NON-SPECIFIC ANTIMICROBIAL AGENTS  Carbapenems and Drug affecting

protein synthesis or DNA

DRUG RESISTANCE synthesis have long PAE against
Single Step Mutation – Streptomycin and Rifampicin G- bacteria.
Multi Step Mutation- Erythromycin, Tetracyclin and  Rifampicin prolongs the PAE of
Chloramphenicol Isoniazid
Drug Resistance can be transferred by:
FACTORS AFFECTING THE CHOICE OF AN
1. Conjugation ANTIMICROBIAL AGENT
 Contact between bacteria
 MULTIDRUG RESISTANCE 1. AGE
chloramphenicol and streptomycin  Chloramphenicol Gray Baby
2. Transduction Syndrome
 Transfer via bacteriophage  Sulfonamides Kernicterus in NB
 Penicillin, Erythromycin and  ½ Life of Aminoglycosides are
Chloramphenicol prolonged in the elderly
 Exhibited by S. aureus  Tetracyclines accumulate in the teeth
3. Transformation and bones of children
 Transfer through environment 2. PREGNANCY
 Exhibited by Pneumococci and Neisseria  Penicillins , most cephalosporins and
Macrolides appear safe
MECHANISM OF RESISTANCE 3. IMPAIRED HOST DEFENSES
 Bactericidal drugs are a must in
 Decreased affinity for the target immunocompromised patients
o Altered PBPs 4. RENAL FUNCTION
 Development of Alternative Metabolic Pathway Contrainidcated In Dose Reduction Safe
o Resistance to Sulfonamides due to the use Renal Disease is Necessary
Cephalotin Aminoglycosides Penicillin
of preformed folic acid instead of
Cephaloridine AMB Rifampicin
synthesizing it from PABA Nitrofurantoin Vancomycin
 Enzymes which Inactivate the drug Nalidixic Acid Ethambutol
o Aminoglycosides- Aminoglycoside Tetracyclines
(EXCEPT Doxycycline
Inactivating Enzymes
o Beta Lactams- B-Lactamases
5. LIVER FUNCTION
o Chloramphenicol- Chloramphenicol Acetyl
Contraindicated Dose Reduction Required
Transferase Erythromycin Estolate Chloramphenicol
 Decreased drug permeability due to loss of Tetracyclines Isoniazid
specific channels Pyrazinamide Rifampicin
Pefloxacin Clindamycin
o Aminoglycosides and Tetracycline
 Development of Efflux pumps
o Tetracyclines, Erythromycin and
Fluoroquinolones
6. GENETICS
SUPERINFECTION  Hemolysis in G6PD Deficient Patients:
 Primaquine
 Appearance of a new infection as a result of  Chloroquine
antimicrobial therapy (Broad Spectrum  Quinine
Antibiotics)  Chloramphenicol
 Commonly seen in Immunocompromised  Nitrofurantoin
patients  Fluoroquinones
o Oropharynx  Dapsone
o Respiratory Tract  Sulfonamides
o GU Tract
 Organisims involved: Antimicrobials Secreted in Bile
o C.albicans Penicillins (Ampicillin, Nafcillin)
o C. difficile Pseudomembranos Colitis Cephalosporins (Ceftriaxone, Cefoperazone)
(most commonly due to 3td Generation Doxyxline
Cephalosporins); DOC: Metronidazole Rifampicin
o Staphylococci Erythromycin
o Proteus
o Pseudomonas CLASIIFICATION OF ANTIBIOTICS ACCORDING TO
 CDK VS. TDK TYPE OF ACTION AND MECHANISM OF ACTION
o CDK (Conscentration Dependent Killing BACTERIOSTATIC BACTERICIDAL
 Aminoglycosides and Protein Synthesis Inhibitors Protein Synthesis Inhibitors
 Tetracyclines  Aminoglycosides
Fluoroquinolones
 Tigecycline  Streptogramins
 SINGLE LARGE DOSE  Chloramphenicol
o TDK (Time Dependent Killing)  Macrolides
 B-Lactams and Macrolides  Lincosamides
 Multiple dosage are required  Linezolid
Drugs Affecting DNA Drugs Affecting DNA
o PAE
 Nitrofurantoin  Quinolones
 Most antimicrobilas have long  Novobiocin  Metronidazsole
PAE against G+ bacteria Drugs Affecting Metabolism Drugs Affecting Cell Membrane
  Sulfonamides
 Dapsone
 PAS
 Trimethoprim
 Ethambutol
Protein Synthesis Inhibitors
Polypeptide Antibiotics 1. DNA Gyrase (Eukaryotes)- Nicks the double
 Polymixin B stranded DNA, Intoduces negative
 Colistin

