Antibiotics

MUTHANNA
ALLAMI
G.S.M
MEDICAL EDUCATION
BILAL
HUSSEIN
DR HARITH ALAWADI LECTURES

G.S.M MEDICAL LECTURES /ANTIBIOTICS DR HARITH ALAWADI
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G.S.M
MEDICAL EDUCATION
Antimicrobial or antibiotics
There are the following antibiotic groups according to the
mechanism of action

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1-cell wall synthesis inhibitors: they can be
-Peptidoglycans synthesis inhibitors: they are Glycopeptides
(vancomycin, bacitracin)
-Peptidoglycan-cross-linking inhibitors: they include
1-Penicillinase-sensitive penicillin’s: penicillin G,V and ampicillin,
amoxicillin
2-Penicillinase-resistant penicillin’s: oxacillin, nafcillin,
dicloxacillin
3-Antipseudomonals: ticarcillin and piperacillin
4-Cephalosporins(I-V):1st
-cefazolin, 2nd
-cefoxitin, 3rd
-ceftriaxon,
4th
-cefepime, 5th
-ceftaroline
5-Carbapenems: imipenem, meropenem, ertapenem,
doripenem.

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6-Monobactams: aztreonam
2-cell membrane destruction: by daptomycin and Amphotericin
B etc.
3-folic acid synthesis and reduction: in the cells, there is PABA
(para aminobenzoic acid), which is very important for the
formation of DHF (dihydrofolic acid) and then THF
(tetrahydrofolic acid) and those are important for DNA synthesis
*The formation of DHF can be blocked by Sulfonamides which
include (sulfamethoxazole, sulfisoxazole, sulfadiazine)
*The formation of THF can be blocked by: Trimethoprim
4-DNA integrity: can be destroyed by Metronidazole
5-mRNA synthesis (RNA polymerase) can be blocked by
Rifampin

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6-DNA gyrase: it’s important to cuts the DNA strands while dna
replications it can be blocked by
-Fluoroquinolones: ciprofloxacin, levofloxacin
-Quinolone: nalidixic acid
7-protein synthesis can be blocked by 2 ways:
-50S subunits inhibitors which include:
*chloramphenicol, clindamycin, linezolid
*Macrolides: azithromycin, clarithromycin, erythromycin
*Streptogramins: quinupristin, dalfopristin
-30S subunits inhibitors which include:
*Aminoglycosides: gentamicin, neomycin, amikacin,
tobramycin, streptomycin

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*Tetracyclines: tetracycline, doxycycline, minocycline
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How to select the prober antibiotic?
1-you should be able to recognize the source of infection
2-you should be able to know the site of infection
3-select the safest drug according to the patient situation
4-you should carefully know the history of the patient to
prevent anaphylaxis (opposite reaction of the body against the
drug) by asking or testing about history of allergy
5-you should know the situation of kidney and liver, if a woman,
you have to know if she is a pregnant or not and you should ask
about the history of recent operations
*Prophylaxis drug: a drug which is given to people who have a
close contact with patients will infectious disease such as TB.

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*Drug resistance: when the drug isn’t affective against the
particular microorganism, such as in case of beta-lactamase
which is produced by that microorganism and it cleaves the
beta-lactam drugs, so they are called resistant bacteria

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-Bactericidal drugs: they kill the bacteria directly and include:
1-aminoglycosides, 2-penicillins, 3-cyclosporine, 4-vancomycin,
5-fluroquinolones, 6-carbapenems, 7-cephalosporines
*they are mostly cell wall synthesis inhibitors
-Bacteriostatic drugs: they slow the growth or the reproduction
of the bacteria and include:
1-chloramphenicol, 2-riferantoin, 3-clindamycin, 4-tetracycline,
5-erythromycin, 6-trimethoprine, 7-lincomycin
*they are mostly protein synthesis inhibitors

