Tuberculosis: Prevention and Treatment

Tuberculosis: Prevention and Treatment Tuberculosis (TB) is an airborne infectious disease which is caused by strains of mycobacteria, mainly Mycobacterium tuberculosis1. There are roughly one third of the worlds population are infected with tuberculosis where nine millions of new cases reported annually2. Although tuberculosis can be prevented and treated, it continues to cause millions of deaths every year2. When infected individual coughs, sneezes or spits, M. tuberculosis is propelled into the air and infected those who breathed in the bacteria that existed in droplets of saliva3. Primarily, tuberculosis will affect the lungs, known as pulmonary tuberculosis3. It will also affect other parts of body, for instance lymph nodes, bones, brain and kidneys3. Once a person is infected with tuberculosis, there are basically three possible ways may occur. Firstly, the immune system plays a vital role and strong enough to kill the bacteria3. Secondly, immune system is not strong enough to fight off the bacteria but is able to b uild a defensive barrier against the bacteria3. Individuals who are latently infected with M. tuberculosis show asymptomatic where these bacteria lie dormant in the lungs and able to reactivate after years1. The disease is often reactivated in those who are immunocompromised or generally weakened. Lastly, the immune system fails to kill bacteria causing the bacteria to grow and spread towards other parts of body which is called active tuberculosis3. In the fight of tuberculosis, World Health Organisation (WHO) recommends universal Bacille Calmette-Guà ©rin (BCG) vaccination in the countries with high TB burdens4. BCG vaccine contains weakened form of M. tuberculosis which will induce human antibodies to fight against this type of bacteria. The efficacy of BCG vaccination can be ranging from 0% to 84%5. This may be due to the frequency of TB exposure and quality of vaccine used, leading to arguments on BCG vaccination efficacies4. One of the greatest arguments is that BCG vaccination causing positive reactions to tuberculin skin testing and hence interfere with the diagnosis of latent TB4. Existence of evidences showing the rates of efficacy also depends on geographical location, age at vaccination and form of TB further complicate the situation. Currently, TB chemotherapy is made up of combination of a list of first-line drugs isoniazid (INH), rifampicin (RIF), pyrazinamide (PZA) and ethambutol (EMB) 6. If the treatment fails d ue to bacterial drug resistance, or patient unable to tolerate, second-line drugs for instance para-aminosalicylate (PAS), fluoroquinolones, ethionamide and cycloserine are introduced6. These are considered as second line drugs generally either less potent with larger doses regimen or more toxic with serious side effects6. Tuberculosis is presently treated in two phases, namely initial phase and continuous phase7. In initial phase, the patient will be treated with concurrent use of four first line drugs, with the aim to eradicate or control bacteria population to replicate in rapid motion and also avoid the emergence of bacteria resistance7. The treatment choices available for initial treatment include isoniazid, rifampicin, pyrazinamide and ethambutol7. Streptomycin is used rarely but can be used in patients who infected with bacteria that are resistant to isoniazid before the therapy is commenced7. The duration for initial phase is 2 months whereas the continuous phase takes 4 months7. During the four months of continuous phase, patients are treated with isoniazid and rifampicin at same doses7. Most of the TB treatment is supervised where drug administration needs to be fully supervised by healthcare professions since lengthy duration of treatment causing incompliance in patients7. These patients who are unlikely to be compliance will be given the drugs three times a week until the course is completed while patients who able to comply with the treatment will not be supervised7. Despite the chemotherapy treatment and BCG vaccine, TB remains as a significant infectious disease due to increasing emergence of drug resistant TB and co-infection with Human Immunodeficiency Virus (HIV) 6. Since the host defense in HIV patients is suppressed, they are more susceptible to TB infections. Moreover, drug- drug interactions between antiviral therapy and anti-TB also causing complications in treating co-infected patients6. Drug resistant TB has evolved mainly because of improper treatment or incompliance