THE SCRIBES SLIDE ANTIBIOTICS classification and types

EkeohaMichael 5 views 91 slides Feb 27, 2025
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About This Presentation

Antibiotics


Slide Content

ANTIBIOTICS
A PRESENTATION BY EKEOHA
MICHAEL
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 1

Objectives
By the end of this lecture you should be able to:
1)Classify commonly used antibiotics into six major antibiotic classes
of;
a)Beta lactams
b)Aminoglycosides
c)Fluoroquinolones
d)Macrolides
e)Tetracyclines
f)Glycopeptides
g)Metronidazole
2)Understand the mechanism of action of each antibiotic class.
3)Understand clinical use of each class of antibiotic
4)Possible major side effects.
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 2

There are Three important Relationships
Drug
Bacteria
Infection
Host defence
Host
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Improving the probability of positive outcomes
•Window of opportunity
•Early recognition and treatment of infection
•Selection of appropriate antibiotic
(e.g. through in vitrosusceptibility determination)
•Optimization of DOSE using Pharmacodynamic
principles
•Use optimized dosing that would allow for the
minimization of selecting further resistance
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 4

Mechanism of Action of Antibiotics
•Agents that inhibit synthesis of bacterial cell walls
Penicillins& cephalosporins
Cycloserine,
Vancomycin
Bacitracin
Azole antifungal agents (clotrimazole, fluconazole, itraconazole)
•Agents that actdirectly on the cell membranes of the microorganisms
Polymixin
Polyene antifungal agents
(Nystatin, Amphotericin B)
They Alter cell membranePermeability, cause leakage of intracellular
components
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 5

Mechanism of Action of Antibiotics
•Agents that affect the function of 30S or 50S ribosomal subunits
to cause a reversible inhibition of protein synthesis
•Bacteriostatic drugs
Chloramphenicol, Tetracyclines,
Erythromycin, Clindamycin,
Pristinamycins
•Agents that bind to 30S ribosomal subunit & alter protein
synthesis, which eventually leads to cell death
Aminoglycosides
•Agents that affect bacterial nucleic acid metabolism.
Rifampycinswhich inhibit RNA polymerase
Quinolones which inhibit topoisomerases
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 6

Mechanism of Action of Antibiotics
•Anti-metabolites
including trimethoprim & sulphonamides
•Antiviral agents
Nucleic acid analogues,
Non-nucleoside reverse transcriptase inhibitors,
Inhibitors of viral enzymes
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 7

CLASSIFICATION BASED ON THE
TYPE OF ACTION
Bacteriostatic Agents
Bactericidal Agents
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Antibiotics
Actions
▪Bactericidal
➢Kills bacteria, reduces bacterial load
▪Bacteriostatic
✓Inhibit growth and reproduction of bacteria
▪All antibiotics require the immune system to work properly
▪Bactericidal appropriate in poor immunity
▪Bacteriostatic require intact immune system
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 9

CLASSIFICATION BASED ON THE
TYPE OF ACTION
Bacteriostatic Agents
Sulphonamides
Tetracyclines
Chloramphenicol
Erythromycin
Ethambutol
Bactericidal Agents
Penicillins/Cephalosporins/Carbapenems
Aminoglycosides
Rifampin
•Isoniazid
•Pyrazinamide
Cephalosporins
Vancomycin
Nalidixic acid
Ciprofloxacin
Metronidazole
& Cotrimoxazole
Some primarily static drugs may become cidalat higher
concentrations (as attained in the urinary tract) & vice-versa.
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 10

CLASSIFICATION BASED ON THE
SPECTRUM OF ACTIVITY
Narrow spectrum
Broad spectrum
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 11

CLASSIFICATION BASED ON THE
SPECTRUM OF ACTIVITY
Narrow spectrum
Penicillin G
Streptomycin
Broad spectrum
Tetracyclines
Chloramphenicol
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 12

