ANTIMYCOBACTERIAL DRUGS
Galya Stavreva and Diana Pendicheva (2012)
Faculty of Medicine, Medical University – Pleven
Introduction
Mycobacteria are aerobic, Gram-positive rod-shaped bacteria with lipid-rich cell walls. The
most common types of mycobacterial infections include tuberculosis, leprosy, and
mycobacterium avium complex.
Tuberculosis (TB), an infectious disease caused by
various
strains
of
mycobacteria,
usually
Mycobacterium tuberculosis, is a major health problem
in developing countries. According to WHO in 2010
8.8 million people fell ill with TB and 1.4 million died
from TB (it currently holds the seventh place in the
global ranking of causes of death). Mycobacterium
avium complex (MAC) is an opportunistic infection
caused by M. avium and M. intracellulare that can
produce severe illness in people with advanced AIDS,
but rarely affects others.
The treatment of infections caused by Mycobacteriа
presents therapeutic problem and involves the use of
drug combinations to delay the emergence of
resistance and to enhance antimycobacterial efficacy.
Many factors such as the development of resistance;
the intracellular location of infection; the formation of
slow-growing granulomatous lesions, and the chronic
nature of mycobacterial disease; and the patient compliance make chemotherapy of
mycobacterial infections complicated.
Antimycobacterial agents are divided into three groups: antitubercular drugs, antileprotic
drugs, and drugs used for atypical mycobacteria.
Classification of drugs used in tuberculosis


First line drugs: Isoniazid (INH), Rifampin (Rifampicin), Ethambutol,
Pyrazinamide, and Streptomycin. These drugs are use routinely; have high
antitubercular efficacy; and low toxicity.
Second line drugs: Ethionamide, Para-aminosalicylic acid (PAS), Capreomycin,
Cycloserine, aminoglycosides (Kanamycin and Amikacin), other rifamicins
(Rifabutin and Pifapentine), fluoroquinolones (Ciprofloxacin, Ofloxacin,
Levofloxacin, Moxifloxacin), macrolides (Azithromycin and Clarithromycin),
Linezolide. These drugs are no more effective than the first-line agents; their toxicities
are often more serious or both; are particularly active against atypical strains of
mycobacteria.
Mechanisms of action and pharmacological effects of antitubercular drugs
First line drugs
1. Isoniazid (INH), a synthetic analogue of pyridoxine, is the most potent tuberculocidal
drug. It is an essential component of all regimens, unless the patients are not able to
tolerate it or bacteria are resistant. INH is bactericidal for multiplying tubercle bacilli,
but is less effective against dormant organisms. It acts against extracellular as well as
intracellular bacteria and is active in acidic and alkaline medium. Its mechanism of
action involves inhibition of synthesis of mycolic acids, an unique fatty acid
component of mycobacterial cell wall. This explains the selective effect of INH for
mycobacteria and the absence of such to other microorganisms. INH is a prodrug that
is activated by mycobacterial catalase-peroxidase (KatG). The targeted enzymes are
acyl carrier protein reductase (InhA) and a ketoacyl-ACP synthase (KasA). The
activated drug covalently binds to and inhibits these enzymes, which are essential for
the synthesis of mycolic acid. For bacilli in a resting phase, isoniazid is bacteriostatic,
but for rapidly dividing organisms, it is bactericidal. Resistance can emerge rapidly if
the drug is used alone. High-level resistance is associated with mutation of katG gene
that codes for a enzyme KatG involved in the bioactivation of isoniazid. Low-level
resistance occurs via deletions in genes that encode the "target enzymes". INH is
completely absorbed orally and penetrates all body fluids and tissues, tubercular
cavities, placenta and meninges. INH is metabolized in the liver; it undergoes Nacetylation and hydrolysis, resulting in inactive products. Acetylation is genetically
regulated: slow inactivation is inherited as a homozygous autosomal recessive trait,
while fast inactivation is due to either a homo- or heterozygous dominant gene. Fast
inactivation is inherited as an autosomal dominant trait. The metabolites are excreted
through glomerular filtration. Slow acetylators excrete more of the parent compound.
Impaired renal function results in accumulation of the drug, primarily in slow
acetylators. Fast acetylators may require higher dosage than slow acetylators for
equivalent therapeutic effects. There is a large variation of the slow acetylator
phenotype among ethnic groups: 40-70% of Caucasians and African-Americans, 1020% of Japanese and Canadian Eskimo, more than 80% of Egyptians, and certain
Jewish populations are slow acetylators.