in patients who stop taking their medications before the bacteria is being fully eradicated since the duration of treatment is lengthy which takes 6-9 months8, 9. The mechanism involved includes chromosomal mutations in genes that responsible for drug targets encoding9. When there is a sequential accumulation of mutations, multi-drug resistant tuberculosis (MDR-TB) emerges where the M. tuberculosis strains will resistant to two of the most commonly used drugs, Isoniazid and Rifampicin9. Patients with MDR-TB are then relying on the second-line drug classes, fluoroquinolones and the three injectable agents namely amikacin, capreomycin, and kanamycin10, 11. The chances to cure would dramatically be reduced for patients who infected with extensively drug-resistant tuberculosis (XDR-TB), a situation where the isolated strains are resistant against any one of fluoroquinolones and at least one of three injectable drugs6. In order to combat with the MDR-TB or XDR-TB and optimize the tuberculosis drug regimen, it is crucial to understand the mechanism of action of current using first-line drugs and how resistance is developed against these drugs. Isoniazid (INH) or isonicotinic acid hydrazide is discovered in 1952, a bactericidal agent which active against organism of the genus Mycobacterium, especially M. tuberculosis, M. bovis and M. kansassi6, 12. In vivo, INH has shown to be bactericidal in culture over the first 48 hours which become bacteriostatic after this particular time frame12. This indicates that INH is bacteriostatic for slow replicating bacilli but is bactericidal against rapidly dividing mycobacterium. The minimal tuberculostatic concentration is 0.025 to 0.05ug/ml13. INH is a prodrug that needs to be activated by catalaseperoxide hemoporotein, KatG before acts by inhibiting mycolic acid synthesis and cell wall disruption in susceptible mycobacterium13, 14. This inhibitory action is only targeted to mycobacteria since other bacteria do not contain mycolic acid in the cell wall13. INH acts by inhibit enoyl acyl carrier protein (ACP) reductase, InhA, and a beta-ketoacyl-ACP synthase, KasA that are crucial in fatt y acid synthesis system for mycolic acid15. Resistance to INH is believed due to mutations in gene encoding catalaseperoxidase katG or InhA or lacking KatG 9, 14. Isoniazid is metabolised in the liver, mainly by acetylation and dehydrazination where slow acetylator may experience higher concentration leads to potential toxicity before excreted in the urine within 24 hours13. Rifampicin (RIF), discovered in 1963, is a lipophilic semisynthetic derivative of rifamycin antibiotic which is produced by the fermentation of a strain of Amycolatopsis mediterranei6, 9, 16. RIF has bactericidal activities against a broad spectrum of microorganisms including gram-positive and gram-negative. RIF will inhibit the action of DNA-dependent RNA polymerase of mycobacteria that is encoded by rpoB through formation of a stable drug-enzyme complex9. This will suppress the initiation chain formation in RNA synthesis and hence prohibit protein synthesis in M. tuberculosis9. Development of resistance to RIF is mostly due to mutation in 81 base pair region of rpoB gene thus facilitate a straightforward approach to detect MDR-TB since 85-90% RIF-resistant strains are also resistant to INH9. RIF produces peak plasma concentration of 7ug/mL in 2 to 4 hours after ingestion of 600mg17. It also distributed well to most of the body tissues and fluids, including cerebrospinal fluid since it is lipophilic17. Following absorption from the gastrointestinal tract, RIF is eliminated rapidly in the bile with fewer amounts excreted through urine17. Pyrazinamde (PZA) is discovered in 1954 and it produces excellent sterility effects against semidormant tubercle bacilli at slightly acidic pH6, 9. The antimicrobial activity of PZA is through interference with mycolic acid synthesis in M. tuberculosis by pyrazinoic acid, an active moiety of PZA9. Conversion of PZA to pyrazinoic acid is mediated by pyrazinamidase enzyme that is encoded by pncA gene in M. tuberculosis, thus indicating that these bacilli are sensitive to PZA9. Resistance against PZA evolved when mutation occur at pncA gene that is responsible for pyrazinamidase, hence affecting the activity of this enzyme9. PZA is well absorbed from gastrointestinal tract and is widely distributed to most tissues and fluid too17. The oral administration of 500 mg PZA produces plasma concentrations of 9-12ug/ml after two hours and 7ug/ml after 8 