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Related Obligate Pathogens, The Mycobacterium Tuberculosis Complex, Comprising M. Tuberculosis. The Human Tubercle Bacillus - M. Bovis - The Bovine Tubercle Bacillus, -agricanu

related obligate pathogens, the mycobacterium tuberculosis complicated, comprising M. tuberculosis. The human tubercle bacillus - M. bovis - the bovine tubercle bacillus, -agricanum - a heterogeneous kind located principally in effuational Africa with properties intermediate between the former two species and M-microti-a uncommon cause of illness involves as well as other modest mammals but attenuated for humans. Humans are the usual, but not special, host of M. tuberculosis. M. bovis causes illness in cattle and also in badgers, deer, as well as other mammals. Humans are incidental hosts, usually acquiring infection by drinking contaminated milk although infection of farm workers may possibly occur by aerogenous route. Human might transmit M. bovis to cattle but human to human is hardly ever reported (PDO D awis et al, 2003). The annual tuberculosis infection rate or annual risk of infection may be the ideal single indicator of the status and trend of tuberculosis in both developed and creating countries. It indicates the proportion of the population that will primarily infected or reinfected in the course of 1 year and is usually expressed as a percentage. The risk of tuberculosis infection in developed countries is now very low, getting less than 0.5% per annum in the majority, 0.1-0 % in most and much less than 0.1% in a few countries. The risk of tuberculosis in these countries is declined by about 10% per year. In creating countries much greater rates are identified. The annual threat of infection for the richest and poorest countries is shown in following table. In most industrialized countries the annual rate of infection is now below 0.1% and continues decline by 10% per annum. In Africa, the annual danger of infection might be considerably as 2.5% or a lot more, and within the present context of increasing tuberculosis, notification as a result of HIB epidemic is growing as opposed to decreasing. Annual danger of infection Areas Current Level Annual decline Trend (%) Health resource Availability Industrialized 0.04-0.1 >10 Excellent Middle income Latin America West Asia 0.5-1.5 5-10 Good Middle income East and South Eest Asia 1.0-2.five <5 Good Sub-Saharan Africa Indian Subcontinent 1.0-2.5 0-3 Poor                                                                                                 (A Gordon Leitch, 2000) In 1990 the commission on Health Research for development stated that "the magnitude of tuberculosis problem is matched only by is relative neglect by the international community". A decade later 2000 ministers of Health and Finance from 20 countries that have 80% of world's tuberculosis cases met in Amsterdam and issued the Amsterdam Declaration". This stated that the global situation was both alarming and unacceptable" and that we commit ourselves to accelerate action against tuberculosis through expansion of coverage of population with the World Wellness Organization (WHO) recommended strategy to combat tuberculosis Direct observe treatment strategy (DOTS), providing for at least 70% detection of infectious cases by the year 2005" (Philip C Hopwell, 2002). EPIDEMIOLOGY About 8 million people developed tuberculosis in 1990 and two.6 to two.9 million people died of it, mostly in Asia. It is estimated that one third of world's population (1700 million) is infected with mycobacterium tuberculosis. The disease is not limited to Asia alone and its prevalence is increasing in developed countries also where it linked to acquired immunodeficiency syndrome (AIDS). According to estimate, approximately 160,000 children die from tuberculosis annually worldwide. The situation in creating countries is different where malnutrition and tuberculosis co-exist (Nizami SQ, 1998). Developing countries in Asia have an estimated 50-100/100,000 cases of smear positive tuberculosis annually. The 1990 incidence of tuberculosis disease in Pakistan has recently been reported at 250/100,000 of which 45% are likely to be smearing positive pulmonary tuberculosis. At these rates, Karachi, a city of approximately 100,000 would have among 5000 and 11250 new cases of smear positive disease annually. Analyzed causes of deaths among adults, age 15-50 years in impoverished Karachi communities, tuberculosis, is identified as the second leading cause of adult death at an annual rate of 30/100,000 which is consistent with incidence -estimates, assuring