• Antimicrobial drugs have caused a dramatic change not only
of the treatment of infectious diseases but of a fate of
• Microorganisms were found to be responsible for a variety of
infectious diseases that had been plaguing humanity from
• Accordingly, chemotherapy aimed at the causative organisms
was developed as the main therapeutic strategy.
• The ﬁrst antimicrobial agent in the world was salvarsan,
– a remedy for syphilis that was synthesized by Ehrlich in
• In 1935, sulfonamides were developed by Domagk and other
• In 1928, Fleming discovered penicillin.
– came into clinical use in the 1940s.
– an outstanding agent in terms of safety and efﬁcacy,
– led in the era of antimicrobial chemotherapy by saving
the lives of many wounded solders during World War II.
• Antimicrobial therapy takes advantage of the biochemical
differences that exist between microorganisms and human
• Their selective toxicity; i.e., they have the ability to injure or
kill an invading microorganism without harming the cells of
• In most instances, the selective toxicity is relative rather than
• The more closely related the undesirable cells are to normal
– the more difﬁcult the task of ﬁnding a drug to that cell.
– E.g., it is easier to cure malaria than cancer.
Definition of terms
– is the use of chemicals against invading organisms (i.e.
bacteria).The term is used for both treatment of cancer
and treatment of infection.
– is a chemical that is produced by one microorganism and
has the ability to harm other microbes, also include
synthetic agents (eg. Sulfa drugs).
• Selective toxicity:
– is the ability of a drug to injure a target cell or organism
without injuring other cells or organisms that are in
Definition of terms cont…
• Narrow spectrum anti-infectives:
– affect only a few bacterial types.
– E.g., The early penicillin drugs.
• Broad-spectrum anti-infectives:
– affect many bacteria.
– E.g., Imipenem.
• Bactericidal Drugs:
– Antibiotics that can aggressively cause bacterial death.
– Penicillins, Cephalosphorins, Metronidazole, Aminoglycosides,
• Bacteriostatic drugs:
– Anti-infectives that interfere with the ability of the cell to
reproduce/replicate without killing them.
– E.g., Tetracyclines, chloramphenicol.
Definition of terms cont…
• Empiric therapy:
– treatment of an infection before specific culture
information has been reported or obtained.
– An infection occurring during antimicrobial treatment for
another infection, resulting from overgrowth of an
organism not susceptible to the antibiotic used.
– A secondary infection that occurs due weakening of the
patients immune system by the first infection.
• Initial therapy is usually empirical,
– the regimen is adjusted according to the results of culture
and sensitivity testing.
• Drug and its regimen may be changed several times during
• For example,
– severe nausea and high severity of illness may necessitate
initial parenteral antibiotic administration.
– when the patient is clinically stable, may be switched to
Managing Chemotherapy cont…
• Treatment must be continued for several days after objective
signs and symptoms of infection have resolved.
• Patients should be instructed to continue antibiotics for the
full duration indicated, even if they feel better.
• If delayed recovery from what is reasonably expectable, the
diagnosis should be reconsidered.
Misuse of Antibiotics
Antibiotics are misused in the following conditions;
• Treatment of untreatable infections
– Treatment of common cold/flu
– Take rest, but not antibiotic
– Viral infections don't respond to antibiotics and are self
• upper respiratory tract infection
• Therapy of fever of unknown origin
– Most instances of pyrexia of short duration are due to
• Improper dosage - suboptimal dose.
Types of Antimicrobial Resistance
• Generally there are tow types of resistance as a defense
mechanism for bacteria against the action of antibiotics:
1. Natural Resistance
• Some microorganisms are naturally resistant to the action of
• Cells without peptidoglycan are naturally resistant to
• Viruses, fungi, human cells are naturally resistant to
2. Acquired resistance
• Make lots of trouble to human kind.
• Bacteria become resistant after some modifications.
Classification By Mechanism Of Action
• Drugs that inhibit bacterial wall synthesis or activate
enzymes that disrupt the cell wall.
• Drugs that increase cell membrane permeability (causing
leakage of intracellular material).
• Drugs that inhibit bacterial protein synthesis.
• Drugs that inhibit bacterial synthesis of nucleic acids.
• Antimetabolites (disruption of specific biochemichal
reactions--> decrease in the synthesis of essential cell
Inhibitors of Bacterial Cell Wall Synthesis
• Also called Cell wall active agents.