Successful Antimicrobial Therapy
•Concentration:
•site of infection
Concentration should inhibit
microorganisms
simultaneously it should be below the
level toxic to human beings.
•Host Defences
Immunity intact -Bacteriostatic Agents
Impaired immunity -Bactericidal Agents
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 13

15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 14
AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS

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AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS

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AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS

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AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS

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AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS

ß-Lactams
Β-Lactam
Ring
Thiazolidine Ring
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 19

ß-Lactams
ß-Lactams
Penicillin
Narrow Spectrum
•Benzylpenicillin (Penicillin G)
•Phenoxymethylpenicillin (Pen V)
•Flucloxacillin
Broad Spectrum
•Amoxicillin/Co-amoxiclav
•Ampicillin
•Piperacillin with Tazobactam
(Tazocin)
Cephalosporin
•Cefalexin
•Cefuroxime
•Cefotaxime
•Ceftriaxone
Carbapenem
•Meropenem
•Imipenem
•Doripenem
•Ertapenem15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 20

Mechanisms of Action
•Anti Cell Wall Activity
•Bactericidal
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Beta Lactams Against Bacterial Cell
Wall
Cell wall
Osmotic
Pressure
Antibiotic against cell wall
Osmotic
Pressure
Cell membrane
Rupture
Cell Membrane
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Spectrum of Activity
•Very wide
•Gram positive and negative bacteria
•Anaerobes
•Spectrum of activity depends on the agent and/or its group
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 23

Adverse Effects
Penicillin hypersensitivity –0.4% to 10 %
•Mild: rash
•Severe: anaphylaxis & death
•There is cross-reactivity among all Penicillins
•Penicillins and cephalosporins ~5-15%
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Resistance to ß-Lactams
•ß-Lactamase
•Other mechanisms are of less importance
•Augmentin
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Important Points
•Beta lactams need frequent dosing for successful
therapeutic outcome
•Missing doses will lead to treatment failure
•Beta lactams are the safest antibiotics in renal and
hepatic failure
•Adjustments to dose may still be required in severe
failure
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Summary
•Cell wall antibiotics
•Bactericidal
•Wide spectrum of use
•Antibiotics of choice in many infections
•Limitations
•Allergy
•Resistance due to betalactamase
•Very safe in most cases
•No monitoring required
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15/11/2024 10:05 ANTIBIOTICS EKEOHA MICHAEL 28
AGENTS THAT INHIBIT
SYNTHESIS OF BACTERIAL CELL
WALLS
A 52-year-old man (weight 70 kg) is brought to the hospital emergency department in a confused and delirious
state. He has had an elevated temperature for more than 24 h, during which time he had complained of a severe
headache and had suffered from nausea and vomiting. Lumbar puncture reveals an elevated opening pressure,
and cerebrospinal fluid findings include elevated protein, decreased glucose, and increased neutrophils. Gram
stain of a smear of cerebrospinal fluid reveals gram-positive diplococci, and a preliminary diagnosis is made of
purulent meningitis. The microbiology report informs you that for approximately 15% of S pneumoniae isolates
in the community, the minimal inhibitory concentration for penicillin G is 20 mcg/mL.
1. Treatment of this patient should be initiated immediately
with intravenous administration of
(A) Ampicillin-sulbactam
(B) Cefazolin
(C) Cefotaxime plus vancomycin
(D) Nafcillin
(E) Ticarcillin
2. The primary mechanism of antibacterial action of the penicillinsinvolves inhibition of
(A) Beta-lactamases
(B) N-acetylmuramic acid synthesis
(C) Peptidoglycan cross-linking
(D) Synthesis of cell membranes
(E) Transglycosylation

15/11/2024 10:13 ANTIBIOTICS EKEOHA MICHAEL 29
AGENTS THAT INHIBIT PROTEIN
SYNTHESIS

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AGENTS THAT INHIBIT PROTEIN
SYNTHESIS

