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Isoniazid (Isonicotinic acid hydrazide,H):

Essential component of all anti TB regimen (except intolerance to H or resistance)

-It is tuberculocidal , kills fast multiplying  organism  &  inhibit slow acting organism

-Acts both on intracellular ( present in macrophages ) &  extracellular bacilli

-Atypical mycobacteria are not inhibited byINH.

Not active against any other micro-orgs.

Mechanism of Action :

Inhibit synthesis of mycolic acid ( uniquefatty acid component of mycobacterial cellwall .)

-INH enters the bacilli by passive diffusion. Itmust be activated to become toxic to bacilli.

It became toxic by Kat G (multifunctionalCatalase - peroxidase , a bacterial enzyme ) which catalyzes the product from INH anIsonicotinoyl radical that subsequentlyinter-acts with mycobacterial NAD & NADPto produce dozen of adducts , one of thesea nicotinoyl NAD isomer which  ↓ the activityof enoyl acyl carrier protein reductase (Inh A) & β- ketoacyl carrier proteinsynthase ( Kas A) , inhibition of these enzymes↓ the synthesis of mycolic acid an essential component of the mycobacterial  cell wall &  causes cell death.

(another adduct , a nicotinoyl –NADP isomer potentially mycobacterial dihydrofolate reductase → interfere with nucleic acid synthesis .

These adducts also produce H2O2 ,   NO radical & other free radicals which are toxic to bacilli )

-          If INH is given alone , inherent resistant  bacilli proliferate selectively &  after 2-3 months an apparently resistant infection  emerges .

(Mutation of the catalase –peroxidase gene in bacilli do not generate the active  metabolite of INH )

-  Combination therapy with INH has good resistance preventing action .There is no cross resistance

Pharmacokinetics :

-Completely absorbed orally , penetrate all  body tissues, tubercular cavities , placenta& meninges .

-          Metabolized in liver by acetylation &  metabolites are excreted in urine .

-          Rate of acetylation shows genetic variation

( fast acetylators > 30% Indians - t½ -1 hr

Slow acetylators >60% Indians -t ½- 3 hrs)

ADRs -

Well tolerated drug

1.Peripheral neuritis & other neurologicalmanifestations- parasthesia  , numbness, mental disorientation & rarely convulsion   ( due to interference with utilization of

pyridoxine & ↑ excretion in urine )Due to this Pyridoxine given prophylactically

-10 mg/day which prevents neurotoxicities(INH neurotoxicity treated with Pyridoxine-100 mg/ day )

2. Hepatitis – more common in older   patients & alcohlics ( reversible)

3. Rashes , fever , acne & arthralgia .

RESISTANCE:

Genetic studies in Mycobacterium smegmatis identified the inhA-encoded, NADH-dependent enoyl acyl carrier protein reductase as the primary target for this drug. A reactive form of isoniazid inhibits InhA by reacting with the NAD(H) cofactor bound to the enzyme active site forming a covalent adduct (isonicotinic acyl NADH) that is apt to bind with high affinity. Resistance can occur by increased expression of InhA or by mutations that lower the enzyme's affinity to NADH. Both of these resistance mechanisms are observed in 30% of clinical tuberculosis isolates. Mutation in katG, which encodes catalase peroxidase, is the most common source for resistance. MARKET FORMULATIONS :

Brand names: Nydrazid
Drug class(es): hydrazide derivatives

Brand names: Rifater
Drug class(es): antituberculosis combinations

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Intro

Tuberculosis is a chronic granulomatous  disease. In developing countries it is a major health problem. ≈ 30% of world population is infected with Myc. Tuberculosis infection. In India > 2 million people develop active disease every year & half million die.

Mycobacterium tuberculosis is the bacteria that cause tuberculosis (TB). It is an aerobic bacillus, which means that it is rod shaped microorganisms (bacillus) that requires a lot of oxygen for it to grow and flourish (aerobic).