hours17. PZA is metabolized in liver whereas the metabolites are excreted through renal glomerular filtration17. Ethambutol (EMB) is discovered in 1962, acts as bacteriostatic agent and is active against undergoing cell division6, 18. EMB primarily targets on impairment of cell wall polymerization by inhibits arabinosy transferase, a vital enzyme responsible for mycobacteria cell wall biosynthesis9, 18. Since arabinosy transferase enzyme is encoded by embC-embA-embB genes, resistance against EMB evolved is believed due to mutation of these genes9. EMB is currently used as one of the first-line treatment for tuberculosis mainly because of its synergistic effect with other front-line drugs and its low toxicity property18. There is roughly 75-80% of an oral dose of EMB is rapidly absorbed in gastrointestinal tract with absorption unaffected when administered with foods19. In addition, EMB is distributed widely to body tissues and fluid, including cerebrospinal fluid before being metabolized in the liver and excreted in urine19. Streptomycin (SM) is an aminoglycoside antibiotic, used as first line treatment for TB when it first discovered in 19441, 6. Streptomycin is isolated from the bacteria Streptomyces griseus and its antimicrobial effects against M. tuberculosis is highly effective when use in combination with other first line agents20. However, SM is no longer considered as first line treatment as resistance against it has developed rapidly1. The optimum pH for SM is at pH8 where its bacteriostatic activity will reduce with increasingly acidic environment20. SM acts by binding tightly to A site of 16S ribosomal RNA subunit, interferes with mRNA translation, causing faulty protein being produced1, 9. Resistant emergence when the mutation occurs at gene rpsL and rrs that encoded for 16S and S12 ribosomal protein1, 9. Upon administration, SM is poorly absorbed from gastrointestinal tract and mostly administered parentally1. SM is mostly excreted in urine and patients with low renal profile might experienc e toxicity such as neurotoxic reactions1. When the first line treatment is no longer suitable for patients or patients develop multi-drug resistance TB, second line drugs will then be introduced in combating the TB. Second line drugs that are mostly used include Ethionamide (ETH), Cycloserine (CS), Para-Aminosalicylic Acid (PAS) and Fluoroquinolones (FQ). ETH has been in use since 1960s, is a structural analogue of INH and it targets at inhibition of mycolic acid biosynthesis in tubercle bacilli9, 21. INH however is much more potent than ETH since the minimal inhibitory concentration for ETH is 0.5-5.0ug/mL21. Resistance evolved due to mutation at gene InhA and ethA which encode for oxygenase enzyme in activation of ETH 9. In vitro, CS has inhibitory effect on M. tuberculosis at 5-200ug/mL and there is no cross resistance occurred between CS and other drugs13. CS acts by interfereing the biosynthesis of bacterial cell wall13. CS is well absorbed in gastrointestinal tract and also widely distributed to body tissues and fluid including cerebrospinal fluid13. PAS was first introduced as first line drug but being replaced by Ethambutol in 1960s1. It acts bacteriostatically with possessing inhibitory effect at concentration less than 1mg/ml by interfere with folic acid metabolism in bacteria1. PAS is readily absorbed from gastrointestinal tract and distributed well throughout the body. Approximately 80% of the drugs will be excreted via kidney after being metabolized to acetylated form1. Moxifloxacin and Gatifloxacin are both been synthesized and evaluated as excellent bactericidal agents through inhibiting DNA gyrase, an ATP-dependent enzymes topoisomerase II which is responsible in bacteria DNA transcription9. DNA gyrase is consisted of two subunits that is arranged in a complex, is encoded by two different genes, gyrA and gyrB where mutations at gyrA will normally cause bacteria resistance to these new generation of flouroquinolones9. Due to the increasing incidence of multidrug resistance TB, it is highly desirable to develop new drugs that are not only potent and effective against current resistant strains of M. tuberculosis but also possess shorter treatment duration since most of the incompliance of patients is brought up by lengthy TB treatment. Most of the mechanisms of action of current treatments are involved in interfering the bacterial DNA synthesis, protein and mycolic cell wall biosynthesis. The enzymes that participate in these pathways could also be the target of