overall case fatality ratios of 50% for untreated and 15% for treated tuberculosis (Marsh et al., 1996). PATHOGENESIS: INDEX CASE WITH INFECTOUS TUBERCULOSIS Cough and generate droplet nuclei, which are inhaled by a contact Primary Onset of CMI response Bacillimia                                      Apical Implant                             Sterilization of the primary complicated Immunosuppressive event Multiple of tubercle bacilli Restoration of CMI Cessation of necrosis         Infectous tuberculosis Figure: Schematic representation of the basic events inside the pathogenesis of tuberculosis. CMI: Cell mediated immune. (VB Balasurbramanian et al., 1994). DIAGNOSIS OF TUBERCULOSIS The different diagnostic methods are as follows: 1.                History and clinical features. two.                2Blood CP and ESR. 3.                Chest radiography. 4.                Sputum for AFB (Acid Fast Bacilli). (Sputum is stand with Zeihl Neilson (ZN) stain. five.                Culture on Lowenstein Jensen medium. 6.                Bronchoscopy if no sputum is available. 7.                Biopsy with histological examination. (Saurders, 1998). DRUG TREATMENT OF TUBERCULOSIS Tuberculosis is among the top ten trigger of global mortality and affects low-income countries in particular. The treatment of smear positive tuberculosis using World Health Organization (WHO) directly observed treatment, short course, Direct observe treatment strategy (DOTS) has far highest impact while BC immunization reduces childhood tuberculosis mortality (Martien W Borgdorff et al. 2002). Drugs used inside the treatment of tuberculosis can be divided into two major categories. First line after combined the greatest level of efficacy with unacceptable degree of toxicity. These include isoniazid, rifampin, ethambutol, streptomycin and pyrazinamide. Excellent results for patients with non drug resistant tuberculosis can be treated with 6 month course of treatment, for the first 2 months, isoniazid, rifampin and pyrazinamide are given, followed by isoniazid and rifampin for remaining 4 months (William A Petri Jr, 2001). STREPTOMYCIN Streptomycin is tuberculocidal, but much less effective than isoniazid or rifampin, acts only on extracellular bacilli (because of poor penetration into cells). Thus, host defense mechanisms are needed to eradicate the illness. It penetrates tubercular cavities, but doesnot cross to the cerebrospinal fluid (CSF), and has poor action in acidic medium. Resistance developed rapidly when streptomycin was used alone in tuberculosis most patients had a relapse (Tripathi, 2003). Streptomycin is bactericidal for tubercle bacillus in vitro. Concentration as low as 0.4 mg/ml may inhibit the growth. vast majority of strains of mycobacterium tuberculosis are sensitive to 10mg/ml (William A Petri Jr, 2001).  It crosses the placenta and fetal serum levels are half of those in maternal blood, the drug is excreted almost entirely by glomerular filtration and dosage must be modified in renal failure to avoid toxicity (A Gordan Leitch, 2000). Untoward effects include rash and fever, auditory and vestibular function of eighth cranial nerve is affected (William A Petri Jr, 2001). Popularity of streptomycin in treatment of tuberculosis had declined because of need for intramuscularly injections and lower margins of safety because ototoxicity and nephrotoxicity especially in the elderly and those with impaired renal function. Streptomycin is ototoxic and nephrotoxic. Vertigo and hearing loss are most common side effects and may possibly be permanent. Toxicity is dose related and threat is increased inside the elderly. As with all aminoglycosides the dose must be adjusted according to renal function. Toxicity can be reduced by limited therapy to no far more than 6 months (Henry FC, 2001). Minor adverse effects are pain, rash, swelling and pus formations at injection site, numbness around the mouth and tingling soon after the injection. Major adverse effects are cutaneous hypersensitivity, vestibular and auditory nerve damage to the patient and in a pregnant woman, also in fetus, renal damage (A Harries, 2003). Apart from hypersensitivity reactions such as fever and rash, Streptomycin also potentiate neuromuscular blocking agents used during anesthesia and should be avoided in-patient with myasthenia gravis (T Frieden and M Espinal, 2003). Significantly rare adverse effects of aminoglycosides include fever, rash, neuromuscular blockade, hypokalemia and hypomagnesaemia (Edward D Chan et al.,2004). MATERIAL AND METHODS This study was carried out inside the department of Pharmacology and Therapeutics, Free T.B Clinical of Muhammad Medical College Mirpurkhas SINDH, Pakistan, under kink supervision of Dr,. SHAMIM-UR-REHMAN, Head of Department from January 2005 to June 2005. The 100 newly diagnosed patients of pulmonary tuberculosis, enrolled is this study after taking informed and written consent. The patients were selected as diagnosed cases of pulmonary tuberculosis from medical chest OPD and chest ward of Muhammad medical college mirpurkhas. Out of these 97 patients were associated through out the study period. Out of remaining three have not come for follow up.                             