This bacteria needs highly oxygenated area body and most commonly affect lungs, growing ends of bones, and the brain (cerebral cortex), with the kidney, liver, and genitourinary tract.

History

First successful drug for treating TB wasPAS (Para- aminosalicylic acid) developed by Lehman in 1943.

Dramatic success came when Waksman & Schutz  discovered Streptomycin which has made remarkable progress.Followed by Thiacetazone by Domagk in   in 1946

In  1952 Isoniazid came into being Pyrazinamide by Kushner & colleagues   in 1952 & later on Rifampicin in 1957    by S. Margalith  has totally  changed thestrategy in the chemotherapy.

Ethambutol came in 1961 by Lederle -laboratories

Fluoroquinolones  , newer macrolides & congener of Rifampicin →Rifabutin arerecent addition in antimycobacterial drugs.

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- Obtained from S. archidacces & is a chemical analogue of D- alanine

-↓ Bacterial cell wall synthesis

-Tuberculostatic & ↓ other G -ve organisms ( E. coli , Chlamydia)

-Resistance develop slowly , no cross resist.

-CNS toxicity is high , sleepiness , headache, tremor , psychosis & convulsions

-Rarely used (only in resistance cases)

Dose :
- 250 mg BD

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-It is Chemically≡ INH

-It is weak tuberculocidal, more active in acidic medium.

-More lethal to intracellular bacilli & to those at sites showing an inflammatory response.

- Therefore effective in first two months of therapy where inflammatory changes are present.

-Good sterilizing activity

-It’s use enabled total duration of therapy to be shortened & risk of relapse to be reduced.

-Mechanism
≡ INH - ↓ fatty acid synthesis but by interacting with a different fatty acid synthesis encoding gene.

-PZA is thought to enter M. tub. by passive diffusion and converted to pyrazinoic acid (its active metabolite) by bact. pyrazinamidase enz.

-This metabolite inhibits mycobact. fatty  acid synthase -I enz. and disrupts mycolic acid synthesis needed for cell wall synthesis

-Mutation in the gene (pcn A) that encodes  pyrazinamidase enzyme is responsible for drug resistance
( minimized by using drug combination therapy) .

PANCREATIC KIDNEY TRANSPLANTATION:

-Absorbed orally, widely distributed ,Good penetration in CSF.

-Metabolized in liver & excreted in urine.

-t½ -6-10 hrs

ADVERSE DRUG REACTIONS :
-Hepatotoxic -dose related

-Arthralgia , hyperuricaemia, flushing , rashes , fever & anaemia

-Loss of diabetic control

DOSE:
– 20-30 mg /kg daily , 1500 mg if > 50 kg

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Amikacin is an antibiotic used for a number of bacterial infections. This includes joint infections, intraabdominal infections, meningitis, pneumonia, sepsis, and urinary tract infections. It is also used for the treatment of multidrug-resistant tuberculosis.It is used either by injection into a vein or muscle.Amikacin was patented in 1971 and came into commercial use in 1976. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. The wholesale cost in the developing world is 13.80 to 130.50 USD for a month. In the United States a typical course of treatment costs 25 to 50 USD. It is made from kanamycin.