newly designed drugs such as TMC207, one of the new drugs which are currently under investigations and clinical trials. TMC207 is a member of diarylquinoline class of compound which target at adenosine triphosphate (ATP) synthase by binding to subunit C of the synthase, blocking the energy pathway of mycobacteria22, 23. In vitro, TMC207 not only possesses ability to inhibit both drug sensitive and resistant M. tuberculosis isolates, but also able to sterilize the patient through killing the dormant bacilli bactericidally22. TMC207 showed a minimum inhibitory concentration of 0.03ug/mL against M. tuberculosis, suggesting a more potent agent compared to current first- line treatments such as isoniazid and rifampicin23. Apart from that, its synergistic effect with pyrazinamide could promise as effective drug combination for sterilizing the patients against TB22. A phase I clinical trials which involved short terms administration of TMC207 in healthy individuals showing no adverse effects and the subjects are well tolerated with it23. However, it is essential to investigate the selectivity of TMC207 again st mammalian ATP synthase with longer periods to ensure the patients safety when administered with TMC207. Thiacetazone (TAC) is widely used as second line anti-TB agent against multiresistant tuberculosis at present24. TAC acts by interferes the biosynthesis pathway of mycolic acid in tubercle bacilli24. The fact that M. tuberculosis has been difficult to eradicate and remains persistent is due to its cell wall that composed of mycolic acid which is resistant against chemical injury, dehydration and also has low permeability to antibiotics24. Mycolic acid contains cyclopropane rings that is activated through cyclopropane mycolic acid synthase (CMASs), has a significant contribution to tuberculosis24. By inhibiting the cyclopropanation, the cell wall biosynthesis will then be interrupted, introducing the bactericidal effects24. The aim of this research is to synthesis and evaluates the analogues of Thiacetazone which might be potential anti tuberculosis agents. The analogues will be tested against different strains of mycobacteria in lab. The target actions of these analogues will also be identified based on the structure of the analogues. The above analogue is synthesized when a benzylaldehyde reacts with a primary amine. This is a condensation process and an imine is produced. The changes at position R1 to R3 with different electron withdrawing groups are first planned to be evaluated. However, the plan is prohibited since the corresponding structures are either unavailable or too expensive that falling outside the budget. After revised on the previous analogues that were discovered and their respective MIC values obtained from lab, the structures of new analogues that are going to be evaluated are finally sorted out. The R1 to R3 positions would be replaced by either a -chloro or a -methoxy with R8 position would either be an amine, a methyl or a benzene ring. A chloro is used at position R1 to R3 since it is electron withdrawing, big and lipophilic molecule whereas the methoxy group is electron donating, small and quite lipophilic. For R8 position, an amine is selected because it is electron withdrawing and small. A methyl is also selected since it is quite lipophilic, small and electron donating. On the other hand, benzene ring which is highly lipophilic, neither electron donating nor withdrawing group might have a different effect on the analogue synthesized. References: Patrick Brennan, Douglas Young (2008). Tuberculosis. 88(2), 85-86, 137-138, 162-163. Health Protection Agency. http://www.hpa.org.uk/HPA/ National Health Services. http://www.nhs.uk/Pages/HomePage.aspx Zaida Araujoa, Jacobus Henri de Waard, Carlos Fernà ¡ndez de Larrea, Rafael Borges, Jacinto Convit (2008). The effect of Bacille Calmette-Guà ©rin vaccine on tuberculin reactivity in indigenous children from communities with high prevalence of tuberculosis. Vaccine 26, 5575-5581. Hart and Sutherland (1977). BCG and vole bacillus vaccines in the prevention of tuberculosis in adolescence and early adult life. Br Med J2(6082), 293-295. Global Alliance for TB Drug Development. http://www.tballiance.org/home/home.php 57th edition of British National Formulary: Section on Tuberculosis drugs, 316-317. Blumberg, H. M. et al. (2003). American Thoracic Society/ Centers for Disease and Prevention/ Infectious Disease Society of American: treatment of TB. Am.J.Respir.CareMed.167, 603-662. Suhail Ahmad and Eiman Mokaddas (2009). Recent advances in the diagnosis and treatment of multidrug-resistant tuberculosis. Respiratory Medicine 103(12), 1777-1790. Frieden TR, Sherman LF, Maw KL, et al. (1996). A multi-institutional outbreak of highly drug-resistant tuberculosis: epidemiology and clinical outcomes. JAMA 276, 1229-1235. Mukherjee JS, Rich ML, Socci AR, et al. (2004). Program and principles in treatment od multi-drug resistant tuberculosis. Lancet 363, 474-481. Zhang Y. et al. (2003). Isoniazid. Tuberculosis 2, 739-758. Hardmn, J.G., L.E. Limbird, P.B Molinoff, R.W. Ruddon, A.G. Goodman (2006). Goodman and Gilmans The Pharmacological Basis of Therapeutics. 