Fluoroquinolone Antibiotics Guide

Chemotherapy Dr.KPS Gowda PESCP Bengaluru-560050 Page 1
3.Chemotherapy:
(f) Quinolines and Fluroquinolines:
These are synthetic antimicrobial drugs like sulfonamides, but they are bactericidal drugs. They
are now widely used drugs for the treatment of many infectious diseases caused by bacteria.
Older quinolones active against gram negative bacteria, but newer flouroquinolones also effect
on gram positive bacteria.
Classification:
1.Older quinolones: ( 4-quinolones)-Nalidixic acid.(first quinolone antibiotic)
2.Newer quinolones ( fluroquinolones)
a.First generation fluoroquinolones:Norfloxacin, ciprofloxacin, ofloxacin, pefloxacin.
b.Second generation fluoroquinolones: Lomefloxacin, sparfloxacin, levofloxacin, gatifloxacin,
moxifloxacin.
Chemistry of quinolones: The basic structure of all quinolones is shown below. It has one
carboxylic (COOH) group at C3 position and a keto (= O) group at C4 position. The parent
compound nalidixic acid does not contain fluorine (F) atom. Introduction of F at C6 position
increases the clinical effectiveness of the compound against many bacterial infections caused by
gram positive and gram negative bacteria. Introduction of a piperazine ring at C7 position
changes the antibacterial and pharmacokinetic properties.
Nalidixic acid Ciprofloxacin Norfloxacin
MOA: DNA replication takes place during cell division in bacteria. Circular double strand DNA
present in the bacteria, During DNA replication DNA helicase breaks the H bond between the
two DNA strands. The separated DNA strand is called as DNA fork. The DNA polymerase
moves along each DNA strand, initiates the DNA replication, each DNA strand split into two.
During this process there is supercoiling of the DNA strand. The DNA gyrase prevents the
supercoiling of the DNA strand. After DNA replication the circular DNA give rise to
complimentary new circular DNA strand. The newly formed circular DNA remains attached
with old circular DNA strand. At this junction the daughter DNA strand is interlinked with
parent DNA strand. Another enzyme topoisomerase IV (structure is similar to DNA gyrase)
allows the separation of two circular DNA. Two bacteria get separated. This type of cell division
is called binary fission. Quinolone antibiotics act by inhibiting the enzymes DNA gyrase

(topoisomerase II) and topoisomerase IV. This leads to the supercoiling of the DNA strand and
separation of the DNA strands get effected. This leads to the death of the bacteria.
Mechanism of bacterial resistance: Mutations takes place in the bacterial cell, so that the mutated
gene produces the enzymes DNA gyrase and topoisomerase IV. These enzymes become resistant
to quinolone antibiotics.
ADME: Nalidixic acid (4-quinolone) is slowly and incompletely absorbed from GIT. They do
not achieve sufficient blood and tissue concentrations and so ineffective in systemic infections.
The flouroquinolones are well absorbed after oral administration and are widely distributed in
the body tissues and fluids. They are concentrated in urine, bile, kidneys, lungs, bones, prostate,
macrophages (produced in the tissues by the differentiation of monocytes) and neutrophils. They
have greater bioavailability, tissue distribution and cellular penetration than nalidixic acid.Their
peak plasma concentrations (1.5 to 6 micro gram/ml) are obtained within 2h of an oral dose.
They are metabolized in the liver and excreted in urine mainly as glucuronides.
ADRs:
1.GIT side effects: Nausea, vomiting, anorexia, diarrhea, abdominal discomfort.
2.CNS side effects: Confusion, dizziness, headache, nervousness, agitation, hallucinations,
convulsions.
Agitation hallucinations Convulsions