supercoils and Reseasl the ends; in G+
AMB
Cell Wall Synthesis Inhibitors Bacteria Topoisomerase IV
 Fosfomycin- 2. Quinolones (Nalidixic acid and
Enolpyruvate Fluoroquinolones) and Novobiocin
Transferase
B. RNA POLYMERASE INHIBITORS
 Cycloserine- Alanine
Racemase and 1. Rifampicin- inhibits DNA Dependent RNA
Alanine Ligase Polymerase
 Bacitracin- C. NUCLOETIDE/NUCLEOSIDE ANALOGUES
Dephosphorylation 1. Formation of faulty nucleic acids
of Bactoprenol
 Vancomycin-
2. Idoxuridine, Acyclovir, NRTI
Transglycosylase D. DRUGS AFFECTING INTERMEDIARY
 Penicillins- METABOLISM
Transpeptidase 1. Drugs Inhibiting Folic Acid Synthesis
 Cephalosporins-
Sulfonamides, Dapsone and PAS acts as
Transpeptidase
First Line ATT Drugs (EXCEPT competitive inhibitors of Folic Acid Synthase
Ethambutol) 2. DHFRase Inhibitors
 INH  Trimethoprim, Pyrimethanamine, Proguanil
 Rifampicin and Methotrexate
 Pyrazinamide
3. Arabinogalactan Syntheis Inhibitor
 Streptomycin
 Ethambutol
BETA-LACTAMS
-All are BACTERICIDAL
-Inhibit Transpeptidase

