Antimycobacterial drugs. Dr.Naza M.Ali lec Dec 2018
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1 Antimycobacterial drugs Dr.Naza M.Ali lec Dec 2018
2 About one-third of the world s population is infected with M. tuberculosis With 30 million people having active disease. Worldwide, 9 million new cases occur Approximately 2 million people die each year.
3 Antimycobacterial drugs Mycobacteria are rod-shaped aerobic bacilli that multiple slowly, every 18 to 24 hours in vitro. Their cell walls contain mycolic acids Mycolic acids are very long-chain, β- hydroxylated fatty acids. Mycobacteria produce highly lipophilic cell walls that stain poorly with Gram stain. they are termed acid-fast.
4 The most widely encountered mycobacterial infection is tuberculosis the leading cause worldwide of death from infection. Mycobacterial infections are intracellular result in the formation of slow-growing granulomatous lesions that are responsible for major tissue destruction.
5 The major pathogens are: -Mycobacterium tuberculosis cause T.B -Mycobacterium leprae cause leprosy -Atypical mycobacterium M tuberculosis can lead to serious infections of the lungs, genitourinary tract, skeleton, and meninges.
6 Strategies for addressing drug resistance Multidrug therapy is employed when treating T.B in an effort to delay or prevent the emergence of resistant strains. The combination of drugs should prevent the emergence of resistant strains.
7 EX. The intensive phase for 2 months Isoniazid, Rifampin, Ethambutol, Pyrazinamide Then continuation phase for the next 4 months Isoniazid and Rifampin
8
9 Treating T.B presents therapeutic problems. The organism grows slowly; difficult to culture have to be treated 6 months 2 years. Resistant organisms readily emerge, in patients who have had prior therapy or who fail to adhere to the treatment protocol.
10 First-line agents for T.B infection: Called first-line drugs because of their efficacy and acceptable degree of toxicity. 1. Rifamycins 2. Isoniazid (INH) 3. Pyrazinamide 4. Ethambutol 5. Streptomycin
11 Second-line drugs /Alternative drugs: are either less effective, more toxic, they are useful in patients who cannot tolerate the first-line drugs or who are infected with myobacteria that are resistant to the first-line agents.
12 1. Amikacin 2. Fluoroquinolones 3. Ethionamide 4. Capreomycin 5. Cycloserine 6. Macrolides 7. Para-aminosalicylic acid (PAS)
13 One successful strategy for achieving better treatment completion rates is Directly Observed Therapy, known as DOT, in which patients take their medication while being supervised and observed. DOT has been shown to decrease drug resistance as well as relapse and mortality rates and to improve cure rates.
14 1. Rifamycins: Rifampin Rifabutin Rifapentine
15 Rifampin Bactericidal against M tuberculosis Must always be used in conjunction with at least one other anti T.B Rifampin inhibits DNA-dependent RNA polymerase in M tuberculosis( not in human) Resistance develop rapidly if the drug use alone.
16 Pharmacokinetic: Orally is well absorbed distribute to most body tissues and in the CSF even in absence of inflammation. The drug undergoes enterohepatic cycling, metabolized in liver. Urine, feces & other secretions have an orange-red color.
17 Clinical uses: In combination with other anti T.B In leprosy (give monthly delays the develop of resistance to dapsone). Prophylactically for individuals exposed to meningitis caused by meningococci or Haemophilus influenzae.
18 Side effect Rifampin cause hepatitis, GI upset, skin rash If given less often than twice weekly, may a flulike syndrome and anemia. Rifampin induce liver drug metabolizing enzymes ( like anticoagulant, ketoconazole & contraceptive steroid).
19 Rifabutin Is less likely to cause drug interactions and is equally effective as anti T.B It is preferred in the treatment of T.B in HIV patients because it is less potent inducer of cytochrome 450 enzymes.
20 Rifapentine has activity comparable to that of rifampin but has a longer half-life than rifampin & rifabutin which permits weekly dosing
21 2. Isoniazid (INH) Is a prodrug that is activated by a mycobacterial catalase-peroxidase (KatG) Structural similar to pyridoxine Act by inhibition of enzymes required for mycolic acids. Mycolic acid is a unique class of very long-chain, hydroxylated fatty acids found in mycobacterial cell walls. Decreased mycolic acid synthesis lead to loss of acidfastness after exposure to INH.