3. Hypersensitivity reactions: Skin rash, uriticaria, pruritus, drug fever, eosinophilia and
photosensitivity.
Photosensitivity Pruritus Drug fever Keratopathy
4.Cartilage damage (arthropathy) in weight bearing joints of young childrens (below 5y) leading
to stunted growth.
5.Miscellaneous: Leucopenia, keratopathy (corneal opacity), nephrotoxicity.
Contraindications:
1.In young childrens- can cause cartilage damage. 2.Pregnant and lactating women- can effect
foetus and infant’s cartilage. 3.Epilepsy- can precipitate convulsions. 4.In severe renal disease.
Drug interactions:
1.Antacids and sucralfates decrease absorption of fluoroquinolones from GIT.
2.NSAIDS potentiate the CNS adverse effects of fluoroquinolones.
3.Ciproflaxacin inhibits the metabolism of theophylline, this results in increased theophilline
toxicity.
Therapeutical uses: They are used in the following bacterial infections.
1.Urinary tract infections: They are effective in UTIs caused by sensitive microorganisms.
They are also effective in prostatitis caused by sensitive bacteria.
2.Sexually transmitted diseases: FQs especially ciprofloxacin are effective in gonorrhoea,
softsore, urethritis and cervicitis, but they are ineffective in syphilis.

3.GIT infections: They are effective in gastroenteritis, traveller’s diarrhoea, shigellosis and
cholera. Also effective in chloramphenicol resistant typhoid fever.
. 4.Respiratory tract infections: FQs are effective in pneumonias and chronic bronchitis.
5.Bone, joint and soft tissue infections: 6.Eye and ear infections: In conjunctivitis and otitis
media. 7.Other infections:Septicemia (bacteria in the blood), multidrug resistant tuberculosis,
and chloroquine resistant malaria. They are also used in meningitis.
Preparations: 1. Nalidixic acid suspension for the treatment of UTIs: 300mg/5ml
2.Nalidixic acid tablet-500mg 3.Norfloxacin 400mg tabs, 4. Ciprofloxacin 250, 500mg tab,
500mg/100ml i.v.infusion

Nalidixic acid suspension

g.Antifungal antibiotics: These are the drugs used in the treatment of fungal
infections(mycoses).
Types of fungal infections:
1.Superficial mycoses: Dermatophytosis (skin, hair, nailbeds), candidiasis (infection of mucous
membrane of mouth, pharynx, esophagus, intestine, vagina, vulva and skin caused by Candida
albicans.)
2.Subcutaneous mycoses: e.g. Maduramycosis/Madura foot (caused by some species of fungi
producing subcutaneous granuloma (nodules) or chronic skin ulceration.
Madura foot Aspergillosis Blastomycosis
Histoplasmosis Cryptococcosis

3.Systemic (deep) mycoses: e.g. Aspergillosis, blastomycosis, histoplasmosis, cryptococcosis,
etc. Aspergillosis is an infection or allergic response due to the Aspergillus fungus.
Blastomycosis is a rare infection that may develop when people breathe in (inhale) a fungus
called Blastomyces dermatitidis, which is found in soil and wood. Histoplasmosis is an infection
due to Histoplasma capsulatum fungus. Cryptococcosis is an infection caused by two types of
fungi- Cryptococcus gatti and C. neoformans.
Classification of antifungal drugs.
1.Systemic antifungal drugs:
a.Antibiotics- e.g.Amphotericin-B, griseofulvin.
b.Antimetabolite; Flucytosine.
c.Azoles- Ketaconazole, fluconazole.
2.Topical antifungal drugs:
a.Azoles- Econazole, miconazole, clotrimazole, oxiconazole.
b.Antibiotics: Nystatin, amphotericin-B (polyene antibiotics).
c.Miscellaneous drugs: Benzoic acid, salicylic acid, ichthamol, selenium sulfide, tolnaftate, etc.
1.Systemic antifungal drugs:
a.Antibiotics- e.g.Amphotericin-B, griseofulvin.
Griseofulvin: It is an antibiotic obtained from Penicillium griseofulvum.Chemically it is a
heterocyclic benzofuran compound.
MOA: It is fungistatic. It is ineffective against bacteria,Candida albicans and any of deep fungi.
It acts by inhibiting the biosynthesis of microtubules of fungal cells leading to stoppage of
spindle formation during mitosis. This causes the stoppage of fungal reproduction and ultimately

death of fungal cells. It accumulates particularly in the fungally infected keratinized areas of the
skin and its appandages (hair and nailbed).
ADME: Given orally, microfine particles of gresiofulvin are absorbed much faster than those of
ordinary large particles of the drug.Fat in food helps in its absorption. Its metabolic fate is
unknown. It is excreted in urine, while large amounts are excreted unchanged in faeces. Its
plasma half life is about 24h, but it persists in the infected keratin tissue of skin for several
weeks.
Clinical uses: It is used in dermatomycoses, but it is not effective when used topically, but
effective when used systemically (orally).
ADRs: Nausea, vomiting, epigastric pain, diarrhoea, headache, parasthesia, peripheral neuritis,
vertigo (a type of dizziness), mental confusion, lethargy, blurred vision, allergic reactions.
Preparations:

