SUBMITTED TO :

DR. ARIf ULLAH KHAN

SUBMITTED BY :

AIMAN SOHAIL

SAP –NO:

6011

SEMISTEr :

6th

SECTION:

SUBJEct:

PHARMACOLOGY
 Antibacterials
1-Folate antagonist :
 Sulphonamide:
Classification on basis of duration of action:
(i) Long acting

 sulfamethazine (Ruminant)
 sulfamerazine (Dog),
 sulfamethoxypridazine
 sulfaethoxypridazine

(ii) Short acting

 sulfathiazole,
 sulfasomidine
 Intermediate acting-
 sulfasimazole
 sulfamethoxazole
 sulphadiazine
 sulfapyridine
 Classification on basis of pharmacokinetic
(absorption) properties:

(i) Oral absorbable agents

 Sulfisoxazole
 Sulfamethoxazole
 Sulfadiazine
 Sulfadoxine

(ii) Oral non-absorbable agents

 Sulfasalazine

(iii) Topical agents

 Sodium sulfacetamide
 Mafenide acetate
 Silver sulphadiazine

MECHANISM OF ACTION:
ANTIMICROBIAL SPECTRUM:
 Sulfonamides are active against
 A broad spectrum of gram-positive and many gram-negative
bacteria
 Plasmodium and Toxoplasma spp

MECHANISM OF RESISTANCE :
  Synthesizing large amounts of PABA
 Bacterial dihydropteroate synthetase is altered
 Impaired Permeability to sulfonamides

PHARMACOKINETICS:
ABSORPTION: stomach and intestine (orally absorbable)
DISTRIBUTION: Body fluids (CNS, CSF), Placenta, Fetus.
PROTEIN BINDING: 20%-90% .
METABOLISM: Portion of absorb drug is acetylated or glucronidated
in liver.
EXCRETION: Inactive metabolite excreted in urine by GF

CLINICAL USES:
• . URINARY TRACT INFECTION:
sulfamethoxyzole)
• ULCERATIVE COLITIS:
• RHEUMATOID ARTHRITIS:
• OCULAR INFECTION:
• BURN INFECTIONS:
sulfadiazine)
Oral ( sulfisoxazole,
Oral (sulfasalazine)
Oral (sulfasalazine)
Topical (sulfacetamide)
Topical (mafenide, silver
 • TOXOPLASMOSIS: Oral [sulfadiazine plus
pyrimethamine](dihydrofolate reductase inhibitor) plus folinic
acid.
• CEREBROSPINAL MENINGITIS: short acting sulfa.
• PROPHYLAXIS IN EPIDEMICS OF MENINGITIS: long
acting sulfa and sulfadiazine.
• BACILLARY DYSENTERY AND GASTROENTERITIS:
sulfa guanidine, sulfa succidine, and sulfa
phthalidine.
• UPPER RESPIRATORY INFECTIONS (sinustis, bronchitis
and pneumonia): (trimethoprim and short acting sulfonamides)

SIDE EFFECTS:

• GASTRO INTESTINAL TRACT:

 Nausea,
 vomit
 abdominal pain
 NEPHROTOXICITY Albuminurea
 Crystalluria
 hematuria
  ALLERGIC REACTION:
Rashes, urticaria, stevens- Johnson syndrome, more with long acting
 HEMATOLOGICAL: Hemolysis in G6P deficiency

DRUG INTERACTIONS:
 Causing drug potentiation (due to displacement from serum
albumin)
 Tolbutamide (hypoglycemic effect)
 Warfarin (anticoagulant action)
 Methotrexate level may also increase

CONTRAINDICATION:
 Infants less than two months
 Pregnancy

SULFADIAZINE :
 Short acting
 Rapid oral absorption
 Used orally

 used for meningitis
 USES: Toxoplasmosis, burn infections, meningitis
 DOSE: 0.5g QID to 2g TDS

SULFAMETHOXAZOLE:
 Intermediate acting
 Slow absorption orally
 Preffered combined with trimethoprim
 Can cause crystalluria
 USES: UTIs, RTIs
 DOSE: initially: 1g BD for 2 days
 Maintenance: 0.5g BD

SULPHACETAMIDE:
 Highly soluble
 Mild irritation at 30%
 Topical infections of chlamydia
 USES: Ophthalmia neonatorum caused by chlamydial
oculogenitalis, Conjuctivitis, Trachoma
 Very low sensitivity reported
 DOSE: 10%, 20% and 30% eye drops
2-CELL WALL SYNTHESIS INHIBITORS :
1. Penicillin
2. Cephalosporins