Aminoglycosides
Inhibit bacterial protein synthesis by irreversibly binding to 30S
ribosomal unit
•Naturally occurring:
•Streptomycin
•Neomycin
•Kanamycin
•Tobramycin
•Gentamicin
•Semisynthetic derivatives:
•Amikacin (from Kanamycin)
•Netilmicin (from Sisomicin)
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30S Ribosomal Unit Blockage by
Aminoglycosides
•Causes mRNA decoding errors
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Spectrum of Activity
•Gram-Negative Aerobes
•Enterobacteriaceae;
E. coli, Proteussp., Enterobactersp.
•Pseudomonas aeruginosa
•Gram-Positive Aerobes(Usually in combination with ß-
lactams)
S. aureusand coagulase-negative staphylococci
Viridans streptococci
Enterococcussp. (gentamicin)
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Adverse Effects
•Nephrotoxicity
•Direct proximal tubular damage -reversible if caught early
•Risk factors: High troughs, prolonged duration of therapy,
underlying renal dysfunction, concomitant nephrotoxins
•Ototoxicity
•8th cranial nerve damage –irreversible vestibular and auditory
toxicity
•Vestibular: dizziness, vertigo, ataxia
•Auditory: tinnitus, decreased hearing
•Risk factors: as for nephrotoxicity
•Neuromuscular paralysis
•Can occur after rapid IV infusion especially with;
•Myasthenia gravis
•Concurrent use of succinylcholine during anaesthesia
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Prevention of Toxicity
a)Levels need to be monitored to prevent toxicity due to high serum
levels
b)To be avoided where risk factors for renal damage exist
1)Dehydration
2)Renal toxic drugs
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Mechanisms of Resistance
•Inactivation by Aminoglycoside modifying enzymes
•This is the most important mechanism
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Important Points
•Aminoglycosides should be given as a large single dose for a
successful therapeutic outcome
•Multiple small doses will lead to treatment failure and likely to lead
to renal toxicity
•Aminoglycosides are toxic drugs and require monitoring
•Avoid use in renal failure but safe in liver failure
•Avoid concomitant use with other renal toxic drugs
•Check renal clearance, frequency according to renal function
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Summary
•Restricted to aerobes
•Toxic, needs level monitoring
•Best used in Gram negative bloodstream
infections
•Good for UTIs
•Limited or no penetration
•Lungs
•Joints and bone
•CSF
•Abscesses
15/11/2024 09:58 ANTIBIOTICS EKEOHA MICHAEL 38