1. PENICILLIN
 NOT ORALLY EFFECTIVE broken down by
gastric acid
 ACID RESISTANT PENICILLINS (VODKA)
Drug Binds To MOA 1. V- penicillin V
Aminoglycosides 30s and 50s  Freezing of
2. O- Oxacillin
Initiation
 Interference 3. D-Dicloxacilin
with 4. K- Cloxacillin
Polysome 5. A- Amoxicillin and Ampicillin
Formation  Short duration of action due to rapid excretion
 Misreading
of mRNA
from kidney Prevented by adding Probenicid,
code Benzathine or Procaine
 Narrow spectrum G+ ONLY
 New Penicillins with Extended Spectrum
Tetracyclines 30s  Inhibit
Glycylcyclines aminoacyl-
1. Aminopenicillin
tRNA a. Ampicillin
attachment b. Amoxicillin
to A site 2. Carboxypenicillins
Chloramphenicol 50s  Inhibits
a. Carbenicillin
peptidyl
transferase b. Ticarcillin
which 3. Ureidopenicillins
results in a. Mexlocillin
inhibition of
b. Azlocillin
peptide
bond c. Piperacillin
formation  Mnemonic A CT MAP
Macrolides 502s  Inhibits  All are effective against G- like E.coli,
Lincosamides trans-
Streptogramins
Salmonella, Shigella (EXCEPT Amox)
location of
peptide  CT MAP- effective against Pseudomonas
chain from  MAP- effective against Klebsiella
A site to P  Problem of Resistance
site
Linezolid 23s of 50s  Inhibits
 PENICILLINASE RESISTANT PENICILLINS
Initiation a. Cloxacillin
** All drugs inhibiting protein synthesis are b. Oxacillin
bacteriostatic EXCEPT aminoglycosides and c. Nafcillin
Streptogramins d. Dicloxacillin
** PUROMYCIN- inhibits protein synthesis in both e. Methicillin
prokaryotes and eukaryotes ; causes premature
chain termination  Can cause HYPERSENSITIVITY REACTION Most
common cause of Drug Induced Anaphylaxis
DRUGS AFFECTING NUCLEIC ACIDS  Only MONOBACTAM can be administered if
patient has allergy with Penicillin
A. DNA GYRASE INHIBITORS  Pharmacokinetics:
  Ampicillin and Nafcillin are excreted partly 4th Generation
by bile
 Clinical Use  Not active against Anaerobes
 DOC for Syphilis- Pen G
5th Generation
 DOC for Neurosyphilis- Aqueous Penicillin
 DOC for Listeria- Ampicillin  Treatment for CAP and MRSA Infections
 Toxicity o Ceftobiprole is also effective against MRSA
 Hypersensitivity and Pseudomonas
 Ampicillin should be avoided inpatients with
viral illness particularly EBV because it can TOXICITY
cause rashes
 Methicillin- interstitial Nephritis  Hypersensitivity Reactions
 Ampicilin- diarrhes  Cefamandole, Cefoperazone, Moxalactam and
 Procaine Penicillin- Seizures and CNS Cefotetan Hypoprothrombinemia and
abnormalities Disulfram like Reaction
 Oxacilin- Hepatitis  Ceftazidime  Neutropenia
 Nafcillin- Neutropenia
EXTRAS:
 Carbenicillin- high doses can result to
bleeding  Cefotaxime and Ceftriaxone are the most active
cephalosporin against Penicillin Resistant
2. CEPHALOSPORIN Pneumococci
 Has 7 aminocephalosporanic acid nucleus  TOC for Pseudomonas: Ceftazidime
 Pharmacokinetics +Aminoglycoside
 Most are excreted via kidney through
TUBULAR SECRETION 3. MONOBACTAM
 Ceftriaxone and Cefoperazone are secreted  Aztreonam
in the bile  Active against G- Rods ONLY
 Nephrotoxicity is increased with loop  ONLY beta lactam that can beused in patient
diuretics sith severe allergy to penicillins
Gen Organism Remarks
4. CARBAPENEMS
1st G+ (Strep and Staph) Not active against
Penicillin Resistant  Imipenem, Doripenem, Meropenem,
Strain Ertapenem
2nd G- ONLY Cefoxitin,  DOC for Enterobacter, Klebsiella and
Cefmetazole and Acinetobacter
Cefotetan are
effective against  ONLY B-lactams which are reliably efficacious
Bacteriodes against EBSL Producing organism
3rd G+ Bacteria ONLY ceftazidime o Meropenem- Most Active
G- Cocci and Cefoperazone o Ertapenem- Least Active and Inactive
(Gonococci) are effective against
Pseudomonas
against Pseudomonas
G- Bacilli Enterbobacteriaceae, Activity against o Imipenem- rapidly inactivated by RENAL
Serratia Pseudomonas bacteriodes is less DEHYDROPEPTIDASE I, overrided by
than cefoxitin CISLATIN which also inhibits the formation
Anaerobes
(Bacteriodes)
of nepohrotoxic metabolites
4th Same as 3rd More resistant to B-  AE: Seizures and GI Distress
lactamases
1st Generation Cephalosporin VANCOMYCIN AND GLYCOPEPTIDES