Medical uses
Amikacin is most often used for treating severe, hospital-acquired infections with multidrug-resistant Gram-negative bacteria such as Pseudomonas aeruginosa, Acinetobacter, and Enterobacter. Serratia marcescens and Providencia stuartii are also included in the spectrum. Amikacin can also be used to treat non-tubercular mycobacterial infections and tuberculosis (if caused by sensitive strains) when first-line drugs fail to control the infection.
Amikacin may be combined with a beta-lactam antibiotic for empiric therapy for people with neutropenia and fever.
Liposomal amikacin for inhalation is currently in late stage clinical trials for the treatment of respiratory diseases, such as cystic fibrosis,Pseudomonas aeruginosa, non-tubercular mycobacterial infections and bronchiectasis.
Pharmacokinetics data: protein binding is 0-11% having biological half life about 2-3 hours and excreted through kidney
Adverse effects
Side-effects of amikacin are similar to those of other aminoglycosides. Kidney damage and hearing loss are the most important effects. Because of this potential, blood levels of the drug and markers of kidney function (creatinine) may be monitored. Moreover, doses are adjusted specifically based upon serum Creatinine clearance in clinical settings.[citation needed]
Administration
Amikacin may be administered once or twice a day but must be given by the intravenous or intramuscular route or via nebulization. There is no oral form available as amikacin is not absorbed orally. In people with kidney failure, dosage must be adjusted according to the creatinine clearance, usually by reducing the dosing frequency.
Resistance
Amikacin evades attacks by most of the antibiotic-inactivating enzymes that are responsible for antibiotic resistance in bacteria. This is accomplished by the L-hydroxyaminobuteroyl amide (L-HABA) moiety attached to N-1 (compare to kanamycin), which inhibits acetylation, phosphorylation, and adenylation in the distant amino sugar ring (C-2,C-3,C-4). To prevent the development of bacterial resistance to this antibiotic, its use is tightly regulated.