9, 1164-1165. Zhang Y, Heym B, Allen B, Young D, Cole S (1992). The catalase-peroxidase gene and isoniazid resistance by Mycobacterium Tuberculosis. Nature 358, 591-593. Richard A. Slayden, Richard E. Lee and Clifton E. Barry (2002). Molecular Microbiology 38(3), 514-525. Rup Lal, Sukanya Lal (2005). Recent trends in rifamycin research. BioEssays 16(3), 211-216. Hardmn, J.G., L.E. Limbird, P.B Molinoff, A.G Gilman (2001). Goodman and Gilmans The Pharmacological Basis of Therapeutics. 10, 1278-1281. Raghunandan Yendapally and Richard E. Lee (2008). Design, synthesis and evaluation of novel ethambutol analogues. Bioorganic and Medical chemistry Letters 18(5), 1607-1611. McEvoy, G.K. (2007). Admerican Hospital Formulary Service. Besthesda, 551. Selman A. Waksman (1953). Streptomycin: Background, Isolation, Properties and Utilisation. Science, 118(3062), 259-266. Sampson AE, Barry CE (1999). Abstract General Meeting American Society Microbiology. 99, 635. Andreas H.D., Alexander Pym, Martin Grobusch et al. (2009). The Diarylquinoline TMC207 for Multidrug- Resistant Tuberculosis. 360(23), 2397-2405. Anna C. Haagsma, Rooda Abdillahi-Ibrahim, Marijke J. Wagner, Klaas Krab, Karen Vergauwen, Jerome Guillemont, Koen Andries, Holger Lill, Anil Koul, and Dirk Bald (2009). Selectivity of TMC207 towards mycobacterial ATP synthase compared with that towardsthe Eukaryotic homologue. Antimicrobial Agents and Chemotherapy, 53(3), 1290-1292. Anuradha Alahari, Xavier Trivelli, Yann Guà ©rardel, Lynn G. Dover, Gurdyal S. Besra, James C. Sacchettini, Robert C. Reynolds, Geoffrey D. Coxon, Laurent Kremer (2007). Thiacetazone, an Antitubercular Drug that Inhibits Cyclopropanation of Cell Wall Mycolic Acids in mycobacteria. PloS ONE, 2(12): e1343. Mycolic acids are a complex mixture of branched, long-chain fatty acids, representing key components of the highly hydrophobic mycobacterial cell wall. Pathogenic mycobacteria carry mycolic acid sub-types that contain cyclopropane rings. Double bonds at specific sites on mycolic acid precursors are modified by the action of cyclopropane mycolic acid synthases (CMASs). The latter belong to a family of S-adenosyl-methionine-dependent methyl transferases, of which several have been well studied in Mycobacterium tuberculosis, namely, MmaA1 through A4, PcaA and CmaA2. Cyclopropanated mycolic acids are key factors participating in cell envelope permeability, host immunomodulation and persistence of M. tuberculosis. While several antitubercular agents inhibit mycolic acid synthesis, to date, the CMASs have not been shown to be drug targets. We have employed various complementary approaches to show that the antitubercular drug, thiacetazone (TAC), and its chemical analogues, inhibit mycolic acid cyclopropanation. Dramatic changes in the content and ratio of mycolic acids in the vaccine strain Mycobacterium bovis BCG, as well as in the related pathogenic species Mycobacterium marinum were observed after treatment with the drugs. Combination of thin layer chromatography, mass spectrometry and Nuclear Magnetic Resonance (NMR) analyses of mycolic acids purified from drug-treated mycobacteria showed a significant loss of cyclopropanation in both the ?- and oxygenated mycolate sub-types. Additionally, High-Resolution Magic Angle Spinning (HR-MAS) NMR analyses on whole cells was used to detect cell wall-associated mycolates and to quantify the cyclopropanation status of the cell envelope. Further, overexpression of cmaA2, mmaA2 or pcaA in mycobacteria partially reversed the effects of TAC and its analogue on mycolic acid cyclop ropanation, suggesting that the drugs act directly on CMASs. This is a first report on the mechanism of action of TAC, demonstrating the CMASs as its cellular targets in mycobacteria. The implications of this study may be important for the design of alternative strategies for tuberculosis treatment.

