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Effects of Streptomycin in Anti-tuberculosis Therapy

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THE IMPACT OF THE UNTOWAED TOOBSERVE aminoglycosides (streptomycin) COMBINITION anti-TB therapy for the treatment of patients with tuberculosis. Authors: Ghulam Rasool Bhurgri, Shamim-ur-Rehman, Muhammad Taki Syeda Momina, Raj Kumar Chohan. Ghulam Mustafa dhri, Barkat Sheikh. Tutorials: Tuberculosis is a chronic granulomatous disease of humans and other mammals, a group of closely related pathogens mandatory Mycobacterium tuberculosis is composed of M. tuberculosis caused. The tuberculosis bacillus of man - M. bovis - bovine TB agricanum - a heterogeneous type found mainly in Africa, halfway between the properties effuational the first two types, and M microti-a rare cause of disease is weakened and other small mammals, but for the man. People are usually, but not unique, the host of M. tuberculosis. M. bovis causes disease in cattle and badgers, deer and other mammals. Humans are accidental hosts, drink, usually acquire the infection by contaminated milk although infection of farm workers can occur by air. Man M. bovis can be transmitted to cattle, but is rarely reported from human to human (PDO AWIS D et al, 2003). The annual rate of TB infection and annual risk of infection is the best indicator of the status and development of tuberculosis in developed and developing countries. It is the proportion of the population that is primarily infected or reinfected in a year and is usually expressed as a percentage. The risk of TB infection in developed countries is now very low, less than 0. 5% per year in the majority, 0 1-0% and less in most of 0. 1% in some countries.

The risk of TB in these countries by about 10% per year has decreased. In developing countries, to find prices much higher. The annual risk of infection for the richest and poorest countries is shown in the following table. In most industrialized countries, the annual infection rate is now less than 0 1% and continue to decline by 10% per year. In Africa, the annual risk of infection can be much like the 2nd 5% or more, and in the current context of increasing TB notification HIB epidemic rather than diminish. The annual risk of infection declineTrend LevelAnnual current areas (%) 0th health resourceAvailabilityIndustrialized 04-0. 1> 10ExcellentMiddle income in Latin America West Asia0. 5-1. 55-10GoodMiddle income ASIA1 East SouthEest. 0-2. Indian 5 <5GoodSub Subcontinent1 SSA. 0-2. 50-3Poor (A Gordon Leitch, 2000), 1990, the Commission on Health Research for Development, that “the magnitude of the problem of tuberculosis, the relative neglect of the international community has agreed. A decade later, in 2000, Minister of Health and Finance of 20 countries, 80% of cases of tuberculosis in Amsterdam have made and adopted the Declaration of Amsterdam “. He explained that the global situation is both alarming and unacceptable “and that we commit ourselves to accelerate action against tuberculosis through expansion of the scope of the population with the World Health Organization (WHO) strategy the fight against tuberculosis recommended direct observed treatment strategy (DOTS), including the detection of at least 70% of infectious cases by the year 2005 “(Philip C. Hopewell, 2002). EPIDEMIOLOGYAbout 8 million people develop tuberculosis in 1990 and 2 6 to 2, 9 million people died, mostly in Asia. It is estimated that one third of the world population (1700 million) is infected with Mycobacterium tuberculosis. The disease is not confined to Asia, and its prevalence in developed countries, increasingly, from which he comes to the acquired immunodeficiency syndrome (AIDS) combined. estimated that about 160,000 children dying every year worldwide from tuberculosis. The situation in developing countries is different, where malnutrition and tuberculosis exist (SQ Nizami, 1998). developing countries in Asia have had an estimated 50-100/100, 000 cases of smear positive tuberculosis per year. The 1990 incidence of TB disease in Pakistan has recently been reported in 250/100 limit is 000 including 45% of smear positive pulmonary tuberculosis. At these rates, in Karachi, a city of about 100,000 would be 5,000 to 11,250 new cases of smear-positive disease have a year. analyzed the causes of death among adults aged 15 -50 years in poor communities of Karachi, tuberculosis is considered the second leading cause of death among adults at an annual rate of 30/100, 000, calculated in accordance with Estimates of incidence, mortality ratios assured total of 50% in treated and untreated 15% for tuberculosis (Marsh et al., 1996). Pathogenesis: INDEX CASE INFECTOUS TUBERCULOSISCough and generate airborne infection, the implant bacilliRestoration with a touch of the MIC responseBacillimia PrimaryOnset sterilization apical primary complexImmunosuppressive tubers CMICessation multiple cases of necrosis are inhaled tuberculosisFigure Infectous: Schematic representation of key events in pathogenesis of tuberculosis. CMI: cell-mediated immune system. (VB Balasurbramanian et al. In 1994). DIAGNOSIS OF TUBERCULOSISThe different methods of diagnosis as follows: 1 patient history and clinical. 