 Cefazolin the the DOC for Surgical Prophylaxis  BACTERICIDAL; excreted UNCHANGED in the
urine
2nd Generation Cephalosporin  Inhibits Transglycosylase Enzyme (Inhibits chain
elongation)
 Extended gram _ coverage  DOC for:
 Cefuroxime attains higher CSF levels as o MRSA
compared to other 2nd Generation o C.jeikeium
o Serious Infection in Penicillin allergic
3rd Generation patients
 Toxicity: RED MAN SYNDROME (histamine
 Can penetrate BBB EXCEPT Cefoperazone and
Release); MC AE of Vancomycin
Cefixime
o Chills, Ototoxicity and Nephrotoxicity
 Ceftazidime- DOC for Melioidiosis; has the
 TEICOPLANIN
maximum activity against pseudomonas
o Longer ½ life
 Ceftriazone is the 1st Choice drug for gonorrhea
o No Red Man syndrome and
and empirical therapy for bacterial meningitis
Nephroptoxicity
o Long term use can cause Biliary
 Telavancin
Sludging and Cholelithiasis due to
o For complicated skin and skin structure
precipitation in bile
infections
 Cefotaxime is metabolized to an active
o Dalbavancin
metabolite
 Given once a week and being
developed for MRSA and VRSA
 o Demeclocycline and Doxycycline can result
FOSFOMYCIN in photosensitivity
o Minocycline: Dose Dependent Vestibular
 Inhibits Enolpyruvate Transferase Toxicity (↑ in women)
 DOC for uncomplicated UTI o Tetracycline also possess anti-anabolic
effects
BACITRACIN

 Causes MARKED NEPHROTOXICITY

 ONLY for Topical Use

CYCLOSERINE

 2nd Line Drug for TB

 Neurotoxic effect and Neuropsychiatric
Symptoms

DRUGS INHIBITING PROTEIN SYNTHESIS

GLYCYLCYCLINES
Broad Spectrum:
 Tigecycline- more resistant to Efflux pumps
1. Chloramphenicol  For serious complicated skin and skin structures
 Inhibition of peptidyl transferase infections and Intra-abdominal infections
 Undergoes enterohepatic circulation  Ineffective against Proteus and Pseudomonas
 Inactivated by glucoronidation
 Resistance is developed by INACTIVATING Moderate Spectrum:
ENZYMES
MACROLIDES
 AE:
o Superinfection Diarrhea  Erythromycin, Azithromycin, Roxithromycin and
o Dose Dependent reversible BM Clarithromycin
Suppression  Tacrolimus->Immunosuppressant and also a
o Gray Baby Syndrome Decreased macrolide
RBC, Cyanosis and CV Collapse  Blocks the translocation of peptide chain from A
2. Tetracyclines to P site
 Inhibit the binding of aminoacyl tRNA to the A  Similar action with Ketolides and Lincosamides
site  Have anti-inflammatory action ; responsible for
 Oral absorption of tetracyclines is impaired by the use of macrolides in the prevention of cystic
food and multivalent cations fibrosis exacerbation
 Crosses the Placenta that is why it is CI in o Erythromycin is secreted by biliary
pregnant women route
 Undergo Enterohepatic Circulation o Clarithromycin- Renal and Biliary Route
 All are excreted in the urine EXCEPT o Azithromycin – Urine
DOXYCYCLINEFeces  DOC for: (CLAW)
 Resistance is due to development of Efflux o Chancroid by H.ducreyi (Azithromycin
pumps 1dose)
 DOC for: (TETRACYCLINE) o Legionella
o Atypical Pneumonia
o Whooping Cough
 Clinical Use of Azith and CLinda:
o CHAT
 C-Chlamydia
 H- H.influenza
 A- mAc
 T- Toxoplasma
 Azithromycin
o More active against H.influenza and
Neisseria
o MAC prophylaxis
 Clarithromycin
o Prophylaxis and Treatment of MAC
 Spiramycin
o DOC: Toxoplasmosis in pregnancy
 Toxicity:  Toxicity
o Superinfection Diarrhea and o Erythromycin- Diarrhea due to
Pseudomembranous Colitis; GI SE are most stimulation of motilin receptors
common SE o E.Estolate- acute cholestatic hepatitis in
o CI in Pregnancy: Tooth Enamel Dysplasia pregnant females
and Irregularities in fetal bone growth o AE: MACRO
o High doses can lead to Hepatic Necrosis  M- Motilin receptor Agonist
o Expired drugs can cause FANCONI  A- Allergy
Syndrome (Renal Tubular Acidosis)  C- Cholestasis
  RO- Reversible Ototoxicity (IV  Vestiubular: Streptomycin and
Erythromycin) Gentamycin
 Netilmicin is the least ototoxic
Narrow Spectrum aminoglycoside
 Nephrotoxic- proximal Tubular Cells
LINCOSAMIDES
(Reversible)
 Clindamycin and Lincomycin  Neomycin- most nephrotoxic
 Anaerobes  Gentamicin- Most nephrotoxic
 DOC: Severe, Invasive Group A Strep among the systemic
 Alternative for Prophylaxis against dental aminoglycosides
procedures  Streptomycin is the least
 Clindamycin nephrotoxic
 NM Blockade
 Reversed by IV Calcium
 Neomycin and Streptomycin
CI in MG