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β lactams
β. lactams contain 7 groups, 5 are penicillin groups, the difference
between them is in the R group of their chemical structure.
- penicillin groups:
1- Natural penicillin: penicillin G (IM, IV) and penicillin V(oral)
- Mechanism: block transpeptidase (which connects the peptides of
peptidoglycans, they are called (D-ala D-ala).
- These drugs make pore in the wall of the bacteria, then it activates
autolytic enzymes.
- Clinical use: gram+ (streptococcus pyogens, streptococcus
pneumonia, actinomyoces)
Gram – cocci (N. meningitides), spirochetes (T. pallidum)
- Adverse effects: hypersensitivity1, direct coomb’s + hemolytic
anemia

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- Resistance mechanism: penicillinase in bacteria (an enzyme that
destroy the beta lactam ring in penicillin)
*jarisch-herxheimer reaction allergic reaction appears in syphilis
patients after treating with penicillin G (flue like symptoms such as
headache, fever, myalgia) due to killed bacteria because some
killed bacteria have toxins in their wall.
2- penicillinase sensitive penicillin:
Aminopenicillins (amoxicillin and ampicillin)
- Mechanism: same as penicillin, wider spectrum, penicillinase
sensitive. Also combine with clavulanic acid to protect against
destruction by β-lacatamase.
- Clinical use: extended spectrum penicillin. H. influenza, H. pylori, E.
coli, listeria monocytogenes, proteus mirabilis, salmonella,
shigella, enterococci.

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*aminopenicillins HHELPSS to kill Enterococci used as mnemonic
for the bacteria that is treated by this antibiotic.
- Adverse effects: hypersensitivity reaction, rash,
pseudomembranous colitis.
- Mechanism of resistance: penicillinase in bacteria cleaves beta
lactam ring.
*beta lactamase inhibitors: clavulanic acid, sulbactam,
tazobactam
*combinations: Augmentin= amoxicillin + clavulanic acid
Unasyn= ampicillin + sulbactam

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3- penicillinase resistant penicillin
Anti-staphylococcus aureus. Dicloxacillin, nafcillin, oxacillin,
methicillin) *NAF to kill STAPH
- Mechanism: same as penicillin narrow spectrum,
penicillinase resistant because of bulky R group block
access of beta lactamase to beta lactam ring.
- Clinical use: staph. Aureus except (MRSA resistant because
of altered penicillin binding protein target site)
- Adverse effects: hypersensitivity reaction, interstitial
nephritis

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Antipseudomonal penicillin’s:
Piperacillin, ticarcillin
Mechanism: same as penicillin, extended spectrum.
Clinical use: pseudomonas spp. And gram – rods, susceptible to
penicillinase, use with beta lactamase inhibitors.
Adverse effects: hypersensitivity reaction.
*combination: timentin = ticarcillin + clavulanic acid
Zosyn = piperacillin + tazobactam

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Beta lactamase inhibitors:
Include Clavulanic Acid, Sulbactam, Tazobactam.
*often added to penicillin antibiotics to protect the antibiotic
from destruction by beta lactamase (penicillinase)
*mnemonic CAST
Cephalosporins(I-V)
Mechanism: beta-lactam. Inhibit cell wall synthesis, but less
susceptible to penicillinase.
-I generation: cefazolin, cefalexin
*for Gram (+) cocci, proteus, E. coli, K. pneumoniae
*given pre-surgical to prevent staph. Aureus wound infections
-II generation: cofactor, cefoxitin, cefuroxime

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*for Gram (+) cocci, H.influnzae, Enterobacter aerogenes,
Neisseria spp., Serratia macescens, proteus, E. coli,
K.pneumonia
-III generation: ceftriaxone, cefotaxime, ceftazidime
*for serious Gram (-) bacteria resistant to other beta-lactams
-IV generation: cefepime
*for Gram (-) with high activity to pseudomonas
Note: all those 4 generations can’t treat LAME {Listeria, Atypical
(mycoplasma, Chlamydia), MRSA, Enterococcus}
-V generation: ceftroline
*broad spectrum {Gram(+),Gram(-)including MRSA}, but it
doesn’t treat pseudomonas
-Adverse effects: hypersensitivity 1, autoimmune hemolytic
anemia, disulfiram like reaction, vitamin k deficiency,