All patients, in this study, were selected according to following criteria:  INCLUSION CRITERIA Diagnosed cases of pulmonary tuberculosis. Age in between 20 to 70 years. Sex either male or female. EXCLUSION CRITERIA Patients suffering from liver disease. Patients suffering from cardiac disease. Patients suffering from renal illness. Patients suffering from diabetes mellitus. Patients suffering from other respiratory illness. Patients suffering from HIV infections. Pregnant or nursing women. Patients with previous multiple drug resistance. The study period extended up to 24 weeks and 12 follow up visits of patients were taken. The required information such as name, age, sex, occupation, address, details of follow up visits and laboratory investigations etc, of each patients were recorded on proforma especially designed for this study. The selected patients were divided according to untoward effects of drugs during study period. Group A:         In this group those patients were included who manifested the nephrotoxicity in different age group and gender. Group B:         In this group those patients were included who manifested the ototoxicity in different age group and gender. MATERIALS: Streptomycin -- 15 mg/kg - maximum 1 gm D/syringes Ophthalmoscope Rhinoscope DETERMINATION OF CREATININE Take a five cc disposable syringe. Take a cotton spirit swab. Clean the arm with spirit swab. Prick the needle incubital vein. Take 3-5 ml of blood. Put the blood sample into plain tube. Wait for clotting the sample for ½ to 1 hour. The sample was centrifuged and collected the serum. PRINCIPLE             Protein free filtrate (pH beneath 2) in treated with alkaline picrate solution (Jaffe’s reaction ) to yield red colour of creatinine picrate. This colour is on account of tautomer of creatinine picrate and is dependent on formation of a salt and ketoenol changed creatinine molecule. The red yellow colour thus formed is compared photometrically to a series of standards prepared from pure solution of creatinine. Reagents Sodium tungstate 5%:   Dilute 1:1 10% Sodium tungstate. Sulfuric acid:                 2/3N Picric acid:0.04 M        (9.16g/l) It may possibly be dried between filter paper or an allowance of 10-12% made for the added water. Sodium hydroxide:        0.75N Stock standard:            (1mg/ml) dissolve 1 g of pure creatinine in 0.1 N hydrochloric acid and make up to 1 litre with the acid. The solution is stable indefinitely. Working standard:        (0.two mg/ml): Dilute two ml stock standard to 1dl. PROCEDURE: A)    For plasma/serum creatinine: Protein precipitation / sample preparation: ·        2 ml plasma + two ml distilled water + 2 ml sodium tungstate. Mix and let stand for 5 minutes, and the centrifuge. ·        To the 3 ml of above protein free filtrate add 1 ml picric acid, heat in biling water bath for about 45 minutes. ·        Make up to volume 4 ml with distilled water after heating. Add 1 ml NaOH. Let stand for 15 minutes and read with standards.

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COLOUR DEVELOPMENT Materials Standards S1 to S6 Total creatinine Blank Wouking standard 0.five 50 3.0 ml - - Distilled water Up to 3 ml - 3.0 ml Protein-free       filtrate - 3.0 ml - Picric acid 1.0 ml to each tube Sodium hydroxide 1.0 ml to each tube Let stand for 15 minutes and then read at 520 nm against blank. CALCULATION                                         OD of test                                                                          100 Creatinine (mg/dl)  =     ___________              X         Amount of Std           X     _________                                         OD of Std                                                                   Sample used Creatinine = (Total creatinine – preformed creatinine) 1.16 (Where 1.16 is the ratio of the molecular weight of creatinine to creatine). DETERMINATION OF BLOOD UREA NITROGEN (BUN) PRINCIPLE             Diacety1 monoxime is hydrolyzed in acidic medium to diacety1, which