Never Ending War is Never Ending Power :: Patriot Act, The Bush Administration

The executive branch and president Bush had expanded their authority and power beyond what the framers could have envisioned. In doing so the checks and balances that had existed no longer function as designed and has created a loop of power and control in the executive branch under the theory of the unitary executive. Many of the powers that the executive branch wield come from Congress giving the Bush administration extraordinary powers following 9/11 with the Patriot Act. The Patriot Act that takes away the protection of habeas corpus, due process, privacy, reversal of innocent until proven guilty (p. 272, 274). It also grants the use of sneak and peak searches allowing for looking first and getting a warrant later which violates the 1st and 4th amendment (p. 271). National security letters requiring providing information for records and then not allowing that person to tell anyone but a lawyer (p. 271). All of these powers were given under the idea of â€Å"war powers†, typically war time is a limited amount of time that accept more extreme security measures, but with the prospect raised by the Bush administration of a new era of never ending conflict means these powers might not end. Another tipping of the scales towards the executive branch and president is the use of signing statements. The signing statements allow legislation passed by congress to be applied how the executive branch sees fit which directly contradicts the legislative role is creating laws ("Aba: Blue-ribbon task," 2006). In the passage of the Detainee Treatment Act of 2005 the administration tried to disallow federal district courts from hearing challenges by Guantanamo detainees (p. 156). While seemingly allowing for the banning of mistreatment, it also prevented filing by detainees against the government for acts of mistreatment, making it unenforceable (p. 157). The allegations of torture against terrorist suspects violates not only the Geneva Convention but also human rights. Torture is not an effect method to gain information it only works to get those tortured to do admit to anything to make the pain stop (Gibney, 2007) . Some powers the administration took for themselves including NSA wiretaps which are not always used against terrorists (p. 112, Farren & Gibb, 2007) . The Bush administration bypassed the FISA court which could be considered weak oversight enacted by congress and operates in secret. The FISA court was specifically setup for the purposes of warrants in exactly the types of cases that were bypassed.

Life today is better Essay

Nowadays life is more comfortable, convenient and better than it was a century before. Modern facilities for health, education, communication and transport have added a lot in bringing betterment to the life of people. Advances in technology have provided people with many ways to spend their leisure time and they also have more opportunities to utilize their physical and mental abilities to achieve a better living standard. Technology and education have got much better as compared to the past as there are more schools, colleges and universities giving basic and modern education. Subsequently, it has revolutionized all the sectors of society. For instance, in the past 100 years, research surveys indicate that millions of people died due to disease outbreaks and absence of cures and appropriate health facilities. But now the mortality rate has significantly reduced because there are hospitals available almost in every town, equipped with basic emergency requirements. Medical research and inventions have eradicated many diseases from the world. Communication has become much easier and fast as internet, mobile phones, television are available nowadays. There is no need to write long descriptive letters and wait for the response for long time. One can talk and even watch his loved ones with only a single click. They provide a better source of recreation too, thus helping to get rid of boredom. Similarly, infrastructure has been improved hence it has upgraded the standard of travelling. One can travel long distances using airplane in few hours while it was not possible some years ago. People had to travel for days to cover long distances on animals, keeping heavy luggage and food with them. Development in industrial sectors has opened new areas for work to earn a living. It has introduced a wide range of career choices so that one can opt for what he likes to do instead of sticking with the occupation of ancestors. It can be inferred from the above arguments that standard of life is far better than it was in the past. People have more facilities and choices for spending and maintaining their lives. It has all happened due to the advent of education and technology that was absent in the past.