β-Lactam Antibiotics: Mechanism of Action
• β-Lactam Antibiotics contain the β-lactam ring essential for
the antibacterial activity.
• Cross-linking of adjacent peptidoglycan (murein) strands,
– A transpeptidation reaction.
• Catalyzed by enzyme transpeptidase (also called
Penicillin Binding Proteins, PBPs)
• β-lactam antibiotics;
– Covalently bind the enzyme at the active site,
– Inhibit cell wall synthesis.
• A large group of bactericidal compounds.
• The antimicrobial activity of penicillin resides in the βlactam ring.
• Splitting of the β-lactam ring by either acid hydrolysis or βlactamases results in the formation of penicilloic acid,
– a product without antibiotic activity.
• Addition of various side chains (R) to the basic penicillin
– Gives compounds with the same mechanism of action but
with different chemical and biological properties.
• Penicillins may be classiﬁed into four groups:
– Natural penicillins (G and V) (narrow spectrum),
– Antistaphylococcal (penicillinase-resistant) penicillins
(very narrow spectrum),
– Aminopenicillins (extended spectrum), and
– Antipseudomonal penicillins (very extended spectrum).
Penicillin G (benzylpenicillin)
• an acid-labile compound, poor absorption from GIT.
• Most appropriate for IM or IV therapy.
• Distributes to most tissues.
• Excreted by the kidneys,
– 90% via tubular secretion, 10% by glomerular ﬁltration.
• Half-life = 30 minutes.
Clinical uses of penicillin G
• Endocarditis caused by S. viridans (or Streptococcus bovis),
• pharyngitis (group A β-hemolytic streptococci),
• Cat bite cellulitis (Pasteurella multocida), and
• Syphilis (Treponema pallidum).
• The activity of penicillin G was originally defined in units.
• Crystalline sodium penicillin G contains approximately 1600
units per mg (1 unit = 0.6 mcg; 1 million units of penicillin =
Penicillin G cont…
• Depot intramuscular formulations of penicillin G,
– procaine penicillin and benzathine penicillin,
– decreased solubility, delayed absorption, and a prolonged
• Procaine penicillin:
– Drug is detectable 24 hours after injection, and
• Benzathine penicillin:
– low levels (0.003 units/mL) are detectable 4 weeks after
Penicillin G cont…
• Intravenous penicillin G
– ﬁrst choice for therapy of meningitis caused by
susceptible S. pneumoniae.
• Depot formulation of benzathine penicillin G
– for rheumatic fever prophylaxis.
• Penicillin V
– orally administered phenoxymethyl congener of penicillin
– have an antibacterial spectrum of activity that is similar to
that of penicillin G.
– used to treat streptococcal infections when oral therapy is
appropriate and desirable.
Antistaphylococcal (penicillinase-resistant) Penicillins
• Methicillin, Nafcillin, oxacillin, cloxacillin, and dicloxacillin
• More resistant to bacterial β-lactamases than is penicillin G.
• Effective against streptococci and penicillinase-producing
– used mostly for skin and soft-tissue infections or
documented methicillin-sensitive S. aureus infections.
• Lack activity against Gram-negative bacteria,
– Unable to pass through G-negative bacterial porins due
Antistaphylococcal Penicillins cont…
• Nafcillin (IM, IV)
– T1/2 = 0.8 to 1.2 hrs
– Primarily cleared by biliary excretion.
• Oxacillin (IM, IV)
– T1/2 = 0.4 to 0.7 hrs.
– Eliminated by both the kidney and biliary excretion.
• Indications for nafcillin or oxacillin include,
– severe staphylococcal infections like cellulitis, empyema,
endocarditis, osteomyelitis, pneumonia, septic arthritis.
Antistaphylococcal Penicillins cont…
• Cloxacillin and dicloxacillin:
– Comparable alternatives for oral therapy.
– Eliminated by both the kidney and biliary excretion.
• No dosage adjustment is required for these drugs in
• T1/2 = 0.5 to 0.8 hrs
• Indications for cloxacillin or dicloxacillin include,
– clinically mild staphylococcal infections like impetigo.
Aminopenicillins (extended spectrum)
• Include, Ampicillin and Amoxicillin.