reacts with urea in the presence of ferric ions, to form a condensed coloured molecule. The colour is intensified and stabilized by thiosemicarbazide.The intensity of red colour comples formed is proportion to the quantity of urea present inside the sample. Urea                             = urea nitrogen two.14 Urea nitrogen                = Urea 0.4665 REAGENTS Oxime solution Dissolve 1 gm diacety1 monoxime (also called 2,3 butanedione monoxime), 0.2 gm thioemicarbazide and 9 gm naCI in water and dilute to 1L. Acid solution                Cautiously add 60 ml concentrated sulfurc acid and ten ml 85% orthophosphoric acid to 800 ml distilled water. Add 0.1 gm FeCI3 and dilute to 1I. Standard stock solution: (1mg/ml) 100 mg of urea in 100 ml of distilled water. Standard working (0.01 mg/ml) Dilute 1 ml of stock standard Solution:                       solution up to 100 ml distilled water. PROCEDURE To 0.1 ml serum/plasma add 9.9 ml distilled water. COLOUR DEVELOPMENT Materials Standards S1 to S6 Total creatinine Blank Working standard 0.1 to 1.0 ml - - Distilled water Up to 2 ml 1.5 ml two.0 ml Protein-free    filtrate (PFF) - 0.five ml - Add to each tube two ml of mixed colour reagent and w ml of mixed acid reagent. Heat for 20 minutes in boiling water. Cool and dread at 540 nm (colours are stable for several minutes. CALCULATION                                        OD of test                                                                            100 Urea nitrogen (mg/dl)=  ___________      X     Amount of Std        X     _________                                         OD of Std                                                                   Sample used All the patients examined for optic neuritis before anti-tuberculosis treatment Method Ocular examination Visual acuity Pupil reaction Fundus examination by Keeler direct ophthalmoscope Colour vision Befor antituberculosis therapy Visual acuity                 6/6 - Normal                      6/6 Pupil reaction Round – regular – reactive Fundus Optic disc pale Visible margins Cup / disc ratio 0:3 Normal vascular pattern Macula looks normal Colour vision:   no red /green defect. EXAMINATION OF EAR             Ototoxicity as an acverse effect of streptomycin First we ruled out the, wax, foreing body, or any other ear disease.             Then we cheked the position of tympanic membrane, any kind of perforation of iy. Then we checked the function of middle ear and inner ear. Then we do the test for hearing and balance 1.      Whisper Test: It was done in ENT OPD room (silent), the distance of patient and doctor was about 1 meter and talked slowly and gradually increased voice frequency. 2.      Tunning Fork test a.       Renies test: We see in this test the ear conduction is better than bone conduction. b.      Weber’s test: In this test, we characterized the disease of ear, and function of proni conduction. c.       ABC (Air Bone Conduction test): We rule out the waning proth doctor, and patients. d.      PTA (Pure tone Audionetery): By this method we watch air conduction, bone conduction . Cochlear function tests are infact tests of hearing and include: a)      voice tests. b)      Tuning fork tests. c)      Audiometery. Voice tests are the tests which we do with the gelp of our voice. Depending on the sort of voice which we use they are called the whisper voice test , conversation voice test, and loud voice test, Normal distances from which the various voices should be couuectly heard by the patient are as follows: Whisper                       =          20 feet Conversation                =          40 feet  Loud                            =          100 feet Thesedistances gowever, apply to tests done in a sound proof room and not within the noisy background of the out patient department .             For accurate results of voice tests, 1 has to observe the following rules: Ear getting tested should face the doctor. Patient should be blind folded. Opposite ear should be plugged. Use only forced expiration speedh i.e., words spoken during the expiration following a deep inspiration. Use only phonetically balanced worlds (P.B. words), e.g., ninety nine, fifty five etc. Start from the maximum normal audibility range and then gradually come nearer to the patient. The main merit of the voice tests is that they are simple to perform and do not repiure any specialized equipment.But they are not really accurate and only give a rough idea as to whether the patient is deaf or not. Tuning fork tests tell us about the form of hearing loss, i.e., conductive or perceptive, and include RINNE’s tests, ABC or