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Rifampicin, also known as rifampin, is an antibiotic used to treat several types of bacterial infections. This includes tuberculosis, leprosy, and Legionnaire's disease. It is almost always used along with other antibiotics, except when given to prevent Haemophilus influenzae type b and meningococcal disease in people who have been exposed to those bacteria. Before treating a person for a long period of time, measurements of liver enzymes and blood counts are recommended. Rifampicin may be given either by mouth or intravenously.
Common side effects include nausea, vomiting, diarrhea, and loss of appetite. It often turns urine, sweat, and tears a red or orange color. Liver problems or allergic reactions may occur. It is part of the recommended treatment of active tuberculosis during pregnancy, even though its safety in pregnancy is not known. Rifampicin is of the rifamycin group of antibiotics. It works by stopping the production of RNA by bacteria.
Rifampicin was discovered in 1965, marketed in Italy in 1968, and approved in the United States in 1971. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. It is available as a generic medication. The wholesale cost in the developing world is about 3.90 USD a month. In the United States it is expensive, with a month of treatment being about 120 USD. Rifampicin is made by the soil bacterium Amycolatopsis rifamycinica.
Antibacterial spectrum:
It is a semisynthetic derivative of rifamycin B obtained from STREPTOMYCIN MEDITERRANEI.rifampin is bactericidal to M.TUBERCLOSIS and many other gram-positive and gram-negative bacteria like straph aureus , N.meningitidis, H.influenzae, E.coli,Klebsiella, Pseudomonas,Proteus and Legionella.
MECHANISM OF ACTION :
Rifampicin inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA-dependent RNA polymerase.
Crystal structure data and biochemical data suggest that rifampicin binds to the pocket of the RNA polymerase β subunit within the DNA/RNA channel, but away from the active site The inhibitor prevents RNA synthesis by physically blocking elongation, and thus preventing synthesis of host bacterial proteins. By this "steric-occlusion" mechanism, rifampicin blocks synthesis of the second or third phosphodiester bond between the nucleotides in the RNA backbone, preventing elongation of the 5' end of the RNA transcript past more than 2 or 3 nucleotides.
Mechanism of resistance
Resistance to rifampicin arises from mutations that alter residues of the rifampicin binding site on RNA polymerase, resulting in decreased affinity for rifampicin. Resistance mutations map to the rpoB gene, encoding the beta subunit of RNA polymerase. The majority of resistance mutations in E. coli are in 3 clusters on rpoB. Cluster I is amino acids 509 to 533, cluster II is amino acids 563 to 572, and cluster III is amino acid 687.
When describing mutations in rpoB in other species, the corresponding amino acid number in E. coli is usually used. In Mycobacterium tuberculosis, the majority of mutations leading to rifampicin resistance are in cluster I, in a 81bp hotspot core region called RRDR for "rifampcin resistance determining region". A change in amino acid 531 from serine to leucine arising from a change in the DNA sequence of TCG to TTG is the most common mutation. Tuberculosis resistance has also occurred due to mutations in the N-terminal region of rpoB and cluster III.
An alternative mechanism of resistance is through Arr-catalyzed ADP-ribosylation of rifampicin. With the assistance of the enzyme Arr produced by the pathogen Mycobacterium smegmatis, ADP-ribose is added to rifampicin at one of its ansa chain hydroxy groups, thereby inactivating the drug.
Resistance in tuberculosis
Mycobacterial resistance to rifampicin may occur alone or along with resistance to other first line anti-tubercular drugs. Early detection of such multi-drug or extensively drug-resistant tuberculosis is critical in improving patient outcomes by instituting appropriate second-line treatments, and in decreasing transmission of drug-resistant TB. Traditional methods of detecting resistance involve Mycobacterial culture and drug susceptibility testing, results of which could take up to six weeks. Xpert® MTB/RIF assay is an automated test that can detect rifampicin resistance, and also diagnose tuberculosis. A Cochrane review updated in 2014 concluded that for rifampicin resistance detection, Xpert® MTB/RIF was accurate, that is (95%) sensitive and (98%) specific.
Pharmacokinetics
Orally administered rifampicin results in peak plasma concentrations in about two to four hours. 4-Aminosalicylic acid (another antituberculosis drug) significantly reduces absorption of rifampicin,[42] and peak concentrations may be lower. If these two drugs must be used concurrently, they must be given separately, with an interval of eight to 12 hours between administrations.
Rifampicin is easily absorbed from the gastrointestinal tract; its ester functional group is quickly hydrolyzed in bile, and it is catalyzed by a high pH and substrate-specific esterases. After about six hours, almost all of the drug is deacetylated. Even in this deacetylated form, rifampicin is still a potent antibiotic; however, it can no longer be reabsorbed by the intestines and is eliminated from the body. Only about 7% of the administered drug is excreted unchanged in urine, though urinary elimination accounts for only about 30% of the drug excretion. About 60% to 65% is excreted through feces.
The half-life of rifampicin ranges from 1.5 to 5.0 hours, though hepatic impairment significantly increases it. Food consumption inhibits its absorption from the GI tract, and the drug is more quickly eliminated. When rifampicin is taken with a meal, its peak blood concentration falls by 36%. Antacids do not affect its absorption. The decrease in rifampicin absorption with food is sometimes enough to noticeably affect urine color, which can be used as a marker for whether or not a dose of the drug has been effectively absorbed.
Distribution of the drug is high throughout the body, and reaches effective concentrations in many organs and body fluids, including the cerebrospinal fluid. Since the substance itself is red, this high distribution is the reason for the orange-red color of the saliva, tears, sweat, urine, and feces. About 60% to 90% of the drug is bound to plasma proteins.
Interactions
Rifampicin is the most powerful known inducer of the hepatic cytochrome P450 enzyme system, including isoenzymes CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP3A4, CYP3A5, and CYP3A7. It increases metabolism of many drugs and as a consequence, can make them less effective, or even ineffective, by decreasing their levels. For instance, patients undergoing long-term anticoagulation therapy with warfarin have to increase their dosage of warfarin and have their clotting time checked frequently because failure to do so could lead to inadequate anticoagulation, resulting in serious consequences of thromboembolism.
Rifampicin can reduce the efficacy of birth control pills or other hormonal contraception by its induction of the cytochrome P450 system, to the extent that unintended pregnancies have occurred in women who use oral contraceptives and took rifampicin even for very short courses (for example, as prophylaxis against exposure to bacterial meningitis).
Other interactions include decreased levels and less effectiveness of antiretroviral agents, everolimus, atorvastatin, rosiglitazone, pioglitazone, celecoxib, clarithromycin, caspofungin, voriconazole, and lorazepam.Rifampicin is antagonistic to the microbiologic effects of the antibiotics gentamicin and amikacin.
Medical use
Mycobacteria Rifampicin is used for the treatment of tuberculosis in combination with other antibiotics, such as pyrazinamide, isoniazid, and ethambutol. For the treatment of tuberculosis, it is administered daily for at least 6 months. Combination therapy is utilized both to prevent the development of resistance and to shorten the length of treatment. Resistance of Mycobacterium tuberculosis to rifampicin develops quickly when it is used without another antibiotic, with laboratory estimates of resistance rates from 10−7 to 10−10 per tuberculosis bacteria per generation.
Other bacteria and protozoans Rifampicin is sometimes used in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) in combination with fusidic acid, including in difficult-to-treat infections such as osteomyelitis and prosthetic joint infections. It is also used as preventive treatment against Neisseria meningitidis (meningococcal) infections. Rifampicin is also recommended as an alternative treatment for infections by the tick-borne pathogens Borrelia burgdorferi and Anaplasma phagocytophilum when treatment with doxycycline is contraindicated, such as in pregnant women or in patients with a history of allergy to tetracycline antibiotics.
Viruses Rifampicin has some effectiveness against vaccinia virus
Adverse effects
The most serious adverse effect is hepatotoxicity, and patients receiving it often undergo baseline and frequent liver function tests to detect early liver damage.The more common side effects include fever, gastrointestinal disturbances, rashes, and immunological reactions. Taking rifampicin usually causes certain bodily fluids, such as urine, sweat, and tears, to become orange-red in color, a benign side effect that nonetheless can be frightening if it is not expected. This may also be used to monitor effective absorption of the drug (if drug color is not seen in the urine, the patient may wish to move the drug dose farther in time from food or milk intake). The discolorization of sweat and tears is not directly noticeable, but sweat may stain light clothing orange, and tears may permanently stain soft contact lenses. Since rifampicin may be excreted in breast milk, breast feeding should be avoided while it is being taken.
Other adverse effects include:Liver toxicity — hepatitis, liver failure in severe cases
Respiratory — breathlessness
Cutaneous — flushing, pruritus, rash, hyperpigmentation,[27] redness and watering of eyes
Abdominal — nausea, vomiting, abdominal cramps, diarrhea
Flu-like symptoms — chills, fever, headache, arthralgia, and malaise. Rifampicin has good penetration into the brain, and this may directly explain some malaise and dysphoria in a minority of users.
Allergic reaction — rashes, itching, swelling of the tongue or throat, severe dizziness, and trouble breathing.