Classification of Penicillins:-
1. Natural penicillins
 Penicillin G
 Penicillin K
 Penicillin N
 Penicillin O
 Penicillin V

2. β-lactamase-resistant
 Methicillin
 Nafcillin
 Oxacillin
 Cloxacillin
 Dicloxacillin
 Flucloxacillin
3. Aminopenicillins
 Ampicillin
 Amoxicillin
 Pivampicillin
  Hetacillin
 Bacampicillin
 Metampicillin
 Talampicillin

4. Carboxypenicillins
 Carbenicillin
 Ticarcillin
 Temocillin
5. Ureidopenicillins
 Mezlocillin
 Piperacillin
 Azlocillin

MECHANISM OF ACTION :
Inhibit bacterial cell wall synthesis by inhibiting trasnpeptidation
process through interfering the penicillin binding protein (PBP an
enzyme), Halting peptidoglycan synthesis and the cell dies.

RESISTANCE TO PENICILLIN:
 Production of Beta – lacatamases (Many 100 types)
 Reduced permeability of drug
  Modification of penicillin binding proteins. (PBP)
 Efflux pump

ANTIBACTERIAL SPECTRUM:
Gram-positive: non-beta-lactamase producing gram-positive cocci
(including viridans streptococci, group A streptococci, Streptococcus
pneumoniae, anaerobic Streptococcus), Enterococcus spp., non-
penicillinase producing strains of Staphylococcus aureus, coagulase
negative Staphylococcus aureus, Clostridium spp. (excluding C.
difficile), Actinomyces spp.
Gram negative: Neisseria meningitides, non-penicillinase producing
Neisseria gonorrheae, Pasteurella multocida.

PHARMACOKINETICS:
Penicillin has low protein binding in plasma, the bioavailability of
penicillin depends on the type; penicillin G has a low bioavailability,
below 30%, whereas penicillin V has a higher bioavailability between
60 and 70%. Penicillin has a short half life and is excreted via the
kidneys

CLINICAL USES:
  Streptococcal infection
 Staph. Infection
 Pneumococcal infection
 Gonococcal infection
 Meningococcal infection
 Haemophilus influenzae infection
 UTI + Lungs & Blood infection
 Prophylactic uses:
 Rh. Fever
 Bact. Endocarditis
 Prosthetic heart valves
 Joint prosthesis

DRUG INTERACTION OF PENICILLIN:

 Penicillins & Aminoglycosides
 Pen & bacteriostatic drugs
 Probenicid, indomethacin, sulfinpyrzaone
 Ampicillin & Allopurinol

ADVERSE EFFECT :
(a). Hypersensitivity reactions :
 Ac anaphylaxis (incid: 0.01 – 0.5 % of Pen.administered pts).
 Ac. Urticaria (Late) 5 – 10 %
 Angioedema
 Serum sickness
 Drug fever
 Joint swelling
 Pruritis
 Skin rashes
 Eosinophilia

b). Toxic effects:

 Pain & irritative inflam at site of I/M inj
 Convulsions
 Super inf → Amp & Amoxy
 GIT upset → NV & Diarrhoea
 Hepatitis → Oxacillin
 Hypokalemia → Carbenecillin
 Na + overloading → Carbenecillin + other Na salts
 Non Allergic Skin Rash → Ampicillin & Amoxycillin
 Granucocytopenia → Nafcillin
 Interstitial nephritis → Methicillin
 Decr. platelet agg. → Bleeding diathesis more with
Carbenecillin & Ticarcillin.
 Bone marrow depression & granulocytopenia (rare) →
 Nafcillin & Oxacillin
 Thrombophlebitis on I/V adms
PENICILLIN G:
 Benzylpenicillin, also known as penicillin G, is an antibiotic used
to treat a number of bacterial infections.
 This includes pneumonia, strep throat, syphilis, necrotizing
enterocolitis, diphtheria, gas gangrene, leptospirosis,
 Effectiveness mainly against Gram-positive organisms. Some
Gram-negative organisms such as Neisseria gonorrhoeae and
Leptospira
 Adverse effects can include hypersensitivity reactions including
urticaria, fever, joint pains, rashes, angioedema, anaphylaxis,
serum sickness-like reaction. Rarely CNS toxicity including
convulsions