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nephrotoxicity with aminoglycosides, exhibit penicillin cross
reactivity: it means, if the patient is sensitive to penicillin, he or
she is also sensitive to cephalosporins
-high penicillin sensitivity: don’t give the drug
-low penicillin sensitivity: you can give the drug
*resistance of bacteria: the bacteria make transpeptidase with
different structure, so the cephalosporins can’t recognize it and
the bacteria become resistant
Carbapenems
They include imipenem, meropenem, ertapenem, doripenem
-mechanism: Imipenem is a broad spectrum, beta-lactamase
resistant carbapenem. Always administered with Cilastatin

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(inhibitor of renal dehydropeptidase I) to lower the inactivation
of drug in renal tubules
-clinical use: Gram (+) cocci, Gram (-) rods and anaerobic. Wide
spectrum but significant side effects limit use to life threatening
infections of after drugs have failed.
*meropenem has low risk of seizures and is stable to
dehydropeptidase I.
-adverse effect: GI distress, and CNS toxicity(seizures)at high
plasma levels
Note: ertapenem+doripenem are limited pseudomonas
coverage.

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Monobactam
They include 1 drug Aztreonam
-mechanism: less susceptible to beta-lactams
Prevents peptidoglycan cross linking by binding to
penicillin-binding protein 3.
Synergistic with aminoglycosides.
No cross allergenicity with penicillin
-clinical use: Gram (-) rods only. No activity against Gram (+)
rods or anaerobes
*for penicillin allergic patients and those with renal
insufficiency who can’t tolerate aminoglycosides.
-adverse effects: usually nontoxic, occasional GI upset.

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Vancomycin
-mechanism: inhibits cell wall peptidoglycan formation by
binding D-ala D-ala protein of cell wall precursors.
*bactericidal against most of bacteria, (bacteriostatic against C.
difficile)
-clinical use: Gram (+) bugs only-serious, multidrug resistant
organisms including MRSA, S. epidermidis, sensitive
enterococcus species, and clostridium difficile(oral dose for
pseudomembranous colitis)
-adverse effects: well tolerated in general, but not trouble free,
nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing-
red man syndrome (can largely prevented by pretreatment with
antihistamines and slow infusion rate)
-mechanism of resistance: occurs in bacteria through acid
modification of D-ala D-ala to D-ala D-alc” pay back 2D-

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alas(dollars)for Vandalizing (Vancomycin)”
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Protein synthesis

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The process starts by transcription to form mRNA, which is the base for
ribosomes, the 30S and 50S attach to it and also the initiator
tRNA(which contain an amino acid as a base for the attachment of A,P
and E), then the initiation complex formation starts by entering of tRNA
through A, then the new amino acid attach to the already founded on P
, by peptidyl transferase then the empty tRNA moves to E and goes out
of the machinery by translocation process then the process is repeated
by entrance of a new tRNA containing a new amino acid and so on...
• The attachment of 50S can be blocked by linezolid (bacteriostatic)
• The initiation complex formation can be blocked by
aminoglycosides. 30S = bactericidal
• The peptidyl transferase can be blocked by chloramphenicol (50S)
bacteriostatic

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• The translocation can be blocked by macrolides 50S and
clindamycin 50S= bacteriostatic
• The A site tRNA binding (the repetition of the process) van be
blocked by tetracycline 30S= bacteriostatic
Aminoglycosides
They include: gentamicin, neomycin, amikacin, tobramycin,
streptomycin.
-mechanism: bactericidal, irreversible inhibition of initiation
complex through binding of 30S subunit. Can cause misreading
of mRNA. Also block translocation. Require O2 for uptake,
therefore ineffective against anaerobes.
-clinical use: severe Gram (-) rod infections. Synergistic with
beta-lactam antibiotics(monobactams).
*neomycin is used for bowel surgery.

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-adverse effect: nephrotoxicity, neuromuscular blockade,
ototoxicity {especially when used with loop diuretics
(furosemide, torsemide)}, teratogen.
-mechanism of resistance: bacterial transferase inactivates the
drug by acetylation, phosphorylation or adenylation
Tetracyclines
Tetracycline, doxycycline, minocycline
-mechanism: Bacteriostatic, bind to 30S and prevent
attachment of aminoacyl-tRNA. Limited CAN penetration.
Doxycycline is eliminated with feces and can be used in renal
failure. Do not take tetracycline with milk (Ca+2), antacids
(Ca+2, Mg+2) or iron- containing preparations because divalent
contains inhibit drug absorption in the gut.