22 Antibacterial spectrum: For bacilli in the stationary phase, INH is bacteriostatic, But for rapidly dividing organisms, it is bactericidal. If it is used alone, resistant organisms develop rapidly Clinical use: in T.B and is a component of most drug combination as prophylaxis for close contacts of patient with active disease
23 Pharmacokinetics Orally is readily absorbed. Drug levels in CSF are about the same as those in the serum. Isoniazid undergoes N-acetylation and hydrolysis Acetylation is genetically regulated, fast acetylators and slow acetylators. Chronic liver disease decreases metabolism Severely depressed renal function results in accumulation of the drug, primarily in slow acetylators.
24
25 Adverse effects 1. Peripheral neuritis as paresthesias of the hands& feet due to pyridoxine deficiency the toxic reactions are corrected by give mg/day of pyridoxine ( vitamin B6) 2. Hepatotoxicity 3. Mental abnormalities, convulsions 4. Optic neuritis
26 3. Pyrazinamide Bactericidal agent used in combination with isoniazid, rifampin, and ethambutol. The mechanism of its action is unknown. Pyrazinamide must be enzymatically hydrolyzed by pyrazinamidase to pyrazinoic acid, which is the active form of the drug.
27 Urate retention can occur and may precipitate a gouty attack.
28 4. Ethambutol Inhibit arabinosyl transferase involved in the synthesis of component of mycobacterial cell walls. Resistance occur rapidly by mutation if the drug use lone Use in combination with other anti T.B
29 Toxicity: Dose-dependent visual disturbances: decreased visual acuity, red green color blindness, optic neuritis possible retinal damage from prolonged use at high doses,
30 Drugs MOA Adverse Effects Rifampin inhibits DNA-dependent RNA polymerase Hepatitis, GI upset, rash INH inhibit mycolic acid synthesis Peripheral neuritis, hepatic enzyme elevation, peripheral neuropathy Pyrizinamide must beenzymatically hydrolyzed by pyrazinamidase hyperuricemia, Gout ( rare) Ethambutol Inhibit arabinosyl transferase Optic neuritis, decreased visual acuity, red green color blindness
31 5. Streptomycin Is used in drug combinations for: life threatening T.B, meningitis, miliary dissemination and severe organ tuberculosis.
32 Alternative drugs 1. Amikacin or kanamycin for T.B suspected to be caused by streptomycinresistance or multi-drug resistance tuberculosis 2. Fluoroquinolones: Ciprofloxacin, moxifloxacin and levofloxacin in multidrug-resistant tuberculosis.
33 3. Ethionamide: This is a structural analog of INH Adverse effects gastric irritation, hepatotoxicity, peripheral neuropathies & optic neuritis. Supplementation with vitamin B6 may lessen the severity of the neurologic side effects.
34 4. Capreomycin: limited use because of nephrotoxicity & ototoxicity. 5. Cycloserine: limited use because of peripheral neuropathy, CNS dysfunction. 6. Macrolides: azithromycin and clarithromycin part of the regimen 7. PAS: is now rarely used due of resistance & toxicity
35 Chemotherapy for Leprosy Leprosy is rare in United States About 70 % all cases in the world are located in India. Infection is aquired by prolonged contact with patients with lepromatous leprosy,
36 Who discharge M. leprae in large numbers in nasal secretion and from skin lesions. Then bacilli enter susceptible individuals via abraded skin or the respiratory tract. The triple-drug regimen for 6 to 24 month ( Dapsone, Clofazimine, and Rifampin)
37 The triple-drug regimen for 6 to 24 month ( Dapsone, Clofazimine, Rifampin)
38
39 Sulphones include: Dapsone, Acedapsone Is structurally related to sulfonamides act by inhibit folate synthesis via dihydropteroate synthetase
40 Dapsone is also used in the treatment of pneumonia caused by Pneumocystis jiroveci in HIV patients. The drug is well absorbed from the GIT, is distributed throughout the body, with high levels concentrated in the skin.
41 Adverse Reactions 1. Hemolysis, in patients with glucose 6-phosphate dehydrogenase deficiency, 2. Methemoglobinemia, 3. Peripheral neuropathy, 4. The possibility of developing a serious and severe skin complication
42 Clofazimine Is a phenazine dye that binds to DNA, Prevents it from serving as a template for future DNA replication. Patients may develop a red-brown discoloration of the skin.
43
44
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