2-CEPHALOSPORINS :
 Similar to Penicillins
 More stable to many Beta Lactamases
 Broader Spectrum of activity

Classification Of Cephalosporins:
1st Generation:
(a). Parentral: (I/V, I/M):
 Cephalothin
 Cephaloridine
 Cephradine
 Cephapirin
 Cefazolin

(b) Oral:
 Cephalexin
 Cephaloglycin
 Cephradine

Both:
 Cephradine (velosef)

2nd Generation:
(a). Oral:
 Cefaclor
 Cefatrizine
 Cefuroxime axetil
 Cefprozil
 Loracarbef

(b) Parentral:
  Cefamendole
 Cefuroxime (Zinacef)
 Cefonicid
 Ceforanide
 Cefprozil
 Cefoxitin (Cephamycin)
 Cefotetan (Cephamycin)
 Cefmetazole (Cephamycin)

3rd Generation:
(a). Oral:
 Cefpodoxime proxetil
 Ceftibuten
 Cefdinir
 Cefixime
(b) Parentral:
 Cefotaxime (Claforan)
 Ceftizoxime
 Ceftriaxone (Rocephin)
 Cefoperazone (Cefobid)
 Ceftazidime
 Cefsulodin
 Moxalactam
4th Generation:
 Cefipime
 Cephalosporins active against MRSA:
 Ceftaroline fosamil Prodrug of Ceftaroline
 Ceftobiprole medocaril Prodrug of Ceftobiprole

MECHANISM OF ACTION :
Inhibit bacterial cell wall synthesis by inhibiting trasnpeptidation
process through interfering the penicillin binding protein (PBP an
enzyme), Halting peptidoglycan synthesis and the cell dies.

RESISTANCE:
 Alt of P.B. Proteins
 Degradation by ß- lactamases (Cephalosporinases)
 Poor influx
 efflux

PHARMACOKINETICS:
Absorption:
  Oral cephalosporins → well abs
 Parentral → poor oral abs so adm. P.A I/V & I/M?

Distribution:
 Distributed to all tissues
 1st & 2nd Gen → poor CNS entry except Cefuroxime
 Some 3rd Gen: → well penetr. of BBB (10 – 30 % of serum)
 Cefoperazone
 Cefotaxime
 Ceftriaxone
 Latamoxef
 Moxalactam
 Protein binding → 17 – 90 %
 Ceftriaxone & Cefoperazone

Excretion:
 Exc. mostly unaltered → kidneys (60 – 100 %)
 Cefoperazone → 75 % in bile (Only 20 % → urine)
 Ceftriaxone → 40 % in bile
 Cephaloridine, Ceftriaxone, Ceftazidime & Moxalactam
→ Negligile tub. Sec
 Elim. t ½ → 0.5 – 8 hrs

ANTIBACTERIAL SPECTRUM:
1st Generation:
G +ve cocci:
 Staphylo

 Strepto

b – Haemolyticus
streptocooci

G +ve bacilli:
Anaerobic cocci:

G –ve m.o:
 E. coli
 Klebsiella Pnumonae
 Proteus mirabilis
2nd Generation:
 Active aginst the microragsnism inhibited by ist gen.
 Inadition they have extended gram neg. coverage
 Sec. gen. are active aginst:

3rd Generation:
Compared to 2nd ge. Have more expanded gram neg spect.
Also crosses bbb.
Active against:
 Citrobacter
 Enterobacteriaceae
 H. influenze (BLP)
 neisseria
 Pseudononas aeruginosa ( Ceftazidime & Cefoperazone)
 B- fragilis ( Ceftizoxime & Moxalactam)
 Serratia mercescens
 Providencia

4th Generation:
  More resistant to B- lactamases e.g. produced by Enterobactor.
 Active against Pseudomonas, Enterobacteriaceae, St aureus
 St. pneumoniae, H. influenzae, & Neisseria
 Penetrates well into C.S.F

CLINICAL USES:
1- Generation
(a). Oral:
 Urinary tract inf.
 Skin, soft tissue inf, osteomyelitis, endocarditis
 Polymicrobial inf e.g. cellulitis, abscesses
(b). parenteral
 Surgical prophylaxis (Cefazolin)
 Klebisiella Pn, staph. & strept. Inf. resistant to Pen.
 Alternative to Pen. in staph & strept inf in allergic pts.
 (other than imediate hypersensitivity

