to decreased GFR Renal proximal tubular cells accumulate and retain drug • Mild proteinuria, appearance of casts, hyaline or granular Proximal tubular cells have regenerative capacity • Neomycin highly toxic- systemic administration contraindicated • Reduced excretion predisposed to ototoxicity • Monitor plasma drug conc. in prolonged and high dose therapy
  13. also interfere with mobilization of centrally located synaptic vesicles to fuse with terminal membrane. (probably by anatagonizing calcium as well as decrease the sensitivity of muscle end plate to Ach. Not manifested ordinarily in clinical settings . However apnoea and fatalities have occurred when these antibiotics were put into pleural or peritoneal cavities after operation especially if curare like drug used for sk muscle relaxation. Neuromuscular blockers should be used cautiously in patients receiving aminoglycosides.
  14. Oldest aminoglycoside antibiotic obtained from streptomyces griseous In intestinal and urinary tract resistant organisms may emerge in 2 days of therapy , E coli, h influenzae, staph aureus, strep pneumoniae and strep pyogenes have become largely resistant. Streptomycin dependence: certain mutuants become dependent on it. Growth promoted occurs when antibitoc induced misreading becomes a normal feature of organism. Adverse effects: 1/5 pt experience vestibular disturbances, auditory disturbances are less common. Streptomycin has lowest nephrotoxicity among aminoglycosides, probably because it is not concentrated in renal cortex. Hypersensitivity reactions are rare , rashes, eosinophilia, fever, exfoliative dermatitis have been noted.anaphylaxis is rare, topical use contraindicated for fear of contact sensitization. Superinfections are not significant, pain at site of injection is common. Paresthesia and scotoma are occasional. Dose: acute infection 1 gm IM BD for 7-10 days TB -1gm or .75 gm IM od or twice weekly for 30-60 days In SABE: 4-6 WEEKS PLAGUE: it effects rapiod cure 7-12 days. May be employed in confirmed cases. Tularemia: drug of choice for this rare disease. Effects cure in 7-10 days. Tetracyclines alternative drugs especially in milder cases In most other situations like UTI, peritonitis, septcaemia etc gentamicin or newer aminoglycoside is preferred due to low potency and wide spread resistance. Oral use for diarrhoea is banned in india.