Flucytosine- It is a fluorinated pyrimidine derivative.
MOA: It is used in deep (systemic) fungal infections. It is fungistatic and not fungicidal. It acts
by converting to 5-fluorouracil and then to 5-fluoro deoxyuridylic acid, which inhibits
thymidylate synthetase during DNA synthesis resulting in stoppage of fungal reproduction
(duplication).
ADME: It is well absorbed from GIT and reaches sufficient concentration in blood and CSF. It
is completely excreted in urine in unchanged form by glomerular filteration.
Uses: It is given along with amphotericin-B for the treatment of systemic mycoses.
ADRs: GIT upsets (nausea, vomiting and anorexia), hepatic damage and bone marrow
depression.
Azoles- Ketaconazole, fluconazole, itraconazole.(Orally)
Ketaconazole: It is an imidazole compound. It is effective orally.MOA: It is a broad spectrum
antifungal drug effective against many superficial and deep (systemic) fungal infections. It is a
fungicidal drug. It acts by interfering with the formation of ergosterol in the cell membrane of
the fungi by inhibiting the enzyme lanosterol 14 α-demethylase. Ergosterol is a cell membrane
stabilizing agent of fungi. Its absence in cell membrane leads to death of fungi.
ADME: It is well absorbed from GIT. Its absorption is retarded in presence of H2 – blockers
(cimetidine and ranitidine). In the plasma it is bound to plasma proteins. It is metabolized in the
liver. Its metabolites and unchanged portions are eliminated through urine.
Clinical uses: Both topical and systemic fungal infections.
ADRs: GIT upset (nausea, vomiting and anorexia), allergic reactions. As it suppresses the
biosynthesis of some steroidal hormones- endocrinal disturbences- gynacomastia, loss of libido,
menstrual irregularities).
Preparations of oral azoles and topical azoles: and tonaftate.

Miscellaneous antifungal agents:
Nystatin- It is effective only against Candida albicans. Benzoic acid and salicylic acid.(used in
dermatophytosis- white field ointment). Ichthammol ( used in dermatomycoses), selenium
sulfide ( for dandruff).
h.Antiviral drugs: These drugs are used in the treatment of viral infections. Viruses have no cell
wall.AQ virus consists of either double stranded DNA or single stranded RNA called a genome,
which is enclosed in a protein coat called capsid. Some viruses also have a lipoprotein envelop.
A DNA virus is a virus that has DNA as its genetic material and replicates using a DNA-
dependent DNA polymerase. The nucleic acid is usually double-stranded DNA (dsDNA) but
may also be single-stranded DNA (ssDNA). Single –stranded DNA is usually expanded to
double–stranded in infected cells. An RNA virus is a virus that has RNA (ribonucleic acid) as its
genetic material. This nucleic acid is usually single-stranded RNA (ssRNA), but may be double-
stranded RNA (dsRNA). Pairing of bases in DNA is - A-T, G-C and in RNA is -A-U, G-C. In
RNA, the sugar is ribose, in DNA deoxyribose. Ribose contains one additional OH group.

A virus is active only when it is within host cell and become inactive (inert) when it is outside a
host cell. Hence viruses are obligate intracellular parasites.Host cell may be mammalian (in
mammalian virus), bacterial (in bacteriophage), insect (in arbovirus0, or plant (in plant virus). A
virus cannot prepare its own food and metabolise. It has to depend on the host cell for these
purposes. QWhen a virus enters the host cell, the host cell works to provide prepared materials
like nucleic acid, protein etc. for the reproduction of the virus. The subsequent release of the
infections progency of the virus from the host cell is called replication of the virus.