2nd Generation:
Oral:
 Otitis media & Sinusitis & lower Resp. tract inf)
 Parenteral:
 Peritonitis, diverticulitis, and pelvic inflammatory disease

3rd Generation:
 Meningitis caused by Pneumo, meningococci &
G –ve aerobes → Ceftriaxone & Cefotaxime.
 H. influenza meningitis (Ceftriaxone & Cefotaxime)
 Sepsis
 gonorrhea

4th Generation:
 uses like 3rd generation
 Penicillin resistant streptococci
 Enterobacter infections

ADVERSE EFFECT:
(a). Allergic reactions:
 Anaphylaxis, skin rashes, drug fever, nephritis, hemolytic anemia,
granulocytopenia
(b). Toxic eff:
 Local irritation can lead to severe pain → I/M inj
 Thrombophlebitis after I/V inj
 GIT upset → oral
 Interstetial Nephritis & tubular necrosis
 Hypoprothrombimemia & bleeding dis-orders
 (Drugs having methylthiotetrazole group)

DRUG INTERACTION:
 Nephrotoxicity of Aminoglycosides ↑ by cephaloridine
 Probenicid ↓ renal exc of some ceph.

CONTRA-INDICATION:
 Hypersensitivity

CEFIXIME:
 Cefixime is an antibiotic useful to treat a number of bacterial
infections
 This includes otitis media, strep throat, pneumonia, urinary tract
infections, gonorrhea
  Cefixime is a broad spectrum cephalosporin antibiotic and is
commonly used to treat bacterial infections of the ear, urinary
tract, and upper respiratory tract.
 Cefixime is contraindicated in patients with known sensitivity or
allergies to cephalosporin class of antibiotics.
 As Cefixime is a third generation cephalosporin, it is not
contraindicated for patients with a true penicillin allergy

3- Protein synthesis inhibiter:

1-Amminogycoside
2-Macrolide

Amminogylcoside:
 Bactericidal
 inhibitors of protein synthesis
 Useful mainly against aerobic gram negative microorganisms
 Useful alone as well as in combination with beta lactam drugs

Aminoglycosides agents:
 Streptomycin
 Tobramycin
 Neomycin
 Kanamycin
 Framycetin (Soframycin)
 Gentamicin
 Sisomicin
 Amikacin
 Netilmicin
 Paromomycin
 ANTIBACTERIAL SPECTRUM:
 Aerobic G –ve bact:- E.coli, proteus , Entarobacter, Klebsiella ,
Brucella, providencia, pseudomonas, serratia species,
Francisella tulorensis & yersinea pestis Acinobactor
 Active against:– H. infl, Schigella, morexella catarhalis
 Active against some G +ve mo. when used in comb. with
 cell wall active drugs eg; sensitive entrococci, strep &
staph.
 Mycobacterium tuberculosis.( Streptomycin & Amikacin )
 Slight difference in spectrum amongst individual drugs

M.O RESISTANCE:
 Production of inactivating enz → By adenylation actylation
& phosplorylation → Netilmicin & Amikacin
are less vulnerable to these enz.
 Impaired entery into the bact cell (Overcome by penicillins &
vancomycin)
 Alteration in receptor on 30–S ribosomal subunit

ADVERSE EFFECT:
Hypersensitivity:
Skin rashes, urticaria, drug fever, dermatitis
Otoxicity:
(a). Auditory:- (cochlear damage)
 Manifested by tinnitus & deafness starting from higher frequency
sounds
 Accumulate in the endolymph & perilymph & cause
damage to hair cells in the organ of corti
 Neomycin, Kanamycin, Amikacin & Paromomycin are
most cochleotoxic
(b).Vestibular toxicity:-
 Vertigo, ataxia, dizziness, loss of balance.
 Streptomycin & Gentamycin are most vestibulotoxic

Nephrotoxicity:-
 Concentrated in renal cortex
 Renal damage progressing to Acute renal tubular necrosis
 Often reversible but may become irreversible
 Manifested by decreased creatinine clearance &
increased serum creatinine level
 ↑ Trough conc. of aminoglycosides
 Potentiated / pptd by other nephrotoxic drugs
 Neomycin, Tobramycin & Gentamycin are most nephrotoxic
 Neuromuscular blockede:- (curare like effect)
 ↓ Ach. Release & ↓ postsynaptic response to Ach.
 Myasthenic pts more at risk
 Reversed by Ca- gluconate or Neostigmine
 May lead to resp paralysis
 But may need resp support