Macrolides
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Macrolides
Erythromycin
Telithromycin
Clarithromycin
Lactone Ring
Azithromycin
15
14
14
14
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Mechanism of Action
•Bacteriostatic-usually
•Inhibit bacterial RNA-dependent
protein synthesis
•Bind reversibly to the 23S ribosomal RNA
of the 50S ribosomal subunits
•Block translocation reaction of the polypeptide
chain elongation
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Spectrum of Activity
•Gram-Positive Aerobes:
•Activity: Clarithromycin>Erythromycin>Azithromycin
•MSSA
•S. pneumoniae
•Beta haemolytic streptococci and viridans streptococci
•Gram-Negative Aerobes:
•Activity: Azithromycin>Clarithromycin>Erythromycin
•H. influenzae, M. catarrhalis, Neisseria sp.
•NO activityagainst Enterobacteriaceae
•Anaerobes: upper airway anaerobes
•Atypical Bacteria
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Mechanisms of Resistance -Macrolides
•Altered target sites
•Methylation of ribosomes preventing antibiotic binding
•Cross-resistance occurs between all macrolides
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Clinical Use
•Cellulitis/Skin and soft tissue
•Beta haemolytic streptococci
•Staphylococcus aureus
•Intra-cellular organisms
•Chlamydia
•Gonococcus
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Summary
•Bacteriostatic
•ALL hepatic elimination
•Gastrointestinal Sideeffects (up to 33 %) (especially
Erythromycin)
•Nausea
•Vomiting
•Diarrhoea
•Dyspepsia
•Best used in atypical pneumonia
•Excellent tissue and cellular penetration
•Very useful in susceptible intracellular infections
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Tetracyclines
•Tetracycline
•Short acting
•Doxycycline
•Long acting
•Inhibit protein synthesis
•Bind reversibly to bacterial 30S ribosomal subunits
•Prevents polypeptide synthesis
•Bacteriostatic
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Spectrum of Activity
•All have similar activities
•Gram positives aerobic cocci and rods
•Staphylococci
•Streptococci
•Gram negative aerobic bacteria
•Atypical organisms
•Mycoplasmas
•Chlamydiae
•Rickettsiae
•Protozoa
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Adverse Effects
•Oesophageal ulceration
•Photosensitivity reaction
•Incorporate into foetal and children bone and teeth
Avoid in pregnancy and children
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Summary
•Very good tissue penetration
•Use usually limited to;
•Skin and soft tissue infections
•Chlamydia
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Glycopeptides
•Vancomycin
•Teicoplanin
MechanismofAction
•Inhibit peptidoglycan synthesis in the bacterial cell wall
•Prevents cross linkage of peptidoglycan chains
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Summary
•Large molecule
•Only active against Gram positive bacteria
•Second choice in all its uses except;
•MRSA
•C.difficile
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AGENTS THAT INHIBIT PROTEIN
SYNTHESIS
1. A 2-year-old child is brought to the hospital after ingesting pills
that a parent had used for bacterial dysentery when traveling
outside the United States. The child has been vomiting for
more than 24 h and has had diarrheawith green stools. He is
now lethargic with an ashen-grey color. Other signs and symptoms
include hypothermia, hypotension, and abdominal distention.
The drug most likely to be the cause of this problem is
(A) Ampicillin
(B) Chloramphenicol
(C) Clindamycin
(D) Doxycycline
(E) Erythromycin
2. The mechanism of antibacterial action of doxycycline involves
(A) Antagonism of bacterial translocase activity
(B) Binding to a component of the 50S ribosomal subunit
(C) Inhibition of DNA-dependent RNA polymerase
(D) Interference with binding of aminoacyl-tRNA to bacterial
ribosomes
(E) Selective inhibition of ribosomal peptidyl transferases

15/11/2024 10:34 ANTIBIOTICS EKEOHA MICHAEL 53
AGENTS THAT INHIBIT PROTEIN
SYNTHESIS
A 24-year-old woman comes to a clinic with complaints of dry cough, headache, fever, and malaise, which have
lasted 3 or 4 d. She appears to have some respiratory difficulty, and chest examination reveals rales but no other
obvious signs of pulmonary involvement. However, extensive patchy infiltrates are seen on chest x-ray film. Gram
stain of expectorated sputum fails to reveal any bacterial pathogens. The patient mentions that a colleague at work
has similar symptoms to those she is experiencing. The patient has no history of serious medical problems. She
takes loratadine for allergies and supplementary iron tablets, and she drinks at least 6 cups of caffeinated coffee per
day. The physician makes an initial diagnosis of community-acquired pneumonia.
3. Regarding the treatment of this patient, which of the following
drugs is most suitable?
(A) Amoxicillin
(B) Clindamycin
(C) Doxycycline
(D) Linezolid
(E) Vancomycin

15/11/2024 10:21 ANTIBIOTICS EKEOHA MICHAEL 54
AGENTS THAT INHIBIT PROTEIN
SYNTHESIS
4. If a patient were to be treated with the macrolide erythromycin,
she should
(A) Avoid exposure to sunlight
(B) Avoid taking supplementary iron tablets
(C) Decrease her intake of caffeinated beverages
(D) Discontinue loratadine temporarily
(E) Have her plasma urea nitrogen or creatinine checked before
Treatment
5. The primary mechanism of resistance of gram-positive
organisms to erythromycin is
(A) Decreased activity of uptake mechanisms
(B) Decreased drug permeability of the cytoplasmic membrane
(C) Formation of drug-inactivating acetyltransferases
(D) Formation of esterasesthat hydrolyzethe lactone ring
(E) Methylation of binding sites on the 50S ribosomal subunit