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-clinical use: borrelia burgdorferi, M. pneumonia, drug’s ability
to accumulate intracellularly makes them very effective against
rickettsia and Chlamydia. Also used to treat acne
-adverse effects: GI distress, discoloration of the teeth and
inhibition of bone growth in children, photosensitivity
*contraindicated in pregnancy
-mechanism of resistance: decrease uptake or increase efflux
out of bacterial cells by plasmid-encoded transport pumps.

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Chloramphenicol
-mechanism: block peptidyl transferase at 50S ribosomal
subunit. Bacteriostatic
-clinical use: meningitis (H. influnzae, Neisseria meningitides,
strept. pneumonia), rocky mountain spotted fever(rickettsia
rickettsia). Limited use owing but often still used in developing
countries because of low cost.
-adverse effect: anemia (dose dependent), aplastic anemia
(dose dependent), gray baby syndrome (in premature infants
because of lack liver UDP-glucaronyl transferase)
-mechanism of resistance: plasmid encoded acetyl transferase
inactivates the drug.

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Clindamycin
-mechanism: block peptide transfer(translocation) at 50S
ribosomal subunit. Bacteriostatic
-clinical use: anaerobic infections (Bacteroides ssp., clostridium
perfringens) in aspiration pneumonia, lung abscesses and oral
infections. Also effective against group A streptococcal
infection.
-Adverse effects: pseudomembranous colitis (C.difficile
overgrowth), fever, diarrhea.

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Oxazolidinones
Linezolid
-mechanism: inhibit protein synthesis by binding to 50s subunit
and preventing formation of the initiation complex.
-clinical use: gram (+) species including MRSA (Methicillin
Resistant Staphylococcus Aureus and VRE (Vancomycin
Resistant Enterococcus).
-Adverse effects: bone marrow suppression (especially
thrombocytopenia), peripheral neuropathy, serotonin
syndrome.
-mechanism of resistance: point mutation of ribosomal RNA

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Macrolides
Azithromycin, clarithromycin, erythromycin
-mechanism: inhibit protein synthesis by blocking translocation
(“MACRO slides”) bind to the 23s rRNA of the 50s ribosomal
subunit. Bacteriostatic
-clinical use: atypical pneumonia (mycoplasma, Chlamydia,
legionella), STIs (Chlamydia), Gram (+) cocci (streptococcal
infection in patients allergic to penicillin) and B. pertussis.
-adverse effect: MACRO, GI Motility issues, Arrhythmia caused
by prolonged QT interval, acute Cholestatic hepatitis, Rash,
eosinophilia, increase serum concentration of theophylline, oral
anticoagulants
*clarithromycin erythromycin inhibits cytochrome p.450
-mechanism of resistance: methylation of 23s rRNA-binding site
binding of the drug.

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YOUR NOTES:
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Folic acid synthesis in bacteria

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1-The process start with PABA (para aminobenzoic acid)
+pteridine is converted into dihydropteroic acid by
dihydropteroate synthase (can be blocked by sulfonamide and
dapsone)
2-Then the dihydropteroic acid is converted into dihydrofolic
acid
3-dihydrofolic acid is converted into tetrahydrofolic acid by
dihydrofolate reductase (can be blocked by trimethoprim and
pyrimethamine)
4-tetrahydrofolic acid will give: purines (DNA, RNA), thymidine
(DNA), methionine(protein)
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Sulfonamides
Sulfamethoxazole (SMX), sulfisoxazole, sulfdiazine
-mechanism: inhibit dihydropteroate synthase, thus inhibiting
folate synthesis.
Bacteriostatic (bactericidal when combine with
trimethoprim)
-clinical use: gram (+), gram (-), nocardia, Chlamydia
SMX: for simple UTI
-adverse effects: hypersensitivity, hemolysis if G6PD deficient,
nephrotoxicity (tubulointerstitial nephritis), photosensitivity,
kernicterus in infants, displace other drugs from
albumin(warfarin).