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SAWBO™ Scientific Animations Without Borders

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Tuberculosis Prevention in English (accent from the USA)

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All SAWBO animations are given out freely. Please donate at http://sawbo-illinois.org/donate.htm in order to help the SAWBO team make more animations and more language variants of our existing animations. Tuberculosis Prevention in English (accent from USA) Tuberculosis is a common infection and contagious disease caused by a bacterium that usually lodges in the lungs.

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Kanamycin can cause severe damage to the kidneys and can also cause hearing loss. You will need to be closely monitored by your health care provider. Be sure your doctor is aware of any other medications you may be taking.

Mechanism of Action :-

Kanamycin interacts with the 30S subunit of prokaryotic ribosomes. It gives birth to substantial amounts of mistranslation and indirectly inhibits translocation during protein synths.

Kanamycin works by interfering with protein synthesis. It binds to the 30S subunit of the bacterial ribosome. This results in incorrect alignment with the mRNA and eventually leads to a misread that causes the wrong amino acid to be placed into the peptide. This leads to nonfunctional peptide chains.

Composition :-

Kanamycin is a mixture of three main components: kanamycin A, B, and C. Kanamycin A is the major component in kanamycin.The effects of these components do not appear to be widely studied as individual compounds when used against prokaryotic and eukaryotic cells.