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AGENTS THAT INHIBIT PROTEIN
SYNTHESIS
6. Regarding the mechanism of action of aminoglycosides, the drugs
(A) Are bacteriostatic
(B) Bind to the 50S ribosomal subunit
(C) Cause misreading of the code on the mRNA template
(D) Inhibit peptidyl transferase
(E) Stabilize polysomes
7.Your 23-year-old female patient is pregnant and has gonorrhea.
The medical history includes anaphylaxis following exposure to amoxicillin. The most appropriate drug to use is
(A) Azithromycin
(B) Cefixime
(C) Ceftriaxone
(D) Ciprofloxacin
(E) Doxycycline
8. Which statement about “once-daily” dosing with aminoglycosides is not accurate?
(A) Convenient for outpatient therapy
(B) Dosage adjustment is less important in renal insufficiency
(C) Less nursing time is required for drug administration
(D) Often less toxic than conventional (multiple) dosing
regimens
(E) Underdosing is less of a problem

AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
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AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
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AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
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AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
15/11/2024 10:52 ANTIBIOTICS EKEOHA MICHAEL 59

Fluoroquinolones
Quinolone pharmacore
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Mechanism of Action
•Prevent:
•Relaxation of supercoiled DNA before replication
•DNA recombination
•DNA repair
•Gram-positive
•Gram-Negative (Enterobacteriaceae H. influenzae, Neisseria sp.
Pseudomonas aeruginosa)
•Ciprofloxacin is most active
•Atypical bacteria: all have excellent activity
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Summary
•Wide range of activity against Gram positive and
negative bacteria.
•Sepsis from Intra-abdominal and Renal Sources
•Coliforms (Gram negative bacilli)
•UTI
•E. coli
•Very good tissue penetration
•Excellent oral bioavailability
•High risk for C.difficile
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Metronidazole
•Antibiotic
•Amoebicide
•Anti-protozoal
•Trichomonas Vaginalis
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Mechanisms of Action
•Molecular reduction
•Nitroso intermediates
•Sulfamides
•Melatbolised
•Bacterial DNA de-stabilised
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Spectrum of Activity & Uses
•Anaerobes
•Bacterial Vaginosis
•Pelvic Inflammatory Disease
•C. Diff
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Bio-Availability
•Oral
•Intra-venous
•Expensive
•Rectal
•Cheap
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Summary
•Wide spectrum of activity
•Anaerobes
•In combination
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AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
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1. Trimethoprim-sulfamethoxazole is established to be effective against which of the following
opportunistic infections in the AIDS patient?
(A) Cryptococcal meningitis
(B) Disseminated herpes simplex
(C) Oral candidiasis
(D) Toxoplasmosis
(E) Tuberculosis
2. A 24-year-old woman has returned from a vacation abroad suffering from traveler’sdiarrhea, and her
problem has not
responded to antidiarrheal drugs. A pathogenic gram-negative bacillus is suspected. Which drug is most
likely to be effective
in the treatment of this patient?
(A) Amoxicillin
(B) Ciprofloxacin
(C) Sulfacetamide
(D) Trimethoprim
(E) Vancomycin