Lifebuoy- Soap of India - 1598 Words

Prepared By – Dhawandeep Singh(331) Neena Sankhyan(325) | NMIMS The LifeBuoy Story While brands have managed to upgrade their image and evolve together with their consumers – Lifebuoy is a great example, having moved from a carbolic, sweaty association to desirable health imagery – there has been no example of a brand that has moved to the top of the pole after residing at the bottom. The relaunch of the soap in 2002, 2004 again in 2006 have been turning points in its history. In 2004, Lifebuoy’s product offering was revamped with contemporary packaging and an upmarket look. While that went down well with existing users, new users were still elusive; they continued to perceive the product as a ‘cheap soap for poor people’. That†¦show more content†¦Although by projecting tough character of the child in the advertisement it again wanted to connect with the audiences on an emotional front .The confidence of ‘Lifebuoy mother’ with regard to the safety of her son underscores the long-standing brand benefit when she says â€Å"naha kar gaya hai... Koi darr nahin†. This transpired into appeal for the whole family which is tough and daring and always ready to take on newer challenges. â€Å"Little Gandhi Ad† The Little Boy picks up a broom; The boy surveys the messy street before sweeping it clean; The kid enjoys the Lifebuoy bath, washing away sweat and toil. The start of the advertisement with the small boy waking up before everybody shows a common child but who gets up on his own, he knows what to do, He has a mission in his mind, starts for work with putting bandana on his head. Shows a person focused and determined to do the work. All portraying the characteristics of a tough child. And he is a leader also trying to portray the soap more synonymous with leaders. He is being portrayed and compared in qualities to Gandhiji with dandi being replaced by a broom and spectacles of the child very much similar to Gandhiji’s. The atmosphere in which he is standing is very gloomy showcasing his fighting against all odds, comparisons with Gandhi. He starts on his own without waiting for anybody else to join him. And the people are shown getting amused by them and slowly other children startShow MoreRelatedLifebuoy in India: Product Life Cycle Strategies1542 Words   |  7 Pagescaution is needed when planning strategies for each product. 2. How did Lifebuoy strategies in the early stages of its PLC enabled the brand to become a leader? When Lifebuoy was introduced in the market, its positioning was a † promise to kill germs and keep the body healthy†, addressing one of the main problems the Indian market had: the plagues, and therefore exploring the market need for hygiene and health protection. Lifebuoy main strategy was to have low prices and low promotion, in order forRead More4ps of Lifebuoy1615 Words   |  7 PagesProduct: Variants Bar Soap: The classic red bar of Lifebuoy soap and its distinctive phenol smell has been synonymous with cleanliness. Body Wash: Lifebuoy Body Wash provides deep cleansing of pores, protecting against the three root causes of skin health problems – clogged pores, over-drying, and infection-causing germs. Lifebuoy ActiFresh variant which envelopes you in its fresh fragrance for up to 12 hours after a bath, protecting you from odor causing germs and helping you keep your activeRead MoreDoc, Docx, Pdf, Wps, Rtf, Odt683 Words   |  3 PagesBrandGuide FMCG Lifebuoy Lifebuoy lt; Lever Ayush.. |    | Liril 2000.. gt; | Lifebuoy | Parent Company | HUL | Category | Personal Care – Soap | Sector | FMCG | Tagline/ Slogan | Healthy hoga Hindustan; Lifebuoy hai jaha tandurusti hai waha | USP | Lifebuoy provides 100% better protection from germs as compared to ordinary soaps | STP | Segment | Personal Care – Soap, Hand Sanitizer, Hand Wash | Target Group | All households, to provide a 100% anti-bacterial soap for complete protectionRead MoreMarketing Strategies Of Soap And Product Life Cycle Of Lifebuoy Soap2252 Words   |  10 Pagessimply reverse the steps instead. â€Æ' Contents Executive Summary 1 Introduction 3 What is Consumer Buying Behaviour? 