2Blood 2nd PC and ESR 3. sputum chest radiograph .. 4th AFB (acid-resistant bacteria). (Sputum is a booth with Zeihl Neilson (ZN) stain. 5th Culture on Lowenstein Jensen medium 6. Bronchoscopy in the absence of sputum is available. 7th biopsy with histological processing. (Saurders, 1998). Pharmacological TUBERCULOSISTuberculosis among the top ten causes of death worldwide and affects low-income countries in particular. The treatment of smear positive tuberculosis World Health Organization (WHO) directly observed treatment, short course treatment strategy shows live (DOTS) has being so far from reducing the greatest impact during the immunization of children in British Columbia can TB mortality (Martien Borgdorff W et al. 2002). drugs to treat tuberculosis in two broad categories. The first line after maximum efficiency combined with unacceptable levels of toxicity. These include isoniazid, rifampin, ethambutol, streptomycin and pyrazinamide. Excellent results for patients with non-resistant TB can be treated with 6 months of treatment, given for the first 2 months of isoniazid, rifampicin and pyrazinamide, followed by isoniazid and rifampin for 4 months (William A Petri Jr, 2001). tuberculocide streptomycin streptomycin, but less effective than isoniazid or rifampicin, acts only on extracellular bacilli (due to poor penetration into cells). Thus, the defense mechanisms necessary to eradicate the disease. It penetrates tuberculous cavities, but doesnot cross the cerebrospinal fluid (CSF), and has a bad effect in the acidic environment. resistance developed rapidly when streptomycin was used alone, most patients relapse of tuberculosis (Tripathi, 2003) had. Streptomycin is bactericidal to tubercle bacilli in vitro. 0th concentration lower than 4 mg / ml can inhibit growth. The vast majority of strains of Mycobacterium tuberculosis are sensitive to 10 mg / ml (a petri dish William Jr., 2001). It crosses the placenta and serum levels fetal half of maternal blood, the drug is almost completely eliminated by glomerular filtration and dose must be in renal failure to avoid toxicity (A Leitch Gordan, 2000). side effects rash and fever, which include auditory and vestibular function remaining eighth cranial nerve is affected (William A Petri Jr rejected, 2001). popularity of streptomycin in the treatment of tuberculosis is due to the need for intramuscular injections and lower margins due to ototoxicity and nephrotoxicity, particularly in elderly patients and patients with renal insufficiency. Streptomycin is ototoxic and nephrotoxic. dizziness and hearing loss are the most common side effects may be permanent. toxicity is dose and the risk is increased in elderly patients. As with all aminoglycosides, the dose according to renal function. toxicity can be reduced by appropriate treatment is limited to a maximum of 6 months (CF Henry, 2001). Side effects include pain, redness , formation of pus and swelling at the injection site, numbness around the mouth and tingling shortly after injection. major side effects are hypersensitivity reactions of the skin, facial nerve and damage to patients and pregnant women, even in the fetus, kidney damage (A Harries, 2003). Apart from hypersensitivity reactions like fever and rash, streptomycin and potentiate neuromuscular blockers used during anesthesia and should be avoided in patients with myasthenia gravis (peace T and M Espinal 2003). Significantly, the aminoglycosides rare side effects include fever, rash, muscle paralysis, hypokalemia and hypomagnesemia (Edward D Chan et al., 2004). MATERIAL AND METHODSThis study was conducted in the Department of Pharmacology and Therapeutics, T. B Free Clinic Medical College of Muhammad, Mirpurkhas Sindh, Pakistan, led by Dr Kink. Shamim-ur- Rehman, head of the department from January 2005 to June 2005. The 100 patients with newly diagnosed pulmonary tuberculosis enrolled, this study provides information after ingestion and written consent. The patients were selected because of pulmonary TB cases diagnosed from OPD in medical and chest Ward