AGENTS THAT AFFECT BACTERIAL
NUCLEIC ACID METABOLISM .
15/11/2024 11:57 ANTIBIOTICS EKEOHA MICHAEL 69
3. Which adverse effect is most likely to occur with sulfonamides?
(A) Fanconi’s aminoaciduria syndrome
(B) Hematuria
(C) Kernicterus in the newborn
(D) Neurologic dysfunction
(E) Skin reactions
4. Supplementary folinicacid may prevent anemiain folatedeficient
persons who use this drug; it is a weak base achieving
tissue levels similar to those in plasma
(A) Ciprofloxacin
(B) Moxifloxacin
(C) Sulfacetamide
(D) Sulfamethoxazole
(E) Trimethoprim

Importanceof Pharmacokinetics in
Treatment
Beta lactams
Good/variable (Dependant on individual
antibiotic)
Soft tissue
Bone and joints
Lungs
CSF
Poor
Abscesses
Examples of good Tissue Penetrators
Tetracyclines
Macrolides
Quinolones
Clindamycin
Aminoglycosides
Good
Circulating organisms
Poor
Soft tissue
Bone and joints
Abscesses
Lungs
CSF
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PHEW!!!
Any Questions?
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS
•3 general categories
• Drug does not reach its target
• Drug is not active
• Target is altered
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS does not reach
its target
Porins
•Absence/mutation
•Reduce drug entry
•Reduced effective drug concentration at the target site.
Efflux pumps
•Transport drugs out of the cell
•Resistance to tetracyclines & β-lactam antibiotics
•Second general mechanism of drug resistance
β-lactam antibiotics -β-lactamase
Aminoglycosides -Aminoglycoside modifying enzymes
•Variant: failure of bacterial cell to convert an inactive drug to its active
metabolite. Resistance to INH in mycobacterium TB
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS does not reach
its target
•Mutation of natural target
•Target modification
The new target does not bind the drug for native target
Resulting in resistance to antibiotic.
Components mediating resistance to β –lactam antibiotics in
psuedomonasaeruginosa
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS does not reach
its target•β–lactam antibiotics hydrophilic
•Must cross outer membrane barrier of the cell via outer membrane
protein (Omp)channel or porins
•Mutation/missing/deleted
•Drug entry slow or prevented.
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS
•β-lactamaseconcentrated between the inner & outer membrane in
the periplasmic space
•constitutes an enzymatic barrier
•Drug destroyed
•Effective concentration not achieved
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS
•Target: PBP penicillin binding protein
•Low affinity for drug
•Altered
•Efflux transporter
•Mex A, Mex B & OprF
•Pumps the antibiotic across the outer membrane
•Reduced intracellular concentration of active drug
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Mutations
•May occur in
•Target protein
•Drug transport protein
•Protein important for drug activation
•Random events
•Survival advantage upon re-exposure to the drug
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•Resistance is acquired by horizontal transferof resistance
determinantsfrom a donor cell, often of another bacterial species by
•Transduction
•Transformation
•Conjugation
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BACTERIAL RESISTANCE TO
ANTIMICROBIAL AGENTS

CROSS RESISTANCE
•Acquisition of resistance to one AMA conferring resistance
to another antimicrobial agent to which the organism has not
been exposed, is called cross resistance
•Seen between chemically or mechanistically related drugs.
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•Resistance to one sulphonamide means resistance to
all others
•Resistance to one tetracyclines means insenstivity to
all others
•Complete cross resistance
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CROSS RESISTANCE

•Resistance to one aminoglycoside may not extend to
others, Gentamycin resistant strains may respond to
amikacin.
•partial cross resistance
•Sometimes unrelated drugs show partial cross
resistance,
e.g. Tetracyclines
& Chloramphenicol
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CROSS RESISTANCE