STREPTOGRAMINS

 Quinpristin-Dalfopristin Penicillin Resistant

Pneumococci, MR E.faecium, MRSA as well as
VRSA PLEUROMUTILINS
 Potent CYP3A4 Inhibitor
 MLS-B Resistance ( Macrolides, Lincosamides  Retapamulin
and Streptogramins) o Topical Tx for Impetigo due to MRSA or
 Venous Irritation Common SE S,pyogenes
 Arthralgia Myalgia Syndrome
ANTIMETABOLITES
OXAZOLIDINONES
1. Sulfonamides
 Linezolid and Tedizolide  Bacteriostatic Agents
 No cross resistance with other protein synthesis  Competitively inhibits folate synthase
inhibiting drugs  Not effective in the presence of pus (contains
 Active against: large amount of PABA)
o MRSA  Undergo Acetylation and can cause Drug
o VRSA Induced SLE
o VAncomycin Resistant E.faecium and Fecalis  Solubility ↓in acidic urine crystalluria
 Major AE of Linezolid: Thrombocytopenia and  Longest Acting- Syulfadoxine; Shortest-
Neutropenia Sulfacytine
o Optic Neuritis  Clinical Use:
o Peripheral Neuropathy  Sulfasalazine and Olsalazine- Ulcerative Colitis
o Lactic Acidosis  Sulfadoxine+Pyrimethamin-Malria
 Sulfadiazine+Pyrimethamine- Tosxoplasmosis
AMINOGLYCOSIDES
and Prophylaxis of P.jiroveci in AIDS
 Streptomycin, Gentamicin, Kanamicin,  Toxicity
Tobramicin,Amikacin,Sisomicin, Netilmicin,  Skin Rash- <ost Common AE
Neomycin and Framycetin  Granulocytopenia, Thrombocytopenia and
 CDK and Prolonged PAE Aplastic Anemia(more common in HIV pts)
 Penetration across the cell wall is dependent on  Acute Hemolysis in G6PD Deficiency patients
O2 Dependent Transport  Kernicterus in the NB- displacement of
o Inactive against anaerobes bilirubin from plasma
 Pharmacokinetics 2. Trimethoprim
o Excreted by glomerular filtration  Bacteriostatic antimetabolite inhibits
o Resistance due to Inactivating Enzymes dihydrofolate reductase
 ONLY AMIKACIN and NETILMICIN are  Similar Drugs: Pyrimethamine, Methotrexate,
resistant to inhibiting enzymes Proguanil and Pentamidine
o Uses:  Attains highest concentration in the prostate
 Gentamicin, Tobramycin and Amikacin and vaginal fluids
 G-  Can be used alone in prostatitis and UTI
 Streptomycin is the 1st line drug for  Toxicity
TB, Plague and Tularemia  Megaloblastic anemia, Leucopenia and
 Amikacin is used for MDR TB Pancytopenia (ALL DHFRase Inhibitors can
o Toxicity cause Megaloblastic Anemia
 Ototoxic  Hyperkalemia (amiloride like action, inhibits
 Hearing Loss: Amikacin, ENaC in Collecting tubules)
Kanamycin and Neomycin
3. Cotrimoxazole  Fluoroquinolones are CONTRAINDICTED in
 Sulfamethoxazole+ Trimethoprin (5:1) Epilepsy