• Effective against a variety of Gram-positive cocci, Gramnegative cocci such as Neisseria gonorrhoeae and N.
meningitidis , and Gram-negative rods such as E. coli and
Haemophilus inﬂuenzae, but their spectrum is limited by
sensitivity to most β-lactamases.
• Have similar pharmacokinetics .
• Both have good oral bioavailability
• Concomitant ingestion of food decreases the bioavailability of
ampicillin but not amoxicillin.
• T1/2; ampicillin= 1.1 to 1.5 hrs, amoxicillin = 1.4 to 2.0 hrs.
• Ampicillin achieves therapeutic concentrations in the CSF only
– Effective treatment for meningitis caused by Listeria
• Amoxicillin does not reach adequate concentrations in the
– not appropriate for meningitis therapy.
• Other indications for ampicillin include serious infections
like enterococcal endocarditis and pneumonia caused by βlactamase-negative H. inﬂuenzae.
• Amoxicillin oral therapy:
– appropriate for clinically acute nonserious bacterial
infections like otitis media and sinusitis.
• Amoxicillin also has use in multidrug regimens for the
eradication of Helicobacter pylori in duodenal and gastric
Antipseudomonal Penicillins (very extended spectrum)
• Mezlocillin, piperacillin, Carbenicillin, azlocillin and ticarcillin
• Achieve only low concentrations in the CSF,
– not among the drugs of ﬁrst choice for meningitis therapy.
• Undergo renal elimination.
• Have comparable spectra of activity against many grampositive and gram-negative pathogens, including most
• Mezlocillin, piperacillin, and ticarcillin;
– have similar clinical outcomes in patients with known or
suspected P. aeruginosa infections.
• Inactivated by β-lactamase (may be combined with β-lactamase
β-Lactamase Inhibitor Combinations
• β-Lactamase Inhibitors;
– Clavulanic acid, sulbactam, and tazobactam.
• Several formulations combine a β-lactam antibiotic with a
β-lactamase inhibitor (ampicillin-sulbactam [Unasyn],
ticarcillin-clavulanic acid [Timentin], amoxicillin–clavulanic
• Combination signiﬁcantly broadens the spectrum of
antibacterial activity against β-lactamase-producing
• These drugs have clinical use in treating infections with
known or suspected mixed bacterial ﬂora, such as biliary
infections, diabetic foot ulcers, endomyometritis, and
β-Lactam Antibiotics in Pregnancy
• All of the penicillin antibiotics are classiﬁed by FDA in
pregnancy category B.
• Obstetricians frequently prescribe,
– ampicillin, penicillin G, and penicillin V
– because they are effective against the infections most
frequently encountered in caring for pregnant women
(e.g., upper respiratory and lower urinary tract
Adverse Effects to Penicillins
• Penicillins are considered among the safest antibiotics.
– a serious, rare allergic response with an occurrence rate
between 0.004% and 0.015% of penicillin courses.
• Allergic cross-reactivity between β-lactam antibiotics is
• Diarrhea: common with extended spectrum.
• Semisynthetic antibiotics derived from products of various
microorganisms, including Cephalosporium and
• β-lactam ring.
– associated with antibacterial activity.
• The different pharmacological, pharmacokinetic, and
antibacterial properties of individual cephalosporins
– Variation in substitution (R).
• More resistant to β-lactamase than penicillins.
• cephalosporinases (β-lactamases speciﬁc for the
– Inactivate cephalosporins
• Cephalosporins are classiﬁed into generations according to
their antibacterial spectrum and stability to β-lactamases.
• The ﬁrst-generation cephalosporins:
– active against streptococci, methicillin-sensitive S. aureus,
and a few gram-negative bacilli.
– Broad spectrum especially against Gm+ve organisms.
– Not effective against pseudomonas.
– Resistant to β-lactamase enzyme.
– Do not cross the meninges so not effective in meningitis.
Figure: The structure of cephalosporins.
Antibacterial Spectrum cont…
• The second-generation cephalosporins:
– have greater stability against β-lactamase inactivation
– possess a broader spectrum of activity to include grampositive cocci, gram-ve organisms, and anaerobes.
– Do not penetrate meninges
• The extended-spectrum, or third-generation, cephalosporins
– high degree of potency and β-lactamase stability
– broader spectrum of action against many common gram-ve
bacteria and anaerobes while retaining good activity
– Less active against staph. than the earlier generations.