CONTRAINDICATION:
 Renal insuff.
 Pregnancy → Deafness in child
 Hypersensitive individuals
 Myasthenia gravis patients

Amikacin:-
 Semisynthetic derivative of Kanamycin → Less toxic
 Less chances of resistance being poor substrate inactivating enz
 Active against the organisms resistant to Gentamycin
 & Tobramycin
 Multidrug resistant & Kanamycin resistant strains of
mycobact T.B are susceptible
  Dose: 7.5 mg /Kg/day / OD or 2 – 3 / wkly in T.d.

 Macrolide:

 Erythromycin
 Clarithromycin
 Azithromycin
 Roxithromycin
 Spiramycin
 Telithromycin

 Erythromycin:-
Isolated from Streptomyces. Erythreus
by Mc. Guire et al. in 1952

ANTIBACTERIAL SPECTRUM:
 Bacteriostatic but may be bactericidal in high concentrations
against very susceptible organisms.
 Effective against aerobic gram positive:
 Pneumococci,staphylococci,streptococci
 Corneybacteria
 Helicobacter pylori
 Mycoplasma pneumonia & Legionella pneumophila
  Chlamydia trachomatis, Ch. Psittaci, Ch.Pneumoniae
 Atypical mycobacteria:-
 M. scrofulaceum.
 M. kansassi
 N. gonorrhoeae
 Pasteurella multocida & borrelia
 Bordetella pertussis

MECHANISM OF ACTION:
 Enter bact cell by passive diffusion
 Bind with on 50-S ribosomal subunit of bact
 Inhibit transcription & elongation of peptide chain

RESISTANCE:
 Reduced permeability of the cell membrane or active Efflux
 Production (enterobacteriaceae) of esterases that hydrolyze
macrolides
 Modification of the of 50-S ribosomal binding site (so called
ribosomal protection)
 Increase efflux

PHARMACOKINETICS:
Absorption:-
 Erythromycin Base:-
 Erythromycin Esters:-
 Estolate:-
Lipid-soluble, acid-stable prodrug
Undergoes hydrolysis in blood or tissues after abs
 Ethyl Succinate:-
Mixed double ester prodrug of erythromycin.
Better oral absorption.
Oral susp for children, without the bitter taste.
 Propionate:-
Lipid-soluble ester of propionic acid.
Better oral absorption.
Erythromycin Salts:-
 Erythromycin Stearate:-
Lipid-soluble salt of stearic acid.
Better oral absorption.
Acid-sensitive. Enteric coated form is Acid-stable.
In small gut base exchange occurs & free erythromycin r
 Erythromycin Lactobionate:-
Water-soluble salt of lactobionic acid
Distribution:-
 Diffuses readily into intracellular fluids
 Activity can be achieved at all sites EXCEPT brain & CSF
  Poor penetration into synovial fluid
 Pr. Binding 70 %
 Concentrated in liver
 t ½ = 1.5 hrs
 Cross placenta
 Highly concentrated in Prostratic fluid, Liver & Bile
 for parenteral dosage forms.
 Erythromycin Gluceptate
 Water-soluble salt of glucoheptonic acid
 for parenteral dosage forms.

Metabolism:-
 Liver by CYP450
Elimination:-
 Mainly in bile as active metabolite
 In bile conc may be 50 times that of plasma
 Undergoes EHC & lost in feces
 Inactive metabolites excreted in urine only 2 – 5 %
 Not removed by dialysis
 Dose needs not be adjusted in renal patients.
 Better abs & longer t₁/₂ :-
Roxithromycin
Clarithromycin
THERAPEUTICS USES:
1. Drug of choice for:-
 Corynae bact inf. (Diphtheria, sepsis, erythrasma)
 Chlamydial inf (resp, eye, genital & new born)
 Respiratory and Throat infections
 ocular or genital chlamydial infection
 Community acquired Pneumonia
 As penicillin substitute in pen. Sensitive pts
2. Prophylaxis of endocarditis prior to dental procedure
Dosage of Erythromycin:-
 Po. 250 – 500 mg x QID (children
40mg/kg/day)
 I/V 0.5 G 8 - 12 hourly .