Replication of the virus: There are various stages in viral replication, which are cell entry
(attachment and penetration), uncoating (release of viral genome), transcription of viral genome,
translation of viral proteins, assembly of viral components and release of new virion from host
cell (by budding or cell lysis).
Examples of DNA virus: Pox virus Small pox
1. Pox viruses (causing small pox)
Herpes virus Herps Chicken pox
2. Herpes virus (herps,), variola virus (chicken pox).
Adeno virus Adeno virus conjuctivitis. Hepatitis B virus cirrhosis of the liver
3. Adeno virus (conjuctivitis, sore throat), hepatitis B virus (cirrhosis of the liver).

Examples of RNA Virus: 1.HIV virus (AIDS)
2.Papilloma virus (warts), rubella virus (German measles)
Warts German meascles
3.Rabdo virus (rabies)
Rabdo virus Rabies

4. Picorna virus (poliomyelitis, meningitis and common cold).
5. Orthomyo virus (influenza):
6. Paramyxo virus: (measles and mumps)
Classification of antiviral drugs: There are three groups
1.Anti herpes virus drugs: Acyclovir, famciclovir, ganciclovir, idoxuridine, sorivudine,
trifluridine and vidarabin.
2.Antiretroviral (anti HIV ) drugs: Zidovudine, stavudine, didanosine.
3.Other antiviral drugs: Amantadine, rimantadine, methisazone, interferon-α and ribavirin.
Acyclovir –MOA- Chemically it is acycloguanosine related to the purines. It is effective in most
of the types of herpes virus.It is virustatic and acts by inhibiting DNA synthesis in herpes
viruses. It enters the virus infected cells. The thymidine kinase produced by herpes infected cells
converts acyclovir to acycloguanosine monophosphte. This is then phosphorylated by human
enzymes to acycloguanosine triphosphate. This inhibits the DNA polymerase of the herps virus
and prevents synthesis of new viral DNA strand during viral DNA replication. In noninfected
host cells thymidine kinase enzyme is not present. Hence there is no formation of
acycloguanosine monophosphate. Hence it is not lethal to host cells.

Antiviral spectrum: Acyclovir is effective against herpes simplex virus type-I (HSV-I), HSV-II,
varocella zoster virus (VZV), it is not effective on cytomegalo virus (CMV), as it lacks the
enzyme thymidine kinase.
ADME: It is partly absorbed after oral administration. It also enters the CSF. Some part of it gets
metabolized in the liver. The metabolites and free form get eliminated through urine. It has
plasma half life of about 6h.
Uses: It is used in the treatment of various types of herpes simplex viral infections- oral herps,
mucocutaneous herps, and genital herps. It is also used prophylactically to reduce the chances of
HIV infections.
ADRS;On oral use : Headache, nausea, insomnia, malaise (feeling of uneasiness) and tremors.
On I.V.Use: Vomiting, skin rash, sweating, hypotension.
On topical use: Stinging and burning sensation after each application.
Preparations: Acyclovir 200mg caps, injection, cream. Famiciclovir200mg tabs.
Ganciclovir inj,

Idoxuridine: It is 5-iodo-2-deoxyuridine (IUDR), acts as a thymidine analogue. (Thymidine or
deoxythymidine is a nucleoside composed of deoxyribose joined to the pyrimidine base-
thymine.) It acts by inhibiting the synthesis of DNA by preventing the utilization of thymidine
(by competition) in the causative viruses. It inhibits both viral and host cell’s DNA synthesis and
hence it has high degree of toxicity when used systemically.
Uses; It is indicated only in H.simplex keratinoconjunctivities.
Prep: Eye drops and ophthalmic ointment.
Vidarabine: Chemically it is adenine arabinoside. It is effective against DNA viruses like herps
viruses. It acts by inhibiting viral DNA synthesis by stopping viral replication. It has more
toxicity than acyclovir.
Uses: It is used in infections caused by herps simplex, varicella zoster and small pox.
Prep; Ophthalmic ointment and i.v. infusion.
2. Antiretroviral (anti HIV ) drugs: Zidovudine, stavudine, didanosine
Zidovudine: MOA: It is a synthetic thymidine analogue (azidothymidineAZT). It has strong
affinity for viral DNA polymerase (reverse transcriptase), but has very low affinity for
mammalian DNA polymerase. It is acted upon by mammalian thymidine kinase (an enzyme) and
is converted to active form azidothymidine triphosphate (by phosphorylation), which
competitively inhibits viral reverse transcriptase and prevents any further elongation of the viral