 Bactericidal sequential blockade at 2 steps in  Recent FDA Reports: can cause peripheral
the DNA Synthesis neuropathy
 Clinical Use:
 DOC: Pneumocytosis and Nocardiosis URINARY ANTISEPTICS
 UTI
 More effective in acidic urine
 RTI
 Nitrofurantoin
 MRSA
 Results in DNA damage
 Middle ear and sinus infections caused by
Hemophilis and Moraxella  Active against most pathogens EXCEPT
 Toxicity: pseudomonas and proteus
 Similar to sulfonamides  AE:
 Diarrhea
FLUOROQUINOLONES  Photoxicity
 Neurotoxicity
 Inhibits DNA Gyrase andTopisomerase IV  G6PD Hemolysis
Inhibits DNA replication  Nalidixic Acid
 Long PAE  Inhibits DNA Gyrase
 AE: Neurotoxicity
1st Gen 2ND Gen 3rd Gen 4th Gen
(Narrow (Gram +) (Broadest
DAPTOMYCIN
Spectrum, Spectrum)
Gram Neg)
Norfloxacin Ciprofloxacin Levofloxacin Moxifloxacin  Lipopeptide bactericidal drug
Lomefloxacin Ofloxacin Gatifloxacin Fleroxacin  Depolarizes bacterial cell membrane with K+
Pefloxacin Garenoxacin efflux and rapid cell death
Sparfloxacin Gemifloxacin
 Gram (+) and against organisms resistant to
Trovafloxacin
linezolid and streptogramins
 Good Oral Bioavailability (EXCEPT norflaxicin) if
 Toxicity: Myopathy
taken on empty stomach
 Antagonized by Pulmonary Surfactant
ROUTE OF EXCRETION
DRUG Kidney Liver Bile MUPIROCIN
All 
Moxifloxacin   Used topically or nasally for eliminating
Trovafloxacin  staphylococcal nasal carriage
Sparfloxacin  
Pefloxacin   POLYPEPTIDE ANTIBIOTICS
 Longest 1/2Life: Sparfloxacin
 Clinical Use:  Affects cell membrane EXCEPT Bacitracin
 Greatest activity against Pseudomonas  Only used topically
(Max: Ciprofloxacin)  Toxicity:
 Ciprofloxacin: DOC for prophylaxis and o Neurotoxic
treatment of anthrax and for prophylaxis o Renal Damage
of meningococcal meningitis
 Levofloxacin- Atypical organisms like IMPORTANT POINTS:
mycoplasma
Elimination
 Respiratory Quinolones: enhanced activity
against gram positive and atypical
organisms
 Levofloxacin
 Gatifloxacin
 Gemifloxacin
 Moxifloxacin
 Effective in TB and can be used for the
prophylaxis of neutropenic patients
 T.PALLIDUM AND NOCARDIA ARE
RESISTANT TO ALL FLUOROQUINOLONES
 Toxicity:
 GI Distress- Most Common followed by CNS
side effects
 Cartlage problems in children <18y/o and
pregnancy
 Phototoxicity
 Moxifloxacin can cause hypoglycemia
 Sparfloxacin and Gatifloxacin can prolong
QT Interval
 Ciprofloxacin can increase the plasma
concentration of methylxanthines thus Drugs effective against anaerobic organisms
amplifying toxicity
Cefmetazole
 NSAIDs can increase CNS toxicity
Cefotetan
 Cefoxitin DOCs
Chloramphenicol
Clindamycin
Metronidazole
Moxifloxacin
Vancomycin