– greatest activity against P. aeruginosa.
– Cross BBB (most agents)
Antibacterial Spectrum cont…
Summary of therapeutic
• Distribute in satisfactory concentrations to most tissues
except the CNS.
• Cefotaxime and ceftriaxone
– antibiotics of ﬁrst choice for the empirical treatment of
brain abscess and meningitis.
• Urinary excretion:
– the major elimination path for most cephalosporins.
– Dose adjustment in patients with renal failure.
• Biliary elimination is important for some cephalosporins.
– Cefoperazone, cefoxitin, and ceftriaxone.
Table: Pharmacokinetic Parameters of Selected Cephalosporins
Clinical Uses of Cephalosporins
• The ﬁrst-generation cephalosporins have activity against
most of the bacterial pathogens that colonize skin and infect
– useful in antimicrobial prophylaxis before surgery.
• Second-generation cephalosporins
– cefoxitin and cefotetan have good anaerobic activity,
• prophylaxis of lower abdominal and gynecological
• Third-generation cephalosporins
– broad spectrum, used in wide range of infections
• Lyme disease (Borrelia sp.), pneumonia, peritonitis,
and sepsis syndrome.
Adverse Effects of Cephalosporins
• The cephalosporins have good safety proﬁles.
• Hypersensitivity reactions.
• Local irritation: severe pain after IM injection and
thrombophlebitis after IV injection.
• Nephrotoxicity especially when used with aminoglycosides.
• Superinfections with Clostridium difﬁcile, enterococci,
MRSA, P. aeruginosa, and Candida albicans.
– inhibits production of active vitamin K.
– Antiplatelet effects.
Protein Synthesis Inhibitors
• Are divided into two groups: bacteriostatic and bactericidal.
– Chloramphenicol, Macrolides, and Tetracyclines are
– Aminoglycosides are bactericidal.
• Mechanisms of action: Inhibit protein synthesis by binding
at different sites of manufacturing process.
• Include: amikacin, gentamicin, kanamycin, netilmicin,
neomycin, streptomycin, paromomycin and tobramycin.
• Are absorbed very poorly from the intact GIT due to their
Streptomycin and amikacin
• effective in the treatment of tuberculosis.
• It is a synergistic companion with beta-lactam antibiotics,
– Pseudomonas, Proteus, Enterobacter, Klebsiella, Serratia,
and other gram-negative rods that may be resistant to a
multiple of other antibiotics.
– used concurrently with penicillin G for bactericidal
activity in endocarditis due to streptococci viridans.
• Creams, ointments or solutions of gentamicin sulfate are used
for the treatment of infected burns, wounds, or skin lesions.
• Very poorly absorbed when given orally.
• Is used in preparation for elective bowel surgery.
• In hepatic coma, it is used to suppress the coliform flora thus
reducing ammonia intoxication.
• Aminoglycosides cause ototoxicity and nephrotoxicity.
• Losses of balance, vertigo are common manifests of
• Include: tetracycline, chlortetracycline, oxytetracycline,
demeclocycline, methacycline, minocycline and doxycycline.
• All tetracyclines have a similar mechanism of action,
– But have different chemical structures.
• Structural analogues synthesized
– to improve pharmacokinetic properties and antimicrobial
• Are broad-spectrum antibiotics.
• Active against many gram-positive and gram-negative
bacteria, including: anaerobes; rickettsiae; active against
• Partially absorbed from the stomach and upper GI tract.
• Tetracyclines mainly differ in their absorption from GIT and
• Doxycycline is better absorbed than tetracycline.
• Absorption is impaired by preparations containing divalent
cations (Ca++, Mg++, Fe++ or Al+++).
• Cross the placenta to reach the fetus and is also excreted in
• Incompletely absorbed tetracyclines remaining in the
– may inhibit sensitive intestinal microorganisms and alter
the normal intestinal ﬂora.
• Penetrate the uninﬂamed meninges
• Doxycycline, minocycline, and chlortetracycline
– excreted primarily in the feces.
– best for elderly patients.
• The other tetracyclines
– eliminated primarily in the urine by glomerular ﬁltration.