DNA. Thus viral DNA terminates prematurely and replication is prevented. It is effective against
HIV-1, HIV-2 and other retro viruses.
ADME: It is well absorbed when given orally. It can also be given by i.v. route. It is distributed
well in tissues and fluids. It can easily penetrate BBB and reaches CSF. About 80% gets
metabolized in the liver by conjugation with glucuronic acid. The metabolites and free form gets
excreted through urine.
Uses: It is used in AIDS caused by HIV.
ADRs:
1. GIT Upset (nausea, vomiting and diarrhea).
2. Bone marrow depression: (anaemia, granulocytopenia and thrombocytopenia).
3. CNS toxicity: (headache, insomnia, agitation and seizures)
4. Myopathy- myalgia.
Preparations: Tabs, caps and iv infusions.

3. Other antiviral drugs: Amantadine, rimantadine, methisazone, interferon-α and ribavirin.
Amantadine: These are tricyclic amines with antiviral activity against influenza virus. They stop
viral replication by preventing uncoating of virus. A virus in order to replicate has to enter the
susceptible host cell, where it is uncoated. This prevents viral replication. They are used as
prophylactic agents against attacks of influenza caused by influenza-A virus. Amantadine is also
used in the treatment of Parkinsonism as dopamine facilitator. It can produce CNS toxicity
(dizziness, slurring of speech, ataxia, insomnia and seizures) and allergic reactions (skin rashes
and pruritus).
Methisazone: It is a semicarbazone. It is mainly effective against small pox viruses. Its mode of
action is unknown. It is used as a prophylactic agent. It has low toxicity.
Interferon-α: These are broad spectrum antiviral agents effective against both DNA and RNA
viruses. The exact mechanism is not known. It probably acts indirectly by binding with specific
cell surface receptors and inducing the production of cellular enzymes which subsequently block
viral replication. It is administered by I.M. or I.V.
Ribavirin: It is an antiviral drug used in severe RSV (a virus causes respiratory tract infections),
hepatitis-C and other viral infections. It is a prodrug. It is converted into active form ribavirin
triphosphate. This inhibits the viral replication by inhibiting the nucleic acid synthesis. It is
administered orally or as aerosol. These are relatively safer drugs.

i) Chemotherapy of tuberculosis and leprosy
Drug therapy of Tuberculosis:
Tuberculosis is a chronic granulomatous infectious disease caused by Mycobacterium
tuberculosis, M.bovis or atypical mycobacteria (collectively called Tubercle bacilli). In 1882
Robert Koch discovered the causative organism of tuberculosis. Tuberculosis is a systemic
disease. e.g. Pulmonary tuberculosis. It also affects the other organs including brain. Its acute
forms are tuberculosis pneumonia and generalized military tuberculosis.
M. bovis
Classification of antitubercular drugs: Two groups
1.Standard drugs ( first line drugs/ primary drugs)
a.Tubeculocidal drugs- Isoniazid, rifampicin, pyrazinamide and streptomycin.