Muhammad Medical College Mirpurkhas. Among these 97 patients were affected by the study period. On the other three were not eligible for monitoring. All patients in this study were following criteria: CRITERIA Admission diagnoses of pulmonary tuberculosis. aged 20 to 70 years. sexes, male or female. EXCLUSION CRITERIA Patients suffering from liver disease. patients with heart disease. patients with renal insufficiency. patients diabetes mellitus. patients with other respiratory diseases. HIV infected patients. Pregnant or nursing women. Patients with a history of multiple drug resistance. The study extended to take 24 weeks and 12 visits patient monitoring. have the information required such as name, age, sex, occupation, address, details of follow-up visits and laboratory tests have been, each patient on a proforma designed specifically for these studies covered. Selected patients were distributed according to adverse drug reactions during the study period. Group A: In this group, patients were included, the nephrotoxic effect of different age groups and occurs between the sexes have been. Group B: Included in this group patients who demonstrated ototoxicity in age groups and genders. MATERIALS: Streptomycin - 15 mg / kg - at most 1 GMD creatinine syringesOphthalmoscopeRhinoscopeDETERMINATION / Take a disposable syringe of 5 cc. Take a ghost swab. Clean arms clean with alcohol. incubital Prick the needle vein. Take 3-5 ml of blood. Put the blood in the regular tube. Wait coagulation of the sample for 1 ½ hour. The sample was centrifuged and the serum collected. PRINCIPLE filtrate protein (pH <2) treatment with a solution of alkaline picrate (Jaffe reaction) to the red performance of creatinine picrate. This color is due to the creatinine picrate tautomer and depends on salt formation and changed ketoenols creatinine molecule. The color red is compared photometrically thus formed to develop a series of standards from the pure solution of creatinine. ReagentsSodium tungstate 5 %: Dilute 1:1 10% sodium tungstate. sulfuric acid and acid 2/3NPicric: 0 04 m (9-16g / l) can be dried between filter paper or a margin of 10-12% for water added . hydroxide: 0 75NStock Standard (1 mg / ml) replaces 1 gram of pure creatinine made in the 0th 1 N hydrochloric acid and a liter of acid. The solution is stable indefinitely. Working standard: (0 2 mg / ml): 1 dl 2 ml of standard stock. Procedure: A) for plasma creatinine serum /: protein precipitation sample preparation /: • Plasma 2 ml + 2 ml distilled water + 2 tungstate ml sodium. Mix and let stand for 5 minutes and centrifuge. To 3 ml of the protein filtrate 1 ml of picric acid, heat in Biling water bath for 45 minutes. · Make up to volume 4 ml of distilled water, after heating. more rest NaOH 1 ml. let stand 15 minutes and read the standards. COLOR materials development standards S1 creatinine S6Total BlankWouking Standard 0th 5 0 50 3 ml - 3 ml distilled water, 3. mlProtein 0-0 3rd filtrate ml picric acid-1. 0 ml of each tubeSodium hydroxide1 rest. 0 ml in each tube for 15 minutes then at 520 nm against the blank. OD-load test 100Creatinine (mg / dl) = ___________ Amount _________ XX Std OD sample usedCreatinine hour = (total creatinine - creatinine preformed) 1 16 (where 1 16 the relationship between the molecular weight of creatine creatinine). a rush of blood urea nitrogen (BUN) PRINCIPLE Diacety1 monoxime is hydrolyzed in acid medium diacety1 reacts with urea in the presence of iron ions to form a condensed colored molecule. The color is enhanced and stabilized by thiosemicarbazide. The intensity of red color is formed proportional completion of the quantity of urea present in the sample. Urea = urea nitrogen urea = 2nd 14Urea 0th 4665REAGENTSOxime solution of 1 g dissolves diacety1 monoxime (also known as butanedione monoxime 2.3), 0 g thioemicarbazide 2 and 9 GM NaCl in water and diluted to 1 liter. acid solution are cautiously 60 ml of concentrated acid and 10 ml sulfurc 85% phosphoric acid to 800 ml of distilled water. Add 1 g diluted FeCI3 0 and 1I. standard solution (1 mg / ml) 100 mg urea in 100 ml of distilled water. normal work (0 01 mg / ml), diluted to 1 ml standard solution: solution to 100 ml of distilled water. 0th PROCEDURETo 1 ml serum / plasma 9th add 9 ml of distilled water. standards TestingCertificates color development creatinine S1 S6Total Blank standard work 1 1 0 0 and ml - distilled water up to 2 ML1. 2 0 5 ml mlProtein filtrate (PFF) -0. 