SCHWABACH’s test, and WEBER’s test, In addition, GELLE’s test also merits description. Lidke any other instrument we must know the correct use of tuning fork which is as follows: Always hold it by its stem. Always hit it gently against one of tour bony points, either elbow or knee cap. While putting it over the external meatus, make sure that the acoustic axis of the fork coincides with the long axis of the external auditory canal. Whenever tou put it over the mastoid, you must block the gearing across the skull bones by making the opposite ear, either with Barany’s nioise box or with a piece of paper. Rinne’s test: Rinne’s test is the test of conductive defness. It compares the air conduction of the ear with its bone conduction. Normally, the air conduction is twice a lot more than the bone conduction (Rinne’s positive). In nerve deafness, the air conduction is much more than the bone conduction but each are reduced (Rinne’s reduced positive).In conductive deafness, the bone conduction is more than the air conduction (Rinne’s negative). Absoluter bore conduction test: A,B,C test or schwabach’s test will be the test of nerve deafness. It compares the bone conduction of the patient with that of the doctor . Normally, the two are equal. Same will be the case in conductive deafness. In nerve deafness, the patient’s bone conduction is reduced and is less than the doctor’s bone conduction. Weber’s test: Weber’s test will be the test of lateralization. In conductive deafness, it is lateralized to the more diseased ear. We take a tuning fork, hit it gently against 1 of our bony points, place it over the middle of patient’s forehead, and ask him as to where does he hear it ideal, Normally, he either hears it greatest inside the middle of the forehead or equally well within the two ears. In conductive deafness, he hears it better within the far more diseased ear. In nerve deafness, he hears it better inside the a lot more normal ear. Gelle’s test: Gelle’s test is the test of stapedial mobility. A vibrating tuning fork is placed over the patient’s mastoid and he is asked to note the intensity. The air pressure inside the esternal auditory canal is then increased either by pressing the tragus or withy the help of siegle’s speculum and he is aked to note the intensiye once again. Afailure to hear the fork better means that the stapes is fixed. Audiometery is testing the hearing with an electrical instrument called the audiometer and plotting the result on a graph paper called the audiogram. It is of three types, namely. a)      Pure tone audiometery. b)      Speech audiometery. c)      Bekesy’s audiometery. d)      Impedance audiometery. Pure tone audiometery will be the 1 which we commonly do in our departments. It uses the pure tones as the sound stimuli and finds the threshold of hearing for the various audible frequencies. Inside the audiogram, the sound intensities are marked on the vertical lines and the sound frequencies, ranging from 250 c.p.s. to 8000 c.p.s. are marked on the horizontal lines. Caloric tests Caloric tests are tests of vestibular function, using hot and cold water for stimulation. Instruments a)      Water can. b)      Kidney tray. c)      Centigrade thermometer. d)      Stop watch. Materials a)      Water at 44*C b)      Water at 30*C. Canal stimulated Lateral semicircular canal. To make it vertical we put a pillow under the head and thus fles the neck by 30*C. Method Run water into the ear for 40 seconds. Notice the after nystagmus, its direction, and its amplitude. The time duration is couted right from the moment we start running water into the ear. N.B. First we complete the test with water at 44*C and then we do it with water at 30*C. In hot water test, the nystagmus is directed towards the ipsilateral side.In cold water test, the nystagmus is directed towards the opposite side. Contra-indications Acute suppurative otitis media. Chornic suppurative otitis media. Perforated ear drum. Labyrinthitis.During the attack of Meniere’s disease, vestivular neuronitis etc. Results Normal value. Normally, the ensuing nystagmus lasts 120-180 second. Plotting. Major abnormalities: Meniere’s illness, canal paresis. Dead labyrinth, no response. In order to poick the nystagmus better, direct observation of the eyes has been replaced by electronystagmography, which depends on detecting the difference in electrical potential among the cornea and retina and gives us an automatically recorded graph, called the electronystagmograph. RESULTS AMD OBSERVATIONS: Table 1 and figure 1 shows nephrotoxicity as an adverse effect. Streptocomycin was main drug to manifest the nephrotoxicity in combined therapy during treatment of pulmonary tuberculosis in combined therapy during treatment of pulmonary tuberculosis patients. Out 97 patients, there were 3 reactions documented in this table. Table two and figure two shows nephrotoxicity in gender after taking the anti tuberculosis drugs. Two males and 1 female was affected during the study.             