Biosynthesis :-

While the main product produced by Streptomyces kanamyceticus is kanamycin A, additional products are also produced, including kanamycin B, kanamycin C, kanamycin D and kanamycin X.

The kanamycin biosynthetic pathway can be divided into two parts. The first part is common to several aminoglycoside antibiotics, such as butirosin and neomycin. In it a unique aminocyclitol, 2-deoxystreptamine, is biosynthesized from D-glucopyranose 6-phosphate in four steps. At this point the kanamycin pathway splits into two branches due to the promiscuity of the next enzyme, which can utilize two different glycosyl donors - UDP-N-acetyl-α-D-glucosamine and UDP-α-D-glucose. One of the branches forms kanamycin C and kanamycin B, while the other branch forms kanamycin D and kanamycin X. However, both kanamycin B and kanamycin D can be converted to kanamycin A, so both branches of the pathway converge at kanamycin.

Side effect :-

Agitation

black, tarry stools

bloody or cloudy urine

bluish lips or skin

blurred vision

burning, crawling, itching, numbness, prickling, "pins and needles", or tingling feelings

chest pain

chills

coma

confusion

continuing ringing or buzzing or other unexplained noise in the ears

cough

decreased urine output

depression

difficulty with breathing

difficulty with moving

dizziness or lightheadedness

dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position

drowsiness

dry mouth

feeling of constant movement of self or surroundings

feeling of fullness in the ears

fever

headache

irritability

lethargy

loss of balance

loss or change in hearing

muscle pain or stiffness

muscle twitching

nausea

not breathing

pain in lower back or side

pain in the joints

painful or difficult urination

pale skin

rapid weight gain

seizures

sensation of spinning

shakiness in the legs, arms, hands, or feet

shortness of breath

sore throat

sores, ulcers, or white spots on the lips or in the mouth

stupor

sweating

swelling of the face, ankles, or hands

swollen glands

thirst

trembling or shaking of the hands or feet

trouble with hearing

troubled breathing with exertion

uncontrolled eye movements

unusual bleeding or bruising

unusual tiredness or weakness

Uses :-

The selection marker kanMX is a hybrid gene consisting of a bacterial aminoglycoside phosphotransferase (kan fromtransposon Tn903) under control of the strong TEFpromoterfrom Ashbya gossypii.

Mammalian cells, yeast, and other eukaryotes acquire resistance to geneticin (= G418, an aminoglycoside antibiotic similar to kanamycin) when transformed with a kanMX marker. In yeast, the kanMX marker avoids the requirement of auxotrophic markers. In addition, the kanMX marker renders E. coli resistant to kanamycin. In shuttle vectors the KanMX cassette is used with an additional bacterial promoter. Several versions of the kanMX cassette are in use, e.g. kanMX1-kanMX6. They primarily differ by additional restriction sites and other small changes around the actual open reading frame.

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Streptomycin may cause severe toxic nerve reactions. The risk is increased in patients with kidney problems. Other severe problems like vision problems, trouble keeping your balance, certain brain problems, and hearing problems (eg, permanent hearing loss) may also happen. The risk of hearing problems may be increased if you have kidney problems or already have hearing problems. It may be increased if you get high doses of streptomycin, or if you get it for a long time. The risk may also be increased in older people, infants, or people who are dehydrated. If you already have kidney problems or hearing problems, tell your doctor. Your doctor will monitor your progress to lower the possibility of these effects. Your doctor may also run certain tests (eg, hearing and/or kidney tests). Discuss any questions or concerns with your doctor.

Do not use streptomycin if you are taking or have recently taken other medicines that can cause nerve, kidney, or hearing problems. This includes amphotericin B, bacitracin, cephaloridine, cisplatin, colistin, cyclosporine, ethacrynic acid, furosemide, paromomycin, polymyxin B, vancomycin, viomycin, or other medicines like this one. There are many other medicines that can do this. Ask your doctor or pharmacist if you are not sure.