Drugs effective against pseudomonas

Beta-Lactams Fluoro Poly- Amino-

peptide glycosides
Carboxypenicillins Cipro, Colistin
Ureidopenicillins Peflo PolyB
Carbapenems
Monobactam
Cepphalosporins
(Ceftazidime,
Cefoperazone,
Moxolactam,
Cefepime,
Cefpirome)
TOC for Pseudomonas:
Ceftazidime+Aminoglycoside

Drugs Effective against MRSA

Cotrimoxazole
Dalbavancin
Daptomycin
Linezolide
Rifampicin
Streptogramins
Teicoplanin
Tetracyclines
Vancomycin

Prophylaxis of Choice
ANTIMICROBIALS FOR SPECIFIC CONDITIONS

ANTI-MYCOBACTERIAL ANTIBIOTICS
Tuberculosis

ISONIAZID (H)

 Prodrug; metabolized via ACETYLATION

 Acts by O2 dependent pathway
 Single MOST IMPORTANT DRUG USED IN TB
 Bactericidal against Rapidly Multiplying
Organisms and Bacteriostatic against Resting
Organisms
 Widely distributed in the body including CSF
 Prophylaxis of Choice for TB and treatment of
latent TB
 Resistance: Kat G Mutation (high level
resistacne) or inhA (Cross resistance to
ethionamide)
 AE:
o Peripheral Neuritis—prevented by
pyridoxine
o Hepatotoxic and Hemolysis in G6PD
Def. Pts
o Inhibits MOA-A; can cause Cheese
Reaction
o Gynecomastia, Drug Induced SLE

RIFAMPICIN (R)

 Bactericidal to BOTH Dividing and Non-Dividing

Mycobacterium
 Inhibits DNA dependent RNA Polymerase
 Enterohepatic circulation and partyly
metabolized by the liver Hepatotoxic to pts
with pre-existing liver disease
 Orange color in the urine
 Safely used in renal dysfunction; eliminated
through the feces
 Penetrates ALL membranes
 ONLY bactericidal drug active dormant bacteria
in solid caseous lesions
 MOST EFFECTIVE and FASTEST ACTING DRUGIN
LEPROSY
 Prophylactic drug for meningococcal and
staphylococcal carrier states
 Toxicity:
o Proteinuria
o Impair antibody responses
o Hepatotoxic- for those with pre-existing
liver disease(Hyperbilirubinemia without
SGPT Elevations)
o Skin rash and flulike syndrome
o Anemia
 RIFABUTIN- lesser drug interactions which can
be used in AIDS with TB; More eefective against
MAC than Rifampicin
 Those on OCP must increase dosage while
taking Rifampicin

ETHAMBUTOL (E)

 BACTERIOSTATIC
 It is not distributed in the CSF
 Toxicity:
o Dose Dependent Visual Disturbances (Loss
of ability to see green and red, Optic
Neuritis)
o Contraindicated in Children
o Hyperuricemia and peripheral neuritis
o Dose adjustment required in renal failure

PYRAZINAMIDE(Z)

 Bactericidal against SLOW REPLICATING

BACTERIA and EFFECTIVE ONLY against
INTRACELLULAR MYCOBACTERIA
 Toxicity:
o Non-Gouty Arthralgia
o Hyperuricemia
o Hepatic Dysfunction
o Porphyria
o Photosensitivity

STREPTOMYCIN(S)

 Aminoglycoside
 Via IM Injection
 ACTIVE ONLY AGAINTS EXTRACELLULAR
BACTERIA
 NOT HEPATOTOXIC
 Contraindicated in Pregnancy

NOTES:

 Ethambutol and Streptomycin DO NOT CROSS

BBB
 Ethambutol and Streptomycin ARE NOT
HEPATOTOXIC
 Ethambutol and Pyrazinamide can cause
HYPERURICEMIA
 Rifampicin is the SAFEST DRUG IN RENAL
FAILURE
 Streptomycin is CONTRAINDICATED IN
PREGNANCY