• Little difference in clinical response among the various
• Their use restricted in pregnancy and in patients under the
age of 8 years
– longer half-life and
– lack of nephrotoxicity,
• choice for patients with preexisting renal disease or
those who are at risk for developing renal insufﬁciency.
• Lack of nephrotoxicity
– related mainly to biliary excretion.
Clinical Uses cont…
– ﬁrst-line agent in the prophylaxis of anthrax after
– choice for the primary stage of Lyme disease in adults and
children older than 8 years.
• Tetracyclines are still the drugs of choice for treatment:
– diseases caused by Rickettsia and Coxiella,
– relapsing fever,
– chlamydial diseases (trachoma, lymphogranuloma
– nonspeciﬁc urethritis.
• Oral admin. - nausea, vomiting, epigastric burning,
stomatitis, and glossitis
• IV injection- phlebitis.
• Staining of both the deciduous and permanent teeth and
retardation of bone growth can occur if tetracyclines are
administered after the fourth month of gestation or if they
are given to children less than 8 years of age.
– may result in oral, anogenital, and intestinal Candida
– Staphylococcus aureus or Clostridium difﬁcile
overgrowth may cause enterocolitis.
• Bacteriostatic, broad-spectrum antibiotic.
• Active against both aerobic and anaerobic gram-positive and
• Active also against rickettsiae.
• Haemophilus influenzae, N. meningitidis, and some strains of
Bacteroides are highly susceptible, and for them
chloramphenicol may be bactericidal.
– changed and unchanged drug excreted by urine.
– A small amount of active drug is excreted into bile or
• Inactivated in the liver by glucuronosyltransferase and is
rapidly excreted (80–90% of dose) in the urine.
Clinical Uses of Chloramphenicol
• Potentially fatal nature of chloramphenicol-induced bone
– restricts its use to a few life-threatening infections in
which the beneﬁts outweigh the risks.
• No longer recognized as the treatment of choice for any
• Since effective CSF levels are obtained,
– a choice for treatment of speciﬁc bacterial causes of
• Haemophilus inﬂuenzae, Neisseria meningitidis, and S.
• Effective against H. inﬂuenzae–related arthritis,
osteomyelitis, and epiglottitis.
Clinical Uses cont…
• A major treatment of typhoid and paratyphoid fever in
• Alternative to tetracycline for rickettsial diseases,
– especially in children younger than 8 years.
Gray baby syndrome:
• Newborn infants(less than a week old and premature infants)
cannot adequately conjugate chloramphenicol to form the
• High levels of free chloramphenicol may accumulate and
cause a potentially fatal toxic reaction.
• This syndrome is characterized by:
– abdominal distention, vomiting, flaccidity, hypothermia,
gray color, shock, and collapse.
• The mortality rate is high.
Bone marrow depression.
• The most publicized adverse affects.
• anemia, sometimes leukopenia or thrombocytopenia.
Drugs that inhibit bacterial synthesis of nucleic acids
• Quinolones: Nalidixic Acid and Fluoroquinolones.
• Rifamycins: Anti-TB drugs.
Quinolones: Nalidixic Acid and Fluoroquinolones.
• Synthetic fluorinated analogs of nalidixic acid.
• Block bacterial DNA synthesis by inhibiting bacterial
topoisomerase II (DNA gyrase) and topoisomerase IV.
• Inhibition of DNA gyrase,
– prevents the relaxation of positively supercoiled DNA that
is required for normal transcription and replication.
• Inhibition of topoisomerase IV
– interferes with separation of replicated chromosomal DNA
into the respective daughter cells during cell division.
• Bactericidal at therapeutic doses.
• The quinolones are now often classiﬁed into generations,
much like the cephalosporins (table below).
• Selectivity of action results from differences in structure b/n
the bacterial and eukaryotic forms of these enzymes.
The ﬁrst-generation and oldest quinolones
– exhibit limited gram-negative activity.
• Nalidixic acid and cinoxacin
– do not achieve systemic antibacterial levels.
– restricted to therapy of bladder infections caused by
urinary pathogens, such as E. coli, Klebsiella and Proteus
• Their use is restricted by resistance.
Gram -ve (including
Pseudomonas species), some
Gram+ve (S. aureus) and
Same as 2nd generation with
extended Gram+ and atypical
Same as 3rd generation with
broad anaerobic coverage
The second-generation drugs
• most reliable activity against gram-negative, including
• Haemophilus spp. and sexually transmitted disease agents,
such as Neisseria gonorrhoeae, Chlamydia trachomatis,
• Possess antipseudomonal activity.