2. Rifampin (Rifampicin) is a semisynthetic derivative of rifamycin, produced by soil
mold Streptomyces mediterranei. Rifampin has a broader antimicrobial activity: in
vitro it is active against gram-positive and gram-negative cocci, some enteric bacteria,
mycobacteria, and chlamydia. Because resistant strains rapidly emerge during therapy,
it is never given as a single agent in the treatment of active tuberculosis. Rifampin
blocks transcription by binding to the beta subunit of bacterial but not human DNAdependent RNA polymerase and thereby inhibits the initiation step of RNA synthesis.
It is bactericidal for both intracellular and extracellular mycobacteria, including M.
tuberculosis, and atypical mycobacteria, such as M. kansasii. It is used
prophylactically for individuals exposed to meningitis caused by meningococci or
Haemophilus influenzae. Rifampin is very active antileprotic drug, but to delay the
emergence of resistant strains, it is usually given in combination with other drugs.
Resistance to rifampin can be caused by alteration of the target site, bacterial DNAdependent RNA polymerase or by decreased permeability. Distribution of the drug
occurs to all body fluids and organs. Since the substance itself is red, this high
distribution in the body is the reason for the orange-red color of the saliva, tears,
sweat, urine, and feces. Tears may stain soft contact lenses orange-red. Rifabutin
(second line drug), an analog of rifampin, has some activity against Mycobacterium
avium-intracellulare complex but is less active against tuberculosis.
3. Ethambutol inhibits the synthesis of arabinogalactan, a component of mycobacterial
cell walls, acting on arabinosyl transferases (encoded by the embCAB operon). It is
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bacteriostatic and specific for most strains of M. tuberculosis and M. kansasii.
Resistance is not a serious problem if the drug is employed with other antitubercular
agents. Ethambutol can be used in combination with isoniazid, rifampin, and
pyrazinamide to treat tuberculosis.
4. Pyrazinamide is a synthetic antitubercular agent used in combination. The drug is
largely bacteriostatic, but the mechanism of its action is unknown. The target of
pyrazinamide appears to be the mycobacterial fatty acid synthase I gene involved in
mycolic acid biosynthesis. Pyrazinamide is the more active in acidic medium; it is
highly lethal to intracellular tubercle bacilli in the acidic environment of lysosomes as
well as in macrophages. Pyrazinamide is enzymatically hydrolyzed to pyrazinoic acid,
which is the active form of the drug. The metabolic conversion via pyrazinamidases
present in M. tuberculosis is encoded by the pncA gene. Resistance occurs via
mutations in this gene and by increased expression of drug efflux systems.
5. Streptomycin is the first antibiotic effective in the treatment of tuberculosis. It is
bactericidal inhibitor of bacterial protein synthesis. Streptomycin acts against
extracellular organisms. It is now used more frequently than before because of the
growing prevalence of drug-resistant strains of M. tuberculosis. Ribosomal resistance
to streptomycin develops readily, limiting its role as a single agent. Infections due to
streptomycin-resistant organisms may be treated with kanamycin or amikacin
(alternative second line drugs).
Second line drugs
1. Ethionamide is a structural analog of INH and also blocks the synthesis of mycolic
acid. It acts on both extra- and intracellular organisms. The major disadvantage is
severe gastrointestinal irritation and adverse neurologic effects at doses needed to
achieve effective plasma levels. It is effective after oral administration, distributes all
over including cerebrospinal fluid. Metabolism is extensive, and the urine is the main
route of excretion. It is seldom used; only in case of resistance to better tolerated
drugs.
2. Para-aminosalicylic acid (PAS) is structurally related to sulfonamides as well as in
mechanism of action. PAS is not active against other bacteria: selectivity may be due
to difference in the affinity of folate synthetase of M. tuberculosis and other bacteria to
PAS. It is rarely used because primary resistance is common. PAS is tuberculostatic
and one of the least active drugs. It only delays development of resistant bacteria and
does not add to the efficacy of more active drugs.
3. Capreomycin is a peptide obtained from Streptomyces capreolus that inhibits protein
synthesis. It is administered intramuscularly for the treatment of multidrug-resistant
tuberculosis. Strains of M. tuberculosis, resistant to streptomycin or amikacin usually
are susceptible to capreomycin.
4. Cycloserine is an orally effective tuberculostatic agent that inhibits cell wall
synthesis. It distributes well throughout body fluids, including the cerebrospinal fluid.