5 ml in each tube, add 2 ml of color reagent and mixed w ml of mixed acid reagent. heat for 20 minutes in boiling water. Cool and terror at 540 nm (the colors are stable for several minutes. COMPUTATION OD test 100Urea nitrogen (mg / dl) = ___________ _________ Amount XX Std OD usedAll patient sample neuritis before anti-TB survey method treatment examinationVisual eye Fundus examination of the pupil of the vision acuity response Keeler ophthalmoscopeColour frount TB treatment, visual acuity 6/6- normal exercise response 6/6Pupil - regularly - margins substantive reactive optical disc paleVisible Cup / midi disk ratio 03 normal vascular pattern seen normalColour Macula Vision: no red / green defect. REVIEW OF streptomycin ototoxicity first ear acverse we excluded the effect, wax, foreign body, or any other disease ear. Then we cheked the position of the membrane, any type of perforation of IY. Then we checked the function of the middle ear and inner ear. Can we take the hearing test and balance Whisper 1st test: It has been mentioned in the ENT OPD space (), was the removal of the patient and the doctor about 1 meter, and said slowly and gradually increase the voice frequency. Tunning Fork 2nd testa. Renier Test: We see in this test The guideline is better than bone conduction. b. Weber test: In this test, we characterized the ear disease, and function of the heat Proni. v. ABC (Air Bone conduction test) : We close the disappearance Proth doctor and patient. d. PTA (pure tone Audionetery): With this method, we observed the air conduction, bone. cochlear function tests infact the hearing and include: One test of votes) are. b) development of tests of the fork. c) Audiometery. Voice-tests are tests that we Gelpi with our voice. Depending on the type of voice we’ll use the voice they whisper test, test voice chat, and more powerful test voice, normal distances, where the different voices must be heard by the patient couuectly are: Whisper = 20 feet = 40 feet made a loud conversation = 100 feetThesedistances gowever, tests in a soundproof room, and not for use in the noisy background of the outpatient department. For detailed results of tests of language, we must remember the following rules: the ear tested, the doctor faces. patient must be blind folded. Compared to his ear. simply means that you should force speedh end, while the words following the expiration of a deep breath. Use only phonetically balanced worlds (PB words), for example, ninety-nine, etc. First fifty-five years the maximum range of audibility Normal and then gradually move closer to the patient. The main merit of the test they perform simple voice and are not repiure no special equipment. But they are not very accurate and give only a rough idea of how to know if the patient is deaf or not. tuning fork tests tell us the type of hearing loss, either conductive or perceptive, and include tests of Rinne, Schwabach ABC or test Weber test, test Gellius also deserves the description. Lidka any other tool we need to know the proper use of the pitch, which reads as follows: you take it from its stem. always slightly on a tour of the bony points, elbow or patella. while placing it on the external ear canal, make sure that the acoustic axis of the fork with the long axis of the collapse of the external ear canal. If tou have to put it on the mastoid, to block transmission through the bones of the skull by the opposite ear, using either NI oise Barany box or a piece of paper. Rinne Test: Rinne test is the test defness driver. He compares the air duct of the ear bone conduction. Normally, the line of the air two times more than the bone conduction (Rinne positive). In deafness, the airline over the bone conduction, but both are reduced (Rinne positive reduced). In a conductive hearing loss, bone conduction on the air line (groove negative). absolute criterion for hole conduction: A, B, C or test Schwabach test is the test for deafness. He compares the patient’s bone conduction with the doctor. Usually, the two are equal. The same is the case of hearing loss. In deafness, bone conduction is reduced and the patient is less than the bone conduction doctor. Test Weber test Weber test lateralized. In a conductive hearing loss, it is more lateralized to the ear affected. We take a pitch, he knocked gently against one of our bone, place it on the center of the patient on the forehead, and ask him where he heard it’s better to be generally understood well in the middle of forehead, or equally in both ears. In a conductive hearing loss, it means better and more patient ear. In the deaf, he hears the better ear is normal. Gelle test: Gelle test is the test of stapes mobility. A vibrating tuning fork is placed over the mastoid process and the patient is asked to note the intensity. The air pressure in the ear canal esternal is then increased by