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-mechanism of resistance: altered enzyme (bacterial
dihydropteroate synthase), decrease uptake or increase PABA
synthesis.
YOUR
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Dapsone
Mechanism: similar to sulfonamides, but structurally distinct
agent
Clinical use: leprosy (lepromatous and tuberculoid),
pneumocystis jirovecii.

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Adverse effects: hemolysis if G6PD is deficient.
Trimethoprim
-mechanism: inhibit bacterial dihydrofolate reductase.
Bacteriostatic
-clinical use: used in combination with
sulfonamides(trimethoprime+sulfamethoxazole) =(TMP-SMX).
Causing sequential block of folate synthesis
*combination used for UTIs, shigella, salmonella, pnemocytis
jiroveci pneumonia treatment and prophylaxis, toxoplasmosis
prophylaxis.
-adverse effects: megaloblastic anemia, leukopenia,
granulocytopenia (may alleviate with supplemental folic acid).
*TMP: Treat Marrow Poorly

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Fluoroquinolones
Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin,
Gemifloxacin, enoxacin
Mechanism: inhibit prokaryotic enzymes topoisomerase II (DNA
gyrase) and topoisomerase IV. Bactericidal. Must not be taken
with antacids.
Clinical use: gram – rods of urinary and GI tracts (including
pseudomonas), Neisseria, some gram + organisms.
Adverse effects: GI upset, super infections, skin rashes,
headache, dizziness, less commonly can cause leg cramps. And
myalgias. Contraindicated in pregnant woman, nursing mothers

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and children less than 18 years old due to possible damage to
cartilage. Some may prolong QT interval. May cause tendonitis
or tendon rupture in people more than 60 years old and in
patients taking prednisone.
Mechanism of resistance: chromosome encoded mutation in
DNA gyrase. Plasmid mediated resistance efflux pumps.
YOUR
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Daptomycin
Mechanism: lipopeptide that disrupts cell membrane of gram +
cocci
Clinical use: S. aureus skin infections (especially MRSA),
bacteremia, endocarditis, VRE.
*not used for pneumonia (avidly binds to and is surfactant)
Adverse effects: myopathy, rhabdomyolysis

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Metronidazole
mechanism: forms toxic free radical metabolites in the bacterial
cell that damage DNA. Bactericidal, anti-protozoal
Clinical use: treats giardia, Entamoeba, trichomonas,
Gardnerella vaginalis, anaerobes (Bacteroides, C difficile). Used
with proton pump inhibitor and clarithromycin for triple therapy
against H. pylori.
Adverse effects: disulfiram-like reaction (severe flushing,
tachycardia, hypotension) with alcohol, headache, metallic
taste.

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MEDICAL EDUCATION
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LECTURES
49
G.S.M
MEDICAL EDUCATION
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LECTURES
50
G.S.M
MEDICAL EDUCATION
Antimycobacterial drugs
*in general the mycobacteria contain in the cell wall mycolic
acid (can be blocked by isoniazid) and arabinogalactan which is
the precursor for the formation of mycolic acid(can be inhibited
by ethambutol)and inside the cell, the RNA polymerase which is
important in RNA polymerization is blocked by(rifambutin or
rifampin)and there is also pyrazinamide which has unclear
mechanism.
bacterium prophylaxis Treatment
M.tuberculosis isoniazid Rifampin, Isoniasid,
Pyrazinamide, Ethambutol
(RIPE for treatment)
M.avium-
intracellulare
Azithromycin,
rifabutin
More drug resistance than
M. tuberculosis
Azithromycin or
clarithromycin+ethambutaol

LECTURES
51
G.S.M
MEDICAL EDUCATION
can add rifabutin or
ciprofloxacin
M.leprae NA Long term treatment with
dapsone and rifampin for
tuberculoid form. Add
clofazimine for lepromatous
form.
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LECTURES
52
G.S.M
MEDICAL EDUCATION
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Rifamycin
Rifampin, rifabutin