4 Overview of Personal Care Industry 5 Company Profile 5 Overview of the product 6 Marketing Strategies of Lifebuoy Soap – STP 7 Product Life Cycle of Lifebuoy Soap 8 Motivation of product 9 Perception of product 9 Learning of product 10 Attitude of product 10 Strength and Weakness 11 Recommendation 11 Conclusion 12 Reference 13 â€Æ' Introduction In the report, it is focusing on the consumerRead MorePlc of Lux1147 Words   |  5 Pages†¢Lux is the brand of UNILEVER INDIA LTD. It has been winning hearts of INDIAN consumersfor 80 years. †¢Lux stands for the promise of beauty and glamour as one of India s most trusted personalcare brands. LUX PRODUCTS : Lux had modified their product into Orchid touch Almond delight Energising fruit Aqua sparkle â€Å"GLAMOUR FACTOR† Introduction STAGE Lux launched the world’s first mass-market beauty soap in the US in 1924 amp; had been launched in India in 1929 †¢At that time thereRead MoreBrand Positioning of Lifebouy4075 Words   |  17 PagesMarket†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦.02 3. About Lifebuoy†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..04 3.1 A catalyst for discovery: The Industrial Revolution†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦04 4. Current Campaign†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..05 4.1 Global Handwahsing Day Coverage†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦05 5. Social Mission†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦06 5.1 5.2 Lifebuoy’s Work†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦06 Local Interventions†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦06 6. Soaps of Lifebuoy†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..07 7. Lifebuoy in Bangladesh†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦.08Read MoreReport on Dettol Soap1208 Words   |  5 PagesCASE STUDY ON Dettol Soap CONCEPT NOTE SUBMITTED TO – BY- Dr. Tanjul Saxena Dr. Yogesh Pande Dr. Vikash k. sinha DATE-24/01/2011 INDUSTRY- Soap Industry COMPANY- Reckitt Benckiser (India) Limited BUSINESSRead MoreHindustan Unilever Marketing Mix7687 Words   |  31 PagesHindustan Unilever [Rural marketing] Product Mix of HUL. HUL is Indias largest marketer of Soaps, Detergents and Home Care products. It has the country’s largest Personal Products business, leading in Shampoos, Skin Care Products, Colour Cosmetics and Deodorants. HUL is also the market leader in Tea, Processed Coffee, branded Wheat Flour, Tomato Products, and Ice cream, Soups, Jams and Squashes. Home amp; Personal Care †¢ Personal Wash †¢ Fabric Wash †¢ Home Care †¢ Oral Care †¢ Skin Care †¢ Hair CareRead MoreMarketing Analysis : Reckitt Benckiser India Ltd970 Words   |  4 Pagesand wounds. Dettol originated from India and launched their first store in 1933. It has been the most trusted brand in India for a long time. Dettol was not only to treat cuts and wounds but it became used in hospitals and nursing homes. Consumers also used it to clean their floor and to bathe. Dettol does not only have the Antiseptic Liquid product but has other product categories that they extended to such as, liquid hand wash, liquid body wash, toilet soaps, shaving creams and plaster stripsRead MoreMarketing Plan for Dettol Liquid Handwash2473 Words   |  10 PagesAPPENDIX†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦...15 　1. Executive Summary Reckitt Benckiser India Ltd (RBIL) is a fully owned subsidiary of Reckitt Benckiser Plc., world’s No.1 Company in household cleaning. Reckitt Benckiser Plc came into being with the merger of Reckitt Colman Plc with Benckiser NV in 1999. The company has operations in 60 countries, sales in 180 countries and has had net revenues in excess of $5.5 billion. Reckitt Benckiser India Ltd (RBIL) manufactures and markets a wide range of products in Personal