Cycloserine is metabolized, and both parent and metabolite are excreted in urine.
Accumulation occurs with renal insufficiency.
5. Fluoroquinolones (Ciprofloxacin, Ofloxacin, Levofloxacin, Moxifloxacin) inhibit
strains of M. tuberculosis in addition to their activity against many gram-negative and
gram-positive microorganisms. They have an important place in the treatment of
multidrug-resistant tuberculosis, especially for strains that are resistant to first-line
agents. Some atypical strains of mycobacteria are also susceptible.
6. Macrolides, such as azithromycin and clarithromycin, are part of the drug
combinations that include ethambutol and rifabutin used for the treatment of infections
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by M. avium-intracellulare complex. Azithromycin is preferred for HIV-infected
patients because does not interfere with the metabolism of antiretroviral drugs.
7. Linezolid is a synthetic antibiotic, an inhibitor of protein synthesis, used for the
treatment of serious infections caused by gram-positive bacteria that are resistant to
other antibiotics. It achieves good intracellular concentrations and has been used in
combination with other drugs to treat patients with multidrug-resistant tuberculisis.
Table 1. Pharmacokinetic parameters
Drug
Isoniazid
Rout of application
Orally (commonly)
i.m.
Rifampin
Orally
Ethambutol
Orally
Tmax; Cmax; t1/2
Tmax 1-2 h; Cmax 3-5
mcg/mL; t1/2 in "fast
acetylators" 60-90 min;
in "slow acetylators" 3-4
h
Tmax 2-4 h; Cmax 5-7
mcg/mL; t1/2 1.5-5 h
Tmax 2-4 h; Cmax 5-7
mcg/mL; t1/2 3-4 h
Pyrazinamide Orally
Tmax 1-2 h; Cmax 30-50
mcg/mL; t1/2 8-11 h;
Streptomycin
Parenterally; i.m.;
i.v.
T max 1 h; C max 25-50
mcg/mL; t1/2 5-6 h
Ethionamide
Orally
PAS
Orally
T max 3 h; C max 20
mcg/mL (at oral dose of
1 g); t1/2 2 h
T max 1,5-2 h; C max 75
mcg/mL; t1/2 1 h
Methabolism, exretion
Liver; phase II reaction by
N-acetylation
Inducer of liver
microsomal enzymes.
Enterohepatic cycling;
partially metabolized in the
liver; 60-65% excretion
through feces
Liver; oxidation followed
by conversion to
dicarboxylic acid. 20-22%
is excreted in feces as
unchanged drug; 8-15% in
urine
Liver; to pyrazinoic acid;
parent molecule and
metabolite are excreted in
the urine
Urine excretion, by
glomerular filtration (89%
within 24 hours).
Liver; to aminosalicylic
acid
Over 80% is excreted in the
urine; 50% as acetylated
compound
Pharmacotherapy of tuberculosis

Isoniazid (INH) is the most important drug worldwide for the treatment of all types of
tuberculosis, unless the patients are not able to tolerate it or bacteria are resistant. It is
used alone for prophylaxis (alternative to INH prophylaxis is rifampin), but for
treatment of active infections, the drug must be used in combination with another
agent. Isoniazid usually is given orally (5 mg/kg), in a single daily dose. Isoniazid may
be used as intermittent therapy for tuberculosis: after a minimum of 2 months of daily
therapy with isoniazid, rifampin, and pyrazinamide, patients may be treated for 4
4





months with twice-weekly doses of isoniazid (15 mg/kg orally) plus rifampin (10
mg/kg, up to 600 mg per dose). Pyridoxine, vitamin B6, (10 to 50 mg per day) should
be administered with INH to prevent the peripheral neuropathy and central nervous
system toxicity.
Rifampin for oral administration is available alone and as a fixed-dose combination
with isoniazid or with isoniazid and pyrazinamide. A parenteral form of rifampin is
available for use when the drug cannot be taken by mouth. Rifampin and isoniazid are
the most effective drugs available for the treatment of tuberculosis. The dose of
rifampin is 600 mg, given once daily (1 hour before or 2 hours after a meal).
Ethambutol has essentially replaced aminosalicylic acid because of a lower incidence
of toxic effects and better acceptance by patients. It can be used in combination with
isoniazid, pyrazinamide, and rifampin in the treatment of tuberculosis. Ethambutol
accumulates in patients with impaired renal function, and adjustment of dosage is
necessary.