Table 3 and figure 3 shows the nephrotoxicity in different age group. In the age group 30-39 1, 40-49 1, and 50-59 1 reaction was documented in this study. Table 22 and figure 22 show the ototoxicity after taking anti tuberculosis drugs. There were 2 reactions recorded in this study. TABLE 1 DRUGS AND NEPHROTOXICITY Drugs Yes No Total Combined therapy* 3 94 97 Streptomycin 3 (3.1%)** 94 97 Pyrazinamide - - - Rifampin - - - Ethambutal - - - Isoniazid - - - *Occurance of nepgrotoxicity is tested by excluding combined therapy. **Percentage in calculated out of 97 patients. TABLE 2 DRUGS AND NEPHROTOXICITY IN GENDER Drugs Male Female Total Combined therapy* 2 1 3 Streptomycin 2 (two.1%)** 1 (1.03%) 3 Pyrazinamide - - - Rifampin - - - Ethambutal - - - Isoniazid - - - *Occurance of nephrotoxicity is tested by excluding combined therapy. **Percentage is calculated out of 97 patients. TABLE 3 DRUGS AND NEPHROTOXICITY ACCORDING TO AGE Drugs 20-29 30-39 40-49 50-59 60-69 Total Combined therapy* 0 1 1 1 3 Streptomycin 0 1 (1.03%)** 1 (1.03%) 1 (1.03%) 3 Pyrazinamide Rifampin Ethambutal Isoniazid *Occurance of nephrotoxicity is tested by excluding combined therapy. **Percentage is calculated out of 97 patients. TABLE 4 DRUGS AND OTOTOXICITY AS AN ADVERSE EFFECT Drugs Yes No Total Combined therapy* two 95 97 Streptomycin 2 (2.1%)** 95 97 Pyrazinamide - - - Rifampin - - - Ethambutal - - - Isoniazid - - - *Occurance of ototoxicity is tested by excluding combined therapy. **Percentage is calculated out of 97 patients. TABLE 1 Frequency of Nephrotoxicity In Anti tuberculosis Drugs FIGURE 2 Nephrotoxicity according to gender in Anti tuberculosis Drugs FIGURE 3 Nephrotoxicity according to Age Groups in Anti tuberculosis Drugs FUGURE 4 Frequency of Ototoxicity in Anti tuberculosis Drugs Table 5 and figure 5 shows the ototoxicity in different gender. There was one reaction in male and female resplectively after taking anti tuberculous therapy. Table 6 and figure 6 shows the ototoxicity in different age group. The age group in between 20-29 and 40-49 were manifested ototoxicity in this study after taking anti tuberculous drugs. TABLE 5 DRUGS AND OTOTOXICITY AS AN ADVERSE EFFECT IN GENDER Drugs Male Female Total Combined therapy* 1 1 two Streptomycin 1 (1.03%)** 1 (1.03%) two Pyrazinamide - - - Rifampin - - - Ethambutal - - - Isoniazid - - - *Occurrence of ototoxicity is tested by excluding combined therapy. **Percentage calculated out of 97 patients. TABLE 6 DRUGS AND OTOTOXICITY ACCORDING TO AGE Drugs 20-29 30-39 40-49 50-59 60-69 Total Combined therapy* 1 0 1 0 0 2 Streptomycin 1 (1.03%)** 0 1 (1.03%) 0 0 two Pyrazinamide Rifampin Ethambutal Isoniazid *Occurance of ototoxicity is tested by excluding combined therapy. **Percentage is calculated out of 97 patients. FIGURE five Ototoxicity according to gender In Anti tuberculosis Drugs FIGURE 6 Ototoxicity according to age Groups in Anti tuberculosis Drugs DISCUSSION: Streptomycin (1 g per day) – it was started with other drugs. After 3-7 weeks of medication, 3 patients complaint of oliguria and two patients presented during follow up with hearing deficit. These reactions proved clinically and laboratory investigations. Nephrotoxicity was recorded in these patients two in male and 1 in female. According to age group 1 in 30-39, two 40-49 and 1 50-59 side effects were documented in this study. Drug was stopped for 3 weeks and identified that blood urea nitrogen and creatinine levels were decreased, therefore this drug was permanently stopped and the remaining four drugs were continued. The proximal renal tubule cells may possibly accumulate aminoglycoside, accounting for nephrotoxicity associated with aminoglycosides. The mechanism of renal toxicity is hypothesized to by the inhibition of intracellular phospholipase inside the proximal tubule. The renal insufficiency is typically characterized by the nonoligouric decrease in glomerular filtrate rate occurring after at least taking a week therapy. Baseline and periodic surveillance of analysis blood urea nitrogen levels, creatinine values is indicated (Edward et al., 2004). Streptomycin is nephrotoxic and should used with caution in patients with renal impairment. If reaction is trouble some which is an infrequent