b.Tuberculostatic drugs- Ethambutol and thiacetazone.
2. Researve drugs (second line/ secondary drugs).
a.Tuberculocidal drugs- Capreomycin, kanamycin and FQs (cipro, o and sparfloxacin).
b.Tuberculostatic drugs-Ethionamide, cycloserine and PAS (para-amino salicylic acid)
Reserve drugs are used in resistant cases of tuberculosis. Antitubercular drugs are always used in
combinations of 2,3, or 4 drugs . The single drug usage leads to the rapid development of
resistance.
Isoniazid (INH)- It is a synthetic drug. Chemically it is the hydrazide of isonicotinic acid. Its
structure is similar to pyridoxine (Vit B6).
It is a highly potent antitubercular drug, but it is ineffective in TB caused by atypical
mycobacteria. It does not act against any other microorganism. It is more effective in rapidly
multiplying organisms as compared to dormants. It is the main drug in antitubercular regimens. It
is given in combination with other antitubercular drugs to prevent mycobacterial resistance. In
tubercular meningitis it is given in double doses.
MOA- Mycolic acids are essential membrane lipids made up of long fatty acids present in the
cell wall of Mycobacterium tuberculosis. Mycolic acids are composed of a shorter beta-hydroxy
chain with a longer alpha alkyl side chain. Each molecule contains between 60 and 90 carbon
atoms. The exact number of carbon atoms varies by species. Most mycolic acids also contains
various functional groups. M.tuberculosis produces three types of mycolic acids; alpha, methoxy
and kito mycolicm acids. Alpha-mycolic acids comprise of about 70%. It consists of several
cyclopropane rings. Methoxy mycolic acids (10- 15 %) contains several methoxy groups and the
remaining keto-mycolic acids (10-15%) contains several keto groups. The isoniazide acts by
inhibiting the enzyme ‘mycolase synthatase’, which is required for the synthesis of mycolic acid.
This damages the cell wall of the mycobacteria. It is primarily tuberculocidal but may be
tyberculostatic at lower concentration. It acts on both extracellular and intracellular tubercle
bacilli. It has no action on dormants.

Drug resistance- In a susceptible mycobacterial population 1 in 107
are resistant mutants, which
donot allows isoniazide penetration. To prevent emergence of mutants, isoniazid should not be
used alone but always used in combination with other antitubercular drugs.
ADME- It is rapidly and completely absorbed from GIT. It is widely distributed in all body
tissues and fluids including brain and CSF. It crosses the placental barrier and is secreted in milk.
It is metabolized in the liver by acetylation, which is under genetic control. In slow acetylators it
leads to neurotoxicity (pheripheral neuritis) and in fast acetylators it leads to hepatotoxicity (due
to acetyl hydrazine- a metabolite). To prevent peripheral neuritis pyridoxine is combined with
isoniazid in the treatment of tuberculosis. The acetylated metabolites and glycine conjugates and
free form are eliminated through urine.
Clinical uses of isoniazid- It is used in all types of tuberculosis. It is the drug of choice of
tubercular meningitis.
Preparations- Isoniazid 100, 300 mg tablets, isoniazid syrup 100mg/5ml, injection 100mg/ml.
ADRs-1.Neurotoxicity and hepatotoxicity. The neurotoxicity is due to pyridoxine deficiency
caused by competition between isoniazid and pyridoxine for the enzyme pyridoxyl kinase.

2. Allergic reactions- Skin rashes, drug fever, lymphdenopathy and jaundice.
3. Ideosyncratic reaction- It can cause hemolysis in patients with G6-PD deficiency.
Drug interactions; Isoniazide is a hepatic microsomal enzyme inhibitor. It inhibits the
metabolism of drugs like phenytoin, carbamazepine, etc leading to their toxicity.
Rifampicin- it is a semisynthetic derivative of the antibiotic ‘Rifamycin B’ produced by
streptomyces species. Chemically it is a macrocyclic compound. It is effective in all types of
tubercle bacilli including dormant bacilli. It is also effective against lepra bacilli and many gram
positive and gram negative bacteria. It is also effective in atypical mycobacteria.
MOA- RNA polymerase (RNAP) is an enzyme that produces RNA. In cells RNAP is necessary
for constructing RNA chains using DNA genes by a process called transcription. Rifampicin
inhibits DNA-dependent RNA polymerase in bacterial cells by binding its beta subunit, thus
preventing transcription to RNA and subsequent translation to proteins. The rifampicin interacts
with the beta subunit of RNA polymerase (α2β trimer). This halts mRNA transcription. This
prevents the translation of polypeptides. Its lipophilic nature helps this drug to enter brain; hence
it is indicated in meningitis tuberculosis.
Drug resistance- Rifampicin resistance is either due to bacterial permeability barrier or due to a
mutation of DNA dependent RNA polymerase. If it is used alone, mycobacteria develop rapid
resistant to it. Hence it is used in combination with other antitubercular drugs. There is no cross
resistance with other antitubercular drugs.
ADME- It is administered orally. It is well absorbed from GIT. Food interfers with its absorption
resulting in lower plasma levels. It is widely distributed in various body tissues and fluids
including brain and CSF. 85 % gets bound to plasma proteins. It crosses placental barrier. It is
metabolized in the liver forming desacetyl rifampicin, which is active as rifampicin against