Pyrazinamide. The combined use of pyrazinamide with other antitubercular agents
drugs is an important factor in the success of short-course (6-month) treatment
regimens. Pyrazinamide is given as a single daily dose, but is safe and effective when
administered twice or thrice weekly (at increased dosages).
Streptomycin is now used more frequently than before because of the growing
prevalence of drug-resistant strains of M. tuberculosis. Many clinicians prefer to give
4 drugs, of which streptomycin may be one, for the treatment of life-threatening
tuberculous disease, including meningitis, miliary dissemination, and severe organ
tuberculosis. The dose is given twice daily (not to exceed 1 g per day). Therapy
usually is discontinued after 2 to 3 months, or sooner if cultures become negative.
Second line drugs with antimycobacterial activity are used in cases that are resistant
to first-line agents. They are less effective, and their adverse drug reactions are often
more serious than the first-line agents.
a) The goals of antitubercular chemotherapy are to kill dividing mycobacteria; to kill
persisting bacilli; and to prevent emergence of resistance.
b) Treatment must include at least 2 drugs to which the bacteria are sensitive to prevent the
development of resistance to antimycobacterial agents.
c) The majority of cases of previously untreated tuberculosis is caused by microorganisms
that are sensitive to isoniazid, rifampin, ethambutol, and pyrazinamide.
d) Because of the increasing frequency of drug resistance, the Centers for Disease Control and
Prevention has recommended that initial therapy should be with a 4-drug regimen (isoniazid,
rifampin, pyrazinamide, and ethambutol or streptomycin) pending sensitivity results.
e) Regimens for treating TB disease have an initial intensive phase of 2 months, followed by
the continuation phase of 4 or 7 months (total of 6 to 9 months for treatment).
f) The combination of isoniazid and rifampin for 9 months is equally effective for drugsensitive tuberculosis.
Pharmacotherapy of Mycobacterium avium complex (MAC) infection
a) MAC infection is common in HIV-AIDS patients. The risk of disseminated MAC (DMAC)
is directly related to the severity of immunosuppression.
b) Clarithromycin/azithromycin are the most effective agents against MAC. Clarithromycin or
azithromycin is recommended for prophylaxis in patients with CD4 counts less than 100/mcL.
c) Isoniazid and pyrazinamide have no role in the treatment of MAC infection.
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d) A favoured regiment consists of an intensive phase with clarithromycin or azithromycin
plus ethambutol. Rifabutin and/or a quinolone are added to the above regimen in some cases.
e) Therapy of MAC infection in HIV-infected individuals lasts at least 12 months or should
continue lifelong if the therapy is associated with clinical and microbiological improvement.
g) Drug interactions are a special concern in patients receiving highly active antiretroviral
therapy. The rifamycins induce the metabolism of protease inhibitors and non-nucleoside
reverse transcriptase inhibitors.
Side effects and toxicity
1. Isoniazid: peripheral neuritis (manifesting as paresthesias of the hands and feet), which is
the most common adverse effect, appears to be due to a relative pyridoxine deficiency;
hepatitis and idiosyncratic hepatotoxicity; convulsions in patients prone to seizures; optic
neuritis; hypersensitivity reactions (rashes and fever); hemolysis in G6PDH deficiency.
Interactions: inhibits metabolism of carbamazepine, phenytoin and warfarin.
2. Rifampin: the most common adverse reactions include nausea, vomiting, and rash.
Hepatitis and liver failure is rare (in daily doses of 1.2 grams or greater); a flu-like syndrome
associated with fever, chills, and myalgias, and sometimes with acute renal failure; hemolytic
anemia; and shock. Rifampin induces a number of cytochrome P450 enzymes and can
decrease the half-lives of other drugs that are coadministered and metabolized by this system.
3. Ethambutol: the most important adverse effect is reversible optic neuritis, resulting in
diminished visual acuity and loss of ability to discriminate between red and green (visual
acuity should be periodically examined); exacerbation of gout (urate excretion is decreased).
4. Pyrazinamide: polyarthralgia (40% incidence); hepatotoxicity (elevations of plasma
alanine and aspartate aminotransferases are the earliest abnormalities); hyperuricemia;
myalgia; maculopapular rash; porphyria and photosensitivity; avoid in pregnancy.
5. Streptomycin: vestibular toxicity (nausea, vomiting, and vertigo); paresthesia of face;
rash; fever; urticaria; cochlear toxicity (deafness); angioedema. Although streptomycin is the
least nephrotoxic of the aminoglycosides, nephrotoxicity does occur rarely; avoid in
pregnancy.