pressing either the tragus or assistance of Withy Siegle and it is the Aked intensiye anew. Afailure fork means to hear more clearly that the stirrup. the tests Audiometery fixed the audience with an electric instrument called audiometer and plot the results referred to an audiogram graph paper. It is audiometery three types, namely. A audiometery) pure tones. b) speech. audiometery c) Bekesy’s. d) audiometery impedance. Pure Tone audiometery is one that we usually do, in our departments. He uses the tones that sound stimuli and find the threshold for different sound frequencies. In the audiogram, the sound intensities are on the vertical lines and marked the tone frequency, ranging from 250 to 8000 cps cps are marked on the horizontal lines. testsCaloric caloric testing of vestibular function tests, with hot and cold stimulation. Instrumentsa) water can. b) kidney specialist. c) Celsius thermometer. d) Stopwatch. Materialsa) of water at 44 * C b) water at 30 ° C. Canal stimulated the semicircular canal. To make it vertical, we put a pillow under his head and neck Fles and 30 * C MethodRun water in the ear for 40 seconds. Note to nystagmus, the direction and magnitude. Now is the time from the moment you begin to run couted water in the ear. NB We must first test with water at 44 * C, then we do with water at 30 ° C. Result hot water, is in the direction of nystagmus on the side ipsilateral addressed. test in cold water, the nystagmus in the opposite direction. purulent otitis media is cons-addressed. purulent otitis media Chornice. perforated eardrum. labyrinthitis. During the attack of Meniere’s disease, etc. vestivular neuronitis ResultsNormal value. Usually no nystagmus after 120-180 seconds. conspiracy. major anomalies: Meniere’s disease, paresis channel. Dead Labyrinth, no answer. For more poick nystagmus, the eye has direct observation Electronystagmography to detect the difference in electrical potential between the cornea and retina depends, and gives us a graph was recorded automatically replaced, electronystagmograph said. RESULTS AMD NOTES: Table 1 and Figure 1 shows the nephrotoxicity as an adverse reaction. Streptocomycin was the main drug to manifest nephrotoxicity have been combined therapy in the treatment of pulmonary tuberculosis in combination for the treatment of patients with pulmonary tuberculosis. Out 97 patients, there are 3 reactions in this table. Table 2 documents and 2 shows sex nephrotoxicity after taking anti-TB drugs. Two men and a woman in the study. Table 3 and Figure 3 shows the nephrotoxicity in different age groups affected. In the 30-39 1 1 40-49 years, 50-59 and 1 reaction to this study. Table 22 and Figure 22 show documented that, after taking anti-TB drugs ototoxicity. There are 2 responses were recorded in this study. 1DRUGS TABLE AND NEPHROTOXICITYDrugsYesNoTotalCombined therapy * 39497Streptomycin 3 (3 1%) ** 9497Pyrazinamide — — — — * accident Ethambutal rifampin isoniazid nepgrotoxicity by exclusion of combination therapy tested. ** Percentage calculated in 97 patients. 2DRUGS and nephrotoxicity TABLE GENDERDrugsMale treatment FemaleTotalCombined 213Streptomycin * 2 (2 1%) ** 1 (1st 03%) — — — — 3Pyrazinamide * isoniazid rifampicin Ethambutal incidence of nephrotoxicity was tested by exclusion of combination therapy. ** Calculated from 97 patients. TABLE 3DRUGS and nephrotoxicity of age Drugs20-2930-3940-treatment from 4950 to 5960-69TotalCombined 01113Streptomycin * 01 (1st 03%) ** 1 (1st 03%) 1 (1st 03%) * 3PyrazinamideRifampinEthambutalIsoniazid occurrence of nephrotoxicity was tested by the exclusion of combination therapy. ** Percentage of the 97 patients was calculated. TABLE 4DRUGS and ototoxicity as a side effect of treatment 29597Streptomycin EFFECTDrugsYesNoTotalCombined * 2 (2 1%) ** — — — 9597Pyrazinamide accident isoniazid rifampicin Ethambutal * — ototoxicity is excluding from the combination therapy tested. ** Percentage is calculated on 97 patients. TABLE 1Frequency nephrotoxicity in the fight against TB by sex DrugsFIGURE 2Nephrotoxicity 3Nephrotoxicity DrugsFIGURE TB by age groups in the fight against tuberculosis DrugsFUGURE 4Frequency shows ototoxicity drugs against tuberculosis transacted Table 5 and Figure 5 ototoxicity in sex opposite. It was a response in male and female resplectively after taking a treatment for tuberculosis. Table 6 and Figure 6 shows ototoxicity in different age groups. The age group 20-29 and 40-49 were evident in this study ototoxicity after taking anti-TB drugs. TABLE 5DRUGS and ototoxicity as a side effect in effect GENDERDrugsMale FemaleTotalCombined 112Streptomycin therapy * 1 (1st 03%) ** 1 (1st 03%) 2Pyrazinamide — — — — * case Ethambutal rifampin Isoniazid ototoxicity was tested by the exclusion of a combination therapy. ** Percentage of 97 patients calculated. 