tubercle bacilli. It undergoes enterohepatic circulation. It is excreted mainly in urine and faeces.
It makes urine, faeces and saliva orange red color during excretion.
Clinical uses: It is mainly used in the treatment of tuberculosis and leprosy in combination with
other drugs. It is also used in the treatment of brucellosis and serious staphylococcal septicaemia.
ADRs: Leucopenia, eosinophilia,
Skin rash diarrhoea dizziness Hepatitis in elderlies
Flu like syndrome
Preparations: Rifampicin 150, 300mg caps, rifampicin syrup 100mg/5ml.
Drug interactions: Rifampicin is a hepatic microsomal enzyme inducer. It increases metabolism
of drugs like digoxin, dapsone, oral contraceptives and hydrocortisone leading to decreased
efficacy of these drugs.
Pyrazinamide: Chemically it is pyrazinoic acid amide. It is a structural relative of nicotinamide.
Nicotinamide

It is active only against M.tuberculosis like isoniazid. It is a tuberculocidal drug. Its mechanism
of action is not known. It is effective against M.tuberculosis of human type but ineffective
against the bovine and atypical forms of tubercle bacilli. It shows antitubercular activity in an
acidic pH (<6.0) and is effective only against tubercle bacilli within macrophages (where the pH
is acidic).Resistance develops rapidly if it is used alone and hence it is given along with other
anti TB drugs.
.
Macrophage
ADME: It is well absorbed from GIT. It is widely distributed in the body tissues and fluids
including brain and CSF. It is metabolized in the liver by deamination. It is excreted in urine as
metabolites and unchanged form.
Preparations: Pyrazinamide 500mg tab, syrup 250mg/5ml.
ADRs: Metallic taste, anorexia, nausea, vomiting, skin rashes, fever, photosensitivity, jaundice,
precipitation of gout.

Ethambutol: It is a tuberculostatic drug. Its mechanism is not known. It is effective against
mycobacteria resistant to isoniazid, streptomycin ethionamide and PAS. It acts mainly against
rapidly multiplying mycobacteria in the walls of the tuberculosis cavities.
ADME: It is given by oral route. It is well absorbed in the GIT. It is distributed in the body
tissues and fluids. It also enters the CSF. It is partly metabolized in the liver. About 50 % of the
drug is excreted unchanged in urine. The metabolites are excreted through urine and faeces.
Uses: It is used in TB in combination with other anti TB drugs.
Preparations: Ethambutol 400,800mg tablets.
ADRs: Oulotoxicity (optic neuritis, red-green blindness, loss of vision and retinal damage).
Other adverse effects are nausea, vomitin, anorexia, dizziness, peripheral neuritis and allergic
reactions.
Thiacetazone: Chemically it is a derivative of thiosemi-carbozone. It is a tuberculostatic drug.
Its mechanism is not known. It is a cheap drug and preferred in long course regimen. It is given
orally. Well absorbed in the GIT. It is widely distributed in body tissues and fluids It is partly
metabolized in the liver. The metabolites and unchanged form are excreted through urine. It is
used only in tuberculosis in combination with other anti TB drugs. It can produce nausea,
anorexia, exfoliative dermatitis, hepatitis, hepatotoxicity, etc.
Ethionamide: It is a tuberculostatic drug. It probably acts by inhibiting the synthesis of mycolic
acid synthesis in mycobacteria. It is also effective in atypical mycobacteria. If it is used alone
resistance develops rapidly, hence it is given along with other anti TB drugs.
ADRs: Nausea, vomiting, anorexia, skin rashes, hepatitis, peripheral neuritis, optic neuritis,

Cycloserine: Chemically it is related to amino acid alanine. It is a tuberculostatic drug. It acts by
inhibiting the cell wall synthesis. It is effective against M.tuberculosis and atypical
mycobacteria. It is well absorbed orally and distributed to various body tissues and fluids
including brain and CSF. It is metabolized in the liver and excreted in urine as both metabolites
and unchanged form. It is given along with other ant TB drugs. The main ADRs are
neurotoxicity, hepatotoxicity and convulsions.
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Fluoroquinolone Antibiotics Guide

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