6. Capreomycin: nephrotoxicity and ototoxicity.
7. Ethionamide: gastric irritation, hepatotoxicity, peripheral neuropathies, and optic neuritis.
8. Cycloserin: CNS disturbances; epileptic seizure; peripheral neuropathies (but they respond
to pyridoxine).
Classification of drugs used in leprosy




Sulfone: Dapsone
Phenazine derivative: Clofazimine
Antitubercular drugs: Rifampin and Ethionamide
Other antibiotics: Ofloxacin, Minocycline, and Clarithromycin
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Mechanisms of action and pharmacological effects of antileprotic drugs
1. Dapsone (diaminodiphenylsulfone) is the most active drug against M. leprae.
Dapsone is bacteriostatic for M. leprae. Dapsone is a competitive inhibitor of
dihydropteroate synthase and inhibits folate synthesis. Because of increasing reports of
resistance, it is recommended that the drug be used in combinations with rifampin
and/or clofazimine. Dapsone can be given orally, penetrates tissues well, undergoes
enterohepatic cycling, and is eliminated in the urine, partly as acetylated metabolites;
t1/2 is 1-2 days.
2. Clofazimine is a phenazine dye with leprostatic and antiinflammatory effects with
unclear mechanism of action. It acts probably by interfering with template function of
DNA in M. leprae. Clofazimine is absorbed by the oral route and appears to
accumulate in tissues and then slowly released. It is used as a component of multidrug
therapy of leprosy.
Pharmacotherapy of leprosy (Hansen's disease)
a) M. leprae does not grow on artificial media; conventional methods cannot be applied to
determine its susceptibility to potential therapeutic agents in vitro. Animal models have
permitted laboratory tests for evaluation of drugs.
b) Leprosy is a disease caused by the bacteria M. leprae which causes damage to the skin and
the peripheral nervous system.
b) M. leprae multiplies very slowly and the incubation period of the disease is about five
years. Symptoms can take as long as 20 years to appear.
b) The global registered prevalence of leprosy at the beginning of 2011 stood at 192246 cases,
approximately 70% of all cases in the world are located in India.
c) Leprosy is curable and treatment provided in the early stages averts disability.
d) The World Health Organization recommends the triple-drug regimen of dapsone,
clofazimine, and rifampin for 6 to 24 months.
Side effects and toxicity
1. Dapsone: common adverse effects include gastrointestinal irritation, fever, skin rashes, and
methemoglobinemia. Hemolysis may occur, especially in patients with G6PDH deficiency.
2. Clofazimine: patients treated with clofazimine may develop icthyosis and red discoloration
of the skin, which may be very distressing to light-skinned individuals. Eosinophilic enteritis
has also been described as an adverse reaction to the drug.
OUESTIONS1
1. The main reason for the use of drug combinations in the treatment
tuberculosis is to: A) Decrease the incidence of adverse drug reactions;
Prevent the emergence of resistance; C) Prevent other bacterial infections;
Shorten the duration of therapy to less than 6 months.
2. Which one of the following antitubercular agents is not first line drug?
Isoniazid; B) Rifampin; C) Ethambutol; D) Ethionamide.
1
of
B)
D)
A)
Answers: 1 B; 2 D; 3 B, C; 4 A, B, D; 5 C; 6 C; 7 B; 8 A; 9 C. 10 D.
7
3. Which of the followings are accurate? A) Rifampin inhibits mycolic acids
synthesis; B) Isoniazid inhibits mycolic acids synthesis; C) The reduced
expression of katG gene is a mechanism of high-level isoniazid resistance; D)
Metabolism of streptomycin is genetically regulated.
4. Which of the followings statements about rifampin are accurate: A) For
tubercular infection it is used along with isoniazid, pyrazinamide, and
ethambutol; B) When used alone, there is a risk of the emergence of resistant
mycobacteria; C) Orange discoloration of body fluids is serious adverse drug
reaction; D) It is very effective antileprotic drug.
5. All of the followings statements are correct, EXCEPT: A) Isoniazid is the most
potent tuberculocidal drug; B) The most important side effect of ethambutol is
optic neuritis; C) Pyrazinamide is second line antitubercular drug; D)
Ethionamide is a structural analog of INH.