occurrence, the dose might be reduced (NCG,2002). Ototoxicity – there were two reactions recorded in this study. According to gender, 1reaction was in male and 1 in female was documented in this study. Side effects of streptomycin were recorded. One in age group 20-29 and 1 in 40-49. The drug was astopped and patients were advised to consult in Ear Nose and Throat OPD. Remaining other drugs were continued. Interestingly, the damage could be fairly isolated to either the choclear or vestibular component, or hardly ever each. The mechanism for the cochlear toxicity is unclear, despite the fact that the target site is considered to the outer hair cells of the organ of corti. Aminoglycoside induced cochlear dysfunction is generally considered to be irreversible. Infury to the hair cells of the ampullar cristae by aminoglycosides is the mechanism of the vestibular toxicity. Sign and symptoms of vestibular toxicity include nausea, vomiting, vertigo and nystagmus (Edward et al., 2004). It proved that like other anti-biotic streptomycin must be careful to continue in combination therapy of Anti-Tuberculosis Therapy. Tuberculosis is a granulomatous disease, caused by mycobacterium tuberculosis. As world Health Organization estimates far more than 300,000 new cases of tuberculosis develop in Pakistan every year. Cure of infectious cases of tuberculosis will be the key to effective control of the illness. Treatment of tuberculosis patients reduces suffering and, if adequately, prevents death from tuberculosis. The first tine of drugs used inside the treatment of tuberculosis consists of isoniazid, pyrazinamide, rifampin, streptomycin, and ethambutol. The major side effects are those giving rise to serious health hazards, and require discontinuation of the drug and referral to chest physician. Minor side effects Trigger relatively little discomfort; they often respond to symptomatic or simple treatment but occasionally persist for the duration of drug treatment. Chemotherapy should be stopped or temporarily interrupted only of severe drug intolerance toxicity occurs. In fact tuberculosis drugs are relatively toxic and mild side effects are not uncommon but most do not warrant drug withdrawal. REFERENCES A Harries. What are the most common adverse drug events to first line tuberculosis drugs, and what is procedure for reintroduction of drugs. Bulletin of WHO 2004; 154-158. Agordon Leitch. “Management of Tuberculosis”, Crofton and Douglas’s Respiratory Illness 5th edition 2000; 444-564. Agordon Leitch. “Tuberculosis”, Crofton and Douglas’s Respiratory Disease 5th edition, 2000; 476-505. Balasubramanian V CH, Weigeshaus BT Taylor and Smith DW. Pathogeneses of tuberculosis pathway to apical localization. Tubercle and Lung Illness 1994; 75:168-178. BTS “Adverse reactions to tuberculosis therapy”. Joint Tuberculosis Committee of British Thoracic Society. Thorax 1998; 3:536-548. D Marsh, B Hashim, F Hassany and L Hussain. Front line management of pulmonary tuberculosis: analysis of tuberculosis and treatment practices in urban Sindh, Pakistan. Tubercle and Lung Illness 1996; 77:86-92. Edward D Chan, Celphi Chaterjee, Michael D Iseman. Pyrazinamide, ethambutol, Aminoglycosides 2nd edition, Philadelphia, Lippincott William and Wilkins 2004; 573-589. Henry F, Chambers. “Antimycobacterial drugs”. In: Basic and Clinical Pharmacology, eight edition ,edited by Bertram G Katzung International edition Lame Medical books New York 2001; pp. 803-8114. Martein W Borgdorf. “ Annual danger of tuberculosis infection time for an up date” . Bullentin of WHO 2002; 501-503. Nizami SQ. Childhood TB. J Pak Med Assoc 1998;48:88. PDO Dawis, DJ uirling and JM Grange. Pulmonary disease IN: Infectious desease 6th edition, Lippincott Williams and Wilkins, Philadelphia 2003; pp. 1644-657. Pelletier, Yee et al. Incidence of serious side effects from first line antituberculosis drugs among patients treated for active tuberculosis. AJP and Crit care Med 2003. Philip C Hopwell. Tuberculosis control how the world has changed since 1990. Bulletin of WHO 2002; 427-728. Saunder Pocket “Diagnosis of tuberculosis”. In: Wssential of Clinical M edicine 2nd edition, New Delhi, Japee Brothers 2003; pp.698-708. Tripathi KD. “Antitubercular drugs” In: Essentials of Medical Pharmacology 5th edition, New Dehli, Japee Brothers 2003; pp.698-708. William AP Jr. “Anticicrobial agents” Goodman and Gilmans the Pharmacological bases of therapeutics 10th edition, (Joe1 G Hardman, Ph.D. Lee E. Limbird et a1). McGraw Hill Medical Publishing Division, New York 2001, pp.1273-1295.

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