Third and fourth generations,
• Greater activity against gram +ve, such as S. pneumoniae.
• MRSA and Enterococcus faecium are resistant.
• Also possess activity against anaerobes.
• Quinolones are rapidly and almost completely absorbed
• Half-life for most quinolones is 3 to 4 hours.
• Elimination through glomerular ﬁltration and tubular
• Moderate to severe renal insufﬁciency,
– quinolone dosages should be modiﬁed.
• Metabolized by hepatic conjugation and glucuronidation.
• All quinolones interact with multivalent cations,
– Form chelation complexes resulting in reduced
• Inhibit CYP1A2 (enoxacin, ciprofloxacin)
– elevated theophylline concentrations cause toxicity.
• Therapeutic uses of the quinolones include:
– urinary and respiratory tract infections,
– GI and abdominal infections, STDs, and
– bone, joint, and soft tissue infections.
• Nalidixic acid
– effective for urinary tract infections.
• In general, they are well tolerated.
• Most frequently reported side effects
– nausea, vomiting, diarrhea, and abdominal pain.
• CNS effects,
– drowsiness, weakness, headache, dizziness, and in severe
cases, convulsions and toxic psychosis.
• Sparﬂoxacin, moxiﬂoxacin
– can cause QT prolongations.
– Fulminant hepatotoxicity result in acute liver failure,
– Use limited to life-threatening infections.
• Damage growing cartilage and cause an arthropathy.
– Contraindicated in patients under 18 years of age.
• Sulfonamides are broad-spectrum antimicrobials
• effective against gram-positive and some gram-negative
organisms of the Enterobacteriaceae.
– E. coli, Klebsiella, Salmonella, Shigella.
• Not active against Pseudomonas aeruginosa and Serratia spp.
• Also effective against Chlamydia spp.
• Used in treating infections caused by Toxoplasma gondii and
occasionally chloroquine-resistant Plasmodium falciparum.
• Sulfonamides are usually given orally,
• Except for compounds designed for local gut effects, the
sulfonamides are rapidly absorbed from the intestinal tract,
primarily from the small intestine.
• pass the placental barrier and enter CSF even in the absence
• Readily distribute throughout body ﬂuids.
• Half-lives range from 2.5 to 17 hours.
• Metabolized by acetylation and oxidation (slow acetylators
are liable to toxicity).
• The parent compound and the metabolites are excreted in the
• Sulfonamides are infrequently used as single agents.
– meningococci, pneumococci, streptococci, staphylococci,
and gonococci, are now resistant.
• The fixed-drug combination of Trimethoprim–
– the drug of choice for infections such as Pneumocystis
jiroveci pneumonia, toxoplasmosis, nocardiosis,
genitourinary, GI, and respiratory tract infections caused
by susceptible bacteria.
• Current indications are more limited,
– especially to the treatment of urinary tract and ear
infections, because of frequently encountered resistance
and the availability of better and safer agents.
Clinical Uses cont…
• Sulfadiazine, in combination with pyrimethamine,
– Treatment choice for symptomatic toxoplasmosis.
– Patients should be well hydrated to prevent crystalluria.
• Topically active sulfonamides are useful in preventing
infections in burn patients.
Adverse Effects and Drug Interactions
• At high concentrations,
– the free drug or its metabolites may form crystals and
cause bleeding or complete obstruction of the kidneys.
• Hypersensitivity reactions (e.g., rashes, eosinophilia, and
• Other rare allergic reactions include,
– Vasculitis, photosensitivity, agranulocytosis, and
thrombocytopenia, hemolytic or aplastic anemia.
• Stevens-Johnson syndrome
– fever, malaise, erythema multiforme, and ulceration of the
mucous membranes of the mouth and genitalia.
Adverse Effects and Drug Interactions cont…
• Sulfonamides compete for sites on plasma proteins that are
responsible for the binding of bilirubin.
– less bilirubin is bound, and
– in the newborn the unbound bilirubin can be deposited in
the basal ganglia and subthalamic nuclei,
• causing kernicterus, a toxic encephalopathy.
– Should not be given to newborns or to women during the
last 2 months of pregnancy.
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