6. All are features of ethambutol toxicity, EXCEPT: A) Retrobulbar neuritis; B)
Colour vision disturbances; C) Arrhythmogenic effect; D) Hyperuricemia
7. A pregnant woman develops tuberculosis. Which one of the following drugs
should not be used? A) Isoniazid; B) Streptomycin; C) Ethambutol; D)
Rifampin.
8. Which of the followings statements concerning antileprotic drugs is LEAST
accurate? A) Resistance develops to dapsone when it is used in combination
with rifampin and clofazimine; B) Dapsone inhibits folate synthesis; C)
Clofazimine may cause skin discoloration; D) Ethionamide, ofloxacin, and
clarithromycin are alternative drugs for leprosy.
9. A patient with AIDS has pulmonary disease that is due to M. avium complex.
The optimal decision is to: A) Give azithromycin for prophylaxis of
dissemination of infection; B) Treat with isoniazid, clarithromycin, and
pyrazinamide at least 6 months; C) Treat the patient with clarithromycin,
ethambutol, and rifabutin at least 12 months; D) Treat the patient with
clarithromycin, ethambutol, and rifabutin at least 6 months.
10. Bactericidal and the fastest acting drug in leprosy is: A) Dapsone; B)
Clofazimine; C) Isoniazid; D) Rifampin.
Conclusions:





An initial four-drug regimen (INH, rifampin, pyrazinamide and either ethambutol or
streptomycin) is recommended for empiric treatment of tuberculosis. Neither ethambutol
nor streptomycin adds considerably to the overall activity, but they are given in
combinations to prevent emergence of resistance.
An isoniazid-rifampin combination given for 9 months will treat 95-98% of cases of
tuberculosis caused by susceptible strains.
The addition of pyrazinamide to an isoniazid-rifampin regimen for the first two months
allows the total duration of therapy to be reduced to 6 months without loss of efficacy.
Multidrug-resistant organisms (resistant to both INH and rifampin) should be treated with
3 or more drugs to which the organism is susceptible for a period of more than 18
months, including 12 months after sputum cultures become negative.
M. avium complex (includes M. avium and M. intracellulare) is the common cause of
disseminated disease in late stages of AIDS. Combinations of drugs are required to
suppress dissemination of the disease (clarithromycin or azithromycin plus ethambutol;
rifabutin and/or a fluoroquinolone are added to the above regimen in some cases).
8

The combination of dapsone, rifampin, and clofazimine is recommended for initial
therapy of leprosy.
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Brown M J Clinical pharmacology (10th ed.) London: Churchill Livingstone; 2008. Benson CA et al. (2003)
Clin Infect Dis. 37:1234. Center for Disease Control and Prevention (2006) Morb Mort Wkly Rep. 55: 301-5.
Field SK et al. (2004) Chest 126(2):566-81. Gandhi NR et al. (2006) Lancet 368:1575-80. Karakousis PC et al.
(2004) Lancet Infect Dis. 4:557. Katzung BG (Editor) Basic & Clinical Pharmacology (11th ed.) New York: The
McGraw-Hill; 2009. Keshavjee S et al. (2008) Lancet 372:1403. Lambev I and Boyadjieva N (Editors)
Pharmacology (2nd ed.) Sofia: APCO; 2010 (in Bulgarian). Nahid P et al (2006) Proc Am Thorac Soc. 3(1):10310. Rang HP et al. Pharmacology (7th ed) London: Chirchill Livingstone; 2011. Samson I (2005) Thorax 60:495.
Sharma HL and Sharma KK Principles of Pharmacology (1st ed.) New Delhi: Paras Medical Publisher; 2007.
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World Health Organization WHO report 2011 Global Tubeculosis Control. Zimhony O et al. (2000) Nat Med.
6:1043-7.
Drugs used in tuberculosis
Generic Name (Trade Name)
Ethambutol
Ethionamide
Isoniazid (Isonid, Rimicid)
Pyrazinamide
Rifampicin (Tubocin)
Streptomycin
Dosage Forms
Tablets 250 mg
Tablets 250 mg
Tablets 100 and 300 mg; amp. 50 mg/2 ml
Tablets 500 mg
Capsules 150 and 300 mg
Powder in vials 600 mg for IV injection
Powder in vials 1 g for IM injection
Drugs used in leprosy
Generic Name (Trade Name)
Clofazimine
Dapsone
Ethionamide
Rifampicin (Tubocin)
Dosage Forms
Capsules 50 mg
Tablets 25 and 100 mg
Tablets 250 mg
Capsules 150 and 300 mg
Powder in vials 600 mg for IV injection
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