ANTIMYCOBACTERIAL
(TB & LEPROSY DRUGS)
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ANTIMYCOBACTERIAL
(TB & LEPROSY DRUGS)
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ANTIMYCOBACTERIAL
(TB & LEPROSY DRUGS)
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A 21-year-old woman from Southeast Asia has been staying with family members in the United States for the last
3 moand is looking after her sister’s preschool children during the day. Because she has difficulty with the English
language, her sister escorts her to the emergency department of a local hospital. She tells the staff that her sister
has been feeling very tired for the last month, has a poor appetite, and has lost weight. The patient has
been feeling somewhat better lately except for a cough that produces a greenish sputum, sometimes specked
with blood. With the exception of rales in the left upper lobe, the physical examination is unremarkable and she
does not seem to be acutely ill. Laboratory values show a white count of 12,000ML and a hematocritof 33%.
Chest x-ray film reveals an infiltrate in the left upper lobe with a possible cavity. A Gram-stained smear of the
sputum shows mixed flora with no dominance. An acid-fast stain reveals many thin rods of pinkish hue. A
preliminary diagnosis is made of pulmonary tuberculosis. Sputum is sent to the laboratory for culture.
1. At this point, the most appropriate course of action is to
(A) Hospitalize the patient and start treatment with isoniazid plus rifampin
(B) Hospitalize the patient and start treatment with 4 antimycobacterial drugs
(C) Prescribe isoniazid for prophylaxis and send the patient home to await culture results
(D) Prescribe no drugs and send the patient home to await culture results
(E) Treat the patient with isoniazid plus rifampin
2. Which drug regimen should be initiated in this patient when
treatment is started?
(A) Amikacin, isoniazid, pyrazinamide, streptomycin
(B) Ciprofloxacin, cycloserine, isoniazid, PAS
(C) Ethambutol, isoniazid, ofloxacin, streptomycin
(D) Ethionamide, pyrazinamide, rifampin, streptomycin
(E) Isoniazid, rifampin, pyrazinamide, ethambutol

ANTIMYCOBACTERIAL
(TB & LEPROSY DRUGS)
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3. The primary reason for the use of drug combinations in the
treatment of tuberculosis is to
(A) Delay or prevent the emergence of resistance
(B) Ensure patient compliance with the drug regimen
(C) Increase antimycobacterial activity synergistically
(D) Provide prophylaxis against other bacterial infections
(E) Reduce the incidence of adverse effects
4. Risk factors for multidrug-resistant tuberculosis include
(A) A history of treatment of tuberculosis without rifampin
(B) Recent immigration from Asia and living in an area of
over 4% isoniazid resistance
(C) Recent immigration from Latin America
(D) Residence in regions where isoniazid resistance is known
to exceed 4%
(E) All of the above

ANTIFUNGALS
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ANTIFUNGALS
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ANTIFUNGALS
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ANTIFUNGALS
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A 37-year-old woman with leukemiawas undergoing chemotherapy with intravenous antineoplastic drugs.
During treatment, she developed a systemic infection from an opportunistic pathogen. There was no erythema
or edemaat the catheter insertion site. A white vaginal discharge was observed. After appropriate specimens
were obtained for culture, empiric antibiotic therapy was started with gentamicin, nafcillin, and ticarcillin
intravenously.
This regimen was maintained for 72 h, during which time the patient’s condition did not improve significantly.
Her Throat was sore, and white plaques had appeared in her pharynx.
On day 4, none of the cultures had shown any bacterial growth, but both the blood and urine cultures grew out
Candida albicans.
1. At this point, the best course of action is to
(A) Continue current antibiotics and start amphotericin B
(B) Continue current antibiotics and start flucytosine
(C) Stop current antibiotics and start amphotericin B
(D) Stop current antibiotics and start ketoconazole
(E) Stop current antibiotics and start terbinafine
2. Interactions between this drug and cell membrane components
can result in the formation of pores lined by hydrophilic
groups present in the drug molecule.
(A) Amphotericin B
(B) Flucytosine
(C) Griseofulvin
(D) Itraconazole
(E) Terbinafine

CONCLUSION
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A good knowledge of Antibiotic therapy is important for
proficiency in managing patients especially in the tropics, it is
the striking difference between you the Doctor and Uncle Ikes
Chemist shop or Abiola Nature Therapy, Learn!!!
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