6DRUGS and ototoxicity TABLE BY AGEDrugs20-2930-3940-4950-5960 69TotalCombined treatment 101002Streptomycin * 1 (1st 03%) ** 01 (03% 1st) * accident 002PyrazinamideRifampinEthambutalIsoniazid ototoxicity is tested by the exclusion of a combination therapy. ** Percentage is calculated on 97 patients. Figure 5Ototoxicity by gender in TB TB 6Ototoxicity DrugsFIGURE DrugsDISCUSSION transacted by age group: streptomycin (1 g per day) - It started with other drugs. After 3-7 weeks of treatment, 3 patients complained of oliguria and 2 patients during the follow-up shows a deficit of hearing. These reactions proved clinically and laboratory examinations. nephrotoxicity was recorded in these patients, two males and 1 female. were in age group 1 in 30-39, 40-49 and 50-59 2 1 Effects Side documented in this study. drug was stopped for 3 weeks and found that blood urea nitrogen and creatinine levels were reduced, so was the drug stopped permanently, and four other drugs were continued. can accumulate proximal tubule cells aminoglycosides, which is associated nephrotoxicity of aminoglycosides. The mechanism of renal toxicity is due to inhibition of intracellular phospholipase in the proximal tubule hypothesis. Renal failure is usually due to the decrease in glomerular filtrate nonoligouric rate occurring after at least one week under treatment. Baseline and regular monitoring characterized the analysis of blood levels of urea nitrogen, reported values of creatinine (Edward et al., 2004). streptomycin nephrotoxic and should be used with caution in patients with renal failure is not used. If the reaction of some problems which is rare, the dose may be reduced (NCG 2002). Ototoxicity - 2 reactions have been recorded in this study. Sex, 1reaction has been documented in males and 1 female in this study. Side effects of streptomycin have been recorded. One in the group of 20-29 years and 40-49 in. The drug was a astopped and patients were encouraged to consult ear, nose and throat medical OPD. Remaining other medications were continued. Interestingly, the component of damage is relatively choclear or vestibular, or are rarely isolated. The mechanism of cochlear toxicity is unclear, although the site is targeted to the outer hair cells of the organ of Corti taken into account. aminoglycoside-induced cochlear dysfunction in general, be irreversible. Infury hair cells of the ampullary crest of the vestibular toxicity of aminoglycosides. Signs and symptoms of vestibular toxicity include nausea, vomiting, vertigo and nystagmus (Edward et al., 2004). demonstrated that, as with the antibiotics streptomycin others must be careful in the combination treatment of anti-tuberculosis. Tuberculosis is still a granulomatous disease caused by Mycobacterium tuberculosis. The WHO estimates that more than 300,000 new cases of TB develop each year in Pakistan. curing infectious TB cases is the fight against diseases key to effectiveness. treatment of TB patients and reduction of pain, if necessary to prevent death from tuberculosis. The first tine of drugs used in the treatment of tuberculosis consists of isoniazid, pyrazinamide, rifampicin, streptomycin and ethambutol. The most important side effects such as the cause of serious health hazards and require discontinuation of the drug and the doctor of mediation in the chest. Minor side effectsCause relatively little discomfort, they often respond to symptomatic treatment or simple, but sometimes for the duration of drug therapy. chemotherapy should be stopped or temporarily interrupted by drug toxicity intolerance is abundant. Indeed, the anti-TB drugs are relatively toxic side effects are mild and most often justified, but not drug treatment. REFERENCESA Harries. What are the most common adverse events for frontline TB drugs, and what is the procedure for the reintroduction of the drug. WHO Bulletin 2004; 154-158. Agordon Leitch. “Tuberculosis Management”, Crofton and Douglas respiratory 5th edition 2000, 444 - 564th Agordon Leitch. “Tuberculosis”, Crofton and Douglas respiratory 5th Edition, 2000, 476-505. Balasubramanian V CH, LV Weigeshaus and Taylor Smith DW. pathogenesis of tuberculosis to apical localization. tubercle and respiratory diseases, 1994, 75 :168-178. BTS “Side effects of therapy.” Joint committee of the British Thoracic Society TB. Thorax 1998; 3:536-548. Marsh D, Hashim B, F and L Hassany Hussain. Front Line Management of pulmonary tuberculosis: analysis

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