ADVERSE EFFECT:
GIT upset:-
 Anorexia, nausea, vomiting & diarrhea → oral adm
 Directly simulates motilin receptors on GIT smooth
muscles
Liver Toxicity:-
Estolate salt (More than 14 days) → acute cholestatic
hepatitis (fever, jaundice, impaired LFTs) probably
 .
Other Hypersensitivity reactions:-
 Fever, eosinophilia and skin eruptions.
Cardio toxicity:-
 Erythromycin can cause cardiac arrhythmias, with
QT prolongation. (esp. in patients with underlying
cardiac disease)

DRUG INTERACTION:
 Erythromycin → cause Microsomal Enz inhibition
(cytochrome P450 enzymes):
 ↑ conc of warfarin, theophylline, Methylprednisolone &
Cyclosporine.
 serum levels of oral digoxin due to bioavailability

4- Nucleic acid synthesis inhibitor:

 Quinolones

CLASSIFICATION:
1st Generation (quinolones)
 Nalidixic acid
 Oxolinic acid
 Cinoxacin

2nd Generation( Fluorinated Quinolones)

1.Agent with least activity against G-ve& G+ve Bacteria

Norfloxacin
2. Agents with excellent activity against G-ve & moderate to good
activity against G+ve Bacteria :
 Ciprofloxacin
 Enoxacin
 Lomefloxacin
 Levofloxacin
 Ofloxacin
 Pefloxacin

3. Agents with excellent activity against

 G-ve& improved activity against G+ve Bacteria:
 Gatifloxacin
  Moxyfloxacin
 Sparfloxacin
 Trovafloxacin
4. Agents with additional activity against anaerobic Bacteria:
 Moxyfloxacin
 Trovafloxacin

MECHANISM OF ACTION:
 Quinolones block bacterial DNA synthesis by inhibiting the
bacterial enzymes:
 DNA gyrase (Topoisomerase II): inhibition of which prevent
relaxation of positively supercoiled DNA, required for normal
transcription and replication
 b-Topoisomerase IV: inhibition of which interfere with separation
of replicated chromosomal DNA into the respective daughter cells
during cell division

RESISTANCE:

 Mutation of DNA gyrase (binding region of the targeting

enzyme)
 Decreased accumulation due to
 a. Change in permeability
b. Increased efflux of drugs

ANTIBACTERIAL SPECTRUM:
 Bactericidal
 Broad spectrum.
 More effective against G-ve.
 Specially useful for Resistant micro organisms

SUSCEPTIBLE MICRO-ORGANISMS:
 Enterobacter species
 Pseudomonas aeroginosa,
 Streptococcus Pneumonae
 Salmonella typhi
 Shigella
 E.coli,
 Niesseria meningitidis, Campylobactor
 Haemphilus sp.

PHARMACOKINETICS:
 Floroquinolones after oral adm. are well absorbed (80-95%)
 Widely distributed in body
 Half life ranges from 3-10 hrs
  Elimination mostly takes place by renal mechanism (either tubular
secretion or glomerular filtration

CLINICAL USES:
 UTIs (Prostatis, Urethritis & Cervicitis).
 Typhoid fever
 Bacterial diarrhea by Shigella, Salmonella, Toxigenic Ecoli.
 Gonorrhoea resistant to other drugs.
 Soft tissue, bones and joint infections.
 Intrabdominal infections (peritonitis). TB : Ciprofloxacin &
Levofloxacin
 Respiratory tract infections (pneumonia, bronchitis and sinusitis)
 Anthrax (ciprofloxacin)

ADVERSE EFFECT:
 GIT upsets (nausea, vomiting and diarrhea)
 CNS abnormalities (headache and dizziness)
 Cardiac arrhythmias (Prolongation of QT interval)
 Hyperglycemia--- Gatifloxacin
 Reversible Arthopathy (damage growing cartilage)
 Tendinitis (adult tendon rupture)
 Allergic reactions (skin rashes)
 Hepatotoxicity (impairment of liver function)
  Photosensitivity

DRUG INTERACTION:
Floroquinoles causes enzyme inhibition of CyP450- Increased levels
of Theophylline, caffeine, Warfarin and cyclosporins

CONTRAINDICATION:
 Children below 18 yrs : Damage to growing cartilage.
 Patients of arrhythmias
 Nursing mothers
 Pregnancy
 Patients with hepatic failure