LECTURES
53
G.S.M
MEDICAL EDUCATION
-mechanism: inhibit DNA-dependent RNA polymerase
-clinical use: M. tuberculosis, delay resistance to dapsone when
used for meningococcal prophylaxis and chemoprophylaxis in
contact of children with H. influnzae type B
-adverse effects: minor hepatotoxicity and drug interaction
(increases cytochrome P-450). orange body fluids (non-
hazardous side effect).rifabutin is favored over rifampin in
patients with HIV infection due to less cytochrome P-450
stimulation.
-mechanism of resistance: mutations reduce drug binding to
RNA polymerase. Monotherapy rapidly leads to resistance.
Pyrazinamide

LECTURES
54
G.S.M
MEDICAL EDUCATION
-mechanism: uncertain mechanism, it is a prodrug. That is
converted to the active compound pyrazinoic acid. Works best
in acidic PH (in host phagolysosomes)
-clinical use: M. tuberculosis
-adverse effect: hyperuricemia, hepatotoxicity
Ethambutol
-mechanism: decrease carbohydrate polymerization of
mycobacterium cell wall blocking arabinosyl transferase
-clinical use: M. tuberculosis
-adverse effects: Optic neuropathy (red-green color blindness).”
pronounce a eyethembutal”.
Streptomycin
-mechanism: interferes with 30S component of ribosome

LECTURES
55
G.S.M
MEDICAL EDUCATION
-clinical use: M. tuberculosis (2nd
line)
-adverse effects: tinnitus, vertigo, ataxia, nephrotoxicity
Isoniazid(B6)
-mechanism: decrease synthesis of mycolic acid. Bacterial
catalase-peroxidase (encoded by KatG) needed to convert INH
(IsoNicotinoyl Hydrazide) to active metabolite.
-clinical use: M. tuberculosis. The only agent used as solo
prophylaxis against TB. Also used as monotherapy for latent TB.
-adverse effects: hepatotoxicity, P-450 inhibition, drug induced
SLE (systemic lupus erythromatous), vitamin B6 deficiency
(peripheral neurotherapy, sideroblastic anemia) administers
with pyridoxine(B6).
-mechanism of resistance: mutations leading to under
expression of KatG.

LECTURES
56
G.S.M
MEDICAL EDUCATION
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LECTURES
57
G.S.M
MEDICAL EDUCATION
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Antimicrobial prophylaxis:

LECTURES
58
G.S.M
MEDICAL EDUCATION
Prophylaxis in HIV patients:
Clinical scenario medication
High risk for endocarditis and undergoing
surgical or dental procedures
Amoxicillin
Exposure to gonorrhea Ceftriaxone
History of recurrent UTIs TMP-SMX
Exposure to meningococcal infection Ceftriaxone, ciprofloxacin or
rifampin
Pregnant woman carrying group B strep. Intrapartum penicillin G or ampicillin
Prevention of gonococcal conjunctivitis in
newborn
Erythromycin ointment on eye
Prevention of post surgical infections due
to S. aureus
cefazolin
Prophylaxis of strep pharyngitis in
children with prior rheumatic fever
Benzathine penicillin G or oral
penicillin V
exposure to syphilis Benzathine penicillin G

LECTURES
59
G.S.M
MEDICAL EDUCATION
Cell count Prophylaxis Infection
CD4less than 200 cells/mm3 TMP-SMX Pneumocysitis
pneumonia
CD4 less than 100 cells/mm3 TMP-SMX Pneumocysitis
pneumonia and
toxoplasmosis
CD4 less than 50 cells/mm3 Azithromycin or
clarithromycin
Mycobacterium avium
complex
Treatment of highly resistant bacteria:
MRSA: vancomycin, daptomycin, linezolid, tigecycline,
ceftaroline.
VRE: linezolid and streptogramins (quinupristin, dalfopristin).
*multi drug resistance P. aeruginosa multi drug resistance
Acinetobacter baumanii. Polymyxins B and E (colistin).

LECTURES
60
G.S.M
MEDICAL EDUCATION
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LECTURES
61
G.S.M
MEDICAL EDUCATION
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LECTURES
62
G.S.M
MEDICAL EDUCATION
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LECTURES
63
G.S.M
MEDICAL EDUCATION
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LECTURES
64
G.S.M
MEDICAL EDUCATION
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