Severe muscle problems and severe breathing problems have happened with streptomycin. The risk of these problems may be increased if you are getting certain medicines used to put you to sleep or to relax your muscles. The risk is also increased if you are getting a certain type of blood transfusion. Discuss any questions or concerns with your doctor.

Mechanism of Action :-
Streptomycin is a protein synthesis inhibitor. It binds to the small 16S rRNA of the 30S subunit of the bacterial ribosome, interfering with the binding of formyl-methionyl-tRNA to the 30S subunit. This leads to codon misreading, eventual inhibition of protein synthesis and ultimately death of microbial cells through mechanisms that are still not understood. Speculation on this mechanism indicates that the binding of the molecule to the 30S subunit interferes with 50S subunit association with the mRNA strand. This results in an unstable ribosomal-mRNA complex, leading to a frameshift mutation and defective protein synthesis; leading to cell death.Humans have ribosomes which are structurally different from those in bacteria, so the drug does not have this effect in human cells. At low concentrations, however, streptomycin only inhibits growth of the bacteria by inducing prokaryotic ribosomes to misread mRNA.Streptomycin is an antibiotic that inhibits both Gram-positive and Gram-negative bacteria and is therefore a useful broad-spectrum antibiotic.

History :-

Streptomycin was first isolated on October 19, 1943, by Albert Schatz, a PhD student in the laboratory of Selman Abraham Waksman at Rutgers University in a research project funded by Merck and Co.Waksman and his laboratory staff discovered several antibiotics, including actinomycin, clavacin, streptothricin, streptomycin, grisein, neomycin, fradicin, candicidin, and candidin. Of these, streptomycin and neomycin found extensive application in the treatment of numerous infectious diseases. Streptomycin was the first antibiotic cure for tuberculosis (TB). In 1952 Waksman was the recipient of the Nobel Prize in Physiology or Medicine in recognition "for his discovery of streptomycin, the first antibiotic active against tuberculosis".Waksman was later accused of playing down the role of Schatz who did the work under his supervision.

At the end of World War II, the United States Army experimented with streptomycin to treat life-threatening infections at a military hospital in Battle Creek, Michigan. The first patient treated did not survive; the second patient survived but became blind as a side effect of the treatment. In March 1946, the third patient—Robert J. Dole, later Majority Leader of the United States Senate and Presidential nominee—experienced a rapid and robust recovery.

The first randomized trial of streptomycin against pulmonary tuberculosis was carried out in 1946 through 1948 by the MRC Tuberculosis Research Unit under the chairmanship of Geoffrey Marshall (1887–1982). The trial was both double-blind and placebo-controlled. It is widely accepted to have been the first randomised curative trial

Results showed efficacy against TB, albeit with minor toxicity and acquired bacterial resistance to the drug.

side effect :-

Black, tarry stools

burning, crawling, itching, numbness, prickling, "pins and needles", or tingling feelings

chest pain

chills

clumsiness

cough

dizziness or lightheadedness

feeling of constant movement of self or surroundings

fever

large, hive-like swelling on the face, eyelids, lips, tongue, throat, hands, legs, feet, or sex organs

nausea

painful or difficult urination

sensation of spinning

shortness of breath

sore throat

sores, ulcers, or white spots on the lips or in the mouth

swollen glands

unsteadiness

unusual bleeding or bruising

unusual tiredness or weakness

vomiting

Therapeutic Uses :-

This medication is used with other medications to treat active tuberculosis (TB) infection if you cannot take other drugs for TB or if you have a type of TB that cannot be treated with other drugs (drug-resistant TB). Streptomycin belongs to a class of drugs known as aminoglycoside antibiotics. It works by killing the organisms that cause the infection.

This drug may also be used to treat other serious infections (e.g., Mycobacterium avium complex-MAC, tularemia, endocarditis, plague) along with other medications.

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